UNIT 1

Introduction: Understanding abnormal behaviour Understanding classification: DSM & ICD

(Latest versions), Clinical assessment.

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Definition of abnormal behaviour (or criteria of abnormal
behaviour) (Psychopathology / mental disorder/ psychological disorder)

"If you talk to God, you are praying; If God talks to you, you have schizophrenia. If the dead talk to you,
you are a spiritualist; If you talk to the dead, you are a schizophrenic." (Szaz, 1973)

The word ‘abnormal’ cannot be defined precisely. In an article by Rosenhan (1973) "On Being
Sane in Insane Places" Rosenhan demonstrated that ideas of normality and abnormality are not
as clear and accurate as people think. He and colleagues faked the single symptom of hearing
voices to gain admission to mental hospitals in five states. They abandoned the symptom once
admitted. They found hospitalization to be dehumanizing. Admitted with the diagnosis of
paranoid schizophrenia, they were discharged with the diagnosis of paranoid schizophrenia
in remission (under control).

Core issues in defining abnormal behaviour

• Categorical vs dimensional models of abnormality: Some models of abnormal

behaviour clearly distinguish normal and abnormal behaviours and are seen as falling
in two distinct categories (categorical models). However, dimensional models
emphasize a continuum of abnormality, accepting that the cut-off between normal and
'abnormal' behaviour is not clear-cut.

• Cultural relativism vs. universalism: There are two views on how culture influences
psychopathology:

1. Cultural relativism: abnormal behaviors can only be understood in the

cultural framework within which they occur.

2. Universalism: There are universalities in the underlying psychological

mechanisms and subjective experiences of many psychological disorders;

Research provides evidence that psychopathology across cultures contains both universal and
culturally specific components. Some disorders are considered to be universal (e.g. depression,
schizophrenia, manic-depression, certain types of anxiety disorder and dementia), but there are
cultural differences in the way that symptoms are express. On the other hand there are some
disorders (such as Dhaat syndrome in India) which may be localized to a particular culture
(called ‘culture bound syndromes’) and not found in other cultures.

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Any adequate definition of abnormality must take into account the issues of cultural relativism
as well as universalism.

Criteria of normality and abnormality

a) Deviance from cultural norms: undersirability. Abnormal behavior is defined as that which
breaks current social or cultural norms and hence is considered undesirable by that culture.
Thus depression, would be regarded as abnormal because it is not expected of us (except in
particular situations such as bereavement, and then too for a certain period of time.

Evaluation

1. Through this approach abnormal behavior can never have a universal meaning as
judgments will vary from society to society. E.g. Hearing voices is considered
abnormal in most societies but in some communities it is seen as a sign of spiritual
enlightenment.
2. Even within the same society, cultural norms keep changing and hence what is
normal or abnormal will also keep on changing. Until 1980 homosexuality was
considered a psychological disorder by the World Health Organisation (WHO) but
today is considered acceptable.
3. This approach equates normality with conformity yet many non-conformists are
valuable and without whom significant advances would never be made

b). Deviance from statistical norms. ‘Abnormality’ would refer to any behaviour that is
statistically infrequent or is not seen very often in society. This principle of statistical deviance
is frequently used in the interpretation of psychological test scores where a value below a cutoff
point is considered abnormal.

Evaluation
1. There is no agreed definition of how much a behavior must deviate from the
norm before it is considered abnormal.
2. Many behaviors that are statistically rare are desirable and healthy such as
very low levels of stress and anxiety etc.
3. Statistically infrequent in one culture may be statistically frequent in another
culture and hence no universal definition of abnormality. For e.g. one
criterion of schizophrenia is hearing voices but in some cultures this is
considered normal and even desirable.
4. This approach too equates normality with conformity.

c). Deviation from ideal mental health: This approach considers abnormal behavior in terms of
deviations from ideal mental health. Humanists’ school such as Abraham Maslow and Carl Rogers
suggested that the ideal goal is self actualization and deviations from it are unhealthy. Jahoda (1958)
proposed a set of criteria for mental health. Abnormality could be indicated by their absence. These
criteria are as follows:

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Evaluation:

This is a useful way of identifying those people who would benefit from psychological help.
1. Most of us would probably fail to meet all of these criteria.
2. Cultural variation may also be a problem. For example, collectivist societies do not
value autonomy in the same way that Western, individualist societies do.

d) Distress or suffering. Distress, refers to an experience of intense stress that is unresolved,

and therefore distracting and difficult to manage. Abnormal behaviour can be defined in
terms of the degree of distress and discomfort that the disorder causes to the individual.

Evaluation
Distress may be illusive concept to evaluate because many individuals may not be
aware of the distress that their disorder is causing them. Many manic patients
experience ‘minimal’ distress but may cause significant distress to others.

e) Dysfunction/disability/maladaptive. Dysfunction refers to a breakdown in functioning of

the individual due to which he is not able to accomplish goals in his life. Dysfunction may
occur in many areas:

• Cognitive dysfunction: this may occur when for example the psychotic person
experiences hallucinations due to which the person is not in touch with reality.

• Emotional dysfunction: people who suffer from depression suffer extreme

feelings of hopelessness, helplessness and sadness due to which they withdraw
from others and may even become suicidal.

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 • Behavioral dysfunction: This is quite apparent in two areas of abnormal
behaviour: social (or interpersonal) and occupational. The person with
depression may withdraw from friends and family (social dysfunction), and may
be unable to work for weeks or months (occupational dysfunction).

Evaluation:
1. However, not all disorders involve maladaptive behavior. Consider the con
artist with antisocial personality disorder. He may be able to talk people out
of their life savings, but is this behavior maladaptive? Not for him, because
it is the way he makes his living. We consider him abnormal, however,
because his behavior is maladaptive for and toward society.

2. It is very judgemental. E.g- one may not have a job because one is lazy, this
does not mean that one is abnormal.

f). harmful dysfunction. Jerome Wakefield (19921 suggests that the proper definition of
abnormality requires both social and biological criteria. Wakefield (1997) proposed the idea of
abnormal behaviour as “harmful dysfunction.” Wakefield classifies “harm” in terms of social
values (e.g., suffering, being unable to work, etc.). And he considers “dysfunction” within an
evolutionary perspective in which some underlying biological mechanism fails to perform
according to its (presumably evolutionary) “design” by natural selection. For example, Panic
Disorder is abnormal, according to Wakefield, because it is viewed by society as harmful and
(2) the fear system was not evolutionarily designed to respond with intense anxiety in the
absence of objective danger.

Evaluation: His analysis assumes that all disorders involve failures of psychological or
physiological systems. Yet some disorders, such as anxiety disorders, probably represent
evolved defensive reactions to subjectively perceived threats.

g) Rosenhan and Seligman’s (1984) criteria. Rosenhan and Seligman (1984) suggested that there are seven
criteria that could be used to decide whether a person or a behavior is normal or not.

1. Suffering – does the person experience distress or discomfort?

2. Maladaptiveness – does the person engage in behaviors that make life difficult for him
or her rather than being helpful?
3. Irrationality – is the person incomprehensible or unable to communicate in a reasonable
manner?
4. Unpredictability – does the person act in ways that are unexpected by himself, herself
or other people?
5. Vividness and Unconventionality – does the person experience things that are different
from most people?

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 6. Observer discomfort – is this person acting in a way that is difficult to watch or that
makes other people embarrassed?
7. Violation of moral or ideal standards – does the person habitually break the accepted
ethical and moral standards of the culture?
Evaluation:

• Some of the criteria depend on subjective judgments of other people. For example
observer discomfort and violation of moral standards involves subjectivity.
• The criteria of irrationality, unpredictability, loss of control and unconventionality
apply to people who choose an unconventional life. This does not mean they are
abnormal.

h) Undesirable behaviours. According to this subjective values model, abnormal conditions are
those deemed by society to be undesirable in some way.

Evaluation: Although many or most abnormal conditions are perceived as undesirable—it does
not explain why many socially undesirable behaviors, such as rudeness, laziness, and even
racism, are not perceived as pathological.
i) Evolutionary definition. Proponents of a biological model, such as R. E. Kendell (1975),
contend that abnormality should be defined by strictly biological criteria, such as those
characterized by a reduced life span, reduced biological fitness the capacity of an organism to
transmit its genes to future generations), or both.

Evaluation; A biological model is subject to numerous counterexamples. For example, being a

soldier in a war may reduce one's longevity but is not a disorder.

j) Anti-psychiatry movement. Since the 1960’s it has been argued by anti -psychiatrists (Arieti,
R.D. Laing, Thomas Szasz) that the entire notion of abnormality or mental disorder is merely
a social construction used by society. An illness must have an objectively demonstrable
biological pathology but psychiatric disorders are not. The medical profession uses various
labels e.g. depressed, schizophrenic to exclude those whose behaviour fails to conform to society’s
norms. Labels and consequently treatment can be used as a form of social control and represent
an abuse of power. Thomas Szasz in his ‘myth of mental illness’ views classification of mental
illness as reason to justify political repression, an extreme position that causes us to examine
assumptions about what's normal and what isn't.

k) An Acceptable definition of abnormality: An eclectic approach. Most people take a 'multiple

perspectives' approach, that is, they evaluate a behaviour using each of the following criteria
before reaching a decision about whether it is 'abnormal' or not.

l) The four D's. Modern definitions of abnormality are influenced by interaction of the four
Ds (Comer, 2005):
1. Deviance: Refers to behaviours that are unacceptable or not common in society.

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 2. Distress: Refers to negative feelings experienced by the individual with the
disorder.
3. Dysfunction/disability/maladpativeness: Behaviors are dysfunctional when they
interfere with person's ability to function in daily life, to hold a job, or form
relationships.
4. Danger: abnormal behaviour involves dangerous or violent behaviour directed at
the individual (e.g. suicidal intent), or others in the environment. Some mental
disorders can cause people to behave in a manner that puts society or themselves
at risk, although typically, most abnormal behaviors do not. For example; delusions
can cause a person to have irrational thoughts and become defensive if they feel
they need to protect themselves from impending dangers.

m). DSM 5 definition. The DSM-5 definition of a mental disorder emphasizes harmful
dysfunction and also the role of disability and distress in differentiating normal and abnormal
behavior

• Psychobiological dysfunction: A mental disorder is a syndrome characterized by

clinically significant disturbance in an individual’s cognition, emotion regulation, or
behavior that reflects a dysfunction in the psychological, biological, or developmental
processes underlying mental functioning.

• Significant distress or disability: Mental disorders are usually associated with

significant distress (e.g., a painful symptom) or disability (i.e., impairment in one or
more important areas of functioning). An expectable or culturally approved response to
a common stressor or loss, such as the death of a loved one, is not a mental disorder.

• Social deviance or conflicts with society: Socially deviant behavior (e.g., political,
religious, sexual) and conflicts that are primarily between the individual and society are
not mental disorders unless the deviance or conflict results from a dysfunction in the
individual, as described above.

It is worth noting that DSM-5 describes people with mental disorders as “usually" experiencing
significant disability or distress—they may not always show both characteristics. Some patients
may experience tremendous emotional pain, but they do not show marked impairment in their
social or academic functioning. Others may drop out of school, abuse alcohol and other drugs,
and/or engage in criminal behavior but do not report anxiety, depression, or low self-esteem.
Although most people with mental health problems experience both distress and impairment,
only one feature is required for most DSM-5 diagnoses.

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 Classification
The term classification refers to any effort to construct groups or categories and to assign objects or people
to these categories or groups on the basis of their attributes, characteristics or relations.

Emil Kraepelin (late 19th century): The "father of psychiatry" (Weckowicz, 1984) gave the first truly
comprehensive system medical classification scheme. In it he defines two major groups of mental
disorders: the manic-depressive psychoses, and dementia praecox (i.e. schizophrenia) with further
subdivisions. Kraepelin's system is important because it defined the discipline of psychiatry as distinct
from neurology, and as a part of the general field of medicine.

Why do we need to classify? Any classification system will help the clinician to arrive at a diagnosis.
This provides a valuable framework for clinicians as it may be used in communicating and generating ideas
that will allow for a greater understanding of a patient’s condition as well as its possible origins and likely
future path.

Criteria of a good Classification system (Sprock & Blashfield, 1983):

1. Exhaustive system: the classification system should be comprehensive in that it should classify all the
types of abnormal behavior that we encounter.
2. Mutually exclusive categories: The disorder should fall into one and only one class and additionally
the symptoms between different disorders should not overlap. The overlapping of symptoms between
various disorders is referred to as co-morbidity. Thus, for e.g. the symptoms between schizophrenia and
bipolar disorders should not overlap.
3. Reliability: For a good classification system, it must show reliability. This takes two forms: inter-judge
reliability (or inter-rater reliability) and test-retest reliability. Inter-judge reliability refers to the fact that if
different clinicians were to diagnose the same person, that person should always be classified with the
same disorder (inter rater reliability). A diagnostic system would not be reliable if, for example, one
clinician used it to diagnose someone as having obsessive-compulsive disorder whereas another clinician
interviewed the same person and diagnosed them with schizophrenia. The classification system should also
show test-retest reliability, which involves the same patients being diagnosed the same at two different
times by the same clinician. The reliability of clinician’s diagnoses can be substantially improved by the
use of explicit diagnostic criteria.
4. Validity: A classification system needs to be valid. The system may be considered valid if the diagnosis
corresponds with observed behavior (construct validity). For example, people diagnosed with social phobia
should show abnormal levels of anxiety in social situations. Discriminant validity occurs when the
disorders is distinct from other disorders i.e. symptom overlap between the various disorders is minimum
and hence co-morbidity is minimum. Researchers have pointed out that as per current DSM, some of the
core features of GAD overlap with all anxiety disorders as well as mood disorders, reducing the overall
discriminant validity. Another type of validity is predictive validity which is concerned with whether we
can predict the future outcomes from the diagnosis including how someone will respond to treatment.
5. Parsimony: the classification system must have a manageable set of categories (Gibbins, 1975).

Classification Models

There are currently two/three basic approaches to classifying abnormal behavior: the categorical,
prototypal (sometimes prototypical is seen as a modified categorical system) and the dimensional.

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A. Categorical classification: The categorical approach assumes:
• Disorders are grouped into categories that have distinct boundaries with distinct symptoms i.e.,
someone either is or is not a member of a category. A disorder can belong to that category only if
it has some ‘necessary’/essential features and these are ‘sufficient’ to be in that category. E.g. in
a categorical classification a creature (e.g. penguin) can be either a ‘bird’ or an ‘animal’ but not
both. Similarly, in terms of psychopathology the symptoms can either be characteristic of anxiety
or depression but not both. This approach similar to traditional, medical disease-based practices in
which a person is considered either to have a given disease or not. Hence, all human behavior can
similarly be divided into the categories of “healthy” and “disordered,”; “normal” and “abnormal”.
Popular and professional language reflects this categorical approach: “Does my child have
ADHD?”
• The different types of disorders that exist within a category are homogeneous.

Conceptualizing people’s psychological problems has certainly many advantages. In fact, some have
argued that categorical thinking is unavoidable and essential to our understanding and communication
about mental disorders: As human beings, we are hardwired to think in categorical terms. However, this
view of psychopathology has failed, as very few disorders can be defined through necessary/essential
features that are always present. A strictly categorical classification system is not possible as the
distinction between normal and abnormal is not clear cut.

Prototypical system (modified categorical approach): A second type of classification system is the
prototypical system that is currently used in the DSMs. Prototypical classification is based on the degree
to which the individual’s signs and symptoms map onto the ideal picture or prototype of the disorder.
A prototype is an idealized picture of the typical features (e.g., a sparrow has all the prototypical
features of the BIRD such as it is small, flies far, lays eggs and eat insects). A sparrow is therefore
closer (or more typical) to the prototype of a BIRD as compared to an Ostrich which is neither small
and nor flies far. Thus, members of a category show some variability in terms of how close or far they
are from the prototype. Similarly, the prototypical classification system assumes that individuals with
a given disorder may show some variability; not all people with the disorder will manifest it in exactly
the same way. For e.g., in the case of Schizophrenia, an individual must meet at least two of five
possible symptoms. Some patients may have all typical features (all five) while others may have only
the essential characteristics (only two of the five). Schizophrenia can manifest itself differently for each
individual, and two clients may share only one or two symptoms but still qualify for the same diagnosis.

As opposed to categorical classification, categories in the prototype model have fuzzy or

unclear/overlapping boundaries. For e.g. in a prototypical category there may be a creature which has
features of both birds and animals (e.g. penguins). So, penguins can lie in both the categories which is
unlike the categorical classification. Similarly, disorders such as anxiety and depression share some
overlapping symptoms (e.g. difficulty concentrating, sleep issues, fatigue, and loss of interest) leading
to co-morbidity.

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Shedler, Westen and Bradley (2006) have suggested that the DSM should provide a narrative description
of a prototype rather than a list of symptoms. The Shedler-Westen Assessment Procedure
or SWAP (SWAP II, 2012) uses such a system and combines prototypical with dimensional systems. The
manual presents a brief narrative description (instead of a specific diagnostic criteria set) of a prototypic
case of each personality disorder. The task of the clinician is then to use a 5-point scale to indicate the
degree to which the current patient’s presentation “matches” the prototype for each disorder (1 =
description does not apply; 2 = only minor features of prototype; 3 = significant features of prototype; 4 =
strong match, patient has the disorder; and 5 = exemplifies the disorder, prototypic case)

B. Dimensional
DSM -5 has partially adopted the dimensional approach to classification. It differs from the categorical
approach in that it neither assumes distinct categories nor assumes homogeneity of disorders within a
category.

This system involves describing the intensity or severity of the individual’s distress on several dimensions
or continuum. Ratings ranging from mild to severe can be obtained on various dimensions. These
dimensions are the same for everyone irrespective of normal/abnormal categories and cuts across various
disorders. These dimensions may include mood, emotional stability, aggressiveness, gender identity,
anxiousness, interpersonal trust, clarity of thinking and communication, social introversion, and so on. A
dimensional approach therefore focuses on the degree to which a person has a symptom and asks the
question “how much?” i.e. disorders are conceptualized quantitatively rather than qualitatively different
from normal.

Profiles can be generated based on the ratings and high/low values can be marked on them. “Normal” can
be discriminated from “abnormal” in these profiles based on some statistical criteria generated from
representative samples. The clinicians could decide that those who lie on the extremes would be labeled as
“abnormal” (e.g. anything above the 97th percentile on aggressiveness and anything below the 3rd
normative percentile on sociability would be considered “abnormal”).

Of course, in taking a dimensional approach, it would be possible to discover that such profiles tend to
cluster together in types—and even that some of these types are correlated. Certain forms of
psychopathology tend to lend themselves to the dimensional model more than do others. Specifically, a
growing body of research suggests that the personality disorders can be conceptualized quite well using
the dimensional approach based on the Big Five personality factors. Dimensional ratings can thus be
obtained on these 5 factors.

Previous versions of the DSM were criticized for their exclusive reliance on the prototypical approaches
to classification. Consequently, the developers of DSM-5 attempted to incorporate aspects of dimensional
classification into the newest edition of the manual. Dimensional classification is most easily seen in the
DSM-5 ‘Cross-Cutting Symptom Measure’, a rating scale that can be used to evaluate the severity of
children's signs and symptoms. The rating scale allows dimensional classification on 10 broad domains
including physical symptoms and sleep problems, anxiety and depression, anger and irritability, and mania
and psychotic symptoms. Children's severity on each domain can be described on a 5-point continuum
ranging from "none or not at all” to “severe or nearly every day.”

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Strengths

• It helps in the treatment of disorders as clinicians tend to treat the symptoms and not the underlying
disorders. The patient’s profile will normally consist of deviantly high and low points which can
be targeted through therapies to decrease those of excessive intensity (e.g., anxiety) and to increase
those that are deficit (e.g., inhibited self-assertiveness)
• It conveys more information than simple categorical or prototypical classification. For example,
rather than merely diagnosing a child with autism, a clinician can describe the child as having mild
impairment in social communication but severe behavioral impairment (e.g., repetitive actions and
difficulty adjusting to changes in routine).
• It allows clinicians to monitor changes in children’s functioning across time. For example, a child
may continue to meet diagnostic criteria for autism after several years of behavior therapy;
however, his repetitive behavior might improve from “severe" to “mild.”
• Stigma of labeling is less likely to occur - i.e., we say ‘she is highly anxious’ (not she has
‘borderline personality disorder’). The model acknowledges that all of us—the normal and the
abnormal—share the same fundamental characteristics but that we differ in the amounts of these
characteristics that we each possess.

Weakness

• Complexity & lack of uniformity in mental health profession particularly given the number of
dimensions that need to be rated.

Classification systems

There are two classification systems in use currently in the world: DSM and ICD.
1) DSM: The Diagnostic and Statistical Manual of Mental Disorders (DSM) given by American
Psychiatric Association (APA) is widely used in America. (This is different from American psychological
association also referred to as APA). DSM is essentially a starting point for determining the nature of a
client’s problem (diagnostic purpose), as well as providing supportive information on prevalence rates

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within the larger population to inform policy decisions (statistical). It does not suggest treatment
approaches. The current DSM is DSM-5 (2013) and its text revision - DSM-TR (2022).
2) ICD: International Statistical Classification of Diseases (ICD) developed by WHO. The current ICD
is ICD 11 released in 2022 is widely used in Europe and many other countries worldwide.

Both systems are similar in many respects, such as in using symptoms as the focus of classification.

DSM
The DSM specifies what subtypes of mental disorders are currently officially recognized and provides,
for each, a set of defining criteria. As already noted, the system is a prototypal one with much fuzziness
of boundaries and considerable overlap, of the various “categories” of disorder it identifies.

The criteria that define the recognized categories of disorder consist for the most part of symptoms and
signs. The term symptoms generally refers to the patient’s subjective description, the complaints she or
he presents about what is wrong. Signs, on the other hand, are objective observations. that the
diagnostician may make either directly (such as the patient’s inability to look another person in the eye)
or indirectly (such as the results of pertinent tests administered by a psychological examiner). To make
any given diagnosis, the diagnostician must observe the particular criteria—the symptoms and signs
that the DSM indicates must be met.

DSM IV TR states that mental disorders should not classify people rather the classification
system classifies disorders that people have. Thus, one should not use the terms “a
schizophrenic” or “an alcoholic” and instead use “an individual with schizophrenia” or an
“individual with alcohol dependence”.

Evolution of DSM: The DSM has gone through 6 revisions since it was first published
in 1952.

• DSM 1 (1952): This was developed to standardize diagnostic practices in coping with
the widespread mental breakdowns occurring among the military personnel in World War
2.
• The DSM-II (1968): A disease based approach: Classification of disorders was based on
etiology (or causal factors) i.e. classification was ‘theoretical’ and disorders were
reflections of diseases (i.e. related to a specific etiology). The various types of disorders
identified in DSM -II as well as DSM -I were described in narrative and jargon-laden
terms that proved too vague for mental health professionals to agree on their meaning.
The result was a serious limitation of diagnostic reliability;
• DSM-III (1980): a neo-Kraepelinian approach: Diagnosis was made on the basis of
“operational” method i.e. based on specific observable signs and symptoms rather than
etiology (referred to as or operational, atheoretical, descriptive, empirical or
phenomenological system). In a typical case, a specific number of signs or symptoms
from a designated list must be present before a diagnosis can properly be assigned. This
increased diagnostic reliability. Multi axial system was introduced for the first time.
Elimination of Neurotic disorders: The elimination of neurotic disorders removed the
psychodynamic underpinning of DSM.
• DSM 1V (1994): Retained multiaxial system and based on prototypical approach, also
incorporated a comprehensive review of the available empirical research findings

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 • DSM 1V TR (2000): The APA released DSM-TR (text revisions) which contains updated
text but no changes in diagnostic categories.
• DSM-5 (2013): In its latest version, the DSM removes the multiaxial system. Instead
DSM is broken down into three sections. It now has a hybrid dimensional-categorical
model. It also incorporates cultural and ethnic considerations.
• DSM -5TR (2022): DSM-5TR (March, 2022): It comprehensively updates the descriptive
text for each DSM disorder. However, in contrast to DSM-IV-TR, in which updates were
confined almost exclusively to the text, there are a number of significant changes and
improvements in DSM-5-TR. It features a new disorder, Prolonged Grief Disorder, as
well as codes for suicidal behavior and nonsuicidal self-injury.

The number of recognized mental disorders has increased enormously from DSM-I to DSM-5
due both to the addition of new diagnoses and to the elaborate subdivision of older ones.

Characteristics of DSM -5

APA website https://www.psychiatry.org/psychiatrists/practice/dsm

DSM was released by the American Psychiatric Association (APA) in 2013 and integrates current research
findings. In the past, APA used roman numerals (I, II, III, and IV) to differentiate between editions of the
DSM. Beginning with DSM-5, Arabic numbers are now being used. The reason for the change is twofold.
First, the new numbering system allows for the manual to be updated (e.g., 5.1, 5.2, 5.3) more expeditiously
as science and research increase our understanding of mental disorders. The second reason is more practical
in nature. Arabic numbers are more globally recognized than roman numerals. One of the goals of the
DSM-5 is to harmonise with the ICD system, which was not the case for previous DSMs.

1. Elimination of Multiaxial system: DSM-5 no longer uses the multiaxial system that was earlier
used in DSM IV. The DSM IV multiaxial had long been criticized for lack of reliability and
consistency amongst clinicians and hence APA chose to remove this multiaxial system from the
DSM-5. This also makes the DSM-5 more compatible with the World Health Organization’s
International Classification of Diseases (ICD) coding system There were five different axes in
DSM IV: 1. The primary diagnosis (1. mental disorders 2. Personality disorders and/or mental
retardation, 3. Medical problems impacting the individual’s psychological concerns, 4.
Environmental and psychosocial stressors impacting the client’s psychological functioning, (such
as job loss, romantic separations, or deaths), and 5. A 0-100 rating called the Global Assessment
of Functioning (or “GAF”), quantifying the person’s overall level of functioning.

Axis 1, 2 and 3 are now combined together in section 2 of DSM -5 (i.e. all mental disorders,
personality disorders, and medical problems). Instead of Axis 4, in DSM-5, clinicians are advised
to make a separate notation regarding contextual information and they can use formal or informal
assessment to understand clients’ cultural context (e.g. Cultural Formulation Interview, CFI). The
GAF scale (Axis 5) was removed from the DSM-5 because of perceived lack of reliability and poor
clinical utility (APA, 2013) and APA (2013) recommended the World Health Organization

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 Disability Assessment Schedule 2.0 (WHODAS 2.0) as a preferred measure for use in assessing
clients’ functioning in DSM-5.

2. Dimensional approach in classification: Previous editions of DSM used a strictly categorical

model requiring a clinician to determine that a disorder was present or absent. However, the latest
edition of DSM-5 integrates dimensional approaches with the categorical approaches thus
indicating a hybrid approach. The dimensional approach, which allows a clinician more latitude to
assess the severity of a condition and does not imply a concrete threshold between “normality” and
a disorder.
3. Atheoretical, descriptive or phenomenological classification: DSM -5 continues to classify
disorders by clusters of signs and symptoms rather than a theory/etiology and thus DSM1V-TR is
‘atheoretical’, ‘descriptive’ or ‘phenomenological’. The diagnostic categories of DSM-IV-TR are
thus based on observable signs and symptoms. With only a few exceptions, DSM-5 avoids
commitments regarding etiology. Indeed, the Manual explicitly notes, “a diagnosis does not carry
any necessary implications regarding the etiology or causes of the individual’s mental disorder.
4. Biopsychosocial model: In 1977, American Psychiatrist George Engel introduced the BPS Model
which all DSM endorse. The biopsychosocial model is a general model or approach to case
formulation (formulation tells us how the person developed the disorder; for e.g., due to genetic
factors, childhood history etc.) that posits that biological, psychological and social factors
(abbreviated "BPS") all play a significant role in mental disorders. It indicates that the DSM-5 does
not reflect the view of any specific "school" or tradition regarding the cause or origin (also known
as "etiology") of mental disorders.
5. Gender Differences in Diagnosis Gender differences have long been noted for some disorders.
Some disorders show a higher prevalence rate for male patients (such as antisocial personality)
than females; other disorders (such as anorexia) are more prominently found in females. Moreover,
males and females who are diagnosed with the same disorder (such as conduct disorder) often show
different symptom patterns. The DSM-5 allows for gender-related differences to be incorporated
into the diagnosis.
6. Appraisal of Cultural Background In DSM-5.The DSM-5 provides a structured interview that
focuses on the patient’s approach to problems and cultural influences that can influence the
adjustment (referred to as the Cultural Formulation Interview - CFI)
7. Three sections of DSM-5: In its latest version, the DSM-5 is broken down into three sections:

• Section I: Introduction and directions on how to use the updated manual

• Section II: Covers information related to all disorders. Over 300 mental disorders are
organized into 22 chapters in this section.
• Section III: Section III of the text includes discussion of emerging assessment measures,
cultural formation considerations, an alternative DSM-5 model for personality disorders,
and conditions for further study. The assessment measures discussed note that there are
limitations to categorical approaches to diagnosis given that individuals may not present
with symptom clusters that exactly match a DSM-provided criteria and so measurements
with a dimensional perspective are discussed.

Section II

Section II has 20 chapters that outline the documented mental disorders with 2 other related chapters, for
a total of 22 chapters. The last two chapters are not considered mental disorders but rather provide
supportive information for completing a comprehensive diagnostic assessment including “medication

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usage” and “Other Conditions that May be a focus of Clinical Attention” (e.g. relational problems; abuse
and neglect; educational and occupational problems; housing and economic problems etc).

Ordering Diagnoses Individuals will often have more than one diagnosis, so it is important to consider
their ordering. The first diagnosis is called the principal diagnosis-this would be the reason for the visit or
the main focus of treatment. The secondary and tertiary diagnosis should be listed in order of need for
clinical attention.

Subtypes, Specifiers, and Severity Subtypes for a diagnosis can be used to help communicate greater
clarity. For example, ADHD has three different subtypes to choose from: predominantly inattentive,
predominantly hyperactive/impulsive, or a combined presentation. Specifiers are extensions to a diagnosis
to further clarify a disorder or illness The ADHD diagnosis offers only one specifier that is “in partial
remission”. Some diagnoses will offer an opportunity to rate the severity of the symptoms. for e.g. through
rating severity on a dimensional diagnosis. For example, for Autism Spectrum Disorder Severity levels are
classified on three levels of severity “requiring support,” “requiring substantial support,” and “requiring
very substantial support.”

Provisional Diagnosis. Sometimes, the clinician has a strong inclination that a client will meet the
criteria for a diagnosis, but does not yet have enough information to make the diagnosis. This is when
the clinician can make a provisional diagnosis. Once the criteria are later confirmed, the provisional
label can be removed.

Other Specified Disorders and Unspecified Disorders The DSM-IV had a diagnosis of not otherwise
specified (NOS) to capture symptomology that did not fit well into a structured category. In lieu of the
NOS diagnosis, the DSM-5 offers two options when these situations arise. The other specified and
unspecified disorders should be used when a provider believes an individual’s impairment to
functioning or distress is clinically significant; however, it does not meet the specific diagnostic criteria
in that category. The “other specified” should be used when the clinician wants to communicate
specifically why the criteria do not fit. The “unspecified disorder” should be used when he or she does
not wish, or is unable to, communicate specifics. For example, if someone appeared to have significant
panic attacks but only had three of the four required criteria, the diagnosis could be “Other Specified
Panic Disorder—due to insufficient symptoms.” Otherwise, the clinician would report “Unspecified
Panic Disorder.”

Life span approach: In contrast to DSM-IV, the DSM-5, Section II, arranges 22 chapters based on a
lifespan approach, thus keeping disorders that emerge in childhood in the beginning chapters with a
neurodevelopmental perspective and organizing disorders that appear in adulthood toward the end of

15
 the manual with a neurocognitive perspective. The text portion of each chapter also has been expanded
to highlight how the symptoms may unfold across the life span.

Integrating Dimensional approach: In Section II, some disorders are still grouped based on the
categorical approach but other disorders are now grouped together as spectrum disorders (e.g.,
schizophrenia spectrum disorders, autism spectrum disorder etc.). For example, research showed that a
number of the pervasive developmental disorders in DSM IV like autism and Asperger’s (APA, 2000)
actually overlapped a great deal and shared many common symptoms (APA, 2013). The DSM-5 merges
these types of disorders into autism spectrum disorder, providing a severity rating (dimensional approach)
to indicate where the individual is on a continuum of impairment.

Section III

This subsection covers assessment measures, cultural formulation, an alternative DSM-5 model for
personality disorders, highlights changes from DSM-IV to DSM-5, and conditions that warrant further
study, such as Internet gaming disorder, suicidal behavior disorder, and neurobehavioral disorder due
to prenatal alcohol exposure (ND-PAE).

1. Assessment measures (Dimensional):

The Assessment Measures offers “cross-cutting measures” which assess symptoms in a dimensional
manner i.e., the symptoms are rated on a continuum (from mild to severe). The term ‘cross-cutting’ is
used in Section II, because these symptoms cross diagnostic lines and provide a picture of the patient's
presentation without assigning a diagnosis. For instance, the symptoms of sleep disturbance may apply
to several possible diagnoses. This depiction of the patient's symptoms is holistic, and it complements
the categorical system of the diagnostic criteria in DSM-5.

In addition to the two cross-cutting measures, DSM-5 includes two other dimensional measures. The
Clinician-Rated Dimensions of Psychosis Symptom Severity is a
rating scale for the severity of eight symptoms of psychosis. The World Health Organization Disability
Assessment Schedule 2.0 (WHODAS 2.0) is used
to measure the degree of disability in adult psychiatric patients, experienced in everyday life during the
last 30 days. The WHODAS 2.0 has a dimensional scale with a 5-point rating system ranging from
having no problem doing a chore to not being able to do it at all (e.g. physically, grooming oneself, and
interacting with people)

2. Culture Diagnosis:

Different cultures and communities exhibit or explain symptoms in various ways. Section III includes
a Cultural Formulation Interview (CFI) to gather relevant cultural information (e.g. People often
understand problems in their own way, which may be similar or different from how doctors describe
the problem. How would you describe [INDIVIDUAL’S] problem; Some people may explain the
problem as the result of bad things that happen in their life, problems with others, a physical illness, a
spiritual reason, or many other causes.)

The DSM-5 also breaks up what was formerly known as ‘culture-bound syndromes’ into three different
concepts.

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 1. The first concept is cultural syndromes. These are clusters of symptoms that tend to co-occur
among individuals in specific cultural groups and that are recognized locally as coherent patterns
of experience. (e.g. Ataque de nervios (“attack of nerves” is a syndrome found in Latinx cultural
contexts, characterized by symptoms of intense emotional). Dhat Syndrome: Dhat syndrome is a
condition found in the cultures of South Asia (including Pakistan, India, Bangladesh, Nepal, and
Sri Lanka) in which male patients suffer from anxiety or distress as they believe that they
are passing semen in their urine. Ideas about this substance are related to the concept of ‘dhatu’
(semen) described in Ayurveda.
2. The second is cultural idioms of distress, linguistic terms or phrases used to convey suffering
within a specific cultural group. This section also provides some illustrative examples of idioms,
explanations, and syndromes from diverse geographic regions
3. The third concept is cultural explanation or perceived cause, mental disorders unique to certain
cultures that serve as the reason for symptoms, illness, or distress.

Personality Disorders: DSM-5 includes two conceptualizations of personality disorders (PDs). The
classification in Section II is identical to the one found in DSM-IV, and includes 10 categorical PDs. The
model in Section III is referred to as the DSM-5 Alternative Model for Personality Disorders (AMPD)
(dimensional approach) and proposes diagnosis of personality disorders as a three-step process.

1. First, counselors must assess elements of personality functioning e.g. interpersonal functioning
(specifically evaluating empathy and intimacy) on a 4-point Likert-type scale consisting ranging
from 0 (little to no impairment) to 3 (severe impairment). This is a dimensional approach.
(Criterion A)
2. Second, counselors must note the presence of 25 pathological personality traits, grouped into five
broad areas (Based on Five factor model): negative affectivity, detachment, antagonism,
disinhibition, and psychoticism. (Criterion B)
3. Finally, using the information gathered from assessment of personality functioning (Step 1) and
pathological personality traits (Step 2), counselors will identify one of six specific personality
disorders: antisocial, avoidant, borderline, narcissistic, obsessive-compulsive, or schizotypal
personality disorder. Four personality disorders (i.e., paranoid, schizoid, histrionic, and
dependent) were eliminated because of low reliability and validity. This is the “categorical”
approach.

Reclassification of disorders from DSM IV to DSM 5:

DSM-IV and DSM-5 categorize disorders into “classes” with the intent of grouping similar disorders
(particularly those that are suspected to share etiological mechanisms or have similar symptoms) to help
clinician and researchers use of the manual. From DSM-IV to DSM-5, there has been a reclassification of
many disorders that reflects a better understanding of the classifications of disorders from emerging
research or clinical knowledge. E.g.

1) Schizophrenia spectrum and other psychotic disorders: All subtypes of schizophrenia deleted.
2) Anxiety disorders: Separation anxiety disorder and selective mutism are now classified as
anxiety disorders. The DSM-5 chapter on anxiety disorder no longer includes obsessive-
compulsive disorder, posttraumatic stress disorder (PTSD) and acute stress disorder. However,
the sequential order of these chapters in DSM-5 reflects the close relationships among them.

17
 3) Obsessive-compulsive and related disorders: A new chapter on obsessive-compulsive and
related disorders includes new disorders.
4) Trauma- and stressor-related disorders: PTSD is now included in a new section titled "Trauma-
and Stressor-Related Disorders."
5) Mood disorders now are separated in two separate chapters: depressive disorders and bipolar
disorders
6) Sexual and Gender identity disorders have been separated in different chapters 1) sexual
dysfunctions and 2) Gender dysphoria and 3) paraphilic disorders
7) Somatic symptom and related disorders: Somatoform disorders are now called somatic
symptom and related disorders
8) “Eating disorders of Infancy or Early Childhood' are now called “feeding and eating disorders”.
Addition of three disorders (i.e. Pica, Rumination disorders, and ARFID- Avoidant/Restrictive
Food Intake Disorder) previously described in the DSM-IV-TR section.
9) The Autism spectrum: In the DSM-5, four separately classified disorders (autism, Asperger’s,
childhood disintegrative disorder, and pervasive developmental disorder) have been unified
under the header of Autism Spectrum Disorder. The previous 4 categories are no longer in use.
10) Mental retardation" has a new name: "intellectual disability (intellectual developmental
disorder)"

Critical evaluation of DSM

Strengths of classification and DSM -5

1. A classification system helps in the diagnosis so that treatment decisions and prognosis can be
made.
2. A classification system provides a common language with which mental health professionals
can discuss similar patients, regardless of their own geographical location.
3. The new DSM-5 moves away from the problematic multiaxial system of classification which
had low reliability and validity. DSM-5 now uses a more dimensional approach by offering
multiple assessment tools (e.g., severity rating scales, disability measure) in contrast to the prior
categorical focus.
4. DSM-5 now gives more emphasis to cultural factors through
inclusion of an explanation for the cultural formation interview technique, and an updated
Cultural Concepts of Distress appendix.
5. DSM-5 has offered revisions to diagnosis criteria across multiple diagnoses to better reflect
emerging research findings.

Criticism of classification and DSM -5 (or issues in classification)

1. Diagnosis puts a label on a person and stigmatizes a person for life. When a person is labeled
“depressed” or “schizophrenic,” others are more likely to make certain assumptions about that
person that may or may not be accurate. The person may accept a redefined identity and play out
the expectations of that role. S/he may decide that s/he “is” the diagnosis and may thus adopt it as
a life “career.” (“I’m nothing but a substance abuser. I might as well do drugs—everyone expects
me to anyway). They can also have devastating effects on a person’s morale, self-esteem, and

18
 relationships with others. The stigmatizing implications of many psychiatric labels can mark
people as second class citizens with severe limitations that are often presumed to be permanent.

Note: For years the traditional term “patient” was used- a term that is closely associated with
medical sickness and a passive stance, waiting (patiently) for the doctor’s cure. Today many mental
health professionals, especially those trained in nonmedical settings, prefer the term “client”
because it implies greater participation on the part of an individual and more responsibility for
bringing about his or her own recovery.

2. Homogeneity within disorders: Classification imposes homogeneity within disorders and

encourages clinicians to ignore the individual characteristics of a particular patient. For e.g. the
diagnostic criteria for schizophrenia (for example) have been made so broad that, in principle, two
patients could present with totally different symptoms yet they may both receive a diagnosis of
schizophrenia.
3. Lowering the thresholds: Some argue that DSM includes disorders that are better understood as
problems in day-to-day life (such as sleep disorders) than as mental disorders. The thresholds for
other disorders have also been reduced. For example, a person who might have been classed as
healthy but ‘a bit of a worrier’ 50 years ago might receive a diagnosis of generalized anxiety
disorder if they were to be assessed today. The consequence is that the boundaries between
‘normal’ and ‘abnormal’ are becoming blurred. According to L. J. Davis (2000) DSM lists a
madness for everyone. Thomas Szasz postulates that psychiatry is based on pseudo-science not on
science that “virtually all psychiatric diagnoses are economics and politics”.
4. Although DSM-5 has introduced some dimensional measurement yet the manual is still primarily
a categorical approach classifying disorders on the basis of clustering of symptoms as opposed to
viewing symptoms as occurring along a continuum.
5. Comorbidities and symptom overlap: A good classification system should produce mutually
exclusive disorders, yet there is considerable co-occurrence between disorders (known as co-
morbidity). For example, studies indicate that as many as 80% of youths with bipolar disorder also
meet diagnostic criteria for ADHD. There are instances in which the presence of multiple diagnoses
suggest the presence of distinct yet comorbid disorders, but in many cases the co-occurring
diagnoses suggest the presence of common, shared pathologies, notably a negative affectivity
(neuroticism or emotional instability) dimension common to the mood, anxiety, and most
personality disorders.
6. Cultural sensitivity: Very few of the empirical studies considered by the authors of the current
DSM have focused sufficiently on ethnic minorities. Moreover, some DSM critics argue that
Western values (independence and self-sufficiency) are embedded in the DSM and that they don’t
encompass the values of many people from non-Western societies (e.g. interdependence).
7. Gender Bias: Some disorders are diagnosed far more often in males: alcohol use disorder, conduct
disorder, ADHD, and antisocial personality disorder, to name a few. Other disorders are diagnosed
far more often in females: major depression, many anxiety disorders, eating disorders, and others.
Critics of the current DSM have argued that some diagnostic categories are biased toward
pathologizing one gender more than the other suggesting that society, rather than or in addition to
the individual, plays a prominent role in their emergence. Some empirical studies have found that
clinicians define mental health differently for males and females and that clients of different genders
with identical symptoms often receive different diagnoses from clinicians. The controversy over
premenstrual dysphoric disorder (PMDD), which had been rejected from previous editions of DSM
but it is now included as a disorder in DSM-5, has renewed this criticism of DSM authors.

19
 8. Nonempirical Influences: At times, political wrangling and public opinion may have pressured DSM
authors to make certain decisions. For example, once-proposed disorders such as masochistic
personality disorder have been strongly opposed by political organizations. Also drug companies
stand to boost profits when new diagnostic categories, and the new client “markets” that come along
with them, are created.

12 DSM-5 conceptualizes psychopathology as something that exists within the person. However,
childhood disorders are often relational in nature. Considerable research indicates that the quality of
parent-child interactions plays an important role in the development of oppositional defiant disorder.
Furthermore, treatment for this disorder relies heavily on parental involvement. However, in the
DSM-5 system, oppositional defiant disorder is diagnosed in the child. The DSM-5 approach to
diagnosis can overlook the role caregivers, other family members, and peers play in the development
and maintenance of children’s problems.

ICD 10

ICD website: https://icd.who.int/en

The International Classification of Diseases (ICD) is published by the WHO in Geneva, Switzerland.
The latest ICD is ICD-11 (2022). This classification system includes diagnoses for all the systems in
the human body.

Characteristics of ICD 11

• International Applicability: The ICD-11 offers guidance for its use with different cultures as
well as translations into 43 different languages. ICD-11 is used globally by clinicians while
DSM an important diagnostic instrument within the US mental health care system. ICD is a
free and open resource for public health benefit while DSM while DSM is the intellectual
property of APA.
• The ICD-11 and DSM-5 share many similarities on mental disorders. The DSM however, is
solely focused on mental health concerns, while the ICD covers all parts of the body and mind
in addition to mental disorders.
• ICD provides codes for each diagnosis which tells a client’s insurance company why you
provided the client with the services you did, helping to justify the services. The DSM doesn't
have its own codes, but rather, publishes the corresponding ICD codes for each mental health
diagnosis. For instance, the DSM-5 uses both ICD-9 and ICD-10 codes.

ICD 10 and 11 Mental Disorder Codes

• ICD 10 codes: Decimal system of coding

A. “Mental, behavioral or neurodevelopmental disorders” were covered in

Chapter V and codes started from ‘F’ in ICD 10.

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 B. ICD 10 uses an open alpha-numeric system in the form FXX . XX. The
letter 'F 'identifies indicates that it is a mental disorder; the first two digits
refers to the broad category and subcategory followed by the decimal point
and then the other details

(F20-F29)-------Schizophrenia, schizotypal and delusional disorder

✓ F20.2---- F(mental disorder), 20(schizophrenia), 2(Catatonic Type);

✓ F21---- F(mental disorder), 21(Schizotypal disorder)

• ICD 11 Codes: New coding system

Mental disorders are covered in Chapter 6 and codes started from ‘6A’.

Schizophrenia or other primary psychotic disorders (6A20-6A2Z)

Y or Z indicates more codes could be added to indicate details of disorder by adding a stem
(e.g. negative symptoms)

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 • Dimensional Approach: Another enhancement of the ICD-11 is that it's based on a dimensional
approach like DSM. 2022 The dimensional potential is robustly realized in the classification of
personality disorders and is similar to DSM-5.
• Lifespan approach to the grouping of disorders just like DSM
• Culture-related information was systematically incorporated based on a literature review on
cultural influences.

ICD 11 categories and changes in the ICD-11

ICD 11 categories

1. Neurodevelopmental disorders (ICD Code: 6A00-6A0Z)

2. Schizophrenia or other primary psychotic disorders (ICD Code: 6A20-6A2Z)
3. Catatonia (6A40-6AZ)
4. Mood disorders (6A80-6C46)
5. Anxiety or fear-related disorders (6B0to 6B0Z)
6. Obsessive-compulsive or related disorders (OCRD)
7. Disorders specifically associated with stress
8. Dissociative disorders
9. Feeding or eating disorders
10. Elimination disorders
11. Disorders of bodily distress or bodily experience
12. Disorders due to substance use or addictive behaviours
13. Impulse control disorders
14. Disruptive behaviour or dissocial disorders
15. Personality disorders and related traits
16. Paraphilic disorders
17. Factitious disorders
18. Neurocognitive disorders
19. Mental or behavioural disorders associated with pregnancy, childbirth or the puerperium
20. Secondary mental or behavioural syndromes associated with disorders or diseases classified
elsewhere

ICD-11 Added Diagnoses: The following diagnoses are now included in the ICD-11.

• Attention Deficit Disorder: Attention-deficit hyperactivity disorder (ADHD) was finally added
to the ICD-11 after not being included in the ICD-10.3 This diagnosis has primarily been made
in the United States and is already included in the DSM-5, so this is a significant change that
may impact rates of ADHD diagnoses worldwide.
• Gaming Disorder: Gaming disorder is newly defined in the ICD-11 as “a pattern of persistent
or recurrent gaming behavior ('digital gaming’ or ‘video-gaming’).

ICD-11 Deleted Diagnoses: The following disorders were removed from the ICD with the publication
of the ICD-11.

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 • Personality Disorders: The section on personality disorders has been completely overhauled.
There is now one diagnosis of "personality disorder" as it was found that there was much
overlap in clinical practice. This diagnosis is labeled as mild, moderate, or severe, and measured
in terms of six trait domain areas to retain some of the earlier specificity of the diagnosis. This
is a fairly significant departure from the original ICD personality disorder diagnosis.

Four Different versions of ICD:

Because ICD-10 is used for several purposes, it exists in several forms each of which is derived from, and
compatible with, the core version (CDDG).

1) Clinical Descriptions and Diagnostic Guidelines (CDDG). Also referred to as the ‘blue book’. The
ICD-10 CDDG is intended for use by psychiatric-clinicians in their everyday practice. It is based on
‘pattern recognition approach’. This is flexible for clinical purposes and comprises a general
description of disorders. It requires that case characteristics be matched with the general
pattern/theme given in the ICD clinical criteria. All the above descriptions are characteristics of
CDDG.
2) Diagnostic criteria for Research (DCR). based on ‘Symptom checklist’. This is far more precise and
strict and intended to be used by researchers. It consists of symptoms with explicit criteria– similar
to DSM–IV. It has advantages in increased reliability, but is relatively cumbersome so that many
clinicians do not bother to apply the criteria rigorously.
3) ICD Primary health Care (ICD- PHC). A simplified classification for use in primary care is also
there. It has only broad categories and no subtypes. ICD 10 categories which were chosen for ICD
PHC included groups of disorders of public health importance, had a high prevalence rate, associated
with significant disablement, morbidity or mortality and for which it is possible to provide effective
and acceptable management in PHC setting.
4) Multiaxial presentations of ICD (for adults, adolescents and childhood): This version has a Tri-axial
framework for psychiatric disorders as described below:

• Axis I: Clinical diagnoses: mental disorders and physical disorders

• Axis II: Disability: (rating on specific areas of functioning e.g. personal care, social functioning).
• Axis III Contextual factors: environmental and life style factors relevant to pathogenesis and
course of patient's illness (problems related to unemployment)

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 Psychological assessment
Psychological assessment refers to a procedure by which clinicians, using psychological tests,
observation, and interviews, develop a summary of the client’s symptoms and problems. The
information gathered in an assessment is used to determine the appropriate diagnosis for a person’s
problems. Psychological assessment also helps in planning the treatment. Treatment planning involves
making use of assessment information to generate a treatment plan and evaluating its effectiveness for
e.g. which therapy will be most effective. Finally, we need to know if the treatment we employed
worked. This will involve making assessments before any treatment is used and then measuring the
behavior while the treatment is in place.

Basic elements in assessment

1. Presenting problem/chief complaints – The clinician in the first instance needs to know the
major symptoms the client is experiencing. The chief complaint is the patient’s responses to
the question, “What brings you to see me/to the hospital today?” or some variant thereof. The
clinician then goes on to take a detailed description of the various symptoms reported by the
client as well as his own observations of the client.
2. Relationship between Assessment and Diagnosis: The purpose of psychological assessment is
to make a diagnosis and then make a recommendation for treatment. Clinical diagnosis is the
process through which a clinician arrives at a general “summary classification” of the patient’s
symptoms by following a clearly defined system such as DSM-5 or ICD.
3. Social or Behavioral History: Assessment should include a description of the social and
behavioral history and also relevant long-term personality characteristics. Social history
includes a person's family relationships and other important relationships - reasons for discord
within the family should be explored. It is also important to assess the kind of environmental
demands (job, family, occupation, family) are placed on the person etc. Assessment should
also be made about the patient’s personality prior to the first episode of mental disorder; this
is sometimes called the ‘premorbid personality’. The diverse bits of information must then be
integrated into a meaningful picture called a “dynamic formulation”. This formulation not only
describes the current situation but also includes hypotheses about what is driving the person to
behave in maladaptive ways. This case formulation then guidesfuture treatment.
4. Ensuring Culturally Sensitive Assessment Procedures: It is critical for the psychologist to be
informed of the issues involved in multicultural assessment (often referred to as cultural
competence) and to use testing procedures that have been adapted and validated for culturally
diverse clients. In using Westerndeveloped tests, users need to take into account the dominant
language, socioeconomic status, ethnicity, and gender of their clients
5. The Influence of Professional Orientation: How clinicians go about the assessment process
often depends on their basic treatment orientations. For example, a biologically oriented
clinician—typically a psychiatrist or other medical practitioner—is likely to focus on
biological assessment methods aimed at determining any underlying organic malfunctioning
that may be causing the maladaptive behavior. A psychodynamic or psychoanalytically
oriented clinician may choose unstructured personality assessment techniques, such as the
Rorschach inkblots or the Thematic Apperception Test (TAT), to be described to identify
intrapsychic conflicts.

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 6. Trust and Rapport Between the Clinician and the Client: The clinician should develop a
trusting relationship. S/he should explain to the patient what will happen during assessment
and assure confidentiality. Providing feedback about the test is also an important element in
the treatment process.

Assessment methods

1.The General Physical Examination:

In cases in which physical symptoms are part of the presenting clinical picture, a referral for a medical
evaluation is recommended. A physical examination consists of the kinds of procedures most of us have
experienced when getting a “medical checkup.” This part of the assessment procedure is of obvious
importance for disorders that entail physical problems, such as a psychologically based physical
condition, addictive disorders, and organic brain syndromes.

2.The Neurological Examination:

Electroencephalogram (EEG):

An EEG is a graphical record of the brain’s electrical activity and may indicate some
irregularities. For example, recent research has supported a link between resting frontal EEG
asymmetry and depression and anxiety.

Anatomical Brain Scans

A brain scan shows brain structure, and brain activity which cannot be detected otherwise.

1. Computerized axial tomography (CAT) scan (also called CT scan): This uses X-rays to
show the structure of the brain to reveal and disease or injuries. The resultant images are two
dimensional and of comparatively low resolution. CT is a useful tool for assisting diagnosis in
medicine, but it is a source of ionizing radiation, and it can potentially cause cancer.
2. Magnetic resonance imaging (MRI). MRI exams use magnetic fields and radio waves to take
images of the structure of the brain to determine if the person has injured or unhealthy tissue.
MRI can create clear, detailed pictures of the structure of the brain and are superior to CAT
scans. In addition, the MRI procedure is normally far less complicated to administer than a
CAT scan and does not subject the patient to ionizing radiation.
3. PET Scans. Positron emission tomography scanning produces a three-dimensional image of
functional processes in the brain, (not just the brain structure). It uses a special dye with
radioactive tracers to record changes in how the body’s working, such as how it absorbs sugar
or how the brain’s functioning.

4. Functional magnetic resonance imaging (fMRI). As originally developed and employed, the
MRI could reveal brain structure but not brain activity. fMRI can do both. It can also show
which part of the brain is active, or functioning, in response to the patient performing a given
task, by recording the movement of blood flow. At this point the fMRI is not considered to be
a valid or useful diagnostic tool for mental disorders; however, investigators are optimistic that
this procedure shows great promise for understanding brain functioning.

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3 The Neuropsychological Examination

Neuropsychology is a domain of psychology that examines brain–behavior relationships. A This

involves the use of various testing devices to measure a person’s cognitive, perceptual, and motor
performance as clues to the extent and location of brain damage. Neuropsychological assessment shares
some common elements with intelligence testing. In fact, many neuropsychological assessments begin
with a measure of general intelligence (Kolb & Whishaw, 2009). Further, some intelligence scales have
been adapted for neuropsychological purposes; most notably the Wechsler Adult Intelligence Scale-
Revised as a Neurological Instrument (WAIS-R-NI).

Early assessment procedures relied on single, independent instruments to assess brain damage. current
assessment practices utilize a battery approach. With fixed battery approaches all individuals requiring
assessment receive the same set of tests. The majority of fixed batteries have cut off scores that reflect
the degree of severity of the impairment and differentiate between impaired and unimpaired individuals.
Two common fixed neuropsychological batteries are the Halstead-Reitan Battery and the Luria
Nebraska Neuropsychological Battery.

The Halstead-Reitan Neuropsychological Test Battery is a battery of tests used to

evaluate brain and nervous system functioning. It provides individuals with a cut-off score or index of
impairment, which discriminates brain damaged from normally functioning individuals. Information
about specific areas of the brain that are damaged and severity of damage can also be garnered from
this battery. Some of the tests are as follows:

1. Halstead category test: Measures a subject’s ability to remember material and can provide clues
as to his or her judgment.
2. Tactual performance test: Measures a subject’s motor speed, response to the unfamiliar, and
ability to learn and use tactile and kinesthetic cues.
3. Rhythm test: Measures attention and sustained concentration through an auditory perception
task.
4. Speech sounds perception test: Determines whether an individual can identify spoken words.
5. Finger Oscillation Task: Measures the speed at which an individual can depress a lever with
the index finger.

Neuropsychological testing provides a clinician with important behavioral information how organic
brain damage is affecting a person’s present functioning. However, in cases where the psychological
difficulty is thought to result from non-organic causes, psychosocial assessment is used.

4 Psychosocial Assessment

Psychosocial assessment attempts to provide a realistic picture of an individual in interaction with his
or her social environment. Clinicians typically formulate hypotheses and discard or confirm them as
they proceed. Starting with a global technique such as a clinical interview, clinicians may later select
more specific assessment tasks or tests. The following are some of the psychosocial procedures that
may be used.

1. Clinical Interviews

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An assessment interview, often considered the central element of the assessment process, usually
involves a face-to-face interaction in which a clinician obtains information about various aspects of a
client’s behavior. There are interviews for a variety of clinical situations: intake interviews to establish
the nature of someone’s problems and assign a DSM diagnosis (e.g. Mental Status Examination or
MSE), orientation interviews to prepare a client for treatment or research, problem-referral interviews
to address a specific referral question, termination or debriefing interviews to end treatment or research,
and crisis intervention interviews to offer support through a crisis and to decide what, if any
,intervention should be offered next. Often these overlap in practice.

Structure of Interviews. The most fundamental feature of clinical interviews is their structure: the
degree to which the interviewer determines the content and course of the conversation. At one end of
the structure continuum are open-ended, nondirective, or unstructured interviews in which the clinician
does as little as possible to interfere with the natural flow of the client’s speech and choice of topics. At
the other end are structured interviews, which involve a carefully planned question-and-answer format.
In between are many blends, usually called guided or semi-structured interviews.

An unstructured interview is a non-directive interview that does not make use of a set of standardized
questions. Some very general questions are planned in advance but the interviewer does not direct the
interview rather it is the client who gives direction to the interview. Typically, an unstructured interview
relies on open ended questions, spontaneity and follow-up questioning in order to gather detailed
information. Because the questions are asked in an unplanned way, important criteria needed for a
DSM-5 diagnosis might be skipped. Responses based on unstructured interviews are difficult to
quantify or compare with responses of clients from other interviews. Overall, the reliability and validity
of unstructured interviews suffer compared with the reliability and validity of more structured
interviews, but proper training and sensitivity to sources of error can maximize the value of interviews
as a rich source of clinical assessment information.

Structured interviews (or directive interviews) follow a predetermined set of questions and the direction
of the interview is controlled by the interviewer. While structured interviews are increasingly popular,
partly because of their greater reliability and validity, they also have some disadvantages including lack
of flexibility, tendency to miss important information that the interview script did not explore and their
routinized nature can alienate clients especially if rapport has not been established.

The reliability of the assessment interview may be enhanced by the use of rating scales that help focus
inquiry and quantify the interview data. For example, the person may be rated on a 3-, 5-, or 7-point
scale with respect to self-esteem, anxiety, and various other characteristics. Such a structured format is
particularly effective in giving a comprehensive impression, or “profile,” of the subject and her crises—
such as marital difficulties, drug dependence, or suicidal fantasies.

Clinical interviews can be subject to error because they rely on human judgment to choose the questions
and process the information. It is chiefly for this reason that recent versions of the DSM have
emphasized an “operational” assessment approach, one that specifies observable criteria for diagnosis
and provides specific guidelines for making diagnostic judgments.

2. Clinical Observation

27
Observations often occurs during interviews but there are also more formal observational assessment
techniques that differ from interviews.

• Observation in natural vs contrived (analogous) situations: This involves observation of

spontaneous behavior of participants in natural surroundings such as schools, homes, and other
settings. There is no manipulation involved and the researcher observes or assesses particular
kinds of responses to situations. In contrast to observation in natural conditions, observation in
contrived (analogous) involves intervention by clinician to create an artificial environment
(analogous to real life situation) in order to assess responses to certain situations. This can
reduce the time and expense of obtaining reactions to certain circumstances. For e.g., role plays
typically involve simulating a depressive or anxiety-provoking stimulus. Once a child is placed
in such a situation, specific behaviors that are representative of the anxious, fearful, or
depressive responses are observed and recorded.
• Enhancing Observational Validity: Additional measures can also be used during this
assessment:

1. Self-monitoring: The client is often trained in self-monitoring which involves self-

observation and objective reporting of behavior, thoughts, and feelings as they occur
in various natural settings.
2. Self-report measures: A client may also be asked to fill out a more or less formal self-
report or a checklist concerning problematic reactions experienced in various
situations. Many instruments have been published in the professional literature and
are commercially available to clinicians.
3. Rating scales: A rating scale is usually more structured than the observational
technique and hence more reliable and valid. The most useful rating scales are those
that enable a rater to indicate not only the presence or absence of a trait or behavior
but also its prominence or degree. The categories may be “outstanding”,
“satisfactory”, “unsatisfactory”, or other similar categories. Rating scales may be
completed during an observation or at a later time. Ratings like these may be made
not only as part of an initial evaluation but also to check on the course or outcome of
treatment. One of the widely used rating scales is the 24 item Brief Psychiatric Rating
Scale (BPRS, Overall & Hollister, 1982) used to measure psychiatric symptoms such
as anxiety, depression, and psychoses. Ratings are made by a clinician on all 24-items
following an interview with a patient. The Hamilton Rating Scale for Depression
(HRSD) is one of the most widely used procedures for selecting clinically depressed
research subjects and also for assessing the response of such subjects to various
treatments.

3 Psychological tests
Scientifically developed psychological tests (as opposed to the recreational ones sometimes appearing
in magazines or on the Internet) are standardized sets of procedures or tasks for obtaining samples of
behavior. Among the characteristics that these tests can measure are coping patterns, motive patterns,
personality characteristics, role behaviors, values, levels of depression or anxiety, and intellectual
functioning. Impressive advances in the technology of test development have made it possible to create
instruments of acceptable reliability and validity to measure almost any conceivable psychological
characteristic on which people may vary. Moreover, many procedures are available in a computer-
administered and computer-interpreted format.

28
 • Intelligence tests. Intelligence testing determines the patient’s level of cognitive
functioning and consists of a series of tasks asking the patient to use both verbal and
nonverbal skills. A clinician can choose from a wide range of intelligence tests. The
Wechsler Intelligence Scale for Children-Revised (WISC-IV), Wechsler Adult Intelligence
Scale-Revised (WAIS-IV) and Stanford-Binet Intelligence Scale (Kamphaus & Kroncke,
2004). Intelligence tests have been criticized for not predicting future behaviors such as
achievement and reflecting social or cultural factors/biases and not actual intelligence. Also,
can we really assess intelligence through one ratio such as an IQ score?

• Personality Projective tests consist of simple ambiguous stimuli that can elicit an
unlimited number of responses. The Rorschach inkblot test consists of 10 symmetrical
inkblots, some are colored, black and red, or just black. One at a time, the person being
tested is shown each inkblot and asked to describe what they see. There are no right or
wrong answers, and you can see more than one thing. The clinician then records the
responses verbatim. Use of the Rorschach in clinical assessment is complicated and
requires considerable training. Furthermore, the results of the Rorschach can be
unreliable because of the subjective nature of test interpretations. In the hands of a
skilled interpreter, however, the Rorschach can be useful in uncovering certain
psychodynamic issues, such as the impact of unconscious motivations on current
perceptions of others. Some researchers have also raised questions about the norms on
which the Exner Rorschach Comprehensive System, a scoring and interpretation
system, is based (Shaffer et al., 1999; Wood et al., 2001). The Rorschach was shown
to “overpathologize” persons taking the test—that is, the test appears to show
psychopathology even when the person is a “normal” person randomly drawn from the
community. The Thematic Apperception Test (TAT) was introduced in 1935 by its
authors, C. D. Morgan and Henry Murray of the Harvard Psychological Clinic. The
TAT uses a series of simple pictures, some highly representational and others quite
abstract, about which a subject is instructed to make up stories. The content of the
pictures, much of them depicting people in various contexts, is highly ambiguous as to
actions and motives, so subjects tend to project their own conflicts and worries onto it
(see Morgan, 2002, for a historical description of the test stimuli). However, there are
questions about its reliability and validity. Another projective test is the sentence
completion test and asks individuals to finish an incomplete sentence. Examples
include ‘My mother…’ or ‘I hope…’ Sentence completion tests, which are related to
the free association method, a procedure in which the client is asked to respond freely,
are somewhat more structured than the Rorschach and most other projective tests. They
help examiners pinpoint important clues to an individual’s problems, attitudes, and
symptoms through the content of her or his responses. Interpretation of the item
responses, however, is generally subjective and unreliable.

• Objective Personality inventories ask clients to state whether each item in a long list of
statements applies to them, and could ask about feelings, behaviors, or beliefs. Examples
include:
i. Minnesota Multiphasic Personality Inventory (MMPI -2): The Minnesota
Multiphasic Personality Inventory (MMPI -2) was developed in the late 1930’s by
psychologist Starke R. Hathaway and psychiatrist J.C. McKinley at the University of

29
 Minnesota. Today, it is the frequently used clinical testing instrument and is one of the
most researched psychological tests in existence.

ii. Sixteen Personality Factor Questionnaire (or 16PF): This is a multiple-choice

personality questionnaire which was developed by Raymond B. Cattell and his
colleagues. In addition to the sixteen primary traits, these researchers also found five
higher-level "second-order" traits of personality.

iii. Beck Depression Inventory (BDI): The Beck Depression Inventory (BDI) measures
the intensity, severity, and depth of depression in patients with psychiatric diagnoses.
Aaron T. Beck, a pioneer in cognitive therapy, first designed the BDI.

iv. The Millon Clinical Multiaxial Inventory (MCMI): The Millon Clinical Multiaxial
Inventory (MCMI, 1977) is an important assessment instrument used by clinical
psychologists. Butcher and Rouse (1996) reported that, over the past few years, only
the Rorschach and Minnesota Multiphasic Personality Inventory–2 have generated
more published research. The Millon Clinical Multiaxial Inventory-III is a personality
test authored by Theodore Millon, Carrie Millon, and Roger Davis, published in 1977.
The MCMI-III diagnoses Axis 2 (personality disorders) and Axis I disorders of DSM
1V in patients who display midrange psychopathology, instead of those who suffer
from sever mental illness or normal functioning adults.

30
 SOCIAL ANXIETY DISORDER

(Previously called SOCIAL PHOBIA)

Jane , a 28-year old supervisor, has been dreading going to work because of
fears that in meetings she will blush, her heart will race, and her thoughts will
"block" so that she cannot express herself clearly. She is very worried about
being seen to be anxious or uncomfortable, as she believes that her colleagues
will think that she is not able to do her job properly. She has also begun to avoid
eating lunch at work.

When normal slight anxiety at social occasions becomes excessive it is referred to as social
anxiety disorder (social phobia). Social phobia largely concerns a fear of scrutiny of what
other people think. E.g. a glance from someone precipitates panic about being judged as
stupid. Unlike specific phobias, which most often originate in childhood, social
phobias typically begin somewhat later, during adolescence or early adulthood

The term social anxiety disorder has been proposed as a more appropriate label for this
disorder because the problems caused by it tend to be much more pervasive and to interfere
much more with normal activities than the problems caused by other phobias (Liebowitz
et al., 2000).

Clinical Picture/Symptoms DSM Criteria

Social Phobia
A useful mnemonic for Social Anxiety Disorder is FEEAR DSM

(criteria similar as in specific phobia except ‘evaluation’.)

A. Fear or anxiety (excessive) about one or more social situations in which the
individual is exposed to possible scrutiny by others. Examples of social situations:
having a conversation, meeting unfamiliar people), being observed (e.g., eating or
drinking), and performing in front of others (e.g., giving a speech).
B. (Evaluation/Scrutinized) The individual fears that he or she will be negatively
evaluated or scrutinized by others in social situations. The person generally has no
problem performing the activity in the privacy of his or her own home. For

1
 example, the person can comfortably give a speech in front of a mirror or flawlessly
perform a piano concerto as long as there is no audience. The fear in social settings
is that the person will appear foolish (or unsure, weak, crazy, stupid, boring,
intimidating, dirty, or unlikable) and/or develop visible anxiety symptoms (e.g.,
sweating, blushing, trembling, a Panic Attack). The person may various anxious
thoughts:

• Anxiety about offending others—for example, by a gaze or by showing

anxiety symptoms—may be the predominant fear in individuals from
cultures with strong collectivistic orientations. S/he may avoid any eye
contact.
• An individual with anxiety about trembling of the hands may avoid
drinking, eating, writing, or pointing in public;
• An individual with fear of sweating may avoid shaking hands or eating
spicy foods;
• Individual with anxiety about blushing may avoid public performance,
bright lights, or discussion about intimate topics.
• Some individuals anxiety about urinating in public restrooms when other
individuals are present (i.e., paruresis, or “shy bladder syndrome”).

C. (Exposure-anxiety) The exposure to the phobic stimulus almost always

immediately provoke an anxiety response, which may be either a Panic Attack or
symptoms of anxiety.
• The degree and type of fear and anxiety may vary (e.g., anticipatory anxiety,
a panic attack) across different occasions.
• The anticipatory anxiety (i.e. anxiety about anticipating a social situation)
may occur sometimes far in advance of upcoming situations (e.g., worrying
every day for weeks before attending a social event, repeating a speech for
days in advance).
• In children, the fear or anxiety may be expressed by crying, tantrums,
freezing, clinging, or shrinking in social situations
D. (Avoidance of fear) The patient either avoids the phobic stimulus or endures it with
severe anxiety or distress.
• Avoidance can be extensive (e.g., not going to parties, refusing school) or
subtle (e.g., overpreparing the text of a speech, diverting attention to others,
limiting eye contact)
E. (Recognition of fear) The patient realizes that this fear is unreasonable or out of
proportion.

2
 • The anxiety has to be excessive. An individual who becomes anxious only
occasionally in the social situation(s) would not be diagnosed with social
anxiety disorder.
• The individual’s sociocultural context needs to be taken into account when
this judgment is being made. For example, in certain cultures, behavior that
might otherwise appear socially anxious may be considered appropriate in
social situations (e.g., might be seen as a sign of respect).
F. (Duration) The fear, anxiety, or avoidance is persistent, typically lasting for 6
months or more.
G. (Social occupational dysfunctioning) Fear markedly interferes with the patient's
usual social, job, or personal functioning.
• For example, an individual who is afraid to speak in public would not
receive a diagnosis of social anxiety disorder if this activity is not routinely
encountered on the job or in classroom work, and if the individual is not
significantly distressed about it. However, if the individual avoids, or is
passed over for, the job or education he or she really wants because of social
anxiety symptom
H. (Mental disorders exclusion) Exclusion criterion 1: The symptoms are not better
explained by another anxiety or mental disorder.

Associated features:

Individuals with social anxiety disorder may be inadequately assertive or excessively

submissive or, less commonly, highly controlling of the conversation. They may show
overly rigid body posture or inadequate eye contact, or speak with an overly soft voice.
These individuals may be shy or withdrawn, and they may be less open in conversations
and disclose little about themselves. They may seek employment in jobs that do not require
social contact, although this is not the case for individuals with social anxiety disorder,
performance only. They may live at home longer. Men may be delayed in marrying and
having a family, whereas women who would want to work outside the home may live a
life as homemaker and mother. Self-medication with substances is common (e.g., drinking
before going to a party). Blushing is a hallmark physical response of social anxiety disorder

Differential diagnosis: Shyness and social phobia

Although this disorder is often thought of as shyness, the two are not the same. Shy people
can be very uneasy around others, but they don't experience the extreme anxiety in
anticipating a social situation, and they don't necessarily avoid circumstances that make

3
them feel self-conscious. In contrast, people with social phobia aren't necessarily shy at all.
They can be completely at ease with people most of the time, but particular situations, such
as walking down an aisle in public or making a speech, can give them intense anxiety.

Feared social situations in community (Wittchen, 1999)

• • Performing on stage (18%)

• • Public speaking (13%)
• • Talking with others (6%)
• • Social gatherings (5%)
• • Eating/drinking in public (4%)
• • Also: dating, assertiveness/conflict, school

Etiology/causal factors/Dynamics
Psychological Factors:

Social behaviours as learned behaviours

1. Classical conditioning: A conditioning model of social phobia involves the hypothesis

that a traumatic social event has created lasting anxiety associated with social interactions.
Thus, negative experience in a social setting is associated with fear. Children who
experience teasing, bullying, rejection, ridicule or humiliation may be more prone to social
anxiety disorder. In addition, other negative events in life, such as family conflict or sexual
abuse, may be associated with social anxiety disorder. One recent study interviewed a
group of people with social phobia about their images of themselves in social phobic
situations and asked where those images originated (McCabe, 2003). Ninety-six percent of
these people remembered some socially traumatic experience that was linked to their own
current image of themselves in socially phobic situations. The themes of these memories
included having been "criticized for having an anxiety symptom" (e.g. being red or
blushing), and having fell "self-conscious and uncomfortable in public as a consequence
of past criticism" such as "having previously been bullied and called a 'nothing'.

2. Vicarious/ observational learning: Another way of acquiring social fears is vicarious

conditioning or through observation. According to this paradigm, observing others
experiencing anxiety in social situations can lead to the observer fearing these situations.

4
People with generalized social phobia also may be especially likely to have grown up with
parents who devalued sociability, thus providing ample opportunity for vicarious learning
of social fears (Morris, 2001). More generally, parents with anxiety disorders are more
likely than nonanxious parents to tell their children about the potential dangers of a novel
situation such as a ground, and thereby strengthen anxious children's avoidant tendencies
(Morris. 2001). Bruch, Heimberg, Berger & Collins (1988) found that parents of
individuals with social phobia themselves avoided social situations. People with
generalized social phobia also may be especially likely to have grown up with parents who
were emotionally cold, socially isolated, and avoidant.

Social Fears and Phobias in an Evolutionary Context:

Dominance hierarchies (Ohman et al., 1985). According to Ohman (1985) social phobias
may have evolved as a result of dominances hierarchies that are a common social
arrangement among animals like primates. These are established as a result of aggressive
encounters between members of a social group, and a defeated individual typically displays
fear and submissive behaviour but rarely attempts to escape the situation completely.

Most social phobias develop during adolescence and early adulthood which is also the time
during which dominance conflicts are prominent. Socially anxious persons often doubt that
they will be able to successfully compete for dominant positions in the social hierarchy.
Thus, instead of making dominance a primary goal during interactions, they may adopt
secondary goals such as becoming submissive, and remaining affiliated with the group.

Socially anxious people may operate predominantly in the ‘competitive mode’ which has
its core the evaluation of the dominance potential of the other. In competitive interactions,
dominant others are viewed as a threat, and resources are acquired by the individual on the
basis of competition and defending them against the encroachment of others. In contrast,
nonanxious individuals have ‘cooperative’ schemata i.e. one in which the person sees
social interaction in terms of mutually supportive and reciprocating networks,
characterized by cooperation, exploration, care-eliciting and care-giving. The competitive
mode would only be triggered if a person interprets cues as threatening rather than reassur-
ing.

For example, a socially anxious individual may view a conversation with a new coworker
as some sort of competition in which each person looks for weaknesses in the other (e.g.,
who is more attractive, well educated) and as a potential threat to his or her status and self-
esteem. A nonanxious person would be more likely to view the same conversation as an
opportunity to pleasantly pass the time, make a new friend, get input on a project, etc.

5
If social phobias evolved as a by-product of dominance hierarchies, it is not surprising that
humans have an evolutionarily based predisposition to acquire fears of social stimuli that
signal dominance and aggression from other humans. These social stimuli include facial
expressions of anger or contempt, which on average all humans seem to process more
quickly and readily than happy or neutral facial expressions. In a series of experiments
Ohman, Dimberg, and their colleagues demonstrated that subjects develop stronger
conditioned responses when slides of angry faces are paired with mild electric shocks than
when happy or neutral faces are paired with the same shocks (1996).

Perceptions of Uncontrollability and Unpredictability Being exposed to uncontrollable and

unpredictable stressful events (such as parental separation and divorce, family conflict, or
sexual abuse) may often lead to submissive and unassertive behavior, which is
characteristic of socially anxious or phobic people. This kind of behavior is especially
likely if the perceptions of uncontrollability stem from an actual social defeat. It may also
develop, at least in part, as a function of having been raised in families with somewhat
overprotective (and sometimes rejecting) parents (Lieb et al., 2000).

Cognitive variables

Cognitive distortions: Beck and Emery (1985) state that individuals with social phobia
share typical negative beliefs about themselves in social situations (e.g. "I'm boring," "I'll
make a fool out of myself," "I wont have anything to say"). They argued that this leads to
a sense of vulnerability when they are around people who might pose a threat.

Clark and Wells (1995) later further proposed a ‘cognitive model’ for social anxiety. In
this model social situations (e.g., dinner party) provoke
(a) Activates negative assumptions/beliefs. Three categories of assumptions are
provoked: excessively high standards for social performance (e.g., “I must look as
intelligent, calm, and confident by others”), beliefs about social evaluation (e.g., “If
I make a mistake then other people will humiliate me”), and beliefs about the self
(e.g., “I’m not as good as other people”).
(b) Perceived social danger. Influenced by these assumptions, such people appraise
social situations as dangerous. They make predictions that they will fail to meet a
desired standard of performance (e.g. “I will come across as boring”), and evaluate
their performance negatively (e.g. (e.g., "I'm boring," ").
(c) Self as an object: Such negative schemas lead to them to see the “self as an object”
i.e. the focus now shift to the self and its evaluation.
(d) Safety Behaviours; S/he may then engage in safety behaviours (e.g., avoiding eye
contact or moving away from social situation)

6
 (e) Somatic and Cognitive symptoms: Anxious arousal results in a wide range of bodily
sensations including sweating, blushing, shaking, or an unsteady voice. She may
also simultaneously have cognitive symptoms (e.g., blank mind; I don’t look
attractive.”)
A vicious cycle may evolve: This behavior may lead others to react to them in a less
friendly fashion, confirming their expectations.

Other cognitive biases:

• Interpreting ambiguous information in a threatening manner: Another cognitive
bias seen in social phobia is a tendency to interpret ambiguous social information
in a negative rather than a benign manner (e.g., when someone smiles at you, does
it mean they like you or that they think you’re foolish?). Moreover, it is these
negatively biased interpretations that are remembered (Hertel et al., 2008).

• Vulnerable mode Numerous studies have also shown that people with anxiety
disorders pay more attention to signs of threat than people who don't have anxiety
disorders (e.g., Mineka, 1992). In social anxiety disorders, it is possible to

7
 describe the individual as functioning in the vulnerable mode. Vulnerability is
defined by Beck and Emery as "a person's perception of himself as subject to
internal or external dangers over which his control is lacking. When the vulnerable
mode is active, incoming information is processed in terms of weakness instead
of strength and the person finds him/herself more influenced by past events that
emphasise their failures than by factors that may predict success.

• ‘hypervigilance’ The individual with social phobia is also ‘hypervigilant’ to social

threats, constantly evaluating the severity of a potential threat and their ability to
cope with it. Cognitive distortions prevent the individual reaching a reasonable
estimate of either threat or coping means.

Biological Causal Factors

Genetic and Temperamental Factors: The most important temperamental variable is
behavioral inhibition, which shares characteristics with both neuroticism and introversion.
Behaviorally inhibited infants who have heightened sensitivity to novel stimuli, and avoid
unfamiliar situations/people are more likely to become fearful during childhood and, by
adolescence, show increased risk of developing social phobia. For example, one classic
study indicated that children who had been assessed as being high on behavioral inhibition
between 2 and 6 years of age were nearly three times more likely to be diagnosed with
social phobia even in middle childhood than were children who were low on behavioral
inhibition (Hayward et al., 1998).

Results from several studies of twins have also shown that there is a modest genetic
contribution to social phobia; estimates are that about 30 percent of the variance in liability
to social phobia is due to genetic factors (Smoller et al., 2008). Nevertheless, these studies
suggest that an even larger proportion of variance is due to ‘nonshared environmental
factors’ (dissimilar environmental factors that cause them to become dissimilar to each
other), which is consistent with a strong role for learning.

Social factors

Parenting and family environment: The role that parent influence has in the development
of anxiety is a complicated issue that has yet to be completely unraveled. Specifically,
parenting traits such as overcontrol, lack of warmth or rejection, and overprotection are
known to be associated with the etiology of this disorder (Stark et al 1990).

8
Public Self-Consciousness: Some authors (e.g. Buss, 1980) suggest that socially anxious
people may be high on the dimension of "public self-consciousness". This is defined as
awareness of oneself as a social object (Heimberg et al., 1987).

Self-Presentation: Schlenker and Leary (1982) point out people experience social anxiety
when two conditions are met. First, the person must be motivated (or have the objective)
to make a particular impression on others. The second condition necessary for producing
anxiety is that the individual does not believe he or she will be successful in conveying the
impressions they wish to make and as such expect to be regarded in the fashion they desire.

Poor Social Skills: Deficits in social skills, or 'social fluency', may be a cause of some
social anxiety disorder. According to this explanation, such people may be either be unable
or lack confidence to interact socially and gain positive reactions and acceptance from
others. The studies have been mixed, however, with some studies not finding significant
problems in social skills (Rapee, 1992) while others have (Stopa and Clark, 1993). Alden
and Wallace (1995) too found that individuals suffering from social phobias were less
warm and less interested in others.

What does seem clear is that the socially anxious perceive their own social skills to be
low. It may be that the increasing need for sophisticated social skills in forming
relationships or careers, and an emphasis on assertiveness and competitiveness, is making
social anxiety problems more common, at least among the 'middle classes (Segrin, 2005).

One possible interpretation is that social skills deficits lead to social phobia. Another
possible explanation is that the presence of social phobia leads to poor social skills
development.

4. Cultural factors:

Information on sociocultural variations in social phobia is slowly beginning to emerge as

this phenomenon gains more attention. For example, Taijin Kyofusho (TKS) is a form of
social anxiety found in Japan, in which individuals are concerned about offending others
through their appearance or behavior.

Cultural factors that have been related to social anxiety disorder include a society's attitude
towards shyness and avoidance. American children appear more likely to develop social
anxiety disorder if their parents emphasize the importance of others' opinions and use
shame as a disciplinary strategy (Leung et al., 1994), but this association was not found for
Chinese/Chinese-American children. In China, research has indicated that shy-inhibited

9
children are more accepted than their peers and more likely to be considered for leadership
and considered competent, in contrast to the findings in Western countries.

Treatment
Cognitive Behavioral therapies:
Cognitive restructuring techniques have been also used. Here a therapist attempts to help
clients having social phobias by identifying their underlying negative thoughts (“I have got
nothing interesting to say”, or “no one is interested in me”) which are generally irrational.
After helping clients understand these cognitive distortions the client helps the clients to
change their inner thoughts through logical reanalysis.

10
 PANIC DISORDER
A person with panic disorder may have repeated panic attacks in which a person feels
sudden over-whelming fright, usually without any reasonable cause. A panic attack is
generally accompanied by physical symptoms, such as a pounding heart, sweating, and
rapid breathing.

Case history

Simon, a 23 year old male, was a victim of repeated panic attacks with agoraphobia. He
complaints of sudden acute palpitations, vertigo, breathlessness, dizziness, restlessness,
nausea and headache, At least three times a month Simon notices palpitations and becomes
frightened that these palpitations signal a heart attack. He is unable to leave home alone
without his mobile phone and cannot go to busy places such as shopping centers or cinemas
for fear of panic.

DSM-5 criteria/Symptoms/Clinical picture

A. Recurrent unexpected ‘panic attacks’. A panic attack is an abrupt surge of intense
fear or intense discomfort that reaches a peak within minutes, and during which
time four (or more) of the following symptoms occur:

Mnemonic device: STUDENTS FEAR the 2 Cs:

• (STUDENTS )

1. Sweating,
2. Trembling,
3. Unsteadiness/dizziness,
4. Derealization (feelings of unreality) or depersonalization (being detached
from oneself)
5. Elevated heart rate (tachycardia),
6. Nausea,
7. Tingling or numbness (Paresthesias)
8. Shortness of breath,

1
 • (FEAR)

9. FEAR of dying,
10. FEAR of losing control,
11. FEAR of choking,
• ( 2 Cs)
12. Chest pain,
13. Chills or heat sensations

B. At least one of the attacks has been followed by 1 month (or more) of one or both
of the following:

1. Persistent concern or worry about additional panic attacks or their

consequences (e.g., losing control, having a heart attack, “going crazy”). The
worries about panic attacks or their consequences usually pertain to physical
concerns, such as worry that panic attacks reflect the presence of life-threatening
illnesses (e.g., cardiac disease, seizure disorder); social concerns, such as
embarrassment or fear of being judged negatively by others because of visible
panic symptoms; and concerns about mental functioning, such as “going crazy”
or losing control.

2. A significant maladaptive change in behavior related to the attacks (e.g.,

behaviors designed to avoid having panic attacks, such as avoidance of exercise
or unfamiliar situations). The maladaptive changes in behavior represent
attempts to minimize or avoid panic attacks or their consequences. Examples
include avoiding physical exertion, restricting usual daily activities, and
avoiding agoraphobia-type situations, such as leaving home, using public
transportation, or shopping. If agoraphobia is present, a separate diagnosis of
agoraphobia is given.

C.) Exclusion criteria 1: Symptoms not related to another disorder

D.) Exclusion criteria 2: Not due to drug abuse or GMC.

DSM -5 definition of panic attack

Panic disorder refers to recurrent unexpected panic attacks (Criterion A). The essential
feature of a panic attack is an abrupt surge of intense fear or intense discomfort that reaches
a peak within minutes and during which time four or more of 13 physical and cognitive
symptoms occur.

2
• For a diagnosis of panic disorder, the panic attacks need to be recurrent and
unexpected. Cultural interpretations may influence the assignment of panic
attacks as expected or unexpected.
✓ The term recurrent literally means more than one unexpected panic attack.
The frequency and severity of panic attacks vary widely. In terms of
frequency, there may be moderately frequent attacks (e.g., one per week)
for months at a time, or short bursts of more frequent attacks (e.g., daily)
separated by weeks or months without any attacks or with less frequent
attacks (e.g., two per month) over many years. In terms of severity,
individuals with panic disorder may have both full-symptom (four or more
symptoms) and limited-symptom (fewer than four symptoms) attacks, and
the number and type of panic attack symptoms frequently differ from one
panic attack to the next.
✓ The term unexpected refers to a panic attack for which there is no obvious
cue or trigger at the time of occurrence—that is, the attack appears to occur
from out of the blue, such as when the individual is relaxing or emerging
from sleep (nocturnal panic attack). In contrast, expected panic attacks are
attacks for which there is an obvious cue or trigger, such as a situation in
which panic attacks typically occur.

• Eleven of these 13 symptoms are physical (e.g., palpitations, sweating), while

two are cognitive (i.e., fear of losing control or going crazy, fear of dying).
Because most symptoms of a panic attack are physical, it is not surprising that
as many as 85 percent of people having a panic attack may show up repeatedly
at emergency rooms or physicians’ offices for what they are convinced is a
medical problem—usually cardiac, respiratory, or neurological.

• A panic attack can arise from either a calm state or an anxious state, and can
return to either an anxious state or a calm state and possibly peak again.

• A panic attack is distinguished from ongoing anxiety by its time to peak

intensity, which occurs within minutes; its discrete nature; and its typically
greater severity.

• Attacks that meet all other criteria but have fewer than four physical and/or
cognitive symptoms are referred to as limited-symptom attacks

• There are two characteristic types of panic attacks: expected and unexpected.
Expected panic attacks are attacks for which there is an obvious cue or trigger,
such as situations in which panic attacks have typically occurred. Unexpected

3
 panic attacks are those for which there is no obvious cue or trigger at the time
of occurrence (e.g., when relaxing or out of sleep [nocturnal panic attack]). For
Panic disorder diagnosis, the attacks need to be unexpected.

Prevalence, Development and Course

Prevalence In the general population, 12-month prevalence estimates for panic attacks in
the United States is 11.2% in adults. The mean age at onset for panic attacks in the United
States is approximately 22–23 years among adults. However, the course of panic attacks is
likely influenced by the course of any co-occurring mental disorder(s) and stressful life
events. Panic attacks are more common in females than in males, but clinical features or
symptoms of panic attacks do not differ between males an

Although panic attacks themselves appear to come “out of the blue,” the first one frequently
occurs following feelings of distress or some highly stressful life circumstance such as loss
of a loved one, loss of an important relationship, loss of a job, or criminal victimization.

Panic attacks are uncommon, and unexpected panic attacks are rare, in preadolescent
children. Older individuals with “panicky feelings” may have a hybrid of limited-symptom
attacks and generalized anxiety. In addition, older individuals tend to attribute panic attacks
to certain situations that are stressful (e.g., medical procedures, social settings) and may
retrospectively endorse explanations for the panic attack even if it was unexpected in the
moment. This may result in under-endorsement of unexpected panic attacks in older
individuals.

Cultural syndromes also influence the cross-cultural presentation of panic attacks, resulting
in different symptom profiles across different cultural groups. Ataque de nervios (attack of
nerves) is a cultural syndrome among Latin Americans that may involve trembling,
uncontrollable screaming or crying, aggressive or suicidal behavior, and which may be
experienced for longer than only a few minutes.

Also, cultural expectations may influence the classification of panic attacks as expected or
unexpected, as cultural syndromes may create fear of certain situations, ranging from
interpersonal arguments, to types of exertion, to atmospheric wind.

Panic attacks are associated with increased likelihood of various comorbid mental
disorders, including anxiety disorders, depressive disorders, and bipolar disorders.

Distinguishing features of panic and anxiety

4
 • The panic attack is distinguished from other forms of anxiety by its intensity and
its sudden, episodic nature.

• Anxiety in contrast to panic is more complex blend of emotions (negative affect)

and cognitions (e.g., worry about future threat and preparation of dealing with this
danger).

• The panic attacks may occur in relaxed situations, sleep (nocturnal panic) or may
be “situationally predisposed”.

Causal factors/ETIOLOGY/ Dynamics

Biological Causal Factors

Genetic Factors. According to family and twin studies, panic disorder has a moderate
heritable component (e.g., Norrholm & Ressler, 2009). In a large twin study, Kendler and
colleagues (2001) estimated that 33 to 43 percent of the variance in liability to panic
disorder was due to genetic factors. Recently, several studies have begun to identify which
specific genetic polymorphisms are responsible for this moderate heritability (e.g., Strug
et al., 2010), either alone or in interaction with certain types of stressful life events (e.g.,
Klauke et al., 2010), but this preliminary work needs to be replicated.

As noted earlier, this genetic vulnerability is manifested at a psychological level at least

in part by the important personality traits called Behavioral Inhibition and Neuroticism
(which is in turn related to the temperamental construct of behavioral inhibition).

Some studies have suggested that this heritability is at least partly specific for panic
disorder (rather than for all anxiety disorders), but one large female twin study suggested
that there is overlap in the genetic vulnerability factors for panic disorder and phobias
(Kendler, Walters, et al., 1995). People with a history of social or specific phobia are at
heightened risk for developing panic disorder (Biederman et al., 2006). However, another
study suggests overlap in the genetic vulnerability for panic disorder, generalized anxiety
disorder, and agoraphobia (Hettema, Prescott, et al., 2005). Only further research can
resolve these inconsistencies in findings (e.g., Norrholm & Ressler, 2009)

5
Panic and the brain.

Locus Ceruleus and Norepinephrine. Located in the brainstem, the locus

coeruleus (blue in colour) is the brain’s major source of norepinephrine, a neurotransmitter
that triggers the body’s fight-or-flight response. Activation of the locus coeruleus is
associated with anxiety and fear, and research with nonhuman primates has shown that
stimulating the locus coeruleus either electrically or through drugs produces panic-like
symptoms. Research indicates that people having panic attacks may have an unusually
sensitive LC.

Amygdala. The amygdala which is part of the limbic system (processes emotions) is
involved in processing fearful and threatening stimuli, including detection of threat and
activation of appropriate response to threatening or dangerous stimuli. Today it is
recognized that it is increased activity in the amygdala that plays a more central role in
panic attacks than does activity in the locus coeruleus. Stimulation of the central nucleus
of the amygdala is known to stimulate the locus coeruleus as well as behavioral responses
that occur during panic attacks. Other recent research has also implicated the
periaqueductal gray area in the midbrain.

Fear network: Today, scientific evidence indicates that anxiety is the result of connections
between a number of different brain regions — a fear network. No one brain region drives
anxiety on its own. Instead, interactions among many brain areas are all important for how
we experience anxiety. This theory posits that the behavioral symptoms of panic disorder
are mediated by a fear network in the brain, which is centered in the amygdala (part of

6
limbic system) and includes locus coeruleus (lower brain centre), as well as prefrontal
cortex (higher brain centre) and hippocampus. According to this view, panic attacks occur
in people who have an abnormally sensitive fear network that gets activated too readily
activated. Abnormally sensitive fear networks may have a partially heritable basis but may
also develop as a result of repeated stressful life experiences, particularly early in life.
(Gorman, et al., 2000).

According to this theory, panic attacks may arise from abnormal activity in the amygdala.
The anticipatory anxiety and that people develop about having another panic attack
is thought to arise from activity in the hippocampus of the limbic system, which is known
to be involved in the learning of emotional responses. Agoraphobic avoidance, also a
learned response, may also involve activity of the hippocampus and higher cortical centers
(Gorman et al., 2000).

Biochemical Abnormalities & Klein's theory of false suffocation alarm. Over 30 years
ago, Klein (1981) and others (Sheehan, 1982, 1983) argued that panic attacks are alarm
reactions caused by biochemical dysfunctions. This theory was supported by ‘biological
challenge’ procedures. ‘Biological challenge’ procedures are experimental procedures
which produce intense physical sensations, and provoke panic attacks far more often in
panic patients than in patients with other disorders or in healthy volunteers. The biological

7
agents used in these experimental procedures include sodium lactate, caffeine, and carbon
dioxide.

Pitts and McClure (1967) were the first researchers to demonstrate that panic attacks could
be induced in the laboratory by sodium lactate injections. Pitts and McClure (1967)
observed that standard exercise produced characteristic anxiety symptoms (such as
increased heartbeat, increased blood pressure etc.). They hypothesized, that these anxiety
symptoms might have been due to an extremely rapid rise of blood lactate acid occurring
as a consequence of the exercise. Its presence is a sign that the body is straining to meet
oxygen needs. Later, in a classic study Pitts and McClure demonstrated that sodium lactate
injections given to subjects in the lab precipitated panic itself in about four-fifths of people
with panic disorder but only one-fifth of the general population. Lactate sensitivity might
be a sign of genetic susceptibility to panic attacks.

The data generated by the challenge paradigm have been interpreted in two principal ways.
One view holds that challenges directly provoke panic by exacerbating a neurobiological
dysfunction. According to this theory, the norepinephrine system (controlled by SNS) in
the locus ceruleus is unusually sensitive in persons with panic disorder. Thus, according to
this theory, some biological agents (such as lactate and carbon dioxide) cause changes in
either the body or the brain that indirectly activate the norepinephrine system in the locus
ceruleus, precipitating a panic attack. The other cognitive view holds that they provoke
attacks by producing bodily sensations that panic patients are prone to fear, perhaps
because they interpret them as harbingers of imminent catastrophe.

Later research revealed that patients with disorders other than panic disorder, and even
some people free of any disorder, can also give similar responses to the test. Furthermore,
the original idea, that most panic disorder patients have attacks when given sodium lactate,
had to be revised; the revised estimates were that roughly 50% of panic disorder patients
give this response, rather than the 85% originally thought to do so.

Neurotransmitters: There is abundant evidence for abnormalities of the norepinephrine

and serotonin neurotransmitter in anxiety disorders. The majority of evidence supports
reduced serotonin and increased noradrenaline in panic disorders. Increased noradrenaline
in turn increases cardiovascular symptoms associated with panic (Gorman et al., 2000).
Increased serotonin also decreases noradrenaline.

This fits with results showing that the selective serotonin reuptake inhibitors—SSRIs
medicines increase serotonin but also decrease noradrenaline and hence are effective. By

8
decreasing noradrenaline, these medications decrease many of the cardiovascular
symptoms associated with panic that are ordinarily stimulated by noradrenaline (Gorman
et al., 2000).

Dysregulation in GABA might contribute to panic disorder. For example, lowered brain
GABA levels are associated with anxiety like behaviors in animals.

Comprehensive Learning Theory of Panic Disorder (conditioning theories). Certain

investigators have proposed a comprehensive learning theory of panic disorder that
accounts for most of the known findings about panic disorder.

Some of the earlier conditioning theories of PD (Antony and Barlow, 1996) suggested that
panic attacks become classically conditioned to internal bodily sensations of anxiety. PD
according to this theory involves a fear of interoceptive fears – that is a fear of internal
bodily sensations. This has been the result of interoceptive conditioning in which various
internal bodily sensations that have been associated with panic attacks acquire the capacity
to provoke panic. For e.g. heart palpitations may occur at the beginning of a full blown
attack and because they become predictors of a full blown attack they may acquire the
capacity to provoke panic.

Bouton, Mineka, and Barlow’s propose the Modern Learning Theory (200) where they
have expanded the above view. The model has 3 components:

1. Conditioning: In learning theory terminology, when the adverse

unconditioned stimulus (US), the panic attack, is paired with previously
innocuous exteroceptive (environmental) and/or interoceptive (visceral)
conditioned stimuli (CS), an association is learned such that the CS alone
can trigger anxiety and panic when reencountered. Interoceptive and
exeroceptive conditioning can occur to multiple different kinds of cues,
ranging from heart palpitations and dizziness to shopping malls.
2. Anticipatory anxiety and Agoraphobic behaviors: Conditioning to
exteroceptive (external) stimuli therefore can result in agoraphobic
behaviors.
3. Panic attacks: Conditioning to interoceptive (internal) cues can result in
seemingly spontaneous or out-of-the-blue panic attacks or heightened
anxiety on future encounters with similar visceral stimuli.
The elicitation of this conditioned anxiety may potentiate further panic attacks in a vicious
cycle, leading to PD.

9
For example, one young man with panic disorder who was particularly frightened of signs
that his heart was racing experienced a surprising and unexpected panic attack after hearing
that his favorite presidential candidate had won. The panic attack thus occurred when he
was happy and excited (which is what made it so surprising for him). However, from the
standpoint of this theory, the attack was actually not surprising. Because the man was
excited, his heart was racing, which probably served as an internal CS that triggered the
panic (Mineka & Zinbarg, 2006).

Cognitive theories of Panic

Catastrophic thinking (Beck and Emery, 1985; Clark, 1986). According to Clark’s
theory, individuals with panic disorder have a tendency to misinterpret certain bodily
sensations in a ‘catastrophic fashion’ or in a much more dangerous manner than they really
are. For example, palpitations may be misinterpreted as evidence of an impending serious
heart attack. A slight breathing difficulty may be misperceived as impending serious
respiratory failure and consequent death. A shaky feeling may be misinterpreted as losing
control of oneself or going mad.

The cycle is believed to operate this way:

1. Anxiety related bodily sensation (e.g. irregular breathing) caused by some worry,
an unpleasant mental image, or a minor illness.
2. The person responds to the anxiety related sensation by becoming anxious.
3. This results in catastrophic thoughts. The person thinks "I am having a heart
attack" or "I am going insane," or some similar thought. The person is not
necessarily aware of making these catastrophic interpretations; rather, the
thoughts are often just barely out of the realm of awareness (Rapee, 1996). These
automatic thoughts, as Beck calls them, are in a sense the triggers of panic.
4. This leads to more anxiety and as the vicious cycle continues, a panic attack
results. The whole cycle might take only a few seconds, and the individual may
not be aware of the initial sensations or thoughts.
This kind of catastrophic thinking might be due to faulty learning (such as observing
parents having a panic attack). It has also been suggested that this thinking may develop as
a result of how significant others and doctors react to the attack.

The Panic Circle:

10
Evidence: Quite a bit of evidence exists for this theory. For example, activating
catastrophic misinterpretations by simply having clients read aloud pairs of words such as
“palpitations-dying”, “breathless – suffocate” increased anxiety and panic in persons
suffering from panic (Clark, 1997).

Criticisms

• One issue concerned whether catastrophic interpretations cause the attack or simply
occur together with a panic attack. For example, some patients report experiencing
catastrophic thoughts after the panic.
• Another issue concerned whether catastrophic misinterpretations are necessary for
panic to occur. Several studies suggest that full-blown panics may occur in the
apparent absence of catastrophizing (e.g., Aronson, Whitaker- Azmitia, & Caraseti,
1989
• The occurrences of panic attacks that erupt during sleep pose another challenge to
Clark's central hypothesis.

Anxiety sensitivity (AS) theory (Reiss, 1991): Not everyone is equally likely to
misinterpret bodily sensations as catastrophic. Some people may be more predisposed to
making such misinterpretations. Such people may have anxiety sensitivity. Anxiety
sensitivity, as defined by Reiss and McNally (1985), is a personality trait that predisposes

11
the person toward fearing anxiety-related bodily sensations, arising from beliefs that these
sensations have harmful consequences. Such a person would endorse statements such as,
“When I notice that my heart is beating rapidly, I worry that I might have a heart attack.”

Perceived control and safety: Studies indicate that persons with panic disorders
perceived less control in the situation as compared to normal individuals (Rapee and
Barlow, 1989). In yet another study half of the people who suffered from PD could bring
a “safe person’ in the lab while the other half could not. Those who could bring a “safe
person” experienced less distressed when inhaling a panic provoking agent like CO2.

Safety Behaviors and persistence of panic: Seligman (1988) proposed that it was not
possible that people who have survived recurrent attacks would continue to misinterpret
bodily sensations catastrophically. If the cognitive theory were correct, Seligman argued,
catastrophic beliefs should have long been refuted for people who have had many attacks
yet no catastrophes. However, some people have had thousands of panic attacks and each
time believe that they are having a heart attack. This catastrophic thought does not seem to
go away. Recent evidence indicates that panic clients frequently engage in “safety
behaviors” before or during the attack and they tend to attribute the lack of catastrophe to
their having engaged in “safety behaviors”. Safety behaviors are “behaviors which are
intended to avoid disaster.” Examples include checking to make sure that a bathroom or
hospital is close by, taking one’s pulse rate whenever cardiac concerns arise, and carrying
cell phones, religious symbols, smelling salts, a special “safe” object, food or drink.
Perhaps the most common safety behavior is carrying anti-anxiety medication, including
empty pill bottles. Another widespread behavior is bringing along or checking on the
location of a safe person, often a spouse, whose presence provides a sense of reassurance
that facilitates venturing out to places that otherwise would be avoided. The “safe” person
is generally considered as such because they know about the patient’s panic attacks and
can assist if the panic attack becomes overwhelming. For e.g., Simon who thinks he is
having a heart attack during a panic attack slows down his breathing, leans against solid
objects and thinks that he has saved himself from a heart attack.

Temperamental Factors. According to some researchers there may be many

temperamental factors related to PD some of which may be the result of genetic factors but
not necessarily so. The temperament most associated with anxiety disorders, including
panic disorder, is neuroticism (Eysenck, 1967; Gray, 1982), or proneness to experience
negative emotions in response to stressors. A closely linked construct, “negative
affectivity,” is the tendency to experience a variety of negative emotions across a variety
of situations, even in the absence of objective stressors (Watson & Clark, 1984).

12
“Fear of Fear” hypothesis (Goldstein and Chambless, 1978). According to “fear of fear”
(Goldstein and Chambless, 1978) theory, people suffering from panic disorder have a fear
of anxiety related sensations. They respond to these sensations with anxiety and this further
increases the unpleasant sensations leading to more anxiety and this cycle continues till a
panic attack occurs (i.e., panic cycle).

This “fear of fear” should be contrasted from the earlier theory of catastrophic thinking by
Clark, 1997. “Fear of fear” may develop due to two factors i.e. misinterpretations
(cognitive factor as emphasized by Clark, 1997) or may be due to noncognitve factors such
as conditioning which are not taken into account by the earlier theory but are emphasized
by Barlow (1996).

Cognitive biases: There is evidence to indicate that persons suffering from PD are more
prone to interpreting ambiguous information as threatening (Clark, 1977). There is also
evidence to indicate that their attention is drawn more towards threatening information
especially physical threat and that they are very good at detecting their heart beats
(McNally, 1994). One study using fMRI techniques demonstrated that people with panic
disorder showed greater activation to threat words than did normals in brain areas involved
in memory processing of threatening material (Maddock et al., 2003). Whether these
information-processing biases are present before the disorder begins and help to cause it is
as yet unclear, but these biases are certainly likely to help maintain the disorder once it has
begun. For example, having one’s attention automatically drawn to threatening cues in the
environment is likely to provoke more attacks.

Three Vulnerability Factors: Combining research- Several independent lines of

research (Barlow, 1988; Clark, 1986; Ehlers & Margraf, 1989) converged in the 1980s on
the same basic conceptualization of panic disorder as an acquired fear of bodily sensations,
particularly sensations associated with autonomic arousal. Psychological and biological
predispositions are believed to enhance the vulnerability to acquire such fear. These
interacting vulnerabilities have been referred to as “triple vulnerability theory” (Barlow,
1988, 2002).

• Biological vulnerability: First, genetic contributions to the development of anxiety

and negative affect constitute a generalized (heritable) biological vulnerability.

• Psychological vulnerability: Second, evidence also supports a generalized

psychological vulnerability to experience anxiety characterized by a diminished
sense of control arising from early developmental experiences.

• Specific psychological vulnerability: A third factor refers to a specific

13
 psychological vulnerability i.e. early learning experiences as a result of which the
experience of certain somatic sensations becomes associated with a heightened
sense of threat and danger.

THERAPIES FOR PANIC DISORDER:

Biological treatment:

• Anti-anxiety drugs or anxiolytic drugs (benzodiazepines such as Xanax) : these

drugs are taken during or at the onset of panic attacks. One major advantage of
these drugs is that they act very quickly (30–60 minutes) and so can be useful in
acute situations of intense panic or anxiety. However, no benefit is realized by their
regular use (except where panic episodes are experienced regularly), and these
drugs may be habit forming. They are often most effective at the beginning of
treatment when the resistance properties of the antidepressants have not yet built
up, and are generally utilized less and less as other parts of the treatment
(antidepressants, psychotherapy) become more effective. Withdrawal from these
drugs can be very slow and difficult, and it precipitates relapse in a high percentage
of cases.
• Antidepressants (including primarily the tricyclics, SSRIs and most recently the
serotonin-norepinephrine reuptake inhibitors—SNRIs): these are taken regularly
every day, and build a resistance to the occurrence of the symptoms. Although these
medications are described as "antidepressants," nearly all of them have anti-panic
properties as well - many panic sufferers do not have classical symptoms of
depression, and may be misled by the name "antidepressant" into believing these
drugs are not targeted to their symptoms, when they are often the most effective
treatment in combination with psychotherapy. One major advantage is that they do
not create physiological dependence in the way benzodiazepines can, and they also
can alleviate any comorbid depressive symptoms or disorders. However, it takes
about 4 weeks before they have any beneficial effects, so they are not useful in an
acute situation where a person is having a panic attack. Troublesome side effects
(such as dry mouth, constipation, and blurred vision with the tricyclics, and
interference with sexual arousal with the SSRIs) mean that large numbers of people
refuse to take the medications or discontinue their use.

Today the SSRIs are more widely prescribed than the tricyclics because the SSRIs are
generally better tolerated by most patients. Moreover, both are generally preferred by
physicians to benzodiazepines because of the risks associated with the latter ( Roy-Byrne
& Cowley, 2007 ).

14
Psychological treatment:

Behavioral and cognitive therapies. The original behavioral treatment for agoraphobia
from the early 1970s involved prolonged exposure to feared situations, often with the help
of a therapist or family member. Similar to what is done with specific and social phobias,
the idea was to make people gradually face the situations they feared and learn that there
was nothing to fear. One limitation of these original treatments was that they did not
specifically target panic attacks. In the mid-1980s, two new techniques were developed as
clinical researchers increasingly recognized the importance of panic attacks to most people
with agoraphobia.

One technique involves the variant on exposure known as interoceptive exposure , meaning
deliberate exposure to feared internal sensations. The idea was that fear of these internal
sensations should be treated in the same way that fear of external agoraphobic situations is
treated—namely, through prolonged exposure to those internal sensations so that the fear
may extinguish. For example, people are asked to engage in various exercises that bring on
various internal sensations (e.g., spinning in a chair, hyperventilating, running in place)
and to stick with those sensations until they subside, thereby allowing habituation of their
fears of these sensations.

The second set of techniques that were developed is cognitive restructuring techniques, in
recognition that catastrophic automatic thoughts may help maintain panic attacks. One kind
of integrative cognitive-behavioral treatment for panic disorder— panic control treatment
—targets both agoraphobic avoidance and panic attacks. There are several aspects to PCT.
First, clients are educated about the nature of anxiety and panic and how the capacity to
experience both is adaptive. A second part of the treatment involves teaching people with
panic disorder to control their breathing. Third, clients are taught about the logical errors
that people who have panic disorders are prone to making and learn to subject their own
automatic thoughts to a logical reanalysis. Finally, they are exposed to feared situations
and feared bodily sensations to build up a tolerance to the discomfort.

What about the combination of antianxiety medication and cognitive-behavioral therapy?

In the short term, such combined treatment sometimes produces a slightly superior result
compared to either type of treatment alone (Barlow et al., 2007; Mitte, 2005). However, in
the long term, after medication has been tapered (especially benzodiazepine medications),
clients who have been on medication with or without cognitive or behavioral treatment
seem to show a greater likelihood of relapse (Arch & Craske, 2008;). Perhaps this is
because they have attributed their gains to the medication rather than to their personal

15
efforts (Başoğlu et al., 1994; Mitte, 2005). The one medication that has shown promise for
enhancing responsiveness to CBT of panic disorder is D-cyloserine.

16
 Generalized anxiety disorder
UNIT 2
Anxiety disorders (clinical picture & etiology):

a) Generalized anxiety disorder

b) Specific Phobias and Social Anxiety Disorder (social phobia)
c) Panic Disorder

Nervous system

The human nervous system is composed of two parts:

 Central nervous system, which includes the brain and spinal cord and controls activities such
as memory and concentration, sleep, muscle movement etc
 Peripheral nervous system, which is composed of nerves that extend outside of the central
nervous system. The PNS can be further divided into two different systems:
1. Somatic nervous system: The somatic system transmits sensory is responsible for
voluntary movement and carry sensory information to and from CNS and spinal cord.
2. The autonomic system or involuntary NS: This mainly controls functions over which
we have less conscious control such as digestion of food, BP and heart rate. The
autonomic system can be further subdivided into two subsystems known as the
sympathetic and parasympathetic systems.
 Generalized anxiety disorder
Anxiety disorders

Anxiety disorders all have unrealistic, irrational fears or anxieties of disabling intensity as their principal
and most obvious manifestation.

Experience of fear and anxiety:

The term anxiety is usually defined as a very unpleasant feeling or apprehension accompanied by
feelings of impending doom. It is free floating and not attached to a specific object (fear). Anxiety is
often distinguished from fear which is attached to a specific object. Also while anxiety is more future
oriented; fear is more present oriented or related to imminent danger. Lang (1968) classified the
symptoms of fear and anxiety into a system of three-responses: verbal-subjective, overt motor acts, and
somato-visceral activity. In this system, the symptoms of anxiety and fear include

 (verbal-subjective), Worry involves thoughts of future threat. It involves ‘self talk’ is

considered the cognitive element of anxiety. In case of fear it involves fear of imminent threat
 (overt motor acts): Worry involves thoughts avoidance and while fear involves escape
 (somato-visceral activity). In case of anxiety there is a central nervous system hyperarousal
leading to hyperalertness (‘hypervigilance’). This can cause symptoms such as restlessness, and
muscle tension. In case of fear there is the Autonomic hyperarousal (peripheral nervous system)
resulting in overstimulation of the sympathetic system leading to physical symptoms such as
sweating, trembling, heart palpitations, and nausea. This system is associated with ‘flight’ or
‘fight’ reaction.

Fear and anxiety overlap to some extent across anxiety disorders. While specific phobia could be viewed
as the archetype of a ‘fear disorder’, GAD is the prototype of an ‘anxiety disorder’. However, other
disorders are characterized by symptoms of both fear and anxiety (e.g. panic disorder).

Normal versus abnormal anxiety response: Anxiety is a natural and a necessary response to threat or
stress as it alerts the person to carry out certain acts that reduce the danger (e.g. working hard for the
exam). However, anxiety can become a pathologic disorder when it is ‘excessive and uncontrollable’
i.e., if it is developmentally inappropriate (e.g., fear of separation in a 10-year-old child) or if it is
inappropriate to an individual's life circumstances (e.g., worries about unemployment in a successful
business executive).

DSM-5 anxiety disorders

1. Generalized Anxiety Disorder
2. Panic Disorder
3. Specific Phobia
4. Social Anxiety Disorder (Social Phobia)
5. Panic Attack (Specifier)
6. Separation Anxiety Disorder
7. Selective Mutism
8. Agoraphobia
9. Substance/Medication-Induced Anxiety Disorder
10. Anxiety Disorder Due to Another Medical Condition
11. Other Specified Anxiety Disorder
12. Unspecified Anxiety Disorder

ICD: Anxiety or fear-related disorders

(6B00-6B0Z)

1. Generalised anxiety disorder (6B00)

2. Panic disorder (6B01)
3. Agoraphobia (6B02)
4. Specific phobia (6B03)
5. Social anxiety disorder (6B04)
6. Separation anxiety disorder (6B05)
7. Selective mutism (6B06)
8. Other specified anxiety or fear-related disorders (6B0Y)
9. Anxiety or fear-related disorders, unspecified (6B0Z)

Changes from DSM 1V to DSM V

1. Disorders excluded from anxiety disorders in DSM V: OCD (which is included with the obsessive-
compulsive and related disorders), PTSD and acute stress disorder are no longer included in Anxiety
disorders.

2. New disorders included in the category of anxiety disorders in DSM V Separation anxiety
disorder and selective mutism are now classified as anxiety disorders.

CASE STUDY:
Jim is a 31 year old successful salesman. He complains of muscle tension, headaches, and difficulty
sleeping. He worries about not having enough money for his family in the event he dies suddenly or is
fired from his job. He worries about job stability and feels he would be unable to get another job that
paid as well. He has elevated blood pressure, heart palpitations, and has missed several work deadlines.
The Anxiety Disorders

These disorders are characterized by excessive anxiety, and fear. Fear and anxiety overlap to some
extent across anxiety disorders. While specific phobia could be viewed as the archetype of a ‘fear
disorder’, generalized anxiety disorder is the prototype of an ‘anxiety disorder’. However, other
disorders are characterized by symptoms of both fear and anxiety. For e.g., a hallmark of panic disorder
is the experience of panic attacks, episodes of a surge of extreme fear with a feeling of impending doom.
But another key element is anxiety, caused by persistent symptoms of apprehensive anticipation and
continuous worry focused on the reoccurrence of future panic attacks. This section provides a brief
summary of the diagnostic criteria for each of the six main anxiety disorders.

1. Generalized Anxiety Disorder (GAD): The main feature of generalized anxiety disorder is
excessive worry about a number of different domains or activities (e.g., work, finances, family,
and health). The worry must be experienced as difficult to control and be associated with at
least three of six symptoms, which include restlessness, fatigue, impaired concentration,
irritability, muscle tension, and impaired sleep.
2. Panic Disorder: A person with panic disorder has repeated panic attacks. Many sufferers of a
panic attack believe they are dying, going insane or having a heart attack (“catastrophic
thoughts”).
3. Agoraphobias it is the fear of situations where escape is difficult.
4. Specific Phobias: A phobia is an irrational fear that produces a conscious avoidance of the
feared object. Specific phobias (formerly known as “simple phobias”) - fear of specific objects
such as snakes, heights
5. Social anxiety disorder – Social phobia is an excessive or unrealistic fear of social situations.
6. Selective mutism (SM) is a psychiatric disorder in which a person who is normally capable
of speech is unable to speak in given situations or to specific people. Selective mutism usually
co-exists with shyness or social anxiety.
7. Separation anxiety disorder (SAD) is a psychological condition in which an individual
experiences excessive anxiety regarding separation from home or from people to whom the
individual has a strong emotional attachment (e.g. a parent, grandparents, or siblings).
8. Other specified anxiety or fear-related disorders: Patients who have prominent
symptoms of anxiety that don’t meet criteria for any specific anxiety disorder can be
coded as having other specified anxiety disorder—and the reason for not including them
in a better-defined category should be stated. DSM-5 suggests several different
possibilities: Insufficient symptoms. This would include panic attacks or GAD with too
few symptoms; presentation is atypical; cultural syndromes. DSM-5 mentions several
in an appendix.
 Generalised anxiety disorder

GAD: Clinical picture/ symptoms

(Clinical picture refers to what does GAD look like? It includes both subjective as well as objective
symptoms. DSM criteria are more objective criteria.)

The core symptom of GAD is excessive anxiety in the form of worry about a numer of activities. Worry
which involves ‘self talk’ is considered the cognitive element of anxiety. Patients who have GAD tend
to worry ‘excessively’ about many common problems - employment, finances, the health and safety of
family and friends, and the ability to complete chores and errands on time, to give just a few examples.
Often, when asked what they worry about, GAD clients will reply: "What don't I worry about?"

Several features distinguish GAD from nonpathological anxiety.

 Worries associated with GAD are excessive and typically interfere significantly with
psychosocial functioning
 Worries associated with GAD are more pervasive, pronounced, and distressing; have longer
duration; and frequently occur without precipitants.
 Worries associated with GAD are more likely to be accompanied by physical symptoms (e.g.,
restlessness or feeling keyed up or on edge).

DSM -5 criteria

A. Excessive anxiety and worry (apprehensive expectation), occurring more days than not
for at least 6 months, about a number of events or activities (such as work or school
performance).
B. The individual finds it difficult to control the worry
C. The anxiety and worry are associated with three (or more) of the following six somatic
symptoms (with at least some symptoms present for more than 6 months).
Note: Only one item is required in children.
(Mnemonic Device: Mr. Fisc" 3/6- The patient has 3 symptoms for a period of 6 months)
1. M=muscle tension,
2. R=restlessness,
3. F=fatigue,
4. I=irritability,
5. S=sleep (difficulty falling asleep),
6. C=concentration (difficulty concentrating)
D. Social/occupational dysfunction
E. Exclusion criteria 1: Symptoms not related to drug abuse or GMC (e.g.,
hyperthyroidism).
F. Exclusion criteria 2: Not due to another mental disorder (general medical condition).

Associated Features
Associated with muscle tension, there may be trembling, twitching, feeling shaky, and muscle
aches or soreness. Many individuals with GAD also experience somatic symptoms (e.g.,
sweating, nausea, diarrhea) and an exaggerated startle response. Symptoms of autonomic
hyperarousal (e.g., accelerated heart rate, shortness of breath, dizziness) are less prominent in
GAD than in other anxiety disorders, such as panic disorder. Other conditions that may be
associated with stress (e.g., irritable bowel syndrome, headaches) frequently accompany
generalized anxiety disorder.

Prevalence & Age of onset

 Although patients with GAD do not typically seek psychological treatment, the life time
prevalence of this disorder is fairly high. It occurs in about 5 % of the general population
(Kessler, 1994).

 Age of onset is difficult to determine with 60 to 80 % stating that they remember being
anxious all their lives.

 Gender differences: It is twice as common in women as in men (Brown, ‘2001).

 The course of GAD is chronic but fluctuating and often worsen during times of stress (Barlow
et al, al’86).

Comorbidity with other disorders

GAD often co-occurs with other disorders especially other anxiety (such as phobias, panic disorders)
and mood disorder (such as depression).

Etiology/causal factors/dynamics

Psychological Causal Factors

Psychoanalytic Viewpoint: The psychoanalytic theory regards the source of generalized anxiety as a
conflict between unconscious sexual or aggressive urges and corresponding threats from the superego.
As a child Jim had been told that sex was dirty. As he grew up he had normal sexual thoughts towards
the opposite sex. This led to an intense conflict and anxiety. This leads to anxiety. The ego then
mobilizes defence mechanisms to deal with this anxiety. However, in case of GAD the person is unable
to use defense mechanisms if s/he experiences frequent and extreme levels of anxiety. It is also
hypothesized that patients having GAD have weak egos due to separation and loss. Unfortunately this
viewpoint is not testable and has therefore been largely abandoned among clinical researchers

Cognitive View: Cognitive theorists maintain that certain patterns of thinking and schemas make
some people particularly vulnerable to anxiety disorders. They point to the following factors:

Perceptions of Uncontrollability and Unpredictability:

  A number of researchers have suggested that people with GAD may have a history of
experiencing many important events in their lives which are uncontrollable and unpredictable.
For e.g., Jim had a mother who had unpredictable moods and temper tantrums for trivial or
nonexistent reasons. There is some evidence that people with GAD may be more likely to have
had a history of trauma in childhood than individuals with several other anxiety disorder.

 Moreover, such unpredictable events may lead to a lack of safety signals and the person does
not know when it is appropriate to relax and feel safe leading to a sense of chronic anxiety and
hypervigilance.

 Intolerance of Uncertainty (IU) Model of GAD: People with GAD clearly also have far less
tolerance for uncertainty than nonanxious controls than people with panic disorder. This low
tolerance for uncertainty in people with GAD suggests that they are especially disturbed by not
being able to predict the future.

A Sense of Mastery: The Possibility of Immunizing Against Anxiety (Chorpita & Barlow, 1998)

On one end of a continuum, a sense of mastery or personal control is the belief that one can
master, control, and shape one’s own life. At the opposite end of the continuum is perceived
powerlessness, the belief that one’s life is shaped by external forces, such as luck, chance, fate,
or powerful others. High levels of sense of control are linked to an ability to take preventative
action and hence immunizes the person against anxiety. On the other hand, a sense of lack of
control results in anxiety (Chorpita & Barlow, 1998). One factor which may lead to a sense of
lack of control is parental anxiety. High parental anxiety may result in parental overcontrol of
the child i.e. excessive amount of involvement in a child's activities and an encouragement of
dependence on the parents. This serves only to promote their children’s anxious behaviors by
making them think of the world as an unsafe place in which they require protection and have
little control themselves (Craske & Waters, 2005).

Central role of worry and its cognitive function:

1. Positive functions of worry (Borkovec et al. theory of ‘benefit of worry’, 1994, 2006): This
states that worrying has several benefits that people with GAD most commonly think
are::

a. Superstitious avoidance of catastrophe (worrying makes the event less likely).

b. Avoidance of deeper emotional topics (“worrying helps me to avoid thinking
about deep emotional topics).
c. Coping and preparation (“worrying helps me to be prepared for the future”)

2. Cognitive theory of worry (Borkovec et al., 2007): Borkovec asserts that worry helps
such patients to avoid the experience of intense emotions which they find
overwhelming.
 Worry is a mental activity that predominantly involves ‘verbal thought’ and is less
characterized by ‘visual imagery’. ‘Verbal thoughts’ arouse less negative emotions, as
compared to ‘visual imagery’ of the same threatening material. One can understand this
by comparing ‘reading about an accident’ (similar to thinking or “worrying”) versus
‘looking at a photo’ (similar to ‘visual imagery’) of an accident scene. Clearly, the
pictorial version (visual imagery) arouses more emotions and hence more physiological
response/autonomic arousal.

According to this theory, once a distressing ‘visual imagery’ (internal or external) is

detected by a GAD patient it results in powerful negative emotions which the person
finds overwhelming. The individual tries to reduce the negative emotions by turning
attention from ‘visual imagery’ to ‘verbal thought’ (worry). This results in two
consequences.
a. First, ‘worrying in words” prevents the experience of powerful emotions.
b. Second, since the material is not processed fully (as emotional aspect is
not processed) therefore it does not allow the individual completely to
reduce emotional distress and "put it aside." The worrier engages in this
process again and again in an inadequate attempt to cope with aversive
experiences.

3. Negative functions of worry and vicious cycle of anxiety: In spite of these positive
functions that worry serves, some of its effects are clearly negative (Mineka, 2004).
Worry itself is certainly not an enjoyable activity and can actually lead to more anxiety
trapping the person in a vicious cycle of anxiety. Attempts to control worry may
paradoxically lead to increased experience of intrusive thoughts and this increases
perception of being powerless. This further leads to further worry, and so a vicious
circle of anxiety, worry, and intrusive thoughts may develop (Mineka, 2004)
 4. Well’s metacognitive theory of GAD: According to Wells (1999, 2002) metacognitive theory of
GAD, a distinguishing feature of pathological worry is the presence of type 2 or metaworry, that
is, worry about the negative consequences of the act of worrying itself. Wells (1995) has
identified two types of worry experienced by people with GAD: 1) Type 1 worry: these are typical
worries about everyday life worries about health, job, safety etc.). 2) Type 2 worry: this is ‘worry
about worry’ or ‘meta worry’ ('Worrying will drive me mad.’ 'I worry about my worries taking
me over’). Wells (1995) suggested that individuals with GAD are defined by high levels of
negative Type 2 worries.

Cognitive biases for threatening information: Beck’s (1976) cognitive theory of anxiety

Beck proposed that:

 Danger Schemas: Anxiety patients have maladaptive schemas. With generalised anxiety
disorder (GAD) the person has a ‘danger schema” i.e., the belief that "the world is a dangerous
place” and therefore one needs to be ‘hypervigilant’ for possible threat. For e.g., Jim has the
following danger schemas: “It is always best to assume the worst. My survival depends on
always being prepared for danger. Any strange situation should be regarded as dangerous.”
These danger schemas may result in various consequences:

 Effects on attention, memory and information processing: In addition, research has shown that
maladaptive thoughts significantly impact other cognitive domains such as attention, memory,
and information processing. Thus, anxious patients will attend to stimuli which present a
physical or psychological threat, ambiguous stimuli will be interpreted in a threatening fashion,
and threatening information will be retrieved readily from long-term memory. For e.g. in one
experiment (Eysenck et al, 1991) anxious and non anxious subjects were asked to read 32
sentences that could be interpreted in either a threatening or threatening manner. One such
sentence was “ The doctor examined little Emma’s growth” which could mean that the doctor
checked her height or the growth of tumor. The anxious participants interpreted the sentences
in a threatening manner (i.e. as a tumor) more often than non anxious patients
  Cognitive distortions: One of the important consequences of having maladaptive schemas is
that anxious patients are subject to a number of cognitive distortions. According to Beck (1976),
two cognitive distortions which are of particular importance are attention binding and
catastrophising. Attention binding involves a preoccupation with danger and an involuntary
focus on concepts related to danger and to threat. Catastrophising involves focusing on the
worst possible outcome of any given situation.

Humanistic perspective: Humanistic theorists propose that people with GAD arises when
people stop looking at themselves honestly and acceptingly. Repeated denial of their true
thoughts, emotions and behaviors make people feel anxiety and unable to fulfill their potential
as human beings. Carl Rogers believes that children who fail to receive unconditional positive
regard from others may become overly critical of themselves and develop harsh self standards
what Rogers called conditions of worth. They try to meet these standards by repeatedly
distorting and denying their true thoughts and experiences. Despite such efforts threatening
self judgments keep breaking through and cause intense anxiety. This sets the stage for GAD.

Cultural Factors: There is a common belief that Eastern (more collectivistic) cultures display
higher levels of anxiety than do Western (more individualistic) cultures. It is likely that the
underlying experience of anxiety are universal but the surface expression of anxiety, and the
ways in which anxiety interferes with daily functioning, and hence, becomes a disorder are
likely to be at least partly influenced by cultural considerations.

Culture bound anxiety disorders:

 Nervios (“nerves”) disorder of chronic worrying in Latino cultures. Tied to poverty and
poor education.
 Taijin kyofusho: Social phobia like disorder manifested in Japan where the patients feel
they will offend or embarrass others.

Other Psychological Factors

Personality Traits: The most consistent finding in research is that neuroticism occurs frequently across
anxiety disorders.

Parenting: The key parenting variables that have been associated with anxiety disorders are parenting
that is (1) overprotective/controlling and lacking in autonomy granting, (2) negative and lacking in
warmth, and (3) parenting that enhances the child's avoidance of ambiguously threatening situations.
These variables are of most importance in the context of a temperamentally vulnerable child. That is, a
child who is born with a more inhibited temperament and is raised in an environment that discourages
autonomy has an increased risk of developing an anxiety disorder. The ultimate consequence of
overprotective parenting is that the child avoids potentially threatening situations and is prevented from
potentially learning the situation is not as dangerous as predicted and he or she is able to exert some
control in the situation.
Family environment: Families of individuals with anxiety disorders report environments that are lower
in cohesion, expressiveness, and support (Turner et ah, 2003). There is also a strong body of literature
that shows a causal link between interparental conflict and increased anxiety symptoms (Hudson, 2005).
There are also a number or other family-related traumas, such as parental death and intrafamilial sexual
abuse, that have been shown to place an individual at risk for increased anxiety.

Peer Victimization: A number of studies have shown that experiences of teasing and bullying are
associated with increases in anxiety as well as depression (Hawker and Boulton, 2000). To date, most
of the research into peer victimization and anxiety has focused on social anxiety. Further research is
needed to determine whether other forms of anxiety are also associated with victimization.

Biological Causal Factors:

Genetic Causes: Although evidence for genetic factors in GAD is mixed, there does seem to be a modest
heritability, although perhaps smaller than that for most other anxiety disorders except phobias (Kendler
et al., 1992). The largest and most recent of these twin studies using the DSM-IV-TR diagnostic criteria
estimate that 15 to 20 percent of the variance in liability to GAD is due to genetic factors.

The evidence is increasingly strong that GAD and major depressive disorder have a common underlying
genetic predisposition (Kendler et al., 2007). What determines whether individuals with a genetic risk
for GAD and/or major depression develop one or the other disorder seems to depend entirely on the
specific environmental experiences they have. At least part of this common genetic predisposition for
GAD and major depression is best conceptualized as the basic personality trait commonly known as
neuroticism (Kendler et al., 2007).

Neurotransmitter and Neurohormonal Abnormalities (neurotransmitters help in carrying the message

across the synapse; neurohormones are released by neuroendocrine cells in the brain that are secreted
into the blood)

1. Serotonin and GABA deficiency: Anxiety disorders may result from some deficits in the
neurotransmitters such as serotonin and GABA. Whether the functional deficiency in GABA and
Serotonin in anxious people causes their anxiety or occurs as a consequence of it is not yet known.
2. The Corticotropin-Releasing Hormone (CRH) and HPA: The hypothalamic–pituitary–adrenal
axis (HPA axis) consists of: the hypothalamus , the pituitary gland, and the adrenal glands (on top
of the kidneys) and is involved in our anxiety response. When under stress, hypothalamus releases
CRH. CRH stimulates the pituitary gland (endocrine cells) to release ACTH (adrenocorticotropic
hormone). This in turn stimulates adrenal gland to release hormone cortisol from the adrenal gland.
As the levels of cortisol in your bloodstream increase, multiple systems are affected, preparing
your body to fight the stress.
The CRH hormone may play an important role in generalized anxiety through its effects on the bed
nucleus of the stria terminalis (BNST). The BNST is part of the extension of amygdala system of the
brain.

Neurobiological Differences Between Anxiety and Panic: Fear and panic involve activation of the fight-
or-flight response, and the brain areas and neurotransmitters that seem most strongly implicated in these
emotional responses are the amygdala (and locus coeruleus) and the neurotransmitters norepinephrine
and serotonin.

Generalized anxiety (or anxious apprehension) is a more diffuse emotional state involving arousal and
a preparation for possible impending threat; and the brain area, neurotransmitters, and hormones that
seem most strongly implicated are the limbic system (especially the bed nucleus of the stria terminalis,
an extension of the amygdala), GABA, and CRH. Although serotonin may play a role in both anxiety
and panic, it probably does so in somewhat different ways.

Recently, people with GAD have been found to have a smaller left hippocampal region similar to what
is seen with major depression (Hettema et al. 2012); this may represent a common risk factor for the
two disorders

Therapy

The most widely used psychotherapy for GAD seems to be Cognitive behavioral therapy
together with medication.

1) CBT examines distortions in our ways of looking at the world and ourselves. Negative
thoughts lead to negative emotions, so CBT aims to change those negative thoughts before they
trigger psychological difficulties. Deep breathing and progressive muscle relaxation helped
decrease the physical over-arousal. Time management and problem-solving skills are also
effective behavioral techniques for GAD. GAD initially appeared to be among the most
difficult of the anxiety disorders to treat, and to some extent this is still true. However, advances
have been made. The magnitude of the changes seen with cognitive-behavioral treatment was
at least as large as those seen with benzodiazepines, and it led to fewer dropouts (i.e., it was
better tolerated). Finally, CBT has also been found to be useful in helping people who have
used benzodiazepines for over a year to successfully taper their medications.

2) Medication is also used to treat GAD. Anxiolytics, e.g. benzodizapines, (such as Xanax or
Klonopin) are probably the most widespread treatment for generalized anxiety disorder. The
benzodiazepine drugs appear to reduce anxiety by increasing GABA activity in certain parts of
the brain implicated in anxiety, such as the limbic system, and by suppressing the stress
hormone cortisol. However, they can create physiological and psychological dependence and
withdrawal and are therefore difficult to taper. A newer medication called buspirone (from a
different medication category) is also effective, and it neither is sedating nor leads to
physiological dependence. It also has greater effects on psychic anxiety than do the
benzodiazepines. However, it may take 2 to 4 weeks to show results (Roy-Byrne & Cowley,
2002, 2007). Several categories of antidepressant medications like those used in the treatment
of panic disorder are also useful in the treatment of GAD, and they also seem to have a greater
effect on the psychological symptoms of GAD than do the benzodiazepines. However, they
also take several weeks before their effects are apparent.

3 Yoga And Meditation: These have also been found effective in the management of
generalized anxiety and related disorders. Sudarshan Kriya Yoga (SKY) has been foud to be
effective. Similarly, effect of yoga nidrā has also been positive.
 Anxiety Disorders: Specific Phobia
A phobia is an irrational fear that produces a conscious avoidance of the feared object.
The affected person usually recognizes that the reaction is excessive. The treatment and
description of phobias is embedded in history of Psychiatry and Psychology. Indeed,
Freud’s classic analytical case of “Little Hans” showed the typical symptoms of animal
phobia.

Patients with specific phobias have unwarranted fears of specific objects or situations.
Fear is the emotional response to real or perceived imminent threat, whereas anxiety is
anticipation of future threat. The best recognized are phobias of animals, blood, heights,
travel by airplane, being closed in, and thunderstorms. The anxiety produced by exposure
to one of these stimuli may take the form of a panic attack or of a more generalized
sensation of anxiety, but it is always directed at something specific. (However, these
patients can also worry about what they might do—faint, panic, lose control—if they
have to confront whatever it is they are afraid of.) Generally, the closer they are to the
feared stimulus (and the more difficult it would be to escape), the worse they feel.

Patients usually have more than one specific phobia. A person who is about to face one of
these feared activities or objects will immediately begin to feel nervous or panicky—a
condition known as ‘anticipatory anxiety’. The degree of discomfort is often mild,
however, so most people do not seek professional help. When it causes a patient to avoid
feared situations, anticipatory anxiety can be a major inconvenience; it can even interfere
with working. Patients with specific phobias involving blood, injury, or injection often
experience what is called a vasovagal response; this means that reduced heart rate and
blood pressure actually do cause the patients to faint.

Symptoms/Clinical picture/DSM criteria

Diagnostic Criteria (DSM-5) -Mnemonic: FEAR DSM

A. Fear (excessive) Marked fear or anxiety about a specific object or situation (e.g.,
flying, heights, animals, receiving an injection, seeing blood) which may be
termed the phobic stimulus. The fact that the fear is excessive or irrational is
important. The categories of feared situations or objects are provided as
specifiers.

1
 B. (Exposure-anxiety) The exposure to the phobic stimulus almost always
immediately provokes an anxiety response, which may be either a Panic Attack or
other symptoms of anxiety.

 An individual who becomes anxious only occasionally upon being

confronted with the situation or object (e.g., becomes anxious when
flying only on one out of every five airplane flights) would not be
diagnosed with specific phobia.

 The degree of fear may vary (from anticipatory anxiety to a full panic
attack) because of various contextual factors such as the presence of
others, duration of exposure, and other threatening elements such as
turbulence on a flight for individuals who fear flying.

C. (Avoidance) The phobic object or situation is actively avoided or endured with

intense fear or anxiety.
 Active avoidance means the individual intentionally behaves in ways that
are designed to prevent contact with phobic objects or situations (e.g.,
avoids entering a dark room for fear of spiders).

D. (Recognition of fear) The patient realizes that this fear is unreasonable or out of
proportion.
 The individual’s sociocultural context should also be taken into account.
For example, fears of the dark may be reasonable in a context of ongoing
violence, and fear of insects may be more disproportionate in settings
where insects are consumed in the diet.
E. (Duration) The fear, anxiety, or avoidance is persistent, typically lasting for 6
months or more.
F. (Social occupational dysfunctioning) Fear markedly interferes with the patient's
usual social, job, or personal functioning. Prior to assigning a diagnosis of
specific phobia, clinicians need to consider whether a patient's fear is extreme in
the context of a particular culture.
G. (Mental disorders Exclusion) Exclusion criterion 1: The symptoms are not better
explained by another anxiety or mental disorder.

Specifiers: Types of specific phobias (DSM-5) are:

It is common for individuals to have multiple specific phobias. The average individual
with specific phobia fears three objects or situations, and approximately 75% of
individuals with specific phobia fear more than one situation or object. For example, if an

2
individual fears thunderstorms and flying, then two diagnoses would be given: specific
phobia, natural environment, and specific phobia, situational.

1. Animal (Snakes, spiders, dogs, insects, birds)

2. Natural environment (Storms, heights, water)
3. Fear of blood-injection-injury
 Fear of blood
 Fear of injections and transfusions
 Fear of injury
 Fear of other medical care
4. Situational (airplanes, elevators, closed spaces)
5. Other (loud sounds, costumed characters)

Associated Features

Individuals with specific phobia typically experience an increase in physiological arousal

in anticipation of or during exposure to a phobic object or situation. However, the
physiological response to the feared situation or object varies. Whereas individuals with
situational, natural environment, and animal specific phobias are likely to show
sympathetic nervous system arousal, individuals with blood-injection-injury specific
phobia often demonstrate fainting or near-fainting response that is marked by initial brief
acceleration of heart rate and elevation of blood pressure followed by a deceleration of
heart rate and a drop in blood pressure. Current neural systems models for specific phobia
emphasize the amygdala and related structures, much as in other anxiety disorders.

Prevalence, Age of Onset, and Gender Differences

Specific phobias are quite common. Results of the National Comorbidity Survey-
Replication, which used DSM-IV criteria, revealed a lifetime prevalence rate of about 12
percent (Kessler, Chiu, et al., 2005). As compared to other countries, the prevalence rate
in India is relatively lower. Chandrashekhar and Reddy (1998) found the weighted
prevalence rate for phobia to be 4.2 percent. Phobias are always considerably more
common in women than in men. The average age of onset for different types of specific
phobias also varies widely. Animal phobias usually begin in childhood, as do blood-
injection-injury phobias and dental phobias.

Causal factors/Etiology/ Dynamics

Psychological factors

3
Psychodynamic Viewpoint

According to the psychoanalytic view, phobias represent a defense against anxiety that
stems from repressed impulses from the id. Because it is too dangerous to “know” the
repressed id impulse, the anxiety is displaced onto some external object or situation that
has some symbolic relationship to the real object of the anxiety (Freud, 1909). For e.g. in
the case of Little Hans (1964), who had a phobia of horses Freud interpreted that the
horses in the phobia were symbolic of the father, and that Hans feared that the horse
(father) would bite (castrate) him as punishment for the incestuous desires towards his
mother. Freud saw Hans' phobia as an expression of the Oedipus complex. However, this
prototypical psychodynamic account of how phobias are acquired was long criticized as
being far too speculative.

Phobias as learned behaviours

(1) Classical Conditioning theory (Wolpe and Rachman, 1960): Specific phobias can
sometimes develop as a result of classical conditioning as when a traumatic
experience takes place in a feared situation. For example, someone who is bitten
by a dog might develop a fear of dogs, or someone who has a car accident might
develop a fear of driving. In this case the previously neutral stimulus i.e. dog
(CS) elicits fear (CR) as the dog has been associated with a bite (UCS) that
elicits fear (UCR). Eventually, the neutral stimulus (dog) alone can elicit the
state of fear. Soon this fear can be generalized and the person may start fearing
all kinds of dogs and not a specific dog. The study of Little Albert by Watson
and Rayner (1920) has frequently been used as an example of fear conditioning
in humans. In this experiment, a previously unafraid baby was conditioned to
become afraid of a rat. This was done by pairing a loud noise (UCS) with the rat
(CS) so that the baby became afarid of the rat.
(2)Vicarious Conditioning/observational learning: Another way of acquiring social
fears is vicarious conditioning. According to this paradigm, observing others
experiencing anxiety in social situations can lead to the observer fearing these
situations. Studies of people with phobias often showed that they had first
become afraid by observing fear in someone else. In one study (Mineka,
Davidson, Cook, & Keir, 1984), researchers looked at some young monkeys
who had been raised in captivity with their parents. These young monkeys had
never seen a snake, and when they were shown a snake they showed no fear
whatsoever. However, their parents had been raised in the wild and were afraid
of snakes. The researchers showed snakes to the parents while the young
monkeys were watching. Predictably, the adult monkeys showed a lot of fear.
The young monkeys were then shown the snakes again. This time, the young
monkeys showed as much fear as the adults had, and their fear stayed strong for

4
 months. Researchers were able to show that strong fears can be learned simply
by watching others without directly having a negative experience.
3) Individual Differences in Learning: Given all the traumas that people undergo,
why don’t more people develop phobias. Several factors may be responsible for
the development as well as maintenance of these phobias:

 Life experiences and Immunization effects: Life experiences may play an

important role in determining why one person develops a phobia after a dog bite
and the other does not. In the latter case, years of positive interaction with a
friendly dog may have prevented him from developing a phobia whereas a
person who has had several traumatic experiences with a dog in the past is more
likely to develop a phobia.
 Degree of control: Another factor which may determine whether a person
develops a phobia after a traumatic experience depends on the degree of
inescapable and uncontrollable event experienced by a person. A person who has
been bitten by a dog in an attack in which escape was difficult is more likely to
develop a phobia as compared to an individual who has been bitten by a dog in
which he was able to escape.
 Inflation effect: Experiences after the conditioning may effect the conditioned
fear. ‘Inflation effect’ suggests that later information (For e.g. being told ‘You
are lucky you are alive because the man who held you up at the bank last week
is a known killer”) alters the interpretation of a the dangerousness of an earlier
trauma leading to an increase/inflation in the level of fear. For example, the
inflation effect suggests that a person who acquired, a mild fear of driving
following a minor crash might be expected to develop a full-blown phobia if he
or she later were physically assaulted. Even verbal information that later alters
one’s interpretation of the dangerousness of a previous trauma can inflate the
level of fear (e.g., being told, “You’re lucky to be alive because the man who
stole your wallet was a serial killer.” Another way in which fear of a CS can be
inflated following conditioning is if the organism later is exposed to
uncontrollable stress.
 Negative cognitions: It has also been shown that our cognitions, or thoughts, can
help maintain our phobias once they have been acquired. For example, people
with phobias are constantly on the alert for their phobic objects or situations and
for other stimuli relevant to their phobia. In addition, phobics also markedly
overestimate the probability that feared objects have been, or will be, followed
by frightening events.

5
Biological preparedness hypothesis (Seligman, 1971)

This “preparedness theory” (Seligman, 1971) was an early attempt to explain human
fears in the context of evolutionary psychology. The theory (also known as the “selective
association model”) states that humans are biologically “prepared” to acquire the fear of
certain objects or situations that used to threaten the survival of our species. There are
several stimuli that are shared by the most phobic people (heights, insects, crowds, etc.)
Stimuli such as guns, knives, and electrical outlets have not been around long enough for
such preparedness to emerge. This model was developed to explain the rapid acquisition
and seeming irrationality of common phobias, as well as their high resistance to
extinction. Phobic fear was seen as a noncognitive and irrational response that is
fundamentally different from conditioned fear in the laboratory (Seligman, 1971).

The most convincing evidence in support of the evolutionary model of phobias is

provided by fear conditioning experiments using rhesus monkeys. Wild rhesus monkeys
fear snakes while domestic rhesus, unless conditioned, do not. In the experiment,
domestic rhesus monkeys are shown a video in which peers respond fearfully to both
snakes (fear-relevant stimuli) and flowers (neutral stimuli). When exposed to the two
stimuli, the monkeys exhibited a fear response to snakes but not to flowers (Cook and
Mineka, 1990).

Biological Factors

Temperamental and genetic factors:

Genetic and temperamental variables, people are more or less likely to acquire fears and
phobias. For example, Lonsdorf and colleagues (2009) examined two genes: two genes
thought to play a role in anxiety disorders: the serotonin transporter gene and the
gene for the enzyme COMT. In the case of the serotonin-transporter gene, two
variants of this gene have been found. The shorter version of this gene (the s allele)
leads to lesser serotonin in the blood and hence is associated with higher
neuroticism scores and anxious behavior. The gene for the COMT enzyme is
involved in breaking down dopamine. This too has two variants. Those with one of
two variants of a different gene (the COMT met/met genotype) did not show superior
conditioning but did show enhanced resistance to extinction (Lonsdorf & Kalisch, 2011).

Some researchers have suggested that temperament plays an important role in

determining one’s susceptibility to developing a number of anxiety disorders. Children

6
who are behaviorally inhibited (excessively timid, shy etc.) at 21 months are at a higher
risk to develop phobias later (Kagan and his colleagues, 2001).

Several behavior genetic studies also suggest a modest genetic contribution to the
development of specific phobias. For example, a large female twin study found that
monozygotic (identical) twins were more likely to share animal phobias and situational
phobias (such as of heights or water) than were dizygotic (nonidentical) twins (Kendler et
al., 1999b). Very similar results were later also found for men (Hettema et al., 2005).
Heritability represents the percent of variation in a trait (e.g., a fear or phobia) that is due
to genetic factors. The following are estimates of heritability for specific fears: animal
fears (mean = 58%); natural environment fears (mean = 37%); blood-illness-injury fears
(mean = 43%); social fears (mean = 37%); and situational fears (23%; Rose & Ditto,
1983; Stevenson, Batten, & Cherner, 1992).

Treatments

Behavioral Therapies:

Exposure-based therapies: This technique reflects a variety of behavioral approaches that

are all based on exposure to the stimuli that frighten them. It tries to break the association
between the phobic stimuli and fear It generally involves prolonged and graduated
exposure to the specific situations that evoke fear (either alone or with the aid of a
therapist or friend) to their feared situations for long enough periods of time so that their
fear begins to subside. One variant on this procedure, known as participant modeling, is
often more effective than exposure alone. Here the therapist calmly models ways of
interacting with the phobic stimulus or situation (Bandura, 1977, 1997).

Systematic desensitization: This is quite similar to exposure therapy—in fact, exposure to

anxiety-provoking stimuli is one of its key components—but rather than simply
breaking the association between the phobic stimuli and fear, systematic desensitization
involves re-pairing the feared object with a new response (relaxation) that is incompatible
with anxiety. Systematic desensitization involves three steps:

 In the first step, the therapist helps the client build an anxiety hierarchy. This is a
list of anxiety-arousing stimuli related to the specific source of anxiety, such as
flying, academic tests, or snakes. The client ranks the stimuli from the least
anxiety arousing to the most anxiety arousing.
 The second step involves training the client in deep muscle relaxation. This
second phase may begin during early sessions while the therapist and client are
still constructing the anxiety hierarchy.

7
 In the third step, the client tries to work through the hierarchy, learning to remain
relaxed while imagining each stimulus. Starting with the least anxiety-arousing
stimulus, the client imagines the situation as vividly as possible while relaxing. If
the client experiences strong anxiety, he or she drops the imaginary scene and
concentrates on relaxation. The client keeps repeating this process until he or she
can imagine a scene with little or no anxiety. After a particular scene is
conquered, the client moves on to the next stimulus situation in the anxiety
hierarchy. Gradually, over a number of therapy sessions, the client progresses
through the hierarchy, unlearning troublesome anxiety responses.

8
 UNIT-3
EATING DISORDER

EATING DISORDERS
According to DSM-V (APA, 2013) eating disorders are characterized by a persistent disturbance in eating
behaviour. Three of the most important adult eating disorders in DSM-V are:

 Anorexia Nervosa
 Bulimia Nervosa
 Binge- Eating Disorder (BED)

CLINICAL PICTURE OF EATING DISORDERS

ANOREXIA NERVOSA
The term ‘anorexia nervosa’ literally means lack of appetite induced by nervousness. At the heart of Anorexia
Nervosa is a pursuit of thinness that is relentless and that involves behaviors that result in a significantly low
body weight. The DSM-V Criteria for Anorexia Nervosa is as follows:
A) Restriction of energy intake relative to requirements, leading to a significantly low body weight in the
context of age, sex, developmental trajectory, and physical health. Significantly low weight is defined as
a weight that is less than minimally normal or for children and adolescents less than that minimally
expected.
B) Intense fear of gaining weight or of becoming fat or persistent behavior that interferes with weight gain,
even though at a significantly low weight.
C) Disturbance in the way in which one’s body weight or shape is experienced, undue influence of body
weight or shape on self-evaluation or persistent lack of recognition of the seriousness of current low
body weight.
We may think of anorexia nervosa as a modern problem, however it is centuries old. The first known medical
account of anorexia nervosa however, was published in 1689 by Richard Morton.
The disorder did not receive its current name till 1873 till Charles Lasegue in Paris and Sir William Gull in
London independently described the clinical syndrome. Even though they may look painfully their own
emaciated, many patients with anorexia nervosa deny having any problem. Indeed, they come to feel fulfilled
by their weight loss. Despite this, quite satisfaction, however, they may feel ambivalent about their weight.
Efforts are often made to conceal their thinness by wearing baggy clothes to carrying hidden bulky objects so
that they will weigh more than measured. Patients with anorexia nervosa may even resort to drinking large
amounts of water to increase their weight temporarily.
There are two types of Anorexia Nervosa- the restricting type and the binge eating type or purging type. The
central difference between these two types of anorexia concerns the way in which patients maintain their very
low weight. In restricting type, every effort is made to limit the quantity of food consumed. Caloric intake is
tightly controlled. Patients try to avoid eating in presence of others. When they are at the table, they may eat
excessively slowly, cut their food into very small pieces or dispose of food secretly. (Beaumont, 2002)
Patients with binge eating or purging type of anorexia nervosa differ from patients with restricting type anorexia
nervosa because they either binge, purge or binge and purge. A binge involves an out of control consumption of
an amount of food that is far greater than what most people would eat in the same amount of time and under the
same circumstances. These binges may be followed by efforts to purge, or remove from their bodies the food
that they have eaten. Methods of purging commonly include self- induced vomiting or misuse of laxatives,
diuretics and enemas. Other compensatory behaviors that do not involve purging strategies however do not
prevent the absorption of all calories from food.
Indicative of the distorted values of patients with eating disorders, those with the restricting type of anorexia
nervosa are often greatly admired by others with eating disorders. One patient’s belief was that the hallmark of
a truly successful person with anorexia was death from starvation and that the patients who were able to
accomplish this should somehow be reversed.
DISTORTED THINKING IN ANOREXIA NERVOSA

 Bones define who we really are, let them show.

 It’s not deprivation, its liberation.
 An imperfect body reflects an imperfect person.
 I have a rule when I weigh myself, if I gain I will starve myself for the day but if I lose, I starve too.
 Anorexia is not a self-inflicted disease, it’s a self-controlled lifestyle.
Because the artistic standards of their profession emphasize a slender physique, dancers are at a high risk for
eating disorders; this is particularly true for ballet dancers. A study has estimated that just fewer than 20% of
ballets suffer from eating disorder, with anorexia nervosa being the most common problem. (Arcelus et al.,
2014)

A CASE OF ANOREXIA NERVOSA

Eisha
Eisha was 22 years old and in her fourth year of graduate study at a university in the United States when she
first sought treatment. Her eating disorder, however, had begun many years earlier. When she was 14 and at
school in her home country of India, she reported being bullied by her classmates who told her she looked fat in
her new school dress. After this incident, she started to feel that she had become fat and she began to starve
herself to lose weight. By the time she was 18 she was in a physically weak state. She ate only once a day. The
rest of the time she exercised, and refused all other requests to eat food. Occasionally, her restraint would break
down and she would binge eat. After each binge-eating episode she would starve herself for 3 or 4 days to
compensate. Eventually she began to purge routinely after eating any food to make sure she did not gain any
weight. She believed that “to be beautiful you need to be thin” and that eating was bad. After eating, she would
tell herself “you are good for nothing.” (Based on Roy, 2014.)

BULIMIA NERVOSA
Bulimia Nervosa is characterized by uncontrollable binge eating and efforts to prevent resulting weight gain by
using inappropriate behaviour such as self-induced vomiting and excessive exercise. The British psychiatrist G.
F. M. Russel (1997) proposed the term in 1979 and it was adopted into the DSM in 1987. The world ‘bulimia’
comes from the Greek ‘pous’ which means ‘OX’ and ‘limos’ which mean hunger. It is meant to denote a hunger
of such proportions that the person could ‘eat an ox’.
The DSM V Criteria for Bulimia Nervosa is as follows:
A. Recurrent episodes of binge-eating, an episode of binge-eating is characterised by both of the following-
 Eating, in a discrete period of time (for example within any two hour period), an amount of food that is
definitely larger than what most individuals would eat in a similar period of time under similar
circumstances.
 A sense of lack of control over eating during the episode (for example a feeling that one cannot stop
eating or control watch on how much one is eating). Recurrent inappropriate compensatory behaviors in
order to prevent weight gain, such as self-induced vomiting; misuse of laxatives, diuretics, or any
medications; fasting; or excessive exercise.
 B. The binge eating and inappropriate compensatory behavior both occur on average at-least once a week
for three months.
C. Self- evaluation is unduly influenced by body shape and weight.
D. The disturbance does not occur exclusively during episodes of anorexia nervosa.
The clinical picture if the binge eating or purging type of anorexia nervosa has much in common with bulimia
nervosa. The difference between a person with bulimia nervosa and a person with binge eating or purging type
of anorexia nervosa is weight. By definition the person with Anorexia Nervosa is severely underweight; this is
not true of the person with Bulimia Nervosa. There is a far greater mortality rate associated with Anorexia
Nervosa than with Bulimia Nervosa.
People with Anorexia Nervosa and Bulimia Nervosa share a common pre-occupation with their shape and their
weight. However unlike patients with Anorexia Nervosa those with Bulimia Nervosa are typically of normal
weight or sometimes even slightly overweight. Bulimia typically begins with restricted eating motivated by the
desire to be slender. During these early stages the person diets, and eats low calorie foods. Overtime however
the early resolve to restrict gradually erodes and the person starts to eat ‘forbidden foods’ such as potato chips,
pizza, and cake, ice-cream and chocolate.
Of course some patients binge on whatever food is available during an average binge someone with bulimia
nervosa may consume as many as 4,800 calories (Johnson et al, 1982). After the binge in an effort to manage
the breakdown of self-control the person begins to vomit, fast, exercise excessively or abuse laxatives. This
pattern then persists because even though those with bulimia nervosa are disgusted by their behaviour, the
purging alleviates the fear of gaining weight that comes from eating.
Whereas people with anorexia nervosa often deny the seriousness of their disorder and are surprised by the
shock and concern with which others view their emaciated conditions, those with bulimia nervosa are often pre-
occupied with shame, guilt and self-deprecation. They make efforts to conceal their behavior as they struggle
(often unsuccessfully) to master their urges to binge.

A CASE OF BULIMIA NERVOSA

Catherine: Distressed by Her Weight
Catherine is 20 years old. Catherine has been concerned about her weight and shape for several years. As a
teenager she felt plump and was frequently on a diet, even though she was within the normal weight range for
her age and height. As she became older, these concerns became more serious. She severely restricted her food
intake and started punishing exercise regimens. At one stage she became significantly underweight. Medical
help led to weight gain, which was quickly followed by more dieting and, for the first time, she started binge
eating. Distressed by the increase in her weight and by increasingly frequent binge eating, Catherine began
vomiting in a desperate attempt to lose weight. Over the past 6 months Catherine has skipped breakfast and
lunch, eaten a normal evening meal with her family, but gone on to binge eat in the late evening usually two or
three times a week. She binges in response to feeling upset and worried. In a recent typical binge she ate four
slices of toast with butter and jam, six packets of potato chips, three large bars of chocolate, half a box of cereal,
and a large bowl of ice cream. She had been feeling rejected by a friend. Catherine drinks large quantities of
water to help her induce vomiting after binging. More recently she has started to take 30 to 40 laxatives, as well
as vomiting. She has a strenuous exercise regime, including 500 daily sit-ups and an aerobic workout. Food is
divided rigidly into good and bad categories; food in the bad category (such as cookies, chocolate, and cheese)
is not allowed. Catherine has become increasingly self-conscious. She refuses to weigh herself, has given up
swimming (she used to swim on her school team), and if she goes shopping she will not try on clothes unless
she has privacy. Catherine dislikes her body. She is preoccupied with her shape and reports that a little voice in
her head constantly says, “You’re fat and ugly, I can’t stand the way you look.” Catherine worries that her
friends will think less of her if she does not lose weight (when out with friends she avoids eating and sucks her
tummy in to the point of pain in order to appear thinner). She feels very bad about herself if she thinks she has
 gained weight. (Adapted from Cooper, Todd, & Wells (2000). Bulimia Nervosa: A Cognitive Therapy
Programme. London: Jessica Kingsley Publishers.)

BINGE- EATING DISORDER (BED)

Substantial unmet needs exist regarding the awareness, diagnosis, and treatment of binge-eating disorder
(BED). Affecting both men and women and appearing in all ethnic groups, BED is the most prevalent of all the
eating disorders in the United States and worldwide. Left untreated, BED causes significant impairment,
reduced quality of life, and decreased productivity. Many patients are unaware of the disorder and present for
treatment of weight-related issues or comorbid medical and psychiatric conditions. Communication barriers,
such as the reluctance of patients to volunteer information about their eating habits and of clinicians to ask
potentially sensitive questions, may be overcome with the use of diagnostic criteria along with appropriate
assessment questions and screening tools. Early recognition and accurate diagnosis may help mitigate the long-
term impact of BED.
(J Clin Psychiatry 2017;78[suppl 1]:3-8)
From the Department of Psychiatry and Institute for Women’s Health, Virginia Commonwealth University,
Richmond.
This article is derived from the planning teleconference series "Challenges in the Recognition and Treatment of
Binge-Eating Disorder," which was held in May, June, and July 2016, and supported by an independent medical
educational grant from Shire.
Dr Kornstein is a consultant for Pfizer, Eli Lilly, Shire, Takeda, Sunovion, Forest, Allergan, and Palatin
Technologies; has received grant/research support from Allergan, Forest, Takeda, and Palatin Technologies;
and has received other financial support from Guilford Press.
Corresponding author: Susan G. Kornstein, MD, PO Box 980319, Richmond VA
23298 (susan.kornstein@vcuhealth.org).
https://doi.org/10.4088/JCP.sh16003su1c.01
© Copyright 2017 Physicians Postgraduate Press, Inc.
Binge-eating disorder (BED) may not be as well-known as anorexia nervosa or bulimia nervosa due to its more
recent formal recognition as an eating disorder. Although binge-eating behavior was first described by Stunkard
in 1959,1 its first mention in the Diagnostic and Statistical Manual of Mental Disorders (DSM) was not until
the third edition was published in 1980.2 There, binge eating was included as a feature of bulimia nervosa. The
term binge-eating disorder was introduced in the DSM-IV in 1994,3 both under the category of Eating Disorder
Not Otherwise Specified and with full criteria in the appendix of conditions requiring further study. Eventually,
BED was formally recognized as a psychiatric disorder and a distinct eating disorder in the DSM-5,4 published
in 2013.

CLINICAL POINTS

 Clinicians must be familiar with DSM-5 criteria for binge-eating disorder (BED) in order to differentiate it from other
eating disorders, such as bulimia nervosa and anorexia nervosa.
 Many patients are unaware of the BED diagnosis, are reluctant to discuss their eating habits, and seek treatment for weight
management or comorbid medical or psychiatric conditions rather than BED.
 Clinicians can use assessment questions along with screening tools (eg, EDE-Q, QEWP-5, BEDS-7) to identify patients
with BED.

Even with the recent attention and research to develop its epidemiology and diagnostic criteria, BED remains
underrecognized and undertreated.5 However, clinicians who familiarize themselves with the diagnostic
criteria, overcome communication barriers with patients, and incorporate screening tools into clinical
assessment can improve their recognition of BED and help patients begin appropriate treatment.
DIAGNOSTIC CRITERIA
Binge-eating episodes are characterized by eating a larger amount of food in a discrete period than is typical for
most people, while feeling unable to control the eating (Table 1).4 During binge-eating episodes, individuals
often eat very rapidly despite not being hungry, and they eat until they feel uncomfortably full, usually alone
because of embarrassment. Episodes are followed by disgust or guilt and must cause marked distress in the
individual.

Click figure to enlarge

The diagnosis of BED requires the presence of recurrent binge-eating episodes occurring at least once per week
for a period of at least 3 months.4 This frequency was reduced from the DSM-IV criteria3 (which required at
least 2 episodes per week for at least 6 months), because it allowed for better identification of clinically
significant symptoms without a substantial increase in prevalence.6 In contrast to anorexia nervosa and bulimia
nervosa, the binge eating in BED is not associated with recurrent use of inappropriate compensatory behavior,
such as purging, exercising excessively, or misusing laxatives.4
Although not a diagnostic criterion of BED (as in anorexia nervosa and bulimia nervosa), overvaluation of body
shape and weight is commonly seen in patients with BED.7 Overvaluation is more specific than body
dissatisfaction because individuals place undue importance on body shape and weight to the point that these
factors define their self-worth. As a cognitive feature, overvaluation is associated with severity of eating
pathology and psychological distress and has negative prognostic significance.7
Clinicians must distinguish BED from overeating, which is a common phenomenon among Americans (eg, at
holiday meals) but does not meet other BED criteria, such as loss of control or feelings of shame and guilt.
The severity of BED is based on frequency of binge-eating episodes. Mild severity is 1-3 episodes per week,
moderate is 4-7, severe is 8-13, and extreme is 14 or more.4

EPIDEMIOLOGY
Among the eating disorders, BED is the most prevalent, both in the United States and worldwide.

One group in which BED is found is individuals seeking weight loss treatment, such as bariatric surgery.
Prevalence rates for patients with BED prior to bariatric surgery range from 4% to 49%, with the large range
due to different DSM criteria, study designs, and assessment methods. Among 130 obese individuals with BED
who sought weight loss treatment, the majority were found to have experienced 5% or greater weight gain in the
year before seeking treatment. In a study comparing weight changes among 97 overweight and obese patients in
the year prior to seeking weight loss treatment, patients with BED gained an average of 18.3 lb (8.3 kg)
compared with an average of 1.5 lb (0.7 kg) in patients without BED. Thus, rapid weight gain can be a sign to
clinicians to screen for BED.

A CASE OF BINGE EATING

Jenna
Jenna is a 33-year-old single woman who lives alone. She works as a therapist in a school for children with
learning difficulties. She came to the clinic for help with chronic feelings of depression. She also
acknowledged a history of obesity and binge eating dating back to her adolescent years. By the time of her
initial consultation she weighed 260 pounds and had a BMI of 39.5. She was afraid that her weight would
continue to increase unless she found ways to control her eating. Jenna told the therapist that she had “always
been fat.” She was extremely reluctant to talk about her eating habits because to do so made her feel
embarrassed and ashamed. She said that, in addition to eating three substantial meals every day, she snacked
constantly because there were always cookies and cakes available in the teachers’ room at school. She also had
eating binges. These occurred approximately twice a week and were invariably triggered by anything that made
her feel sad, disappointed, or upset. If she had a difficult day at work, she would stop at a convenience store on
her way home, buy candy and cookies, and eat quickly in the car. She would then feel disgusted with herself,
setting the stage for another binge eating episode when she was alone at home. She would prepare large
amounts of food for herself and eat as rapidly as she could until she was so full she was uncomfortable. Jenna
longed to be able to “eat normally” but also acknowledged how reliant she was on food to help her cope with all
the sadness in her life. There was no evidence of any purging, fasting, or misuse of laxatives. Occasionally,
Jenna did try to exercise, although she regarded herself as “too fat to go to the gym.”

ETIOLOGY
As with other disorders, a single factor is unlikely to cause an eating disorder. In all probability, they reflect the
complex interaction between genetic and environmental factors. Several areas of current research like genetics,
neurobiology, sociocultural pressures to be thin, personality, the role of the family, and the role of
environmental stress, suggest that eating disorders result when several influences converge in a person’s life.
However, it is important not to regard these areas as distinct and in competition with each other. The etiology of
eating disorders is affected by biological, psychological, social, and sociocultural factors (Becker, 2004; Kaye,
2009; Tylka & Subich, 2004).

BIOLOGICAL DIMENSION
Biological predispositions in people with eating disorders include genetics, brain features, neurochemical
features, and personality traits such as perfectionism and impulsivity.

I) GENETICS
Like most psychological disorders, eating disorders run in families and thus seem to have a genetic component
(Trace, Baker, Penas-Lledo, & Bulik, 2013). Studies suggest that relatives of patients with eating disorders are 4
to 5 times more likely than the general population to develop eating disorders themselves, with the risks for
female relatives of patients with anorexia higher (Strober, Freeman, Lampert, Diamond, & Kaye, 2000; Strober
& Humphrey, 1987).
Twin studies of eating disorders also suggest a genetic influence. Most studies of both anorexia and bulimia
report higher MZ than DZ concordance rates (Bulik, Wade, & Kendler, 2000) and that genes account for a
portion of the variance among twins with eating disorders (Wade et al., 2000).
Research also suggests that key features of the eating disorders, such as dissatisfaction with one’s body, a strong
desire to be thin, binge eating, and preoccupation with weight, are heritable (Klump, McGue, & Iacono, 2000).
Genetic influences may be triggered by physical changes such as puberty. The eating disorder only shows up
when certain environmental factors interact with the presence of genetic risk factors (Culbert, Burt, McGue,
Iacono, & Klump, 2009; Klump et al., 2007).

II) BRAIN ABNORMAILITES

One brain area that plays an important role in eating is the hypothalamus.
It is reasonable to suggest that the hypothalamus “senses” weight in some way and keeps things in balance with
the ventromedial hypothalamus acting as a “satiety center” and the lateral hypothalamus serving as an “appetite
center.” It is also reasonable to think that the lateral hypothalamus acts as a site that integrates other information
relevant for regulating food intake. The lateral hypothalamus receives information from many parts of the brain,
including the frontal cortex and the amygdala (which is a part of the brain involved in emotion and fear
learning). Animal research suggests that a network involving these (and other) brain areas may be important not
only for overeating in response to environmental cues but for suppressing eating in response to fear (Petrovich,
2011). As research progresses we will learn more about how the pieces of the puzzle fit together to result in
different types of eating disorders.

III) NEUROCHEMICAL FACTORS

Endogenous opioids are substances produced by the body that reduce pain sensations, enhance mood, and
suppress appetite. Opioids are released during starvation and have been hypothesized to play a role in both
anorexia and bulimia. Starvation among people with anorexia may increase the levels of endogenous opioids,
resulting in a positively reinforcing euphoric state (Marrazzi & Luby, 1986). Furthermore, the excessive
exercise seen among some people with eating disorders would increase opioids and thus be reinforcing (Davis,
1996; Epling & Pierce, 1992).
Some research supports the theory that endogenous opioids play a role in eating disorders, at least in bulimia.
Researchers have examined levels of serotonin metabolites among people with anorexia and bulimia. Several
studies have reported low levels of serotonin metabolites among people with anorexia (e.g., Kaye et al., 1984)
and bulimia (e.g., Carrasco et al., 2000; Jimerson et al., 1992; Kaye et al., 1998). Lower levels of a
neurotransmitter’s metabolites are one indicator that the neurotransmitter activity is underactive.
More recently, researchers have examined the role of the neurotransmitter dopamine in eating behavior.
Another study found that women with either anorexia nervosa or bulimia nervosa had greater expression of the
dopamine transporter gene DAT (Frieling et al., 2010). When a gene is “turned on,” or expressed, as it interacts
with different aspects of the environment. The expression of DAT influences the release of a protein that
regulates the reuptake of dopamine back into the synapse. Brain activity or gene expression of certain dopamine
genes is correlated with eating disorders, not that these things cause eating disorders.

IV) SET POINTS

There is a well-established tendency for our bodies to resist marked variation from some sort of biologically
determined set point or weight that our individual bodies try to “defend” (Garner, 1997; Ravussin et al., 2014).
Anyone intent on achieving and maintaining a significant decrease in body mass below his or her individual set
point may be trying to do this in the face of internal physiological opposition, which is aimed at trying to get the
body back close to its original set-point weight.

A) PSYCHOLOGICAL DIMENSION
A number of psychological risk factors have been found to increase an individual’s chances of developing an
eating disorder. These include body dissatisfaction, perfectionism, depression, dysfunctional beliefs, using
control to deal with stressors, and low levels of interpersonal competence (Myers & Crowther, 2009).
Dissatisfaction with one’s body can result in fragile or low self-esteem, depression, and feelings of helplessness.

I) BODY DISSATISFACTION
It has been found to be a strong predictor of the development of disturbed eating patterns (Johnson & Wardle,
2005). Up to one-third of young people (Crow, Eisenberg, Story, & Neumark-Sztainer, 2008; Mission Australia,
2010) and a large percentage of women between the ages of 35 to 65 (McLean, Paxton, & Wertheim, 2010)
indicate significant levels of body dissatisfaction. Women with high body dissatisfaction as compared to body-
satisfied women are more likely to compare their bodies to other women and report lower self-evaluation after
this process (Trampe, Stapel, & Siero, 2010). Similarly, men who score high on appearance-orientation report
lower muscle satisfaction when exposed to commercials with muscular men (Hargreaves & Tiggemann, 2009).
Other evidence suggests that in treating bulimia, reducing the anxiety associated with eating is less important
than countering the tendency to overly restrict food intake and the associated negative attitudes about body
image that lead to bingeing and purging.

II) MALADAPTIVE PERFECTIONISM

Perfectionism (defined as the pursuit of unattainably high standards combined with an intolerance of mistakes)
has long been regarded as an important risk factor for eating disorders (Bruch, 1973). This is because people
who are perfectionistic may be much more likely to subscribe to the thin ideal and relentlessly pursue the
“perfect body.”
Maladaptive perfectionism is composed of two dimensions:
(1)Inflexible high standards
(2) negative self-evaluations involving mistakes
The presence of both is strongly related to eating disorder symptoms when perfectionist standards are imposed
on weight, shape, and/or dieting (Bardone-Cone & Cass, 2007; Bardone-Cone, Sturm, Lawson, Robinson, &
Smith, 2010; Boone, Soenens, Braet, & Goossens, 2010).
Perfectionism may also have a genetic basis. In a twin study, high levels of perfectionism were found in the
twins with anorexia nervosa, as expected. However, high levels of perfectionism were also found in the co-
twins who did not suffer from eating disorders (Wade et al., 2008).

III) PERCEIVED INCOMPETENCE

Perceived Incompetence or the belief that one is inadequate in social relationships has also been found to be
associated with disordered eating (Ferrier & Martens, 2008) and may interact with maladaptive perfection and
body dissatisfaction to create even greater risk for an eating disorder (Ferrier-Auerbach & Martens, 2009).
Individuals with eating disorders often appear to use food or weight control as a means of handling stress or
anxieties (Schwitzer et al., 2001; Walsh & Devlin, 1998).
Dieting may be used to demonstrate self-control and improve self-esteem and body image (Jones, Leung, &
Harris, 2007).
IV) MOOD DISORDERS
Mood disorders such as depression often accompany eating disorders. Rates of affective disorders such as
depression are higher in the relatives of individuals with eating disorders compared with controls, and some
investigators believe that eating disorders represent an expression of a mood disorder (Rutter, MacDonald et al.,
1990). At this point, we still do not know the precise relationship between affective disorders and eating
disorders. Depression may be the result, not the cause, of having an eating disorder.

V) NEGATIVE EMOTIONALITY
Negative affect (feeling bad) is a causal risk factor for body dissatisfaction (Stice, 2002). This seems to be
especially true of individuals with eating disorders, who, like people with depression, tend to show distorted
ways of thinking and of processing information received from the environment (e.g., Butow et al., 1993; Garner
et al., 1997). In many cases, there is widespread negative self-evaluation (e.g., Fairburn et al., 1997). These
cognitive distortions (“I’m fat; I’m a failure; I’m useless”) have the potential to make people feel even worse
about them.
Longitudinal studies have confirmed that depression and general negative affect are predictive of a high risk for
later developing an eating disorder (Johnson, Cohen, et al., 2002; Leon et al., 1997. A major problem is that
after binges patients feel disappointed or even disgusted with themselves.

B) SOCIAL DIMENSION
Remember that anorexia and particularly bulimia are the most culturally specific psychological disorders yet
identified. For many young women, looking good is more important than being healthy. For young females in
competitive environments, self-worth, happiness, and success are largely determined by body measurements
and percentage of body fat, factors that have little or no correlation with personal happiness and success in the
long run. The cultural imperative for thinness directly results in dieting, the first dangerous step down the
slippery slope to anorexia and bulimia.

I) FAMILY INFLUENCES
Clinicians have long been aware that certain problems seem to regularly characterize the families of patients
with anorexia nervosa, prompting many clinicians to advocate a family therapy approach to treatment
intervention (Lock et al., 2001). Echoing this sentiment, more than one-third of patients with anorexia nervosa
reported that family dysfunction was a factor that contributed to the development of their eating disorder (Tozzi
et al., 2003).
Patients with anorexia nervosa perceive their families as more rigid, less cohesive, and as having poorer
communication than healthy control participants do (Vidovic et al., 2005). Family factors have also been
studied in connection with bulimia nervosa. Both white and ethnic minority (black, Hispanic, and biracial)
adolescents with bulimia nervosa perceive their families to be less cohesive than their parents do (Hoste et al.,
2007).
Peer relationships can either serve as a buffer against eating disorders or produce pressure to lose weight. In a
longitudinal study, girls who reported that their friends were “very much” involved in dieting at the beginning
of the study were very likely to engage in extreme dieting and unhealthy weight control behaviors five years
later (Eisenberg & Neumark-Sztainer, 2010).
Figure: ROUTE TO EATING DISORDERS (Social Comparison can lead to development of Eating
Disorders) Adapted from Stice (2001)
 II) MEDIA EXPOSURE TO THE ‘THIN IDEAL’
Another risk factor for eating disorder, especially in Western society, is media promotion of the “thin ideal.”
Young people, especially young girls, are influenced by the media’s depiction of attractiveness and ideal body
type saying that Selena Gomez and Taylor Swift are not overweight. Body types for many celebrities and
athletes seem to set a standard, but many of these “models” are severely underweight and thin. This media ideal
clashes with the fact that size and weight of the average woman have increased over the years. Some of these
girls (and boys) try to achieve the media ideal but in the end they can only do so via severely restricted eating,
excessive exercise, or purging. Media depictions do influence body dissatisfaction and eating disorder
symptoms in children as young as age 5 years (Damiano, Paxton, Wertheim, McLean, & Gregg, 2015)
Moreover, social pressures toward thinness may be particularly powerful in higher socioeconomic backgrounds,
from which a majority of girls and women with anorexia nervosa appear to come (McClelland & Crisp, 2001).

III) CULTURAL DIFFERENCES

In the United States, it was reported at one time that the incidence of anorexia was eight times greater in white
women than in women of color (Dolan, 1991). More recent studies do not support this contention. Indeed there
is a somewhat greater incidence of eating disturbances and body dissatisfaction among white women than black
women (Grabe & Hyde, 2006; Perez & Joiner, 2003), but differences in actual eating disorders, particularly
bulimia, do not appear to be as great (Wildes, Emery, & Simons, 2001).
The relationship between BMI and body dissatisfaction also differs by ethnicity. Compared with African
American adolescents, white adolescents become more dissatisfied with their bodies as their BMI rises
(Striegel-Moore et al., 2000).
The emphasis on thinness and dieting has spread beyond white women of upper and middle socioeconomic
status to women of lower socioeconomic status, as has the prevalence of eating disorder pathology (e.g., Story
et al., 1995; Striegel-Moore et al., 2000).

IV) ETHNIC MINORTIIES AND EATING DISORDERS

Research has also been directed to the influence of cultural standards and values on body dissatisfaction and
eating disorders among ethnic minorities. African American girls and women tend to be more satisfied with
their body size, weight, and appearance than are white females, even though they tend to be heavier than their
white counterparts.
They also have a lower level of negative attitudes toward body size and weight and less motivation for thinness
(Chandler-Laney et al., 2009; Gilbert, 2003; Lovejoy, 2001). Although some show dissatisfaction with their
bodies and weight, more African American college students report satisfaction with their appearance, body size,
and shape compared with their white peers (Harris, 2006; Powell & Kahn, 1995).

V) CROSS CULTURAL STUDIES

Far fewer reports of eating disorders are found in Latin America, South America, and Asia, whereas they appear
to be increasing in European countries, Israel, and Australia (Miller & Pumariega, 2001). Countries or groups
that have been exposed to Western values show an increasing concern over eating and body size (Becker, 2004;
Steiger & Bruce, 2007). Although the standard of beauty among women in South Africa is based on fuller
figures, black teenage girls in this region are drawn to Western standards of thinness, resulting in a dramatic
increase in eating disorders among this group (Simmons, 2002). Asian countries that are exposed to Western
media also report increases in body shape concerns and distorted eating attitudes (Liao et al., 2010). Cultural
values and norms affect views on body shape and size. Weight normalcy is influenced by cultural beliefs and
practices.

C) COGNITIVE BEHAVIOURAL FACTORS

Cognitive behavioral theories of eating disorders focus on understanding the thoughts, feelings, and behaviors
that contribute to distorted body image, fear of fat, and loss of control over eating. People with eating disorders
may have maladaptive schemata that narrow their attention toward thoughts and images related to weight, body
shape, and food (Fairburn, Shafran, & Cooper, 1999).

ANOREXIA NERVOSA
Cognitive behavioral theories of anorexia nervosa emphasize fear of fatness and body-image disturbance as the
motivating factors that powerfully reinforce weight loss. Many who develop anorexia symptoms report that the
onset followed a period of weight loss and dieting. Behaviors that achieve or maintain thinness are negatively
reinforced by the reduction of anxiety about becoming fat. Furthermore, dieting and weight loss may be
positively reinforced by the sense of mastery or self-control they create (Fairburn et al., 1999; Garner, Vitousek,
& Pike, 1997).

BULIMIA NERVOSA AND BINGE- EATING DISORDER

People with bulimia nervosa are also thought to be over-concerned with weight gain and body appearance;
indeed, they judge their self-worth mainly by their weight and shape. They also have low self-esteem, and
because weight and shape are somewhat more controllable than are other features of the self, they tend to focus
on weight and shape, hoping their efforts in this area will make them feel better generally. They try to follow a
pattern of restrictive eating that is very rigid, with strict rules regarding how much to eat, what kinds of food to
eat, and when to eat. These strict rules are inevitably broken, and the lapse escalates into a binge. After the
binge, feelings of disgust and fear of becoming fat build up, leading to compensatory actions such as vomiting
(Fairburn, 1997). Although purging temporarily reduces the anxiety from having eaten too much, this cycle
lowers the person’s self-esteem, which triggers still more bingeing and purging, a vicious circle that maintains
desired body weight but has serious medical consequences.

Figure: Schematic of Cognitive Behavioral Theory of Bulimia Nervosa

D) ADDITIONAL RISK FACTORS

I) GENDER
Eating disorders are much more frequently found in women than in men. Being female is a strong risk factor for
developing eating disorders, particularly anorexia nervosa and bulimia nervosa (Jacobi et al., 2004). Moreover,
the greatest period of risk for these disorders occurs in adolescence. Binge-eating disorder does not follow this
pattern, however. The onset of binge-eating disorder is typically well after adolescence. Binge-eating disorder is
also much more likely to be found in males as well as in females. For men (but not for women) sexual
orientation is a risk factor for disordered eating. As we noted earlier, this may be because gay and bisexual men
are trying to be attractive to men, who (regardless of sexual orientation) typically place great emphasis on
physical appearance.
Distortions of body image in some males can also have tragic consequences. Olivardia, Pope, and Hudson
(2000) have described a syndrome in men, particularly male weight lifters, that they initially termed “reverse
anorexia nervosa.” Thus, although a marked gender difference in typical body image distortion is obvious, with
many women thinking they’re too big and some men thinking they’re too small, both types of distortion can
result in severe psychological and physical consequences (Corson & Andersen, 2002; Kanayama et al., 2006).

II) DIETING
Most people have been on a diet at some point in their lives (Jeffrey et al., 1991). Estimates are that, at any one
time, approximately 39 percent of women and 21 percent of men are trying to lose weight (Hill, 2002). Dieting
is a risk factor for the development or worsening of eating disorders (Jacobi et al., 2004; Striegel-Moore &
Bulik, 2007). In a large sample of adolescent girls, body dissatisfaction and dieting predicted symptoms of
bulimia nervosa at a 1-year follow-up (Johnson & Wardle, 2005).

III) CHILDHOOD SEXUAL ABUSE

Childhood sexual abuse has been implicated in the development of eating disorders (Jacobi et al., 2004).
However, there is some debate about whether sexual abuse is truly a risk factor for eating disorders (see Stice,
2002). In one prospective study, Vogeltanz-Holm and colleagues (2000) failed to find that early sexual abuse
predicted the later onset of binge eating. However, another prospective study found that children who had been
sexually abused or physically neglected had higher rates of eating disorders and eating problems in adolescence
and adulthood (Johnson, Cohen, et al., 2002).
One possibility is that being sexually abused increases the risk of developing other disorders that are comorbid
with eating disorders. This would mean that abuse is a general risk factor for psychopathology rather than a
specific risk factor.

AN INTEGRATIVE MODEL
Although the three major eating disorders are identifiable by their unique characteristics, and the specific
diagnoses have some validity, it is becoming increasingly clear that all eating disorders have much in common
in terms of causal factors. It may be more useful to lump the eating disorders into one diagnostic category,
simply noting which specific features occur, such as dietary restraint, bingeing, or purging. Recently
Christopher Fairburn and colleagues have attempted to develop this approach ( Fairburn et al., 2007; Fairburn &
Cooper, in press). Thus, we have integrated a discussion of the causes of eating disorders.
In putting together what we know about eating disorders, it is important to remember, again, that no one factor
seems sufficient to cause them. Individuals with eating disorders may have some of the same biological
vulnerabilities (such as being highly responsive to stressful life events) as individuals with anxiety disorders
(Kendler et al., 1995; Rojo, Conesa, Bermudez, & Livianos, 2006).
Figure: MULTIPATH MODEL FOR EATING DISORDERS (The dimensions interact with one another
and combine in different ways to result in an eating disorder.)
GENDER DYSPHORIA
Gender dysphoria is discomfort with one’s sex relevant physical characteristics or with one’s assigned gender.
GD is a new term used in DSM-V in place of the previous gender identity disorder, the degree of dysphoria can
vary and may fluctuate over time within the same individual. Gender dysphoria can be diagnosed at two
different life stages, either during childhood (gender dysphoria in children) or adolescents or adulthood (that is
gender dysphoria in adolescents and adults).
Gender dysphoria refers to the distress that may accompany the incongruence between one’s experienced or
expressed gender and one’s assigned gender although not all individuals will experience distress as a result of
such incongruence many are distressed if the desired physical interventions by means of hormones and or
surgery are not available. The current term is more descriptive than the pervious DSM-4 term gender identity
disorder and focuses on dysphoria as the clinical problem, not identity perse.
In DSM-V there is one over-arching diagnosis of gender dysphoria, which separate developmently appropriate
criteria sets for children and for adolescents and adults.

DSM-V criteria for gender dysphoria in children-

A marked incongruence between one’s experienced or expressed gender and assigned gender, of at least 6
months duration, as manifested by at least 6 of the following;
1. A strong desire to be of the other gender or an insistence that one is the other gender (or some alternative
gender different from one’s assigned gender).
2. In boys (assigned gender), a strong preference for cross-dressing or simulating female attire; or in girls
(assigned gender), a strong preference for wearing only typical masculine clothing and a strong resistance to the
wearing of typical feminine clothing.
3. A strong preference for cross-gender roles in make-believe play or fantasy play.
4. A strong preference for the toys, games or activities stereotypically used or engaged in by the other
gender.
5. A strong preference for play-mates of the other gender.
6. In boys (assigned gender), a strong rejection of typically masculine toys, games and activities and a
strong avoidance of rough and tumble play; or in girls (assigned gender), a strong rejection of typically feminine
toys, games and activities.
7. A strong dislike of one’s sexual anatomy.
8. A strong desire for the primary and secondary sex characteristics that matched one’s experienced
gender.
B. The condition is associated with clinically significant distress or impairment in social school or other
important areas of functioning.

DSM-V criteria for gender dysphoria in adolescents and adults-

A marked incongruence between one’s experienced or expressed gender and assigned gender, of at-least 6
months duration, as manifested by at least 2 of the following:
1. A marked incongruence between one’s experienced or expressed gender and primary or secondary sex
characteristics (or in young adolescents, the anticipated secondary sex characteristics).
2. A strong desire to be rid of one’s primary or secondary sex characteristics because of a marked
incongruence with one’s experienced or expressed gender (or in young adolescents, a desire to prevent the
development of the anticipated secondary sex characteristics).
3. A strong desire for the primary or secondary sex characteristics of the other gender.
4. A strong desire to be of the other gender (or some alternative gender different from one’s assigned
gender).
5. A strong desire to be treated as the other gender (or some alternative gender different from one’s
assigned gender).
6. A strong conviction that one has the typical feelings and reactions of the other gender (or some
alternative gender different from one’s assigned gender).
B. The condition is associated with clinically significant distress or impairment in social, occupational or
other important areas of functioning.
Key characteristics of gender dysphoria:

 Boys with gender dysphoria often show a preoccupation with traditionally feminine activities (Cohen-
Kettenis & klink, 2015). They may prefer to dress in female clothing they enjoy stereotypical girl’s
activities such as playing with dolls and playing house. They usually avoid rough and tumble play and
often express the desire to be a girl.
 Girls with gender dysphoria typically prefer traditional boy’s clothing and short hair. Fantasy heroes
often include powerful male figures like batman and superman. They show little interest in dolls and
increased interest in sports, although many girls considered to be ‘tomboys’ frequently have many or
most of these traits, girls with gender dysphoria are distinguished by their desire to actually be a boy or
to grow up as a man.
 Young girls with gender dysphoria are treated better by their peers than are boys with gender dysphoria
because cross-gender behaviour in girls is better tolerated ( Cohen-Kettenis et al, 2003). In clinic-
referred gender dysphoria boys outnumbered girls 5-1 in one study (Cohen-Kettenis et al, 2003) and 3-1
 in another study (Cohen-Kettenis et al, 2006). An appreciable percentage of that imbalance may reflect
greater parental concern about femineity in boys than about masculinity in girls.
 The most common adult outcome of boys with gender dysphoria has been homosexuality rather than
trans-sexualism (Zucker, 2005). In Richard green’s (1987) prospective study of 44 very feminine boys
from the community, only one had sought sex change surgery by age 18. About 3 quarters became gay
or bisexual men who were evidently satisfied with their biological sex however several later studies of
clinic referred children have found that 10-20% boys with gender dysphoria were trans-sexual by age 16
or 18 and about 40-60% identified themselves as homosexuals or bisexuals, a percentage that may have
increased by the time they were older (Zucker, 2005). Several smaller prospective studies of girls with
gender dysphoria have shown that 35-45% may show persistent gender dysphoria (leading to a desire for
sex re-assignment surgery in many), and about half had a homosexual orientation. However largest
prospective study to date which followed 25 girls with gender dysphoria (ages 3-12) into young
adulthood (average age 23), found somewhat lower rates of persistent gender dysphoria and
homosexuality. At follow up, 3 were classified as being dissatisfied with their gender and two of these 3
wanted to have sex re-assignment surgery. However, 32% had homosexual or bisexual fantasies and
24% engaged in homosexual or bisexual behaviour these rates are clearly much higher than expected
from base rates of gender dysphoria in the population but not as high as in boys with gender dysphoria
(Drummond et al, 2008).
Research from non-western cultures shows that stigmatization of gender non-conforming children is not
universal (Vasey & Bartlett, 2007). In Samoa, very feminine males are often considered ‘fa’afafine’ (roughly
meaning ‘in the manner of women’), a kind of third gender, neither male nor female. Fa’afafine are identified as
young children by their behaviour and usually are accepted by their families and culture. As adults these
individuals sexually attracted to other men and typically have sexual relations with heterosexual men. They
generally do not recall that their gender non-conformity was associated with distress. Because of this some have
argued that childhood gender dysphoria should not appear DSM-V (Vasey & Bartlett, 2007).
Very little is known about the origins of gender identity in normal men and women, so it is not surprising that
etiology of gender dysphoria is also poorly understood (Richmond, Carroll & Denboske, 2010). There is some
reason to believe that gender identity is strongly influenced by sex hormones, especially during the pre-natal
period (Diamond, 2009).
Children and adolescents with gender dysphoria are often brought in by their parents for psychotherapy (Zucker
et al. 2008). Specialists attempt both to treat the child’s unhappiness with his/her biological sex with his/her
biological sex and to ease strained relations with parents and peers. Children with gender dysphoria often have
other general psychological and behavioral problems such as anxiety and mood disorders that also need
therapeutic attention (Zucker et al, 2002). Therapists try to improve peer and parental relations by teaching such
children how to reduce their cross-gender behaviour, especially in situations where it might cause interpersonal
problems.
Gender dysphoria is typically treated psychodynamic ally- that is by examining inner-conflicts. If a child will
eventually transition into the other sex, it is beneficial to prevent full sexual maturity from occurring in the
original, unwanted sex. Thus, in the progressive Netherlands under some circumstances early adolescents with
gender dysphoria are given hormonal treatment to delay puberty while they decide how to proceed (Cohen-
Kettenis, 2010 ).
Two related facts about gender dysphoria in children are especially important clinically

 First, most children with gender dysphoria do not become adults with gender dysphoria the problem
generally remits during childhood (Wallien & Cohen-Kettenis, 2008).
 Second, individuals who are gender dysphoric into adolescents are likely to remain so into adulthood
and they are also likely to take medical steps to transform their bodies, the crucial period at which many
children with dysphoria desist or persist appear to be ages 10-13 (Steensma et al, 2011). Increasing
numbers of parents of children with gender dysphoria are cooperating with their children’s wishes and
allowing them socially to assume an identity opposite to their birth sex (Rosin, 2008).
UPD UNIT 4

BINGE EATING DISORDERS

Feeding and eating disorders are characterized by a persistent disturbance of eating or eating-related
behaviour that results in the altered consumption or absorption of food and that significantly impairs
physical health or psychosocial functioning.

Some individuals with eating disorders report eating-related symptoms resembling those typically
endorsed by individuals with substance use disorders, such as craving and patterns of compulsive use.
This resemblance may reflect the involvement of the same neural systems, including those implicated
in regulatory self-control and reward, in both groups of disorders. However, the relative contributions
of shared and distinct factors in the development and perpetuation of eating and substance use
disorders remain insufficiently understood.

ANOREXIA NERVOSA

Diagnostic Criteria

A. Restriction of energy intake relative to requirements, leading to a significantly low body weight in
the context of age, sex, developmental trajectory, and physical health. Significantly low weight is
defined as a weight that is less than minimally normal or, for children and adolescents, less than that
minimally expected.

B. Intense fear of gaining weight or of becoming fat, or persistent behavior that interferes with weight
gain, even though at a significantly low weight.

C. Disturbance in the way in which one's body weight or shape is experienced, undue influence of body
weight or shape on self-evaluation, or persistent lack of recognition of the seriousness of the current
low body weight.

Specify whether:

(F50.01) Restricting type: During the last 3 months, the individual has not engaged in recurrent
episodes of binge eating or purging behavior (i .e., self-induced vomiting or the misuse of laxatives,
diuretics, or enemas). This subtype describes presentations in which weight loss is accomplished
primarily through dieting, fasting, and/or excessive exercise.

(F50.02) Binge-eating/purging type: During the last 3 months, the individual has engaged in recurrent
episodes of binge eating or purging behavior (i.e., self-induced vomiting or the misuse of laxatives,
diuretics, or enemas).

Specify if:

In partial remission: After full criteria for anorexia nervosa were previously met, Criterion A (low body
weight) has not been met for a sustained period, but either Criterion B (intense fear of gaining weight
or becoming fat or behavior that interferes with weight gain) or Criterion C (disturbances in self-
perception of weight and shape) is still met.

In full remission: After full criteria for anorexia nervosa were previously met, none of the criteria have
been met for a sustained period of time.

Specify current severity:

The minimum level of severity is based, for adults, on current body mass index (BMI) (see below) or,
for children and adolescents, on BMI percentile. The ranges below are derived from World Health
Organization categories for thinness in adults; for children and adolescents, corresponding BMI
percentiles should be used. The level of severity may be increased to reflect clinical symptoms, the
degree of functional disabil ity, and the need for supervision.

Mild: BMI < 15 kg/m2

Moderate: BMI 16-16.99 kg/m2

Severe: BMI 15-15.99 kg/m2

Extreme: BMI < 15 kg/m2

Subtypes
Most individuals with the binge-eating/purging type of anorexia nervosa who binge eat also purge
through self-induced vomiting or the misuse of laxatives, diuretics, or enemas. Some individuals with
this subtype of anorexia nervosa do not binge eat but do regularly purge after the consumption of
small amounts of food.

Crossover between the subtypes over the course of the disorder is not uncommon; therefore, subtype
description should be used to describe current symptoms rather than longitudinal course.

Diagnostic Features

There are three essential features of anorexia nervosa: persistent energy intake restriction; intense
fear of gaining weight or of becoming fat, or persistent behavior that interferes with weight gain; and
a disturbance in self-perceived weight or shape.
The individual maintains a body weight that is below a minimally normal level for age, sex,
developmental trajectory, and physical health (Criterion A). Individuals' body weights frequently meet
this criterion following a significant weight loss, but among children and adolescents, there may
alternatively be failure to make expected weight gain or to maintain a normal developmental
trajectory (i.e., while growing in height) instead of weight loss.

Criterion A requires that the individual's weight be significantly low (i.e., less than minimally normal
or, for children and adolescents, less than that minimally expected). Body mass index (BMI; calculated
as weight in kilograms/height in meters2 ) is a useful measure to assess body weight for height. For
adults, a BMI of 18.5 kg/m2 has been employed by the Centers for Disease Control and Prevention
(CDC) and the World Health Organization (WHO) as the lower limit of normal body weight. An adult
with a BMI between 17.0 and 18.5 kg/ m 2 , or even above 18.5 kg/ m , might be considered to have
a significantly low weight if clinical history or other physiological information supports this judgment.

In summary, in determining whether Criterion A is met, the clinician should consider available
numerical guidelines, as well as the individual's body build, weight history, and any physiological
disturbances.

Individuals with this disorder typically display an intense fear of gaining weight or of becoming fat
(Criterion B). This intense fear of becoming fat is usually not alleviated by weight loss. In fact, concern
about weight gain may increase even as weight falls. Younger individuals with anorexia nervosa, as
well as some adults, may not recognize or acknowledge a fear of weight gain. In the absence of another
explanation for the significantly low weight, clinician inference drawn from collateral history,
observational data, physical and laboratory findings, or longitudinal course either indicating a fear of
weight gain or supporting persistent behaviors that prevent it may be used to establish Criterion B.

Often, the individual is brought to professional attention by family members after marked weight loss
(or failure to make expected weight gains) has occurred. If individuals seek help on their own, it is
usually because of distress over the somatic and psychological sequelae of starvation. It is rare for an
individual with anorexia nervosa to complain of weight loss per se. In fact, individuals with anorexia
nervosa frequently either lack insight into or deny the problem. It is therefore often important to
obtain information from family members or other sources to evaluate the history of weight loss and
other features of the illness.

Prevalence

The 12-month prevalence of anorexia nervosa among young females is approximately 0.4%. Less is
known about prevalence among males, but anorexia nervosa is far less common in males than in
females, with clinical populations generally reflecting approximately a 10:1 female-to-male ratio.

Development and Course

Anorexia nervosa commonly begins during adolescence or young adulthood. It rarely begins before
puberty or after age 40, but cases of both early and late onset have been described. The onset of this
disorder is often associated with a stressful life event, such as leaving home for college. The course
and outcome of anorexia nervosa are highly variable. Younger individuals may manifest atypical
features, including denying "fear of fat." Older individuals more likely have a longer duration of illness,
and their clinical presentation may include more signs and symptoms of long-standing disorder.
Clinicians should not exclude anorexia nervosa from the differential diagnosis solely on the basis of
older age.

Many individuals have a period of changed eating behavior prior to full criteria for the disorder being
met. Some individuals with anorexia nervosa recover fully after a single episode, with some exhibiting
a fluctuating pattern of weight gain followed by relapse, and others experiencing a chronic course over
many years.

Hospitalization may be required to restore weight and to address medical complications. Most
individuals with anorexia nervosa experience remission within 5 years of presentation. Among
individuals admitted to hospitals, overall remission rates may be lower.

The crude mortality rate (CMR) for anorexia nervosa is approximately 5% per decade. Death most
commonly results from medical complications associated with the disorder itself or from suicide.

Risk and Prognostic Factors

Temperamental. Individuals who develop anxiety disorders or display obsessional traits in childhood
are at increased risk of developing anorexia nervosa.

Environmental. Historical and cross-cultural variability in the prevalence of anorexia nervosa supports
its association with cultures and settings in which thinness is valued. Occupations and avocations that
encourage thinness, such as modeling and elite athletics, are also associated with increased risk.

Genetic and physiological. There is an increased risk of anorexia nervosa and bulimia nervosa among
first-degree biological relatives of individuals with the disorder. An increased risk of bipolar and
depressive disorders has also been found among first-degree relatives of individuals with anorexia
nervosa, particularly relatives of individuals with the binge-eating/purging type. Concordance rates
for anorexia nervosa in monozygotic twins are significantly higher than those for dizygotic twins. A
range of brain abnormalities has been described in anorexia nervosa using functional imaging
technologies (functional magnetic resonance imaging, positron emission tomography). The degree to
which these findings reflect changes associated with malnutrition versus primary abnormalities
associated with the disorder is unclear.

Culture-Related Diagnostic Issues

 Anorexia nervosa occurs across culturally and socially diverse populations, although available
evidence suggests cross-cultural variation in its occurrence and presentation.
 Anorexia nervosa is probably most prevalent in post-industrialized, high-income countries
such as in the United States, many European countries, Australia, New Zealand, and Japan,
but its incidence in most low- and middle-income countries is uncertain.
 Whereas the prevalence of anorexia nervosa appears comparatively low among Latinos,
African Americans, and Asians in the United States.
 The presentation of weight concerns among individuals with eating and feeding disorders
varies substantially across cultural contexts. The absence of an expressed intense fear of
weight gain, sometimes referred to as "fat phobia," appears to be relatively more common in
populations in Asia,
 Within the United States, presentations without a stated intense fear of weight gain may be
comparatively more common among Latino groups.

Diagnostic Markers

The following laboratory abnormalities may be observed in anorexia nervosa; their presence may
serve to increase diagnostic confidence.

Hematology. Leukopenia is common, with the loss of all cell types but usually with apparent
lymphytosis. Mild anemia can occur, rarely, bleeding problems.

Serum chemistry. Dehydration may be reflected by an elevated blood urea nitrogen level.
Hypercholesterolemia is common. Hepatic enzyme levels may be elevated. Self-induced vomiting may
lead to metabolic alkalosis (elevated serum bicarbonate), hypochloremia, and hypokalemia; laxative
abuse may cause a mild metabolic acidosis.

Endocrine. Serum thyroxine (T4) levels are usually in the low-normal range; triiodothyronine (T 3)
levels are decreased, while reverse T 3 levels are elevated. Females have low serum estrogen levels,
whereas males have low levels of serum testosterone.

Electrocardiography. Sinus bradycardia is common, and, rarely, arrhythmias are noted.

Bone mass. Low bone mineral density, with specific areas of osteopenia or osteoporosis, is often seen.
The risk of fracture is significantly elevated.

Physical signs and symptoms. Many of the physical signs and symptoms of anorexia nervosa are
attributable to starvation. Amenorrhea is commonly present and appears to be an indicator of
physiological dysfunction. If present, amenorrhea is usually a consequence of the weight loss, but in a
minority of individuals it may actually precede the weight loss. In prepubertal females, menarche may
be delayed. In addition to amenorrhea, there may be complaints of constipation, abdominal pain, cold
intolerance, lethargy, and excess energy.
 The most remarkable finding on physical examination is emaciation. Commonly, there is also
significant hypotension, hypothermia, and bradycardia. Some individuals develop lanugo, a fine
downy body hair. Some develop peripheral edema, especially during weight restoration or upon
cessation of laxative.

Suicide Risk

Suicide risk is elevated in anorexia nervosa, with rates reported as 12 per 100,000 per year.
Comprehensive evaluation of individuals with anorexia nervosa should include assessment of suicide-
related ideation and behaviors as well as other risk factors for suicide, including a history of suicide
attempt.

Differential Diagnosis

Other possible causes of either significantly low body weight or significant weight loss should be
considered in the differential diagnosis of anorexia nervosa, especially when the presenting features
are atypical (e.g., onset after age 40 years).

Medical conditions (e.g., gastrointestinal disease, hyperthyroidism, and acquired immunodeficiency

syndrome [AIDS]). Acute weight loss associated with a medical condition can occasionally be followed
by the onset or recurrence of anorexia nervosa, which can initially be masked by the comorbid medical
condition.

Major depressive disorder. In major depressive disorder, severe weight loss may occur, but most
individuals with major depressive disorder do not have either a desire for excessive weight loss or an
intense fear of gaining weight.

Schizophrenia. Individuals with schizophrenia may exhibit odd eating behavior and occasionally
experience significant weight loss, but they rarely show the fear of gaining weight and the body image
disturbance required for a diagnosis of anorexia nervosa.

Substance use disorders. Individuals with substance use disorders may experience low weight due to
poor nutritional intake but generally do not fear gaining weight and do not manifest body image
disturbance.

Social anxiety disorder (social phobia), obsessive-compulsive disorder, and body dysmorphic
disorder. Some of the features of anorexia nervosa overlap with the criteria for social phobia, OCD,
and body dysmorphic disorder. Specifically, individuals may feel humiliated or embarrassed to be seen
eating in public, as in social phobia; may exhibit obsessions and compulsions related to food, as in
OCD; or may be preoccupied with an imagined defect in bodily appearance, as in body dysmorphic
disorder. If the individual with anorexia nervosa has social fears that are limited to eating behavior
alone, the diagnosis of social phobia should not be made, but social fears unrelated to eating behavior
(e.g., excessive fear of speaking in public) may warrant an additional diagnosis of social phobia.
Similarly, an additional diagnosis of OCD should be considered only if the individual exhibits obsessions
and compulsions unrelated to food (e.g., an excessive fear of contamination), and an additional
diagnosis of body dysmorphic disorder should be considered only if the distortion is unrelated to body
shape and size (e.g., preoccupation that one's nose is too big).

Bulimia nervosa. Individuals with bulimia nervosa exhibit recurrent episodes of binge eating, engage
in inappropriate behavior to avoid weight gain (e.g., self-induced vomiting), and are overly concerned
with body shape and weight. However, unlike individuals with anorexia nervosa, binge-eating/purging
type, individuals with bulimia nervosa maintain body weight at or above a minimally normal level.
Comorbidity

Bipolar, depressive, and anxiety disorders commonly co-occur with anorexia nervosa. Many
individuals with anorexia nervosa report the presence of either an anxiety disorder or symptoms prior
to onset of their eating disorder. OCD is described in some individuals with anorexia nervosa,
especially those with the restricting type. Alcohol use disorder and other substance use disorders may
also be comorbid with anorexia nervosa, especially among those with the binge-eating/purging type.

BULIMIA NERVOSA
Diagnostic Criteria

A. Recurrent episodes of binge eating. An episode of binge eating is characterized by both of the
following:

1. Eating, in a discrete period of time (e.g., within any 2-hour period), an amount of food that is
definitely larger than what most individuals would eat in a similar period of time under similar
circumstances.

2. A sense of lack of control over eating during the episode (e.g., a feeling that one cannot stop eating
or control what or how much one is eating).

B. Recurrent inappropriate compensatory behaviors in order to prevent weight gain, such as self-
induced vomiting; misuse of laxatives, diuretics, or other medications; fasting; or excessive exercise.

C. The binge eating and inappropriate compensatory behaviors both occur, on average, at least once
a week for 3 months.

D. Self-evaluation is unduly influenced by body shape and weight.

E. The disturbance does not occur exclusively during episodes of anorexia nervosa.

Specify if:

In partial remission: After full criteria for bulimia nervosa were previously met, some, but not all, of
the criteria have been met for a sustained period of time.
In full remission: After full criteria for bulimia nervosa were previously met, none of the criteria have
been met for a sustained period of time.

Specify current severity:

The minimum level of severity is based on the frequency of inappropriate compensatory behaviors
(see below). The level of severity may be increased to reflect other symptoms and the degree of
functional disability.

Mild: An average of 1 -3 episodes of inappropriate compensatory behaviors per week.

Moderate: An average of 4-7 episodes of inappropriate compensatory behaviors per week.

Severe: An average of 8-1 3 episodes of inappropriate compensatory behaviors per week.

Extreme: An average of 14 or more episodes of inappropriate compensatory behaviors per week.

Diagnostic Features
There are three essential features of bulimia nervosa: recurrent episodes of binge eating (Criterion A),
recurrent inappropriate compensatory behaviors to prevent weight gain (Criterion B), and self-
evaluation that is unduly influenced by body shape and weight (Criterion D). To qualify for the
diagnosis, the binge eating and inappropriate compensatory behaviors must occur, on average, at
least once per week for 3 months (Criterion C).

An "episode of binge eating" is defined as eating, in a discrete period of time, an amount of food that
is definitely larger than most individuals would eat in a similar period of time under similar
circumstances (Criterion Al). The context in which the eating occurs may affect the clinician's
estimation of whether the intake is excessive. For example, a quantity of food that might be regarded
as excessive for a typical meal might be considered normal during a celebration or holiday meal. A
"discrete period of time" refers to a limited period, usually less than 2 hours. A single episode of binge
eating need not be restricted to one setting. For example, an individual may begin a binge in a
restaurant and then continue to eat on returning home. Continual snacking on small amounts of food
throughout the day would not be considered an eating binge.

An occurrence of excessive food consumption must be accompanied by a sense of lack of control

(Criterion A2) to be considered an episode of binge eating. An indicator of loss of control is the inability
to refrain from eating or to stop eating once started. Some individuals describe a dissociative quality
during, or following, the binge-eating episodes. The impairment in control associated with binge
eating may not be absolute; for example, an individual may continue binge eating while the telephone
is ringing but will cease if a roommate or spouse unexpectedly enters the room. Some individuals
report that their binge-eating episodes are no longer characterized by an acute feeling of loss of
control but rather by a more generalized pattern of uncontrolled eating. If individuals report that they
have abandoned efforts to control their eating, loss of control should be considered as present. Binge
eating can also be planned in some instances.

The type of food consumed during binges varies both across individuals and for a given individual.
Binge eating appears to be characterized more by an abnormality in the amount of food consumed
than by a craving for a specific nutrient. However, during binges, individuals tend to eat foods they
would otherwise avoid.

Individuals with bulimia nervosa are typically ashamed of their eating problems and attempt to
conceal their symptoms. Binge eating usually occurs in secrecy or as inconspicuously as possible. The
binge eating often continues until the individual is uncomfortably, or even painfully, full. The most
common antecedent of binge eating is negative affect. Other triggers include interpersonal stressors;
dietary restraint; negative feelings related to body weight, body shape, and food; and boredom. Binge
eating may minimize or mitigate factors that precipitated the episode in the short-term, but negative
self-evaluation and dysphoria often are the delayed consequences.

Another essential feature of bulimia nervosa is the recurrent use of inappropriate compensatory
behaviors to prevent weight gain, collectively referred to as purge behaviors or purging (Criterion B).
Many individuals with bulimia nervosa employ several methods to compensate for binge eating.
Vomiting is the most common inappropriate compensatory behavior. The immediate effects of
vomiting include relief from physical discomfort and reduction of fear of gaining weight. In some cases,
vomiting becomes a goal in itself, and the individual will binge eat in order to vomit or will vomit after
eating a small amount of food. Individuals with bulimia nervosa may use a variety of methods to
induce vomiting, including the use of fingers or instruments to stimulate the gag reflex. Individuals
generally become adept at inducing vomiting and are eventually able to vomit at will. Other purging
behaviors include the misuse of laxatives and diuretics. Individuals with this disorder may take thyroid
hormone in an attempt to avoid weight gain. Individuals with diabetes mellitus and bulimia nervosa
may omit or reduce insulin doses in order to reduce the metabolism of food consumed during eating
binges. Individuals with bulimia nervosa may fast for a day or more or exercise excessively in an
attempt to prevent weight gain. Exercise may be considered excessive when it significantly interferes
with important activities, when it occurs at inappropriate times or in inappropriate settings, or when
the individual continues to exercise despite injury or other medical complications.

Individuals with bulimia nervosa place an excessive emphasis on body shape or weight in their self-
evaluation, and these factors are typically extremely important in determining self-esteem (Criterion
D). Individuals with this disorder may closely resemble those with anorexia nervosa in their fear of
gaining weight, in their desire to lose weight, and in the level of dissatisfaction with their bodies.
However, a diagnosis of bulimia nervosa should not be given when the disturbance occurs only during
episodes of anorexia nervosa (Criterion E).

Associated Features Supporting Diagnosis

Individuals with bulimia nervosa typically are within the normal weight or overweight range (body
mass index [BMI] < 30 in adults). The disorder occurs but is uncommon among obese individuals.
Between eating binges, individuals with bulimia nervosa typically restrict their total caloric
consumption and preferentially select low-calorie ("diet") foods while avoiding foods that they
perceive to be fattening or likely to trigger a binge.

Menstrual irregularity or amenorrhea often occurs among females with bulimia nervosa; it is
uncertain whether such disturbances are related to weight fluctuations, to nutritional deficiencies, or
to emotional distress.

The fluid and electrolyte disturbances resulting from the purging behavior are sometimes sufficiently
severe to constitute medically serious problems. Rare but potentially fatal complications include
esophageal tears, gastric rupture, and cardiac arrhythmias. Individuals who chronically abuse
laxatives may become dependent on their use to stimulate bowel movements. Gastrointestinal
symptoms are commonly associated with bulimia nervosa.

Prevalence

Twelve-month prevalence of bulimia nervosa among young females is 1%-1 .5%. Point prevalence is
highest among young adults since the disorder peaks in older adolescence and young adulthood. Less
is known about the point prevalence of bulimia nervosa in males, but bulimia nervosa is far less
common in males than it is in females, with an approximately 10:1 female-to-male ratio.

Development and Course

Bulimia nervosa commonly begins in adolescence or young adulthood. Onset before puberty or after
age 40 is uncommon. The binge eating frequently begins during or after an episode of dieting to lose
weight. Experiencing multiple stressful life events also can precipitate onset of bulimia nervosa.

Disturbed eating behavior persists for at least several years in a high percentage of clinic samples. The
course may be chronic or intermittent, with periods of remission alternating with recurrences of binge
eating. However, over longer-term follow-up, the symptoms of many individuals appear to diminish
with or without treatment, although treatment clearly impacts outcome. Periods of remission longer
than 1 year are associated with better long-term outcome.

Significantly elevated risk for mortality (all-cause and suicide) has been reported for individuals with
bulimia nervosa. The CMR (crude mortality rate) for bulimia nervosa is nearly 2% per decade.
Diagnostic cross-over from initial bulimia nervosa to anorexia nervosa occurs in a minority of cases
(10%-15%). Individuals who do experience cross-over to anorexia nervosa commonly will revert back
to bulimia nervosa or have multiple occurrences of cross-overs between these disorders. A subset of
individuals with bulimia nervosa continue to binge eat but no longer engage in inappropriate
compensatory behaviors, and therefore their symptoms meet criteria for binge-eating disorder or
other specified eating disorder. Diagnosis should be based on the current (i.e., past 3 months) clinical
presentation.

Risk and Prognostic Factors

Temperamental. Weight concerns, low self-esteem, depressive symptoms, social anxiety disorder,
and overanxious disorder of childhood are associated with increased risk for the development of
bulimia nervosa.

Environmental. Internalization of a thin body ideal has been found to increase risk for developing
weight concerns, which in turn increase risk for the development of bulimia nervosa. Individuals who
experienced childhood sexual or physical abuse are at increased risk for developing bulimia nervosa.

Genetic and physiological. Childhood obesity and early pubertal maturation increase risk for bulimia
nervosa. Familial transmission of bulimia nervosa may be present, as well as genetic vulnerabilities for
the disorder.

Course modifiers. Severity of psychiatric comorbidity predicts worse long-term outcome of bulimia
nervosa.

Culture-Related Diagnostic Issues

Bulimia nervosa has been reported to occur with roughly similar frequencies in most industrialized
countries, including the United States, Canada, many European countries, Australia, Japan, New
Zealand, and South Africa. In clinical studies of bulimia nervosa in the United States, individuals
presenting with this disorder are primarily white. However, the disorder also occurs in other ethnic
groups and with prevalence comparable to estimated prevalences observed in white samples.

Gender-Related Diagnostic Issues

Bulimia nervosa is far more common in females than in males. Males are especially underrepresented
in treatment-seeking samples, for reasons that have not yet been systematically examined.

Diagnostic Markers

No specific diagnostic test for bulimia nervosa currently exists. However, several laboratory
abnormalities may occur as a consequence of purging and may increase diagnostic certainty. These
include fluid and electrolyte abnormalities, such as hypokalemia (which can provoke cardiac
arrhythmias), hypochloremia, and hyponatremia. The loss of gastric acid through vomiting may
produce a metabolic alkalosis (elevated serum bicarbonate), and the frequent induction of diarrhea
or dehydration through laxative and diuretic abuse can cause metabolic acidosis.

Physical examination usually yields no physical findings.

However, inspection of the mouth may reveal significant and permanent loss of dental enamel,
especially from lingual surfaces of the front teeth due to recurrent vomiting. These teeth may become
chipped and appear ragged and "moth-eaten." T

there may also be an increased frequency of dental caries.

In some individuals, the salivary glands, particularly the parotid glands, may become notably enlarged.

Individuals who induce vomiting by manually stimulating the gag reflex may develop calluses or scars
on the dorsal surface of the hand from repeated contact with the teeth.

Serious cardiac and skeletal myopathies have been reported among individuals following repeated
use of syrup of ipecac to induce vomiting.

Suicide Risk

Suicide risk is elevated in bulimia nervosa. Comprehensive evaluation of individuals with this disorder
should include assessment of suicide-related ideation and behaviors as well as other risk factors for
suicide, including a history of suicide attempts.

Comorbidity

 Comorbidity with mental disorders is common in individuals with bulimia nervosa, with most
experiencing at least one other mental disorder and many experiencing multiple
comorbidities.
 There is an increased frequency of depressive symptoms (e.g., low self-esteem) and bipolar
and depressive disorders (particularly depressive disorders) in individuals with bulimia
nervosa.
 In many individuals, the mood disturbance begins at the same time as or following the
development of bulimia nervosa, and individuals often ascribe their mood disturbances to the
bulimia nervosa. However, in some individuals, the mood disturbance clearly precedes the
development of bulimia nervosa.
 There may also be an increased frequency of anxiety symptoms (e.g., fear of social situations)
or anxiety disorders.
 These mood and anxiety disturbances frequently remit following effective treatment of the
bulimia nervosa.
 The lifetime prevalence of substance use, particularly alcohol or stimulant use, is at least 30%
among individuals with bulimia nervosa. Stimulant use often begins in an attempt to control
appetite and weight.
 A substantial percentage of individuals with bulimia nervosa also have personality features
that meet criteria for one or more personality disorders, most frequently borderline
personality disorder.

BINGE-EATING DISORDER

Diagnostic Criteria

A. Recurrent episodes of binge eating. An episode of binge eating is characterized by both of the
following:
1. Eating, in a discrete period of time (e.g., within any 2-hour period), an amount of food that is
definitely larger than what most people would eat in a similar period of time under similar
circumstances.

2. A sense of lack of control over eating during the episode (e.g., a feeling that one cannot stop
eating or control what or how much one is eating).

B. The binge-eating episodes are associated with three (or more) of the following:
 1. Eating much more rapidly than normal.

2. Eating until feeling uncomfortably full.

3. Eating large amounts of food when not feeling physically hungry.

4. Eating alone because of feeling embarrassed by how much one is eating.

5. Feeling disgusted with oneself, depressed, or very gui lty afterward.

C. Marked distress regarding binge eating is present.

D. The binge eating occurs, on average, at least once a week for 3 months.

E. The binge eating is not associated with the recurrent use of inappropriate compensatory
behavior as in bulimia nervosa and does not occur exclusively during the course of bulimia nervosa
or anorexia nervosa.

Specify if:

In partial remission: After full criteria for binge-eating disorder were previously met, binge eating
occurs at an average frequency of less than one episode per week for a sustained period of time.

In full remission: After full criteria for binge-eating disorder were previously met, none of the
criteria have been met for a sustained period of time.

Specify current severity: The minimum level of severity is based on the frequency of episodes of
binge eating (see below). The level of severity may be increased to reflect other symptoms and
the degree of functional disabil ity.

 Mild: 1 -3 binge-eating episodes per week.

 Moderate: 4-7 binge-eating episodes per week.
 Severe: 8-1 3 binge-eating episodes per week.
 Extreme: 14 or more binge-eating episodes per week.

Diagnostic Features

The essential feature of binge-eating disorder is recurrent episodes binge eating that must occur,
on average, at least once per week for 3 months (Criterion D).

An "episode of binge eating" is defined as eating, in a discrete period of time, an amount of food that
is definitely larger than most people would eat in a similar period of time under similar circumstances
(Criteriqn A1). The context in which the eating occurs may affect the clinician's estimation of whether
the intake is excessive. For example, a quantity of food that might be regarded as excessive for a
typical meal might be considered normal during a celebration or holiday meal. A "discrete period of
time" refers to a limited period, usually less than 2 hours. A single episode of binge eating need not
be restricted to one setting. For example, an individual may begin a binge in a restaurant and then
continue to eat on returning home. Continual snacking on small amounts of food throughout the day
would not be considered an eating binge.

An occurrence of excessive food consumption must be accompanied by a sense of lack of control

(Criterion A2) to be considered an episode of binge eating. An indicator of loss of control is the inability
to refrain from eating or to stop eating once started. Some individuals describe a dissociative quality
during, or following, the binge-eating episodes. The impairment in control associated with binge
eating may not be absolute; for example, an individual may continue binge eating while the telephone
is ringing but will cease if a roommate or spouse unexpectedly enters the room. Some individuals
report that their binge-eating episodes are no longer characterized by an acute feeling of loss of
control but rather by a more generalized pattern of uncontrolled eating. If individuals report that they
have abandoned efforts to control their eating, loss of control may still be considered as present. Binge
eating can also be planned in some instances.

Binge eating must be characterized by marked distress (Criterion C) and at least three of the following
features: eating much more rapidly than normal; eating until feeling uncomfortably full; eating large
amounts of food when not feeling physically hungry; eating alone because of feeling embarrassed by
how much one is eating; and feeling disgusted with oneself, depressed, or very guilty afterward
(Criterion B).

Individuals with binge-eating disorder are typically ashamed of their eating problems and attempt to
conceal their symptoms. Binge eating usually occurs in secrecy or as inconspicuously as possible. The
most common antecedent of binge eating is negative affect. Other triggers include interpersonal
stressors; dietary restraint; negative feelings related to body weight, body shape, and food; and
boredom. Binge eating may minimize or mitigate factors that precipitated the episode in the short-
term, but negative self-evaluation and dysphoria often are the delayed consequences.

Associated Features Supporting Diagnosis

Binge-eating disorder occurs in normal-weight/ overweight and obese individuals. It is reliably

associated with overweight and obesity in treatment-seeking individuals. Nevertheless, binge-eating
disorder is distinct from obesity. Most obese individuals do not engage in recurrent binge eating.

In addition, compared with weight-matched obese individuals without binge-eating disorder, those
with the disorder consume more calories in laboratory studies of eating behavior and have greater
functional impairment, lower quality of life, more subjective distress, and greater psychiatric
comorbidity.

Prevalence

Twelve-month prevalence of binge-eating disorder among U.S. adult (age 18 or older) females and
males is 1.6% and 0.8%, respectively.

Development and Course

Little is known about the development of binge-eating disorder. Both binge eating and loss-of-control
eating without objectively excessive consumption occur in children and are associated with increased
body fat, weight gain, and increases in psychological symptoms.

Binge eating is common in adolescent and college-age samples. Loss-of-control eating or episodic
binge eating may represent a prodromal phase of eating disorders for some individuals.

Dieting follows the development of binge eating in many individuals with binge-eating disorder. (This
is in contrast to bulimia nervosa, in which dysfunctional dieting usually precedes the onset of binge
eating.)

Binge-eating disorder typically begins in adolescence or young adulthood but can begin in later
adulthood.
Remission rates in both natural course and treatment outcome studies are higher for binge-eating
disorder than for bulimia nervosa or anorexia nervosa. Binge-eating disorder appears to be relatively
persistent, and the course is comparable to that of bulimia nervosa in terms of severity and duration.
Crossover from binge-eating disorder to other eating disorders is uncommon.

Risk and Prognostic Factors

Genetic and physiological. Binge-eating disorder appears to run in families, which may reflect
additive genetic influences.

Culture-Related Diagnostic Issues

Binge-eating disorder occurs with roughly similar frequencies in most industrialized countries,
including the United States, Canada, many European countries, Australia, and New Zealand. In the
United States, the prevalence of binge-eating disorder appears comparable among non-Latino whites,
Latinos, Asians, and African Americans.

Comorbidity

Binge-eating disorder is associated with significant psychiatric comorbidity that is comparable to that
of bulimia nervosa and anorexia nervosa. The most common comorbid disorders are bipolar disorders,
depressive disorders, anxiety disorders, and, to a lesser degree, substance use disorders. The
psychiatric comorbidity is linked to the severity of binge eating and not to the degree of obesity.

GENDER DYSPHORIA
Diagnostic Criteria

Gender Dysphoria in Children 302.6 (F64.2)

A marked incongruence between one's experienced/expressed gender and assigned gender, of at

least 6 months' duration, as manifested by at least six of the fol lowing (one of which must be Criterion
A1 ):

1 . A strong desire to be of the other gender or an insistence that one is the other gender (or some
alternative gender different from one's assigned gender).

2. In boys (assigned gender), a strong preference for cross-dressing or simulating female attire; or in
girls (assigned gender), a strong preference for wearing only typical masculine clothing and a strong
resistance to the wearing of typical feminine clothing.

3. A strong preference for cross-gender roles in make-bel ieve play or fantasy play.
4. A strong preference for the toys, games, or activities stereotypically used or engaged in by the other
gender.

5. A strong preference for playmates of the other gender.

6. In boys (assigned gender), a strong rejection of typically masculine toys, games, and activities and
a strong avoidance of rough-and-tumble play; or in girls (assigned gender), a strong rejection of
typically feminine toys, games, and activities.

7. A strong dislike of one's sexual anatomy.

8. A strong desire for the primary and/or secondary sex characteristics that match one's experienced
gender.
B. The condition is associated with clinically significant distress or impairment in social, school, or other
important areas of functioning.

Specify if:

With a disorder of sex development (e.g., a congenital adrenogenital disorder such as 255.2 [E25.0]
congenital adrenal hyperplasia or 259.50 [E34.50] androgen insensitivity syndrome).

Coding note: Code the disorder of sex development as well as gender dysphoria.

Gender Dysphoria in Adolescents and Adults 302.85 (F64.1)

A. A marked incongruence between one's experienced/expressed gender and assigned gender, of at

least 6 months' duration, as manifested by at least two of the following:
1. A marked incongruence between one's experienced/expressed gender and primary and/or
secondary sex characteristics (or in young adolescents, the anticipated secondary sex characteristics).

2. A strong desire to be rid of one's primary and/or secondary sex characteristics because of a marked
incongruence with one's experienced/expressed gender (or in young adolescents, a desire to prevent
the development of the anticipated secondary sex characteristics).

3. A strong desire for the primary and/or secondary sex characteristics of the other gender.

4. A strong desire to be of the other gender (or some alternative gender different from one's assigned
gender).

5. A strong desire to be treated as the other gender (or some alternative gender different from one's
assigned gender).

6. A strong conviction that one has the typical feelings and reactions of the other gender (or some
alternative gender different from one's assigned gender).

Specifiers

The posttransition specifier may be used in the context of continuing treatment procedures that serve
to support the new gender assignment.

Diagnostic Features

Individuals with gender dysphoria have a marked incongruence between the gender they have been
assigned to (usually at birth, referred to as natal gender) and their experienced/ expressed gender.
This discrepancy is the core component of the diagnosis. There must also be evidence of distress about
this incongruence. Experienced gender may include alternative gender identities beyond binary
stereotypes. Consequently, the distress is not limited to a desire to simply be of the other gender, but
may include a desire to be of an alternative gender, provided that it differs from the individual's
assigned gender.
Gender dysphoria manifests itself differently in different age groups. Prepubertal natal girls with
gender dysphoria may express the wish to be a boy, assert they are a boy, or assert they will grow up
to be a man. They prefer boys' clothing and hairstyles, are often perceived by strangers as boys, and
may ask to be called by a boy's name. Usually, they display intense negative reactions to parental
attempts to have them wear dresses or other feminine attire. Some may refuse to attend school or
social events where such clothes are required. These girls may demonstrate marked cross-gender
identification in role-playing, dreams, and fantasies. Contact sports, rough-and-tumble play,
traditional boyhood games, and boys as playmates are most often preferred. They show little interest
in stereotypically feminine toys (e.g., dolls) or activities (e.g., feminine dress-up or role-play).
Occasionally, they refuse to urinate in a sitting position. Some natal girls may express a desire to have
a penis or claim to have a penis or that they will grow one when older. They may also state that they
do not want to develop breasts or menstruate.

Prepubertal natal boys with gender dysphoria may express the wish to be a girl or assert they are a
girl or that they will grow up to be a woman. They have a preference for dressing in girls' or women's
clothes or may improvise clothing from available materials (e.g., using towels, aprons, and scarves for
long hair or skirts). These children may roleplay female figures (e.g., playing "mother") and often are
intensely interested in female fantasy figures. Traditional feminine activities, stereotypical games, and
pastimes (e.g., "playing house"; drawing feminine pictures; watching television or videos of favorite
female characters) are most often preferred. Stereotypical female-type dolls (e.g., Barbie) are often
favorite toys, and girls are their preferred playmates. They avoid rough-and-tumble play and
competitive sports and have little interest in stereotypically masculine toys (e.g., cars, trucks). Some
may pretend not to have a penis and insist on sitting to urinate. More rarely, they may state that they
find their penis or testes disgusting, that they wish them removed, or that they have, or wish to have,
a vagina.

In young adolescents with gender dysphoria, clinical features may resemble those of children or adults
with the condition, depending on developmental level. As secondary sex characteristics of young
adolescents are not yet fully developed, these individuals may not state dislike of them, but they are
concerned about imminent physical changes.

In adults with gender dysphoria, the discrepancy between experienced gender and physical sex
characteristics is often, but not always, accompanied by a desire to be rid of primary and/ or secondary
sex characteristics and/ or a strong desire to acquire some primary and/ or secondary sex
characteristics of the other gender. To varying degrees, adults with gender dysphoria may adopt the
behavior, clothing, and mannerisms of the experienced gender. They feel uncomfortable being
regarded by others, or functioning in society, as members of their assigned gender. Some adults may
have a strong desire to be of a different gender and treated as such, and they may have an inner
certainty to feel and respond as the experienced gender without seeking medical treatment to alter
body characteristics. They may find other ways to resolve the incongruence between experienced/
expressed and assigned gender by partially living in the desired role or by adopting a gender role
neither conventionally male nor conventionally female.

Associated Features Supporting Diagnosis

 When visible signs of puberty develop, natal boys may shave their legs at the first signs of hair
growth. They sometimes bind their genitals to make erections less visible.
 Girls may bind their breasts, walk with a stoop, or use loose sweaters to make breasts less
visible.
 Increasingly, adolescents request, or may obtain without medical prescription and
supervision, hormonal suppressors ("blockers") of gonadal steroids (e.g., gonadotropin-
releasing hormone [GnRH] analog, spironolactone).
 Clinically referred adolescents often want hormone treatment and many also wish for gender
reassignment surgery.
 Adolescents living in an accepting environment may openly express the desire to be and be
treated as the experienced gender and dress partly or completely as the experienced gender,
 have a hairstyle typical of the experienced gender, preferentially seek friendships with peers
of the other gender, and/ or adopt a new first name consistent with the experienced gender.
 Older adolescents, when sexually active, usually do not show or allow partners to touch their
sexual organs. For adults with an aversion toward their genitals, sexual activity is constrained
by the preference that their genitals not be seen or touched by their partners.
 Some adults may seek hormone treatment (sometimes without medical prescription and
supervision) and gender reassignment surgery. Others are satisfied with either hormone
treatment or surgery alone.
 Adolescents and adults with gender dysphoria before gender reassignment are at increased
risk for suicidal ideation, suicide attempts, and suicides. After gender reassignment,
adjustment may vary, and suicide risk may persist.

Prevalence

For natal adult males, prevalence ranges from 0.005% to 0.014%, and for natal females, from 0.002%
to 0.003%. Since not all adults seeking hormone treatment and surgical reassignment attend specialty
clinics, these rates are likely modest underestimates. In children, sex ratios of natal boys to girls range
from 2:1 to 4.5:1. In adolescents, the sex ratio is close to parity; in adults, the sex ratio favors natal
males, with ratios ranging from 1:1 to 6.1 :1.

Development and Course

Because expression of gender dysphoria varies with age, there are separate criteria sets for children
versus adolescents and adults.

Criteria for children are defined in a more concrete, behavioral manner than those for adolescents
and adults. Many of the core criteria draw on well-documented behavioral gender differences
between typically developing boys and girls. Young children are less likely than older children,
adolescents, and adults to express extreme and persistent anatomic dysphoria. In adolescents and
adults, incongruence between experienced gender and somatic sex is a central feature of the
diagnosis. Factors related to distress and impairment also vary with age. A very young child may show
signs of distress (e.g., intense crying) only when parents tell the child that he or she is "really" not a
member of the other gender but only "desires" to be. Distress may not be manifest in social
environments supportive of the child's desire to live in the role of the other gender and may emerge
only if the desire is interfered with. In adolescents and adults, distress may manifest because of strong
incongruence between experienced gender and somatic sex. Such distress may, however, be
mitigated by supportive environments and knowledge that biomedical treatments exist to reduce
incongruence. Impairment (e.g., school refusal, development of depression, anxiety, and substance
abuse) may be a consequence of gender dysphoria.

Gender dysphoria without a disorder of sex development. For clinic-referred children, onset of cross-
gender behaviors is usually between ages 2 and 4 years. This corresponds to the developmental time
period in which most typically developing children begin expressing gendered behaviors and interests.
For some preschool-age children, both pervasive cross-gender behaviors and the expressed desire to
be the other gender may be present, or, more rarely, labeling oneself as a member of the other gender
may occur. In some cases, the expressed desire to be the other gender appears later, usually at entry
into elementary school. A small minority of children express discomfort with their sexual anatomy or
will state the desire to have a sexual anatomy corresponding to the experienced gender ("anatomic
dysphoria"). Expressions of anatomic dysphoria become more common as children with gender
dysphoria approach and anticipate puberty.
Rates of persistence of gender dysphoria from childhood into adolescence or adulthood vary. In natal
males, persistence has ranged from 2.2% to 30%. In natal females, persistence has ranged from 12%
to 50%. Persistence of gender dysphoria is modestly correlated with dimensional measures of severity
ascertained at the time of a childhood baseline assessment. In one sample of natal males, lower
socioeconomic background was also modestly correlated with persistence. It is unclear if particular
therapeutic approaches to gender dysphoria in children are related to rates of long-term persistence.
Extant follow-up samples consisted of children receiving no formal therapeutic intervention or
receiving therapeutic interventions of various types, ranging from active efforts to reduce gender
dysphoria to a more neutral, "watchful waiting" approach. It is unclear if children "encouraged" or
supported to live socially in the desired gender will show higher rates of persistence, since such
children have not yet been followed longitudinally in a systematic manner. For both natal male and
female children showing persistence, almost all are sexually attracted to individuals of their natal sex.
For natal male children whose gender dysphoria does not persist, the majority are androphilic
(sexually attracted to males) and often self-identify as gay or homosexual (ranging from 63% to 100%).
In natal female children whose gender dysphoria does not persist, the percentage who are gynephilic
(sexually attracted to females) and self-identify as lesbian is lower (ranging from 32% to 50%).

In both adolescent and adult natal males, there are two broad trajectories for development of gender
dysphoria: early onset and late onset. Early-onset gender dysphoria starts in childhood and continues
into adolescence and adulthood; or, there is an intermittent period in which the gender dysphoria
desists and these individuals self-identify as gay or homosexual, followed by recurrence of gender
dysphoria. Late-onset gender dysphoria occurs around puberty or much later in life. Some of these
individuals report having had a desire to be of the other gender in childhood that was not expressed
verbally to others. Others do not recall any signs of childhood gender dysphoria. For adolescent males
with late-onset gender dysphoria, parents often report surprise because they did not see signs of
genderdysphoria during childhood. Expressions of anatomic dysphoria are more common and salient
in adolescents and adults once secondary sex characteristics have developed.

Adolescent and adult natal males with early-onset gender dysphoria are almost always sexually
attracted to men (androphilic). Adolescents and adults with late-onset gender dysphoria frequently
engage in transvestic behavior with sexual excitement. The majority of these individuals are gynephilic
or sexually attracted to other posttransition natal males with late-onset gender dysphoria. A
substantial percentage of adult males with late-onset gender dysphoria cohabit with or are married
to natal females. After gender transition, many self-identify as lesbian. Among adult natal males with
gender dysphoria, the early-onset group seeks out clinical care for hormone treatment and
reassignment surgery at an earlier age than does the late-onset group. The late-onset group may have
more fluctuations in the degree of gender dysphoria and be more ambivalent about and less likely
satisfied after gender reassignment surgery.

In both adolescent and adult natal females, the most common course is the early-onset form of gender
dysphoria. The late-onset form is much less common in natal females compared with natal males. As
in natal males with gender dysphoria, there may have been a period in which the gender dysphoria
desisted and these individuals self-identified as lesbian; however, with recurrence of gender
dysphoria, clinical consultation is sought, often with the desire for hormone treatment and
reassignment surgery. Parents of natal adolescent females with the late-onset form also report
surprise, as no signs of childhood gender dysphoria were evident. Expressions of anatomic dysphoria
are much more common and salient in adolescents and adults than in children.

Adolescent and adult natal females with early-onset gender dysphoria are almost always gynephilic.
Adolescents and adults with the late-onset form of gender dysphoria are usually androphilic and after
gender transition self-identify as gay men. Natal females with the late-onset form do not have co-
occurring transvestic behavior with sexual excitement.

Gender dysphoria in association with a disorder of sex development. Most individuals with a disorder
of sex development who develop gender dysphoria have already come to medical attention at an early
age. For many, starting at birth, issues of gender assignment were raised by physicians and parents.
Moreover, as infertility is quite common for this group, physicians are more willing to perform cross-
sex hormone treatments and genital surgery before adulthood.

Disorders of sex development in general are frequently associated with gender-atypical behavior
starting in early childhood. However, in the majority of cases, this does not lead to gender dysphoria.
As individuals with a disorder of sex development become aware of their medical history and
condition, many experience uncertainty about their gender, as opposed to developing a firm
conviction that they are another gender. However, most do not progress to gender transition. Gender
dysphoria and gender transition may vary considerably as a function of a disorder of sex development,
its severity, and assigned gender.

Risk and Prognostic Factors

Temperamental . For individuals with gender dysphoria without a disorder of sex development,
atypical gender behavior among individuals with early-onset gender dysphoria develops in early
preschool age, and it is possible that a high degree of a typicality makes the development of gender
dysphoria and its persistence into adolescence and adulthood more likely.

Environmental. Among individuals with gender dysphoria without a disorder of sex development,
males with gender dysphoria (in both childhood and adolescence) more commonly have older
brothers than do males without the condition. Additional predisposingfactors under consideration,
especially in individuals with late-onset gender dysphoria (adolescence, adulthpod}, include habitual
fetishistic transvestism developing into autogynephilia (i.e., sexual arousal associated with the
thought or image of oneself as a woman) and other forms of more general social, psychological, or
developmental problems.

Genetic and physiological. For individuals with gender dysphoria without a disorder of sex
development, some genetic contribution is suggested by evidence for (weak) familiality of
transsexualism among nontwin siblings, increased concordance for transsexualism in monozygotic
compared with dizygotic same-sex twins, and some degree of heritability of gender dysphoria. As to
endocrine findings, no endogenous systemic abnormalities in sex-hormone levels have been found in
46,XY individuals, whereas there appear to be increased androgen levels (in the range found in hirsute
women but far below normal male levels) in 46,XX individuals. Overall, current evidence is insufficient
to label gender dysphoria without a disorder of sex development as a form of intersexuality limited to
the central nervous system.

In gender dysphoria associated with a disorder of sex development, the likelihood of later gender
dysphoria is increased if prenatal production and utilization (via receptor sensitivity) of androgens are
grossly atypical relative to what is usually seen in individuals with the same assigned gender. Examples
include 46,XY individuals with a history of normal male prenatal hormone milieu but inborn
nonhormonal genital defects (as in cloacal bladder exstrophy or penile agenesis) and who have been
assigned to the female gender. The likelihood of gender dysphoria is further enhanced by additional,
prolonged, highly gender-atypical postnatal androgen exposure with somatic virilization as may occur
in female-raised and noncastrated 46,XY individuals with 5-alpha reductase-2 deficiency or 17-beta-
hydroxysteroid dehydrogenase-3 deficiency or in female-raised 46,XX individuals with classical
congenital adrenal hyperplasia with prolonged periods of non-adherence to glucocorticoid
replacement therapy. However, the prenatal androgen milieu is more closely related to gendered
behavior than to gender identity. Many individuals with disorders of sex development and markedly
gender-atypical behavior do not develop gender dysphoria. Thus, gender-atypical behavior by itself
should not be interpreted as an indicator of current or future gender dysphoria. There appears to be
a higher rate of gender dysphoria and patient-initiated gender change from assigned female to male
than from assigned male to female in 46,XY individuals with a disorder of sex development.

Culture-Related Diagnostic Issues

Individuals with gender dysphoria have been reported across many countries and cultures. The
equivalent of gender dysphoria has also been reported in individuals living in cultures with
institutionalized gender categories other than male or female. It is unclear whether with these
individuals the diagnostic criteria for gender dysphoria would be met.

Diagnostic Markers

Individuals with a somatic disorder of sex development show some correlation of final gender identity
outcome with the degree of prenatal androgen production and utilization. However, the correlation
is not robust enough for the biological factor, where ascertainable, to replace a detailed and
comprehensive diagnostic interview evaluation for gender dysphoria.

Functional Consequences of Gender Dysphoria

Preoccupation with cross-gender wishes may develop at all ages after the first 2-3 years of childhood
and often interfere with daily activities. In older children, failure to develop age-typical same-sex peer
relationships and skills may lead to isolation from peer groups and to distress. Some children may
refuse to attend school because of teasing and harassment or pressure to dress in attire associated
with their assigned sex. Also in adolescents and adults, preoccupation with cross-gender wishes often
interferes with daily activities. Relationship difficulties, including sexual relationship problems, are
common, and functioning at school or at work may be impaired. Gender dysphoria, along with atypical
gender expression, is associated with high levels of stigmatization, discrimination, and victimization,
leading to negative self-concept, increased rates of mental disorder comorbidity, school dropout, and
economic marginalization, including unemployment, with attendant social and mental health risks,
especially in individuals from resource-poor family backgrounds. In addition, these individuals' access
to health services and mental health services may be impeded by structural barriers, such as
institutional discomfort or inexperience in working with this patient population.

Comorbidity

Clinically referred children with gender dysphoria show elevated levels of emotional and behavioral
problems most commonly, anxiety, disruptive and impulse-control, and depressive disorders.

In prepubertal children, increasing age is associated with having more behavioral or emotional
problems; this is related to the increasing non-acceptance of gender-variant behavior by others. In
older children, gender-variant behavior often leads to peer ostracism, which may lead to more
behavioral problems. The prevalence of mental health problems differs among cultures; these
differences may also be related to differences in attitudes toward gender variance in children.
However, also in some non-Western cultures, anxiety has been found to be relatively common in
individuals with gender dysphoria, even in cultures with accepting attitudes toward gender-variant
behavior. Autism spectrum disorder is more prevalent in clinically referred children with gender
dysphoria than in the general population. Clinically referred adolescents with gender dysphoria appear
to have comorbid mental disorders, with anxiety and depressive disorders being the most common.
As in children, autism spectrum disorder is more prevalent in clinically referred adolescents with
gender dysphoria than in the general population. Clinically referred adults with gender dysphoria may
have coexisting mental health problems, most commonly anxiety and depressive disorders.
 SCHIZOPHRENIA

Schizophrenia

The word or term ‘schizophrenia’ comes from the Greek word ‘skhizein’ meaning ‘to split’
and Greek word ‘phrenos’ meaning ‘diaphragm, heart, mind.’ schizophrenia is a psychotic
disorder in which the term literally means split mind (the split does not refer to splitting of
personality as in multiple personality disorder) this is because there is a split between
emotion and cognition.

● Schizophrenia is not a single disorder but a syndrome consisting of several different

types of disorders, however, DSM-IV treats it as a single entity.

● This term was coined by Swiss Psychiatrist Eugen Belicuer (1857- 1911) in the year
1911 which was later accepted worldwide. It denotes a severe and complex mental
illness wherein the patient uses the ability to think, feel or behave in a normal way.
The patient perceives a distorted reality but is usually unaware that he/she is ill.

● The patient also suffers from delusions i.e., firmly held but false beliefs and begin to
act on them. As a result of their faulty thinking and perception. Their behaviour
becomes abnormal.

● Nearly 6.7 million Indians suffer from this disorder variously described as ‘cancer of
the mind’ and the greatest disorder of the youth. It starts in the most productive period
of life (15-45 years) and is cosmopolitan in its appearance, meaning it's more
prevalent in the urban areas.

● It is now widely recognized that schizophrenia is a brain disorder. The DSM-IV of the
AIA defines schizophrenia as a clinical mental disorder.

The 17th edition of the Murik Manual defines schizophrenia as follows-

“ a common and serious mental disorder characterised by loss of contact with reality,
delusions, abnormal thinking, flattened affect, diminishes motivation and disturbed
work and social functioning.”

● The National Institute of Mental Health wrote in 2010, people with schizophrenia
may hear voices other people won't hear. They may believe that other people are
reading their minds, controlling their thoughts or plotting to harm them. This can
terrify people with illness and make them withdrawn or extremely agitated.

People with schizophrenia may not make sense when they talk. They may sit for
hours without moving or talking. Sometimes people with schizophrenia seem fine
until they talk about what they are really thinking.
 Schizophrenia: origin of the construct

Epidemiology: it is the study of distribution of prevalence of diseases, disorders, or

health related behaviour in a given situation.

● One of every 140 people alive today survives until at least the age of 55 will develop
the disorder.

● Some people (for eg., those who have a parent with schizophrenia) have a statistically
higher risk for developing the disorder than the orders do.

● There are also other groups of people who seem to have an especially higher risk for
developing schizophrenia. For example, people whose fathers were older (age 45-55
or more) have two or three times the normal risk for developing schizophrenia when
they grow up ( Bryon et. al., 2003)

● The vast majority of cases of schizophrenia begin in late adolescence and early
adulthood with 18-30 years age being the peak time for the onset of the illness
(Tandon et.al., 2009). Interestingly schizophrenia begins early in men (20-24 years)
than in women (35-40 years). This is because of the protective effects of oestrogen
present in women.

● One particularly stable finding often referred to as urban drift has been the association
between living in an urban environment and diagnosis of schizophrenia.

● Males also tend to have a more severe form of schizophrenia. Brain imaging studies
show that schizophrenia related abnormalities of the brain structures are more severe
in male patients than they are in female patients.

● It is prevalent in all cultures, similar incidence across continents.

Clinical pictures: signs & symptoms

The symptoms of schizophrenia fall in three categories (can co occur in some patients):

● Positive symptoms
● Negative symptoms
● Disorganised symptoms ( bizarre behaviour and disorganised speech)

Two general symptom patterns or syndromes of schizophrenia have been different. These are
called negative and positive syndromes of schizophrenia. (Anderson et.al., 1995)
Positive syndrome- signs and symptoms and access or distortion in a normal repertoire of
behaviour and experience in which something have been added to the normal repertoire of the
behaviour and experience presence of characteristic psychotic symptoms for example
hallucination delusions etc it responds to treatment as compared to the negative symptoms

Negative syndrome- by contrast refers to an absence or deficit of behaviours normally

present in a person's stepdaughter. Difficult to treat however not all negative symptoms may
reflect lack of emotions in a study by Kving and Neale 1996, it was found that patients with
schizophrenia may not look emotionally expressive but may be internally experiencing plenty
of emotions as measured by autonomic arousal.

In clinical samples approximately 20 to 25% of patients display primarily negative symptoms

Kirkpatrick et al 2006 patients with negative symptoms need help with everyday tasks.

· Alogia (Poverty of speech): Absence or little speech so that example if you ask a person
with a locator describe a happy life experience the person might respond Getting married
end end failed to elaborate even when asked for additional information.

· Anhedonia (Loss of pleasure from life): There are two types of loss of pleasure,

1. Consummatory pleasure is the amount of pleasure experienced in the moment

or in the presence of something pleasurable. For example the amount of
pleasure you experience while eating a good meal.

2. Anticipatory pleasure Refers to the amount of expected pleasure from future

events or activities. People with schizophrenia tend to have a deficit in
anticipatory pleasure but not consummately pleasure ( Guard et al 2007)

· Apathy: feelings of indifference towards people, activities and events. Many people with
schizophrenia express little interest in the events surrounding them.

· affective blunting (emotional flattening): restricted range of emotions (blunted affect).

The person's fall may remain immobile most of the time no matter what happens and
body language may be unresponsive to what is going on in the environment. For example,
one man set fire to his house then sat down to watch TV. when it was called out to his
attention that his house was on fire, he calmly walked outside. People with blunted affect
may speak in a monotone voice without any emotional expression and may not amke eye
contact with others.

· Avolition: absence of will, ambition or drive to take action or accomplish tasks (including,
work or school, self-care, hobbies or social activities, household chores and may spend
most of the time sitting.)

· Asociality: some people with schizophrenia have severe impairment in social

relationships. They have few friends, poor social skills and very little interest in dealing
with other people. They may not desire close relationships with family, friends or
 romantic partners. Instead, they may wish to spend most of the time alone when around
others, may interact only superficially & briefly, appear aloof or indifferent to social
interaction.

· catatonia: psychologically induced immobility occasionally marked by periods of

excitement.

Disorganised symptoms:

The examples of disorganised symptoms are as follows:

● Echopraxia: imitation of the movement of another person.

● Fighting of ideas: continuous flow of verbalization in which the patient jumps rapidly
from one topic to another.
● Perseveration: persistent adherence to a single topic or idea, verbal repetition of
sentence & phrase, resisting attempts to change topics.
● Ambivalence: holding seemingly contradictory beliefs about some person or situation.
● Associative looseness: fragmented or poorly related thoughts or ideas.
● Echolalia: imitating speech sounds of other people.

A related differentiation with more emphasis on biological variation and speed of onset refers
to essentially the same pattern as Type-I and Type-II schizophrenia (Crow, 1985).

Type-I schizophrenia or positive schizophrenia: characterised by positive symptoms and

tends to respond to medication and treatment. It has a sudden onset and bearable course.
Symptoms tied to biochemical abnormalities.

Type-II schizophrenia or negative schizophrenia: characterised by negative symptoms

associated with structured brain abnormalities and does not respond as well to medications
and treatment. It has an insidious onset and chronic causes.

A third pattern of that disorganised type has been recognized as yet another cluster of
schizophrenia signs independent of the above two. Dolphus et.al., 1996 suggested that there
are at least four discriminable patterns of schizophrenia- positive, negative, disorganised and
mixed.

● Disorganised type: earlier classified as hebephrenic includes severe and excess

disruption in speech, affect and behaviour.
● Disorganised speech: frequent derailment or incoherence; speaking in abstracts.
● Disorganised behaviour: dressing inaptly, crying frequently or catatonic behavior.
● Inappropriate affect: laughing/ crying at inappropriate times.

It has been suggested that the positive and negative symptoms can be conceived of as two end
points of a continuum or even as two independent continua both of which may be included in
schizophrenia.
DSM-5 criteria for schizophrenia:

Schizophrenia spectrum and other psychotic disorders include schizophrenia, other psychotic
disorders and schizotypal and schizotypal (personality) disorder, they are defined by
abnormalities in one or more of the following 5 domains:

1. Delusions
2. Hallucinations
3. Disorganised thinking (speech)
4. Grossly disorganised or abnormal motor behaviour (including catatonia)
5. Negative symptoms

Diagnostic criteria of schizophrenia:

A. Two or more of the following, each present for a significant position of time during a
1-month period (or less, if successfully treated). At least one of these must be present
(1), (2) or (3).
1. Delusions
2. Hallucinations
3. Disorganised thinking (speech)
4. Grossly disorganised or abnormal motor behaviour (including catatonia)
5. Negative symptoms

B. for a significant portion of time, since the onset of the disturbance level of functioning in
one or more major areas such as work, interpersonal relations or self care is remarkably
below the level achieved prior to the onset (or when the onset is childhood/adolescence, there
is failure to achieve expected level of interpersonal, academic/occupational functioning).

C. continuous signs of the disturbance persist for at least six months. This 6 month period
must include at least 6 months of symptoms (or less if successfully treated) that meet criteria
A. i.e, active phase symptoms and may include periods of prodromal or residual symptoms
during these prodromal/residual periods. The signs of the disturbance may be manifested by
only negative symptoms or by two or more symptoms listed in criteria A, present in
attenuated form (e.g., odd beliefs, unusual perceptual experiences).

D. schizo affective disorder and depressive or bipolar disorders with psychotic features have
been ruled out because either:

● No major depressive or manic episodes have occurred concurrently with the active
phase symptoms.

● If mood episodes have occurred during active phase symptoms, they have been
present for a minority of the total duration of the active and residual periods of the
illness.
E. the disturbance is not attributed to the psychological effects of a substance (e.g., drug
abuse, medication) in another medical condition.

F. if there is a history of autism spectrum disorder or a communication disorder of childhood

onset, the additional diagnosis of schizophrenia is made only if predominant delusions or
hallucinations in addition to the other required symptoms of schizophrenia are also present
for at least 1 month or less (if successfully treated).

Culture related diagnostic issues

Cultural and socio-economic factors must be considered particularly when, when the clinician
and the individual do not share the same cultural and socio economic background. Ideas that
appear to be delusional in our culture (e.g., witchcraft) may be commonly held in another
culture.

In some cultures, visual or auditory hallucinations with a religious content (e.g., hearing
god’s voices) are a normal part of religious expression.

In addition, the assessment of disorganised speech may be made difficult by linguistic

variation in narrative styles across cultures, the assessment of affect requires sensitivity to
differences in styles of emotional expression, eye contact and body language which vary
across cultures. If the assessment is conducted in a language that is different from the
individual’s primary language, care must be taken to ensure that alogia is not related to
linguistic barriers. In certain cultures, distress may take the forms of
hallucinations/pseudo-hallucinations and overvalued ideas that may present clinically similar
to true psychosis but are normative to the client’s sub-group.

Main symptoms/ hallmark symptoms of schizophrenia:

Disorganised speech: disorder in the thought form.

Human thinking has three characteristics: stream, form and content. Abnormalities may occur
in any of these.

● stream/flow: how it is being thought about- the amount of speed of thinking.

● Form: abnormalities of the way thoughts are linked together.
● Content: what is being thought about (in case of psychotic disorders, abnormalities in
content may include delusions.)

Schizophrenia is often referred to as a “formal thought disorder” because it was earlier

believed that this is a disorder of form rather than content of thought, however this is no
longer thought to be true, although form disorder is one of the main symptoms of
schizophrenia. Basically, a person fails to make sense despite seeming to explore to the
semantic and syntactic rules governing verbal communication.The failure is not attributable
to low intelligence, poor education or cultural deprivation.

Following are some indicators of disordered thinking which is expressed ion disordered
thinking:

● Cognitive slippage/derailment:

Meenl, 1962 refers to this rapidly shifting from topic to topic making it very difficult
to follow the conversation, this includes at one end of security (circumstantiality) to
word salad at the other end of the scale.

Circumstantiality: the person talks at a length about irrelevant and trivial details (i.e.,
circumstances) and is very delayed at reaching its goal (excessive long windedness).
However, there is a clear association between sentences. A person afflicted with this
condition, when asked about a certain recipe, would give minute details about going
to the grocery store, the shopping experience, etc.

● Tangentiality: Replying to questions in an irrelevant manner and never reaching the

goal, however, there is a clear association between sentences (but end is not reached)
for example, Q. what city are you from? Ans. That is a hard question. I don't know
where my relatives came from, so I don't know if I am French or Irish.

● Word salad (incoherence): Is at the extreme end of the scale. The words are just
words.

● Neologisms: New word formations. For example, “I got so angry, I picked up a dish
and threw it at the geshiker.” , “handshoes (gloves)”

● Echolalia: Echoing other people’s speech. For example, “can we talk for a few
minutes?” “talk for a few minutes, talk for a few minutes.”

● Blocking: The person stops speaking and after a period of seconds, indicates, he or
she is unable to remember what he/she had intended to say. Blocking may give rise to
the delusion that thoughts have been withdrawn from head (thought withdrawal).

● Mutism: refusal or inability to speak.

● Flight of ideas:

Rapidly shifting from one topic to another which are related with the help of
superficial associations. In its extreme forms, it involves cognitive incoherence and
disorganisation. For example,
 Dr.: How are you sleeping at night?
Client: Why would I sleep tonight? Would you be able to do my work? I whistle when
I play and I am happy to do it all. Okay, so that is a haul.

Types of flight of ideas are:

1. Where there is rhyming or clanging. For exmaple, will, hill, bill.

2. Where there is distrcation. For exmaple, a patient talking about his appetite
sees another patient walk past teh window and assumes that the patient is
going for ECT and starts talking about ECT (electrotherapy/ shock therapy)

B. disturbance of thought content: Delusions:

Psychiatrist and philosopher Karl Jaspers was the first one to define the three main criteria for
a belief to be considered delusional. In his book, titled ‘General Psychopathology’, these
criteria are: certainty (held with absolute conviction), incorrigibility (not changebale by
compelling counter argument or proof to the country). Impossibility or falsify of content
(impossible, bizarre or patently untrue).

A delusion is essentially an erronous belief that is fixed and firmly held despite clear
contradictory evidence. The word delusion comes from the latin word- ‘ludere’ which means
to play in essence tricks are played on the mind. People with delusions believe things that
others who share this social, religious and cultural backgrounds do not believe.

T5a delusion therfore involves a disturbance in the content of thought. Not all people who
have delusions suffer from schizophrenia. However, delusions are common in schiziophrenia
occuring in more than 90% of the patients at some time during their illness (Cutting, 1995).

In DSM-IV, a delusion is defined as: ‘A false belief based about external reality is firmly
sustained despite evidence to the contrary. The belief is not one ordinarily accepted by other
members of the person’s culture.

In schizophrenia, the delusions are usually bizarre (comapred to non-bizarre delusions in

delusional disorder). Delusions are considered bizarre if they are clearly implaussible, non
understandable, non-understandable, and not derived from ordinary life experiences (for e.g.,
an individual’s belief that teh stranger has removed his/her internal organs and replaced them
with someone else’s organs without any scars or wounds or when a person believes he has
invisible wings and can fly).

Because of its importance in schizophrenia, delusion has been called ‘the characteristic of
madness’ (Jaspers, 1963). Disturbances in thought usually involve certain types of delusions
or false beliefs.

● persecution - ‘out to get me’

● Control- (someone is controlling the thoughts) for eg., neighbour is an alien and has
the power to control my thinking for evil purposes.

Types:

a. Thought broadcasting (false belief that the affected person’s thought are heard
aloud)
b. Thought insertion (false belief that one’s thoughts are being controlled by
outside forces.
c. Thought withdrawal (false belief that an outside force, person is removing or
extracting one’s thoughts)

● Reference: ‘talking about me.’where some neutral environmental event (such as a T.V.
program or a song on the radio) is believed to have a special or a personal meaning
intended only for the person.

● Grandeur: a person with delusions of grandeur would believe that he is famous and
important (e.g, ‘I invented rock and roll’).

● Nihilistic: belief that something does not exist (for e.g., one's brain, a part of the
world).

● Jealousy : delusion that the individuals sexual partners are unfaitful (morbit jelousy or
Othello syndrome)

● Somatic: usually the false belief is that the body is diseased, abnormal or changed. An
example of a somatic delusion would be a person who believes that his/her body is
infected with parasites.

● Erotomaniac: persona believes that another person, often someone important or

famous, is in love with him/her.

● Capgras: it is the belief that the existence of identical ‘doubles’ who may coexist with
or replace significant others or the patient.

● Cortad: (walking corpse syndrome) it is a very rare neurological disorder. Victims

believe that they are dead or otherwise believe they do not have blood or internal
organs. It can be very dangerous because the victims develop a feeling of immortality
or no longer part in living functions (such as eating or sleeping)

● Mixed type: for example, one woman had multiple delusions including a believe that
celebrities were talking to her through the television. That deceased husband was still
alive and cheating on her and that her internal organs were getting infected (Mahgoub
& Hossain, 2006)
Out of the above the main type of delusion usually seen in schizophrenia includes delusion of
grandeur. A person with delusion or delusions of grandeur would believe that he is famous
and important (such as Mother Teresa or Jesus Christ) and he would be trying to “save the
world”. Sometimes delusions are not just isolated beliefs instead they become elaborated into
a complex delusional system.

DISRUPTION OF PERCEPTION: HALLUCINATIONS ETC

The following perceptual disturbances may take place:

Hallucinations- The word comes from the Latin word hallucinare or allucinere meaning to “
wonder in mind” or “idle talk” (Aleman and Laroy). A hallucinations is a false sensory
perception experienced in the absence of an external stimulus, as distinct from an illusion,
which is a misperception (false impression) of an external stimulus. Usually the
hallucinations are auditory although hallucinations may occur in any sensory modality-
visual, auditory, olfactory, gustatory, tactile or proprioceptive (sense of balance and position
in space)

Auditory hallucinations- Hearing voices when there are no auditory stimulus is the most
common type of auditory hallucination in mental disorders the voice maybe heard either
inside or outside one’s head and is generally considered more severe when coming from
outside one’s head the voices maybe male or female recognized as the voice of someone
familiar or not recognized as someone familiar and maybe critical or positive, in
schizophrenia the content of what the voices say is usually unpleasant and negative. In
schizophrenia a common symptom is to here voices conversing and/or commenting. When
someone hears voices conversing they hear two or more voices speaking to each other
(usually about the person who is hallucinating). In voices commenting the client hears a voice
making comments about his/her behaviour or thoughts typically in third person (such as
“isn’t he silly?”). Sometimes the voices consists of hearing a “running commentary” on the
person’s behaviour as it occurs ( “she is taking a shower”). Other time the voices may tell the
person to do something commonly known as command hallucinations.

Gustatory hallucinations: A false perception of taste (tasting sensations when there is no

stimulus for them). Usually the experience is unpleasant for instance an individual may
complain of a persistent taste of metal, this type of hallucinations is commonly seen in some
medical disorder (such as epilepsy) than in mental disorders

Olfactory hallucinations: A false perception of odor or smell (smelling odors that are not
present). Typically the experience is very unpleasant for example the person may smell
decaying fish, dead bodies or burning rubber. Sometimes those experiencing olfactory
hallucinations believe the odor emanates from them. Olfactory hallucinations are more
typical of medical disorders than psychological disorders.
Somatic (inside one’s body)/ tactile (outside one’s body, for eg bugs are crawling up one’s
back) hallucinations- A false perception (feeling sensations when there is no stimulus for
them or sensation of touch or something happening in or on the body a common tactile
hallucination is feeling like something is crawling under or on the skin (also known as
formication).

Visual hallucinations- A false perception of sight (seeing things that are not present). The
content of the hallucination may be anything such as shapes, color and flashes of light but are
typically people or human like figures, for example one may perceive a person standing
before them when no one is present.

However, auditory hallucinations are by far the most common being present in up to 75% of
patients with schizophrenia (Wing et al 1979, Bauer et al 2011). In contrast visual
hallucinations occur less frequently (39% of patients) and olfactory, tactile and gustatory
hallucinations are even more rare (1-7%). Auditory hallucinations are more common in
women than in men, auditory hallucinations are most common and can range from being
malevolent to being benevolent or having both qualities (Trawer 2004). Research suggests
(Stern 1998) that in some cases people may even act on the hallucinations and do what the
voices tell them to do. Research (McGuire 1996) has indicated that auditory hallucinations
occur when the individual misinterprets his own self generated and verbally mediated
thoughts (inner speech or self talk) as coming from another source. From neuroimaging
studies it was found that Broca’s area (speech production area in the brain) was more active
than vernika’s (speech comprehension area of the brain) during auditory hallucinations.

Breakdown of perceptual selectivity

The person seems unable to seek out and process the mass of sensory information to which
all of us are exposed to. For e.g., “I feel like I am too atest, everything seems to be
compouring at once, my nerves seem super sensitive, things seem so vivid and they come to
me like flood from a broken bank.”

Other:

● Depersonalisation: which is a patient’s feeling that he is not himself, that he is

different and that there is something strange about him and he cannot account for.

● Derealisation: which expresses a patient’s feeling that the environment is somehow

different or strange but he/she cannot account for these changes.

DISTURBED MOTOR BEHAVIOR

Various peculiarities are seen specially in catatonic schizophrenia. Various forms may
include:
● Catatonia: immobility or excited agitation. Catatonia is an even more striking
behavioural disturbance; the patient with catatonia may show a virtual absence of all
movement and speech and be in what is called a catatonic stupor. At other times, the
patient may hold an unusual posture for an extended period of time without a seeming
discomfort.

● Mannerisms: odd/voluntary patterns of behaviour

● Bizarre grimacing: strange smile

● Negativism: resistance to suggestion, tending to do the opposite (as seen in catatonic

schizophrenia).

● Waxy flexibility: it is a psychomotor symptom where a posture which is placed is

indefinitely maintained. For instance, if you were to move the arm of someone with
waxy flexibility, they would keep their arm where you moved it until it is moved
again as if made from wax.

● Echopraxia: is the involuntary repetition or imitation of the observed movements of

another.

● Emotional dysfunction: The person suffers from inappropriate emotions or affect.

● Anho… (check once from the book): it is the inability to experience pleasure from
normally pleasurable life events such as eating, exercise, social interactions, etc.

● Emotional shallowness (or blunting): the person may appear almost emotionless. To
the extent that even the most dramatic event produces at most intellectual recognition
of what is happening. This may reflect lack of expressiveness and not lack of feeling.

● Strong affect: may be shown in certain situations but the emotions clash with the
situation. For example, the patient may react to the parents’ death with gleeful hilarity
(laughter).

● Confused sense of self: a person suffering from schizophrenia may be confused about
his sense of identity and may even have a delusion of the new identity such as
god/christ. He may also be uncertain about the boundaries separating the self from the
rest of the world leading to frightening, cosmic or oceanic feeling of somehow
intimately tied up with universal powers including god or the devil.

● Disrupted violation: disorganised behaviour can show itself in a number of ways.

Goal directed activity is most universally disrupted. The impairment occurs in areas
of routine daily functioning such as work, social relations and self care. To the extent
that the observers note that the person is not herself or himself anymore. For example,
 the person may no longer maintain minimal standards of personal hygiene or may
exhibit a profound disregard of personal safety and health. In other cases, grossly
disorganised behaviour appears as silliness or unusual dress. For example, wearing an
overcoat, scarf or gloves on a hot summer day). Many researchers attribute this
disruption of ‘executive’ behaviour to impairment in the functioning of the prefrontal
region of the cerebral cortex. (Lenzenweger & Dworkin, 1998).

● Retreat to an inner world: this includes disengagement from the external world and
in extreme cases can be seen as a deliberate attempt to avoid being overwhelmed.
There is a rich elaboration of the inner world (fantastic ideas, creating of strange
beings). For example, this person may create strange creatures who interact with him
in various self directed dramas.

ETIOLOGY

Breakdown of perceptual selectivity

Etiology

1. Biological factors
Given the similarity in the symptoms and prevalence of schizophrenia across cultures
and across time it is not surprising that Biological factors have long been thought to
play a strong role in the development of schizophrenia.

A. Genetic factors
It has long been known that disorders of the schizophrenic type are familial and tend
to run in families. There is overwhelming evidence for higher than expected rates of
schizophrenia among biological relatives of index cases, i.e., the diagnosed group of
people who provide the starting point for enquiry (also called propands). There is a
strong association between the closeness of the blood relationship (i.e., level of gene
sharing) and the risk for developing the disorder. For example, the prevalence of
schizophrenia in the first degree relatives (parents, siblings and offspring) of a
proband with schizophrenia is about 10%, for second degree relatives who share only
25% of their genes with the proband (half siblings, aunts, uncles, nieces, nephews,
and grandchildren), the lifetime prevalence of schizophrenia is closer to 3%.
Ofcourse, just because something runs in the families does not automatically
implicate genetic factors. The terms familial and genetic are not synonymous, and a
disorder can run in a family for non genetic reasons. The interpretation of familial
concordance patterns is not completely straight forward, in part because of the strong
relationship between the sharing of genes and the sharing of the environments in
which those genes express themselves. Although they are indispensable in providing a
starting point for researchers, family studies cannot by themselves tell us why a
disorder runs in families. To disentangle the contributions of genes and environment,
we need twin and adoption studies.
i) Family studies
Human genome project has discovered several genetic linkages behind the causal
factors of the disease. Genetic factors are proposed to be responsible for the familial
predisposition of schizophrenia (more than 80%). Studies indicate that the disorder
tends to run in families giving rise to the notion of a tainted gene, the possibility of
developing schizophrenia in the offspring is approximately 25-50% when the mother
is schizophrenic.

The disorder is now understood as the result of multiple genes and their interactions,
specific genes appear to make only minor contribution towards the illness
(Williamson, 2007).

Furthermore, patients who have schizophrenia in their family histories have more
negative symptoms than those whose families are free of schizophrenia (Malaspina et
al., 2000) suggesting that negative symptoms may have a stronger genetic component.
According to a review of family studies, a person with a first degree relative with
schizophrenia is almost 10 times more likely to develop schizophrenia than a person
with no schizophrenia in the immediate family (Schneider and Deldin, 2001).

ii) Twin studies

Schizophrenia concordance rates for identical twins are routinely and consistently
found to be significantly higher than those for fraternal twins or ordinary siblings. The
most famous case of concordance for schizophrenia is the genain quadruplets but the
specific symptoms onset, course and outcomes of the disorder varies substantially
among them (Mirsky, 2000).

Although being a twin does not increase once risk for developing schizophrenia, study
after study has shown a higher concordance for schizophrenia among identical twins
than among people related in any other way including fraternal twins.

Torray is a notes schizophrenia researcher, who has a sister with the disorder, he and
is colleagues in 1994 have published a review of the major literature worldwide on
twin studies of schizophrenia. The overall pair wise concordance rates is 28% in mz
twins and 6% in dz twins. This suggests that a reduction in shared genes from 100%
to 50% reduced the risk of schizophrenia by nearly 80%, also note that sharing 50%
of ones genes with a co-twin with schizophrenia is associated with a lifetime risk for
schizophrenia of 6%. Although this is low in absolute terms it is markedly higher than
the baseline risk of less than 1% found in the general population. Other studies
(Squire et al., 2003) indicate 45-50% concordance rate for identical twins compared to
only 15% concordance rate for fraternal twins, this shows that mz twins are much
likely to develop schizophrenia than dz twins.
 If schizophrenia were exclusively a genetic disorder the concordance rate for identical
rates would ofcourse be 100%. Two conclusions can therefore be drawn: genes
undoubtedly play a role in causing schizophrenia and genes themselves are not the
whole story. Twin studied provide some of the most solid evidence that the
environment plays an important role in the development of schizophrenia but why one
mz twin should develop schizophrenia when their co-twin does not is a fascinating
question. Torray (1994) also found the following differences between schizophrenic
and non-schizophrenic co-twins:

- 30% of the discordant affected twins were described as being different sugesting
CNS dysfunction.
- discordant affected twins showed widespread range changes.
- discordant affected twins showed widespread range changes though they were not
related to clinical aspects of schizophrenia indicating that behavioral manifestation of
schizophrenia was related to some other factors.
A great deal of research attention is now being directed at studying people with a
known genetic liability for schizophrenia. Historically, the most important subjects to
study in this regard have been mz twins who are discordant for schizophrenia. This
investigative strategy was pioneered by Fischer (1971,1973) in an ingenious study.

Other endophynotypic risk markers for schizophrenia include abnormal performance

on measures of cognitive functioning such as tests of working memory by studying
these traits rather than the disorder itself researchers hope to speed up progress in the
search for the genes related to schizophrenia. Major collaborative studies designed to
explore different endophenotypes are now underway (Greenwood et al 2007)
Prenatal exposures
In this section we highlight some environmental risk factors that might either cause
schizophrenia or trigger it in a genetically vulnerable person. Apart from genetic
susceptibilities other biological factors also start playing as early or even before one’s
birth.
● Viral infection: Kraeplin (1919) suggested that “infections in the years of
development might have a causal significance for schizophrenia”. Evidence for the
involvement of infectious diseases in the etiology of schizophrenia first came from the
“season of birth defect” we also know that in the northern hemisphere more people
with schizophrenia are born between January and march (winter months) than would
be expected by chance (Waddington et al 1999). This is thought to be due to the
exposure to viruses during development.

Risk of schizophrenia seems to be greatest when the mother gets flu in the 4th to 7th
month of gestation although the size of the effect is small and influenza clearly
doesn’t account for very many cases of schizophrenia the fact that this association
exists is very provocative but how can maternal influenza set the stage for
schizophrenia in a child two or three decades later? One possibility is that the
mother’s antibodies to the virus cross the placenta and somehow disrupts the neuro
 development of the fetus (Waddington et al 1999). Other maternal infections such as
rubella and toxoplasmosis that occur during this time has also been linked to
increased risk for the later development of schizophrenia (Brown 2011)

• Rh incompatibility: The idea that the mother’s immune system might

somehow damage the developing fetus is not new, Hollister, lang and Mednick 1996
have shown that Rh incompatibility between the mother and child increases the risk of
schizophrenia as this incompatibility may result in oxygen deprivation or hypoxia.
Blood incompatibility between the blood of the mother and the blood of the fetus may
increase the risk of brain abnormalities of the type known to be association with
schizophrenia (Friedman et al 2011)

• Pregnancy and birth complications: patients with schizophrenia are much

more likely to have been born following a pregnancy or delivery that was complicated
in some way (Cannon et al 2002). Although the type of obstetric complications varies
many delivery problems (for example breech delivery, prolonged labour or the
umbilical cord is around the babies neck) effect the oxygen supply of the new born.
The research again points towards damage to the brain at a critical time of
development (early cerebral insult “in the genetically at risk babies’)

• Early nutritional deficiencies: In 1999 Dalmon found sex of risked factors

representing 3 different etiological mechanism that could lead to schizophrenia. These
were: Malnutrition during fetal life, extreme prematurity, hypoxia and lack of blood
supply. This could impair development of the CNS and may lead to schizophrenia this
is supported by the research on children born in the Dutch hunger winter, a period in
the history of Netherlands when there was acute famine due to Nazi blockade (1944).
There was a two fold increase in schizophrenia in children born during this period.
Early prenatal nutritional deficiencies appear to have been the cause.

• Maternal stress: if a mother experiences an extremely stressful event late in

her first trimester of pregnancy or early in the second trimester the risk of
schizophrenia in her child is increased (King et al 2010). For example in a large
population study conducted in Denmark the death of a close relative during the first
trimester was associated with a 67% increase in the risk of schizophrenia of the child
(khashan et al 2008) currently it is thought that the increase in stress hormones that
passed to the foetus via the placenta might have negative effects on the

Twin Studies

Sz concordance rates for identical twin studies are routinely and consistently found to be
significantly higher than those of fraternal twins or ordinary siblings. The most famous case
of concordance for Sz is the genain quadrupalets, but the specific symptoms, onset, course
and oucomes of the disorder varied substatially among them. (Mirskey et. al. 2000).
Although being being a twin does not increase ones risk for developing Sz, study after study
have shown a higher concordance for Sz among identical twins than among people related in
any other way including fraternal twins.

Torrey is a noted Sz researcher who has a sister with the disorder. He and his collegues in
1994have published a review of the major literature, world wide on twin studies of Sz. The
overall pair wise concordance rate is 28%. In M2 twins and 6% in D2 twins. This suggests
thatA reduction in shed genes from hundred percent to 50% reduces the risk of Sz by nearly
80%. Also note that sharing 50% ones genes with co-twin with Sz is associated with the
lifetime risk for Sz of 6%. Although this is low in absolute terms, it is markedly higher than
the baseline risk of less than 1% found in the general population. Other studies (Squire et. al
2003) indicate 45 to 50% concordance rate for identical twins compared to only 15%
concordance rate of fraternal twins.This shows that M2 twins are much likely to develop Sz
than D2 twins.

Is Sz were exclusively a genetic disorder concordance rate of identical twins would of course
be 100% . Two conclusions can be drawn:

- Genes undoubtedly play a role in causing Sz

- Genes themselves are not whole story

Twin studies provide some of the most solid evidence that the environment plays an
important role in the development of Sz. But why one M2 twin should develop Sz when his
or her twin does not is a fascinating question. Torrey (1994) also found the following
differences between schizophrenia and non schizophrenic co-twins.

- 30% of the discordant affected twins were described as having different

suggesting CNS dysfunction.

- Discordant affected twins showed widespread brain changes though they were not
related to clinical aspects of schizophrenia indicating that behavioral
manifestation was related to some other factors.

A great deal of research attention is being directed towards studying people with a known
genetic liability for schizophrenia. Historically, the most important subjects to study in this
regard have been M2 twins who are discordant for schizophrenia. This investigative strategy
was pioneered by Fisher in 1971 and 1973 and and ingenious study.

Fisher reasoned that genetic influence if present could be just as likely to show up in the
offspring of the twins without schizophrenia in discordant pairs. As they would be to show up
in the offspring of the twins with schizophrenia ( because they share all their genes in
common).And in a search of official records in Denmark, Fisher found exactly that. In a
follow up of Fishers report and age corrected incidence rate for Schizophrenia of 17.4 % for
the offspring of M2 twins. This rate which far exceeds normal expectancy was not
significantly different from that for offspring of the Twin studies with schizophrenia in
discordant pairs or from that for offsprings of Dz. Assuming that exposure to an aunt or uncle
with schizophrenia would have at most Limited etilogic significance. These results and
impressive support to the genetic hypothesis. They also indicate that a predisposition to
schizophrenia may remain ‘unexpressed’ ( as in the Twins without schizophrenia and
discordant pairs) unless ‘released’ by unknown environmental factors.

Adoption studies

The assumption that M2 to and D2 twins have equally similar environments can create some
problems when we try to interpret the findings of Twin studies.

Interpretation problems with twin studies

- Challenging equal environmental assumption : Twin studies are based on the

assumption that M2 twins and D2 twins differ only in terms of their genes. Equal
Environmental Assumptions (EEA) states that the environmental conditions of
M2 twins and D2 twins are same. This may not be true as there is evidence to
indicate that monozygotic twins are treated more similarly by their family (have
more similar env).

- Also at least two-thirds of M2 to twins are meaning that, they share the blood
supply as they share one placenta. One study found, that the concordance rate of
search M2 twins was Almost double the concordance rate ( or D2 twins who had
separate placentas) ( Davis and Phelps, 1995).

So the higher concordance rate may not be due to ‘fainted genes’ but due to
intrauterine factors involved in schizophrenia.

- Other factors: Some researchers also suggest that identical twins are identical only
till the splitting of zygote. After that some Amount of influence may be that
affecting the twins differentially such as chromosomal changes, gene mutations,
difference in circulation and oxygenation, different response to exposure agents
etc.

Several studies have attended to overcome the shortcomings of the Twin method in
achieving a true separation of hereditary from environmental influences by using what
is called as the adoption strategy. Hence concordance rates for schizophrenia are
compared for the biological and the adoptive relations of persons who have been
adopted out of the biological families at an early age (Preferably at birth) and have
subsequently developed schizophrenia.If concordance is greater among the patients
biological than adoptive relatives, hereditary influence is strongly suggested. A
reverse pattern would be argued for environmental causations.
The first study of this kind was conducted by Heston in 1966. Heston followed up 47
children who had been born to mothers who were in a state mental hospital suffering
from schizophrenia. The children had been placed with relatives or into Foster homes
within 72 hours of their birth. In his follow-up study, Heston found that 16.6% of
these children were later diagnos with Sz. In contrast none of 50 control children
(selected from among the residents of the same Foster homes whos mothers did not
have Sz) developed Sz. In addition, to the greater probability of being diagnosed with
schizophrenia, the offspring whose mother had schizophrenia are also more likely to
be diagnosed as mentally retarded, neurotic or psychopathic. They also had been
involved more frequently in criminal activities and had spent more time in the penal
institutions. These findings were often taken to suggest that any genetic liability
conveyed by mothers is not specific to schizophrenia but includes a liability of other
forms of psycho-pathology.But we must be careful about drawing such conclusions.
Hestons study provided no information about fathers of the children. We therefore
cannot know to what extent some of the problems the children were facing due
genetic liability conveyed by their father.

Heston studies began With mothers with schizophrenia and then traced what
happened to the adopted avail offsprings. An alternative approach involves located
adult patients with schizophrenia who adopted early in life and then looking into their
biological and adoptive relatives. A large scale adoptive study was undertaken in
Denmark which Danish investigator working in collaboration (Kender et al.1994) as
would be expected on the basis of a genetic model, the data showed a Preponderance
for Schizophrenia and schizophrenia spectrum problem (for ex schizotypal and
paranoid personality disorder). In the biological relatives of adoptees with
schizophrenia more specifically 13.3% of the 105 biological relative had
schizophrenia or schizophrenia spectrum disorders themselves. In contrast only 1.3 %
of 224 adoptive parents showed such problems.

Quality of the adoptive family

In Finland, between 1960 and 1979, a finish adaptive study of schizophrenia was
conducted (Tienari et al. 2004)Provided further evidence of genotypes environment
interaction in schizophrenia. Using interviews, the researcher first look at the quality
of the family and mint in which the doctor children were raised. They then looked at
what happened to the children who were raised in healthy versus dysfunctional
families. The degree of adversity in the family environment predicted later problem in
the adopted children. However, only those children who were raised in dysfunctional
and had high genetic risk of schizophrenia went on to develop schizophrenia related
disorders themselves. Children at high genetic who were raised in healthy family
environment did not develop problem any more frequently than their children at more
genetic risk. These findings are important because they suggest that our genetic
makeup May control how sensitive we are to certain aspects of our environment. If
we have no genetic inclinations certain kinds of environmental influences may not
 affect us very much but if we have high genetic risk we may be much more vulnerable
to certain types of environmental risks such as High communication deviance for
adverse family environment. Finding such as these also raise the exciting possibility
that certain kinds of environment may protect people with genetic susceptibility to
schizophrenia ever developing the illness.The Finnish adoptive family study has
provided strong confirmation of the diathesis stress model as it applies to the regions
of schizophrenia.

Family studies talas schizophrenia runs in families and when an adoption, studies help
us explore the relative contribution of genes and environment. these approaches also
tell us about the genetic heterogeneity of schizophrenia. for example in addition to
higher results of schizophrenia, higher rates of schizotypal personality disorderAre
also found in the relatives of patients with schizophrenia. This supports the idea of the
schizophrenia spectrum and suggest that a genetic liability to schizophrenia can
sometimes manifest itself in a form of Pathology that is “schizophrenia like” but not
exactly schizophrenia itself.

- Molecular genetics

Researchers are now trying to locate and identify the genes that are involved in
schizophrenia using the techniques of molecular genetics. studies are suggesting
specific regions on certain chromosome that may contribute to schizophrenia.
Currently there is a big deal of interest of regions on chromosomes 1, 2, 6, 8, 13 and
22 among others.

Why are there chromosomes of Sachin test? The reason is that in some cases they host
genes that are known to be involved in processes that are believed to be dysfunctional
in schizophrenia. These gemes are known as candidate genes. An example in the Com
T gene. This train is located on chromosome 22 and is involved in dopamine
metabolism. Dopamine is a neurotransmitter that has long been implicated in
psychosis. Interestingly, children who have a genetic syndrome (Velocardiofacial
syndrome) that involves a deletion of genetic material on chromosome 22 are at
higher risk for developing schizophrenia as they move through adolescence (Gothel et
al. 2007). Prior to the onset of any disorder, they often report transient psychotic
syndromes such as auditory hallucination have poor social functioning and reduced
IQ.

Endophenotypes

To simply think researchers are now focusing on less Complex and more homogeneous
phenotypes (such as specific symptom clusters) that may potentially be under the control of a
smaller number of genes.There are also exploring Endophenotypes discrete, stable and
measurable traits thought to be under genetic control by studying different and phenotypes
researchers hope to get closer to specific genes that might be important in schizophrenia
(Gottesman & Gould, 2003, Lenen Weger, 2010).

Accordingly researchers are interested in people who scored high on certain test on measures
that are thought to reflect a predisposition to schizophrenia.One example is subjects who
scored high on a self-report measure of schizophrenia traits involving perceptual aberrations
of Magical ideation (Pert-Mag Scale).Other endophenotype risk markers for schizophrenia
include abnormal performance on measures of cognitive functioning such as test for working
memory. By studying these stress rather than the disordered itself researchers hope to speed
up progress in the search for the genes related to schizophrenia. Major collaborative studies
design to explore different endophenotypes and now under vain (Greenwood et al. 2007).

Prenatal exposures

In this section, we highlight some environmental risk factors that might either cause Sz or
trigger it in a genetically vulnerable person. Apart from genetic susceptibilities, other
biological factors also start playing as early or even before ones birth.

Viral infections

Kraeplin, 1919, suggested that infections in the year of development might have a causal
significance for schizophrenia evidence for the involvement of infectious disease. The
evidence of schizophreniaFirst came from the season of birth defect. We also know that in the
Northern hemisphere there with people with schizophrenia a born between January and
March (winter months) than would be expected by chance (Waddington et al. 1999) this is
thought to be due to exposure to viruses during development.

Rise of schizophrenia seems to be greater when the mother gets the flu in the 4th to 7th
month of gestation. Although, the size of the effect is small and influenza clearly does not
account for very many cases of schizophrenia.The fact that this association exists is very
provocative but how can maternal influenza set the stage for schizophrenia in a child two or
three decades later? one possibility is that the Mother's antibodies to the virus cross the
placenta and somehow disrupt the neurodevelopment of the foetus (Waddigton et al, 1999).
Other maternal infections such as rubella and toxoplasmosis that occurred during this time
have also been linked to increased risk for later development of schizophrenia (Brown, 2011).

RH incompatibility

The full form of RH is the idea that mothers immune system might somehow manage the
developing foetus is not new. Hollister, Laing & Mednick, 1996 have shown that RH
incompatibility between the mother of child increases the risk of schizophrenia as this and
compatibility may result in oxygen deprivation or hypoxia. Research also suggests that
incompatibility between the blood of the mother and the blood of the foetus may increase the
risk of brain abnormality is of the type known to be associated with schizophrenia (Friedman
et al, 2011).
Pregnancy and birth complications

Patients with schizophrenia are much more likely to have been bird following a pregnancy
that was complicated in somewhere Canon et al, 2002). Although the type obstetree
complication varies many delivery problem (for example breech delivery prolonged labour
or the umbilical cord around the neck affect the oxygen supply of the newborn). The research
again suggest damage to the Brain at a critical time of development (early cerebral insult in
the genetically at risk babies).

Early nutritional deficiency

In 1999, Dalwan, found sets of risk factors representing three different etiological
mechanisms that could lead to schizophrenia.These were: malnutrition during fetal life,
extreme prematurity, hypoxia and lack of blood supply. This quote a development of central
nervous system and may lead to schizophrenia. This is supported by the research on children
born in the ‘Dutch hunger winter’ ( period in the history of Netherland when there was a cute
famine due to Nazi blockade 1944). There was a two fold increase in schizophrenia in
children born during this period. Early prenatal nutrition deficiency appears to have been the
cause.

Structural and functional brain abnormalities

Neurocognition

Schizophrenia patients experience many problems with their neurocognitive functioning. For
example they perform much worse than healthy controls on a broad range of
neuropsychological tests (Hoff et al, 2000). Furthermore, patients who have only recently
become ill performed about the same a neuropsychological test as patients who have been ill
for many years (and both groups obviously performed worse than controls).In other words,
cognitive difficulties can be seen right from the start of the illness and so are unlikely to be
due to the effects of external hospitalization or medication.

Other cognitive deficits are also Apparent for example- when asked to respond to established
as quickly as possible.This measure of response time in schizophrenia patients was poor
compared with controls. In addition, they showed deficits on continuum performance tasks
(CPT).

There are also problems with working memory. when they engage in tasks of working
memory patients with schizophrenia show less prefrontal ray activity compared to Healthy
controls Canon et al, 2005).

Somewhere between 54% to 86% of people with schizophrenia also show a tracking
dysfunction and deficits in ability to track a moving target such as a pendulum (Cornblatt et
al, 2004).This is a skill referred to as smooth Pursuit eye movement. Around 50% of the first
degree relatives of schizophrenia patients also show eye tracking problem even though they
do not have schizophrenia themselves. This suggests that disturbances in eye tracking have a
genetic basis and that eye tracking may represent a viable endophenotype for genetic studies.

Perhaps the strongest finding in the area of neurocognition and schizophrenia,However,

concurs psychophysiological measured called P50. When two clicks are cut and close in
succession the brain receiving auditory signal produces a positive electrical response to each
click. This response is called P50. Because it occurs 50 milisrconds after the click. In normal
subjects the response to the second click is less marked the response to the first click because
the normal brain depends on “gates”, responses to repeated sensory events- if they did not
happen, habituation to a stimulus would never occur. Many patients with schizophrenia in
contrast respond almost as strongly to the second click as to the first. This is referred to as
“proffer P50 suppression”( Clementze et al, 1998).It has been suggested that proffer P50
supression if the result of problem with specific receptors in the hippocampus of the medial
temporal lobe (Adler et al. 1998).

Brain volume and ventricular enlargement

Some adults with schizophrenia have been diagnosed as having a decrease in brain volume
due to ventricular enlargement -hollow areas filled with cerebrospinal fluid in the brain
(Anderson et al. 1986). as well as enlarged sulci ( Canon and Marco, 1986). These
enlargements may be an indicator of brain degeneration as it leads to a loss in brain tissue
also there is progressive grey matter loss in schizophrenia.

Specific brain areas

Number of brain imaging and post-mortem studies have shown that abnormal physiology
appears to be involved in the development of schizophrenia (Gur and Pearlson, 1993)
concludes that three brain structures are involved in schizophrenia. Though Canon indicates
only the first two:

1) Frontal lobe

2) Temporary region

3) Thalamus

1) Hypofrontality or reduced frontal lobe activity

The frontal lobe activity which is concerned with thinking planning integrating
information from various paths of the brain same to be reduced (known as
hypofrontality for frontal atrophy)in Sz (Buchpaun & Haier,1907).This may account
for some of the negative symptoms and perhaps to be involved in some attentional
cognitive deficits (Canon et al 1998). There is some evidence that reduced frontal lobe
activity may also occur in persons with bipolar mood disorders, so the specificity of
hypofrontality is not certain.
 2) Thalamus

Is the relay station of the brain. It receives messages and send it to other areas of the
brain. the size of the thalamus is considerable a reduced in schizophrenia and this may
reduce the ability of the individual to filter or “gate” irrelevant information.

3) White matter problems

Evidence is growing that schizophrenia also and valve problems with white matter.
New fibres are are covered in a myelin sheath (which looks white in colour in a
chemically preserved brain). Myelin act as an insulator and increases the speed and
efficiency in between Nerve cells. White matter therefore is crucially important for
connectivity of the brain.If there are Disruptions in the integrity of the white matter
there will be problems in how well off the cells in the nervous system can function.

Studies of patients of schizophrenia show that they have reductions in white matter
volume as well as structural abnormalities in the white matter itself. Interestingly,
these abnormalities can be found in first episode patients and also in people at
genetically higher risk for the disorder. This suggests that they are not a result of the
disease itself or the effects of the treatment. At the clinical level white matter
abnormalities have been shown to be correlated with cognitive impairments (Kubick
et al 2007). In people at high risk of developing schizophrenia white matter changes
in the temporal area of the brain also pedictl late social functioning (Karlsgodt et al
2009).

Brain functioning

Some patience of schizophrenia Show abnormally Low frontal lobe activation known as
hypofrontality when they are involved in mentally challenging tasks or another test generally
though to require substantial frontal lobe involvement. The strain area does not seem to be
able to kick into action when patients perform Complex tasks.Another patient hyperactivation
in frontal brain areas is found suggesting that they are having to work harder to be successful
on the task. In both sets of circumstances, however the brain is not functioning in an optimal
and efficient way (Keshavan et al 2008).

Impaired functioning of the frontal lobes during cognitive tasks is also found in patients in
the early stages of schizophrenia as well as people at high risk for developing the disorder.
However it is important to remember that such alterations in functioning and not
characteristic of all patients. Nonetheless frontal lobe dysfunctionIs believed to account for
some of the negative symptoms of schizophrenia and perhaps to be involved in some
attentional cognitive deficits Canon et al 1998).
This function of the temporal lobe is also found what may be the most important is that that
may be a problem with the way activity in different brain regions gets coordinated.

Cytoarchitecture

This refers to the overall organisation of cells in the brain which seems to be compromised in
schizophrenia to several factors:

- Improper cell migration: It has been suggested that Due to certain factors for
example viral infection that may be in proper cell migration which occurs during
the second trimester with some cells failing to reach their target destinations.

- Disrupted synaptic pruning and neural cell death: Normal individuals have neural
redundancy that is excessive synapses and neural cell that help to to delete
unnecessary neural connections for neural redundancy during development. The
mechanism is not properly understood and may lead to increased or decreased
during density in schizophrenia ( lower densities of neurones in the prefrontal
cortex; abnormalities in the distribution of cells in different layers of the cortex
and hippocampus- Arnold 2007)\

- Decreased inhibitory inter neurones: These neurones are responsible for regulating
the encitatuion of the neurons.It seems the brains in patients having schizophrenia
have a lack of such inhibitory interneurons. Thus, the person is unable to regulate
or decrease over activity in certain key circuits of the brain (Benes 2000).

Neurochemistry or biochemical factors

● Dopamine hypothesis -

The proposed hypothesis states that symptoms of schizophrenia may be related to

over activity in the dopamine system. Increased dopamine actually make the
individual pay more attention to irrelevant stimuli. This is called ‘aberrant salience’
(Kapur,2003).It has been suggested that this aberrance silence causes the positive
symptoms of the disorder (delusions and hallucinations) as the individual sees
meaning where there is none leading to misinterpretation.

However there is much debate in the scientific community as do the exact mechanism
by which dopamine levels are altered. Increased levels of dopamine activity may be
due to increased production of dopamine in the synaps, slow metabolism aur
breakdown of dopamine or by blocking of neural uptake. Recent development in the
idea that is not necessarily too much dopamine activity but rather the dopamine
activity receptors are over sensitive or too dense.There is some evidence in the post
mortem examination of schizophrenic patients, there appears to be an increased
number of dopamine activity receptors (Mckeena, 1997). Although, there are at least
Five types of dopamine receptors (D1 to D5) most of the research has focused on D2
 dopamine receptors and has found an increase in the receptors in patients with
schizophrenia compared with controls (Gjeede & Wong, 1987).

There is much clinical evidence that provide support to the dopamine hypothesis and
amphetamine work by causing the brain to produce more dopamine and have been
shown to produce psychotic like symptoms. In addition traditional antipsychotic drugs
(chlorpromazine) act by blocking dopamine receptors in the brain.

There are four main dopamine tracks (or brain regions where the neurotransmitter is
found). It may be possible that there is over activity in some tracts and under activity
in other tracts. Increased activity in the mysolimbic tract may be responsible for the
negative symptoms of schizophrenia.

Recent research indicates that serotonin and glutamate system may also be involved in
schizophrenia.

Researchers and now are exploring concentrations of glutamate in post-mortem brains

of patients with schizophrenia and finding lower levels of glutamate in both the
prefrontal cortex and the hippocampus compared with controls (Goff and Coyle,
2001). Olney & farber ( 1995) have proposed that diminished activity at certain types
of glutamate receptors known as NMDA receptors may not only trigger schizophrenia
like symptoms but also cause the degeneration of neurons in key brain areas.The
glutamate hypothesis is also prompting the development of new experimental drugs
such as glucine that are designed to activate glutamate receptors. Furthermore, an
overactive dopamine system good result in excessive separation of glutamate leading
to under activity of NMDA receptors which would Trigger schizophrenia like
symptoms and subtle brain damage.

Neuro development models

Two basic models have been suggested-

1) Neurodegenerative model

2) Neurodevelopmental model

Neurodegenerative model states that patients with schizophrenia have the brains that are
normal till about adult life when degenerative changes take place.The focus has shifted to the
neurodevelopmental hypothesis.Neurodevelopmental hypothesis on the other hand proposes
that schizophrenia is the result of early brain lesions (called static lesions) which originate in
the middle stage of interactive life (Murray & Lewis, 1987).The static lesion lies dormant
until it expresses itself in the mature brain. the causes for these lesions are second trimester
exposure to obstetric complications, viral infections leading to cerebral insult or damage.This
may result in an improper cell migration which occurs during second trimester with some
cells failing to reach their target destinations

Developmental precursors/predictors: if the neurodevelopmental model Is valid there would

be certain developmental precursors to the disorder.Attempts have been made to find such
developmental precursors to schizophrenia.( indicators of vulnerability to the disorder before
the elders itself strikes)

- Motor abnormalities, decreased positive emotions and increased negative

emotions:

In a study by Walker et al. 1984 it was found that blind observers investigators
gathered Family home movies made during childhood 32 persons who eventually
develop schizophrenia.Trained observers made blind rating that is the observers were
not informed of outcome of certain dimensions of the emotional and facial
expressions Motor skills and neuromotor abnormalities of the children and of their
healthy outcome siblings from the same movie clips.

Blind observers rated preschizophrenic patients higher on motor abnormalities, lower

on the positive emotions and higher on the negative emotions. Jones19994 and
isohanni 2001Found evidence of delayed speech and delayed motor development at
age 2 two in children who later developed schizophrenia.

- Decreased attention: Children who are at risk for developing schizophrenia show
poor performance on tasks but required attention according to Comblatt et alt
1992 some of their social problems may result from underlying attentional
problems.

Interpreting the biological evidence diathesis stress model

Biological factors undoubtedly play a role in the etiology of schizophrenia but genetic
predisposition can be shaped by environmental factors such as prenatal exposures. The
diocese trust model originates largely from schizophrenia research. According to this model
schizophrenia is produced by the interaction of vulnerable hereditary predisposition
(diathesis) with precipitating events (stress in the environment) Zubin & Spring 1997.

Psychological causes

Psychological dimension includes behaviour attitudes and attributes that contribute to the
symptoms of schizophrenia by increasing the vulnerability of predisposed individuals.
 ● Fromm-Richman’s ‘schizophrenogenic’ mothers ( mothers who generate Sz)

In 1948, Fromm-Richman described the mother of the schizophrenic and established

the term ‘schizophrenogenic mother’. The SM was described as total cold rejecting
possessive individual who creates get and in conjunction with the passive remote and
ineffective father which causes confusion and a feeling of insufficiency to her son and
finally leaves him to schizophrenia. Feminist criticize this because they say it is
wrong to blame parents for schizophrenia.

● Lids’s 1949 ‘marital schism’ & ‘skew’ theory

- Marital schism; refers to a division of the family what the parents

maintaining antagonistic and contrary views. The family is in constant
state of disequilibrium through repeated threats of parental separation.
Parents constantly fight with each other, seek collusion with children,
there by excluding the partner. As a result of this, the child has divided
loyalties.

- Marital skew: the family is skewed with one partner being excessively
dominant and the submissive partner to the eccentricities of the dominant
partner. In these families one of the two parents suffer from a serious
disorder. Family equilibrium is achieved through distorted parental
relationships. The marriage is not under threat due to one excessively
powerful and dominant parent.

(the below theories are in continuation with the above topic)

‘Singer & Wynnes’ “pseudo reciprocity” & “communication deviance” (1966)

● Pseudo reciprocity: the families give the impression of a reciprocal, open,

understanding relation but in reality are emotionally distant. The parents avoid every
disagreement giving a false picture of harmony to the others while in reality they hide
a deeper distance between them. For example, they may make a big drama of giving
presence to each other on occasions but there is an underlying hostility and
disappointment.

● Communication Deviance: Wynne & Singer proposed that families of such patients
have odd and deviant styles of communication and are unable to establish and
maintain a shared focus of attention. For example, peculiar language, change of topic
abruptly with closure.

Double Bind Hypothesis (Bateson, 1959)

Bateson believed that the condition of double Bind occurs when an individual (often a child)
receives repeated contradictory messages from the same parent. For example, a mother telling
her child that she loves him or her while at the same time turning her head away with disgust.
The solution is to create an escape from the double bind, then in the world of delusional
systems.

Psychodynamic approaches

Freud in 1924 believed that schizophrenia developed from two psychological processes- (i)
regression to pre ego stage (ii) efforts to reestablish ego control. He proposed that when the
world is extremely harsh or withholding, for example, when parents are extremely harsh or
cold. People who develop schizophrenia regress to the earliest point in their development to
the pre ego state of primary narcissism, in which they recognise and meet their needs only.
Their near total regression leads to self-centred symptoms such as neologism, loose
associations and delusions of grandeur. Once people regress to such an infantile state, then try
to reestablish ego control and contact with reality. Their efforts give rise to yet other
schizophrenic symptoms. Auditory hallucination may for example, be an individual’s attempt
to substitute for a lost sense of reality.
ROLE OF EXCESSIVE LIFE STRESS AND EXPRESSED EMOTIONS (EE)
EE by George Brown is a measure of family environment that is based on how a family
member speaks about the patient during a private interview with a researcher. It has three
main elements:

● Criticism: which reflects dislike or disapproval of the patient.

● Hostility: indicates the dislike or rejects of the patient as a person.

● Emotional overinvolvement; reflects dramatic or over concerned attitude on the part

of the family member towards the patient’s illness.

EE is important because it has been repeatedly shown to predict relapse in patients with
schizophrenia. In a meta-analysis of 26 studies, Butzlaff & Hooley (1998) demonstrated that
living in high EE homes more than doubled the relapse risk for schizophrenia patients in the
9-12 mnths of hospitalisation. High EE behaviours exhibited by family members are
perceived as stressful by the patients because high EE relatives have been found to be more
behaviourally controlling of patients than low EE relatives are (Hooley & Campbell, 2002)
when they try to help, they sem to do so in rather intensive ways (for example, ‘she would not
go to sleep, so I held her head down to the pillow’ in other words well meaning attempts to
get patients to function better simply backfire. If patients are stressed by what the relatives
do, this could increase cortisol levels affecting important neurotransmitter systems (trigger
dopamine activity & affects glutamate release) and perhaps eventually lead to a return of
symptoms of schizophrenia.
In sum, research has taught us that disturbances and conflict in families that include an
individual with schizophrenia may well be caused by having a severely ill and psychotic
person in the family. Rather than causing schizophrenia, family communication problems
could be the result of trying to communicate with someone who is surely ill and disorganised.
At the same time however, some families do show unusual communication patterns. In the
early years, parents were assumed to have caused their children disorders through hostility,
open rejection or gross parental ineptitude. However, these attitudes are fast changing. As we
know from the Finnish adoption studies, adverse family environments and communication
deviance probably have little pathological consequence if the child who is exposed has no
genetic risk for schizophrenia. (Tienari et.al., 2004; Wahlberg et.al., 1997)

Alternative approaches: existential perspective

An approach broadly known as the anti-psychiatry movement notably most active in the
1960s has opposed the orthodox view of schizophrenia as an illness. Psychiatrist Thomas
Szasz argues that psychiatric patients are not ill but are just individuals with unconventional
thoughts and behaviours that make society uncomfortable. He argues that society unjustly
seeks to control such individuals by classifying their behaviour as an illness and possibly
treating them as a method of social control.
Schizophrenic behaviour is a special strategy that a person invents in order to live in an
unlivable situation (R.D. Laing) similarly psychiatrists Laing, Arieti, Lids and presently
Colin Ross have argued that the symptoms of what is normally called mental illness are
comprehensible reactions to impossible demands that society and particularly family places
on some sensitive individuals.

They were revolutionary in valuing the content of psychotic experience as worthy or

interpretation rather than considering it simply as a secondary but essentially meaningless
marker of underlying psychological or neurological distress.

According to Laing’s existential principles, schizophrenia is actually a constructive process in

which people try to cure themselves of the confusion and unhappiness caused by their social
environment.

Laing said that people are in search of their true selves which is difficult in present day
society and therefore, develop a false self rather than a true self. Some people, those who
develop schizophrenia have faced a lifetime of obstacles and out of desperation they
eventually undertake an inner search, withdrawing from others. Laing believed that left alone
these people would indeed achieve a healthy outcome.

Researchers have speculated that in some cultures schizophrenia or related conditions may
predispose an individual to becoming a Shaman, certainly the experience having access to
multiple realities is not uncommon in schizophrenia and is a core experience in many
Shamanic traditions. Equally. The shaman may have the skill to bring on and direct some of
the altered states of consciousness which psychiatrists label as illness. Speculations around
regarding primary and important religious figures as having schizophrenia. Commentators
such as Paul Kurtz, and others have endorsed the idea that major religious figures experience
psychosis, heard voices and displayed delusions of grandeur.

An additional approach is suggested by the work of Richard Bandler who argues that ‘the
usual difference between someone who hallucinates and someone visualises normally is that
the person who hallucinates does not know he is doing it or does not have any choice about
it.’

He suggests that because visualisation is a sophisticated mental capability, schizophrenia is a

skill or albeit an involuntary or dysfunctional one is being used but not controlled. He
therefore suggests that a significant route to treating schizophrenia might be to teach the
missing skill- how to distinguish create reality from consensus external reality to reduce its
maladaptive impact and ultimately how to experience ultimate control over the visualisation
or auditory process .

Hypnotic approaches have been explored by the physician Milton H. Erikson as a means of
facilitating this.

Socio-cultural factors:

Researchers believe that unless a person has a genetic predisposition towards schizophrenia,
socio-cultural factors have little impact on the development of the disorder.

● urban living: Research suggests that growing up in an urban environment creates a

higher risk for developing schizophrenia (Pederson & Mortensen, 2001). The study
suggests that the more time a person spends before the age of 15 in an urban area, the
higher his/her risk for developing schizophrenia. The ‘sociogenic hypothesis’ suggests
thatcities ‘breed’ or ‘precipitate' psychosis in genetically vulnerable people by the
stress of social isolation and complex cognitive demands that characterise inner city
or urban life. Other possibilities have been suggested that include greater exposure to
pollution, toxic agents and infectious agents. But the associations with urban living
has not received enough attention because current research centres on neural imaging
and pharmacology.

● Immigration: Research is also showing that recent immigrants have a much higher
risk of developing schizophrenia than do people who are native to thecountry of
immigration looking a tthe results of 40 different studies involving immigrant groups
from many different parts of the world, (Cantor- gray and selton 2005 found that first
generation immigrants those born in another country had 2.7 times the risk of
developing schizophrenia; for second generation immigrants (that is those withone or
both parents having been born abroad the relative risk was even higher at 4.5.one
possibility is that immigrants are more likely to receive this diagnosis because of
cultural misunderstandings (Shashi tharan 1993) however there is no convincing
 evidence that this is the case another possibilitythat experiences of being
discriminated against could leave some immigrants to develop a paranoid and
suspicious outlook on theworld which could set the stage for the development of
schizophrenia the stress that results from social disadvantage and social defeat may
have an effect on dopamine release in key neural circuits moreover some of these
biological changes could make people more sensitive to the affects of using illicit
substances this is interesting in light of new evidence linking cannabis abuse to the
development of schizophrenia. Socio-economic status: Morethan 50 studies
conducted in Europe, Asia and North America have found that people of lower
economic status are diagnosed with schizophreniamore frequently than people of
middle or upper SES. Some people believe that stressors associated with being in a
low social class may contribute to the developmentof schizophrenia (called the
sociogenic hypothesis). Another explanation of the correlation between schizophrenia
and lowclass is the social selection theory" which reverses the direction of causality
between social class and schizophrenia. During the course of their developing
psychosis people with schizophrenia may drift into the poverty ridden areas of the
citythe growing cognitive and motivational problems of these individuals may so
impair their earning capabilities that they can not afford to liveelsewhere or may
choose to move to areas where little social pressure would be bought to bare on them
and where they can escape intense social relationships.

Schizophrenia and Ethnicity

Psychotic behaviour observed in countries other than USA or among particular ethnic groups
have been identified as a culture bound syndrome. Allen 1997 h a ssuggested that
schizophrenia seems to occur less often and with diminished severity in traditional, less well
developed cultures Mezzich, Linn, Hughes (2000) summarised some of these psychotic
behaviours:

● Bouffee delirante - A syndrome found in west Africa and Haiti involves a sudden
outburst of agitated and aggressive behaviour, marked confusion and psychomotor
excitementit is sometimes accompanied by visual and auditory hallucinations or
paranoid ideation.

● Ghost sickness- is preoccupation with death and the deceased it is frequently observed
among members of some native American tribes, Symptoms include bad-dreams,
weakness, feelings of danger, loss of appetite, fainting, diziness, fear,anxiety, loss of
consciousness, confusion, feeling of futility and a sense of suffocation.

● Lakura- it refers to a chronic psychosis experiencedby Latinos in US and latin

America symptoms include incoherence, agitation, visual and auditory hallucinations
inability to follow social rules, unpredictability and possible violence
 ● Qi-Gong- psychotic reaction is an acute time limited episode characterizedby
dissociative paranoid or other psychotic symptoms that e participating ni the Chinese
folk health enhancing practice of Qi-Gong especially vulnerable Are those who
become overly involved in the practice.

● Zar- an experience of spirits possessing a person is seen. In Ethiopia,Somalia,Egypt,

Sudan, Iran and other north African and middle eastern societies the afflicted person
may laugh, shout, wail, bang his or her head on the wall or be apathetic and
withdrawn refusing to eat or carry out daily tasks. Such behaviour is not considered
pathologic or abnormal locally.

Ethnicity may also be a factor in a way person responds to psychotropic medications this
difference in response is probably the result of the person's genetic make up. Some people
metabolise certain drugs more slowly so that the drug level in the bloodstream is higher than
desired. African Americans, Caucasian-Americansand Hispanic-Americans appear to require
comparable therapeutic doses of antipsychotic medications Asian clients however need lower.

Ethnicity may also be a factor in a way person responds to psychotropic medications this
difference in response is probably the resultof the person's genetic makeups o m epeople
metabolise certain drugs more slowlyso that the drug level in the bloodstream is higher than
desired. African Americans, Caucasian- Americansand Hispanic- Americans appear to
require comparable therapeutic doses of antipsychotic medications asian clients howeverneed
lower doses of drugs to obtain the same effects (Kudzmarg 19990 therefore they would be
likely to experience more severe side effects fi given the traditional or usual doses.