Clinical Psych
Clinical Psych
Introducing psychopathology:
- Concept of abnormal behaviour
Definition Behaviour that deviates significantly from societal norms or from what is considered typical or healthy. However,
determining what is "abnormal" can be complex because it varies across cultures, contexts, and historical periods.
Key characteristics Statistical Actions or mental processes that are statistically uncommon. However, rarity alone doesn’t
Rarity/deviancy: imply abnormality, they are also rare but not seen as undesirable.
→ Why can the
definition change… Violation of Social Violates societal expectations or cultural standards.
Norms:
Personal Distress Experiences significant distress or discomfort. Some conditions may not cause distress to
(suffering): the person, but might still be harmful to others.
Maladaptive Impairment in a person’s ability to function effectively in everyday life. This could include
Behavior: behaviours that hinder well-being or lead to harmful outcomes.
Unexpectedness and Abnormal behaviour can be characterised by impulsive, unpredictable actions that are
Unpredictability: difficult to understand within a given context.
- Clinical Assessment
Clinical diagnosis and - Assessment data → pattern of symptoms the person presents → consistent with Diagnostic criteria in DSM
classification system & ICD
- Diagnosis only to aid the mental health professional → determining of prognosis, treatment plans and
outcomes (APA 2013)
Disturbance in Cognition, Disorders can manifest in various ways, including irrational thought patterns, emotional
Emotion Regulation, or Behavior dysregulation (such as extreme mood swings), or behaviours that are outside of societal
norms or are harmful.
Associated with Distress or For a behaviour or pattern to be classified as a mental disorder, it generally needs to cause
Disability significant personal distress (such as anxiety or depression) or impairment in critical areas
of functioning, such as social relationships, work, or self-care.
Exclusion of Socially Deviant The DSM-5 clarifies that socially deviant behaviour (e.g., political, religious, or sexual
Behaviour differences) and conflicts between the individual and society are not, by themselves,
mental disorders unless they result from dysfunction within the individual. This distinction
aims to avoid labelling behaviours that might simply deviate from cultural norms as
pathological.
The DSM-5’s definition helps clinicians standardise diagnoses, guiding research, treatment, and communication within mental health
care. However, the definition acknowledges that mental disorders are complex, multifaceted, and influenced by personal, cultural, and
situational factors, making diagnosis a nuanced process.
Prolonged grief F43.8 A new diagnosis characterised by an intense, persistent grief response following the death of a loved one.
disorder Symptoms persist for at least 12 months (or 6 months in children), leading to significant functional
impairment. This includes emotional numbness, yearning, and difficulty in accepting the loss.
Unspecified Mood F39 This category is introduced for situations where mood symptoms cause significant impairment but do not meet
Disorder the full criteria for any specific mood disorder. This inclusion offers flexibility for diagnosing atypical mood
disturbances.
Suicidal behaviour T14.91 This disorder is diagnosed when an individual has made a suicide attempt within the past 24 months. The
disorder attempt was not made solely for attention-seeking purposes, and there is a high risk of further suicidal
behaviour. It can be used as a stand-alone diagnosis or alongside other mental health conditions.
Non-Suicidal R45.88 This new inclusion defines repetitive, intentional self-inflicted harm (e.g., cutting, burning) without suicidal
Self-Injury (NSSI) intent. It causes distress or impairment and is not explained by other disorders (like borderline personality
disorder). This was previously listed under "Conditions for Further Study" in DSM-5 but is now included as a
formal diagnosis.
Stimulant-Induced F15.96 This disorder addresses cognitive impairment caused by prolonged stimulant use, particularly involving drugs
Mild Neurocognitive such as methamphetamine or cocaine. Symptoms include memory difficulties, attention issues, and executive
Disorder function deficits.
Other DSM-5-TR Updates - Gender Dysphoria: Language has been updated to be more gender-inclusive, reflecting a modern
understanding of gender identity. Terms such as "desired gender" are replaced with "experienced
gender."
- Substance Use Disorders: Some diagnostic criteria and descriptors have been updated for clarity and
to reflect the latest research in substance abuse and treatment approaches.
- Cultural Concepts of Distress: Expanded descriptions of how culture affects the presentation,
understanding, and treatment of various mental disorders.
The DSM-5-TR incorporates numerous updates and refinements to better align diagnostic criteria with current research and improve
clarity in diagnosing mental health disorders. Below are the significant changes:
Language Updates Gender Dysphoria: Terminology revised to be more inclusive and precise regarding gender diversity. For example,
for Inclusivity and terms like "desired gender" have been changed to "experienced gender" to better reflect the lived experience of
Precision individuals with gender dysphoria.
Enhanced clarity on gender-neutral language throughout diagnostic criteria for various disorders.
Cultural Concepts of Distress: Expanded descriptions of how cultural and social factors impact the expression and
understanding of mental health disorders.
Updates to Attention-Deficit/Hyperactivity Disorder (ADHD)
Diagnostic Criteria - Criterion A: Clarification on the examples provided for inattention and hyperactivity symptoms across age
for Specific Disorders groups, particularly in adults.
Persistent Depressive Disorder (Dysthymia): Criteria now better distinguish between chronic depression and
intermittent major depressive episodes.
Diagnostic criteria for Cannabis Use Disorder (F12.20) have been clarified to better distinguish between use and
dependence.
Cultural Concepts of Expanded section on the impact of cultural factors on the presentation, diagnosis, and understanding of mental health
Distress conditions.
Greater emphasis on cultural sensitivity and how mental disorders are influenced by sociocultural contexts.
Clarified criteria for mood disorders and anxiety disorders as they present in older adults.
Personality Disorders No major structural changes, but enhanced clarity in the definitions and criteria of personality disorders, especially
concerning comorbid conditions.
Emphasis on dimensional approaches to personality disorders, including more specific guidance on diagnosing
borderline and antisocial personality disorders.
Expanded Greater attention to racial and ethnic disparities in the diagnosis of mental health conditions, with updated guidance on
Consideration of how these factors influence the manifestation of symptoms
Race, Ethnicity, and
Trauma Trauma-Informed Diagnosis: More explicit references to trauma and stressor-related disorders and the impact of
adverse experiences on mental health.
Prevalence (%) Number of active cases in a population during any given time
Unit 2
Anxiety Disorders:
Generalised Anxiety Disorder
Intro - Unreasonable/irrational, chronic, excessive
- Formerly known as free-floating anxiety
- 6 months << , difficult to control
- Mst have 3/6 symptoms
- Chronic worry, tension
- Marked vigilance for possible signs of threat
- Procrastination, checking, calling a loved one
Comorbidity - Stress
- Major Depressive disorder
- Minimal Suicidal tendencies
Psychological - Results from an unconscious conflict between ego and id impulses that are not adequately dealt with
Causal factors because the person’s defence mechanisms have either broken down or have never developed.
- Freud → primarily sexual and aggressive impulses that had been either blocked from depression or
punished upon expression that led to GAD
- Defence mechanism → overwhelmed when a person experiences frequent and extreme levels of anxiety as
might happen if Id impulses are frequently blocked from expression
- Viewpoint is not testable and has therefore been largely abandoned among clinical researchers.
Biological Genetics There is evidence that GAD has a genetic component, with family studies showing that people
causal factor with a family history of anxiety disorders have a higher risk of developing GAD. Genetic
factors can affect neurotransmitter regulation, brain structure, and function, increasing
susceptibility.
Brain structure Studies using brain imaging have shown that individuals with GAD often have differences in
certain brain areas, particularly:
- Amygdala: Involved in fear and emotion processing, it can become overactive in
people with GAD, leading to heightened anxiety responses.
- Prefrontal Cortex: Responsible for decision-making and impulse control, it may be
underactive in GAD, reducing the ability to regulate emotional responses effectively.
- Anterior Cingulate Cortex: This area integrates emotional and cognitive information,
and its dysfunction is also associated with anxiety.
Hormone The Hypothalamic-Pituitary-Adrenal (HPA) axis, which regulates the body’s response to
stress, may be overactive in individuals with GAD, leading to prolonged stress hormone
release (e.g., cortisol) and increased anxiety. Chronic high cortisol levels can have long-term
effects on brain areas like the hippocampus and amygdala.
Definition An intense, irrational fear of a An emotional response to a real, A vague, uneasy feeling about a
specific object, situation, or immediate threat. potential threat or future uncertainty.
activity, often leading to avoidance.
Duration Persistent and long-lasting unless Short-lived and ends once the Can be chronic, lingering for long
treated. threat is gone. periods.
Triggers Specific object or situation (e.g., Immediate, actual danger (e.g., a Often non-specific or related to future
spiders, heights). car approaching fast). events, situations, or uncertainties.
Intensity Often intense and disproportionate Proportionate to the level of threat. Varies from mild to severe, but often out
to the actual threat. of proportion to reality.
Anxiety Disorders
Specific Phobias Definition: Intense, irrational fear of a specific object, situation, or activity (e.g., animals, heights, flying).
Symptoms: Immediate anxiety or panic upon exposure, often leading to avoidance behaviour.
Impact: Can interfere with daily life if the feared object or situation is commonly encountered.
Social Phobias Definition: Extreme fear of social or performance situations where one may be judged or embarrassed.
Symptoms: Sweating, trembling, blushing, nausea, and difficulty speaking in social settings
Impact: This can lead to avoidance of social interactions, impacting relationships, career, and quality of life.
Panic Disorder Definition: Recurrent, unexpected panic attacks (sudden periods of intense fear or discomfort).
Symptoms: Palpitations, shortness of breath, chest pain, dizziness, and feelings of loss of control or impending
doom.
Impact: Fear of future attacks often leads to avoidance behaviours, and can significantly affect daily
functioning.
Agoraphobia Definition: Anxiety about being in situations where escape may be difficult or help unavailable during a manic
episode.
Symptoms: Fear of crowds, open spaces, or situations like using public transportation, often leading to
avoidance.
Impact: Severe cases can lead to individuals becoming homebound, greatly limiting their mobility and
independence.
Social Environment: Peer relationships, bullying, and cultural factors contribute to social anxiety.
Cognitive Patterns: Negative thought patterns, like catastrophic thinking and a heightened sense of threat, are
linked to anxiety.
Treatment Cognitive-Behavioural Therapy (CBT): Helps individuals identify and change distorted thought patterns and
behaviours that fuel anxiety.
Exposure Therapy: Gradual, controlled exposure to anxiety triggers to reduce fear responses.
Medications: SSRIs (Selective Serotonin Reuptake Inhibitors) and benzodiazepines are often prescribed to manage
symptoms.
Mindfulness and Relaxation Techniques: Meditation, deep breathing, and progressive muscle relaxation can help
reduce anxiety symptoms.
Outcomes Efficacy: Many people experience significant relief with treatment, particularly with CBT and medication.
Relapse: Some individuals may experience symptom recurrence, particularly if stress levels increase.
Long-Term Management: Learning coping strategies and maintaining a supportive social network can improve
long-term outcomes and quality of life.
Varied Response: Outcomes can differ widely; some may achieve full remission, while others manage symptoms
on a long-term basis.
Unit 3
- Mental Retardation
Intellectual disability - ICD significant limitation → intellectual functioning and adaptive behaviour >18 age
Intellectual Developmental deficits in general mental abilities and impairment in everyday adaptive functioning, compared to an
Disorder - DSM individual’s age, gender, and socioculturally matched peers.
diagnosis clinical assessment and standardised testing of intellectual and adaptive functions. diagnostic criteria
→ ADL = activity, daily living
Symptoms Deficit in:
- Reasoning
- Abstraction
- Judgement
- Learning
- Adaptive functioning
provisional diagnosis 12-15 hours informant interaction → if SQ is(not) subpar it’s diagnosis can change.
317 F70 Mild 50-55 to 70 → Cognitive deficits include a reduced ability to abstract and egocentric thinking
→ Children with milder intellectual disabilities may function academically at the high
elementary level and may acquire vocational skills sufficient to support themselves in
some cases
→ Social assimilation may be problematic
→ Communication deficits, poor self-esteem, and dependence may further contribute
to a relative lack of social spontaneity
318.0 F71 Moderate 35-40 to 50-55 → Communication skills develop more slowly, and social isolation may ensue in the
elementary school years.
→ Academic achievement is usually limited to the middle-elementary level
→ Children with moderate intellectual deficits benefit from individual attention
focused on the development of self-help skills
→ these children are aware of their deficits and often feel alienated from their peers
and frustrated by their limitations
→ they continue to require a relatively high level of supervision but can become
competent at occupational tasks in supportive settings
318.1 F72 Severe 20-25 to 35-40 → preschool years
→ affected children have minimal speech and impaired motor development
→ some language development may occur in school-age years
→ generally need extensive supervision
318.2 F73 Profound Below 20-25 → requires constant supervision and is severely limited in both communication and
motor skills
→ adulthood - some speech development, and simple self-help skills may be acquired
→ isolation
→ hyperactivity
→ low frustration tolerance
→ aggression
→ affective instability, repetitive and stereotypic motor behaviours, and self-injurious
behaviours.
Causes
Genetic factors Intellectual disabilities tend to run in families
Malnutrition & - Dietary deficiencies in protein and other essential nutrients during the early development of the foetus
other biological could do irreversible physical and mental damage
factors - A limited number of cases of intellectual disability are associated with organic brain pathology.
Autism
Diagnostic Deficits in Social Challenges in social reciprocity (e.g., abnormal conversation flow, limited sharing of emotions
criteria: Communication or interests)
and Interaction
Issues with nonverbal communication (e.g., poor eye contact, atypical gestures, or lack of
facial expressions)
Difficulties in forming and maintaining relationships (e.g., struggles with adjusting behaviour,
limited imaginative play, or lack of interest in peers).
Developmental Symptoms begin in early development, though may not be fully apparent until social demands
Onset: increase.
Significant Impact Symptoms must lead to noticeable difficulties in social, occupational, or other functional areas.
Not Due to Other The symptoms should not be better explained by other intellectual or developmental disorders.
Conditions
Prevalence - 1% and 2% of the population, with similar estimates in child and adult samples.
- Internationally prevalence is close to 1% (0.62% median) with minimal variation across regions, ethnicities,
or age groups.
- Globally, ASD is diagnosed more in males than females, with a male-to-female ratio of 3:1, though there are
concerns about under-recognition in women and girls.
Comorbidity - Intellectual disabilities, language disorders, and learning challenges, including difficulties in literacy,
numeracy, and coordination.
- Psychiatric conditions commonly co-occur with ASD, with about 70% of individuals having at least one
additional mental disorder, such as anxiety, depression, or ADHD.
- Restricted eating patterns are also frequent.
- In nonverbal individuals, changes in sleep, eating, or behaviour may indicate anxiety, depression, or pain
from undiagnosed medical issues.
- Common medical conditions with ASD include epilepsy and constipation.
Levels
Level 3: Requiring Social Communication: Severe verbal and nonverbal deficits; minimal initiation or response to social
Very Substantial interactions.
Support
Restricted/Repetitive Behaviours: Extreme inflexibility; significant distress with changes, impacting all
areas of functioning.
Level 2: Requiring Social Communication: Marked deficits in communication despite support; limited interactions focused on
Substantial specific interests.
Support
Restricted/Repetitive Behaviours: Inflexible behaviour is observable, causing distress and functional
interference across contexts.
Level 1: Requiring Social Communication: Noticeable communication difficulties without support; trouble with initiating and
Support maintaining social interactions.
- ADHD
Definition - Categorised by a pattern of diminished sustained attention and increased impulsivity or hyperactivity.
- Significant impairment in academic functioning as well as in social and interpersonal situations.
- Often associated with comorbid depressive disorders, including LD, Anxiety disorders, mood disorders
and disruptive behaviour disorders
History - The early 1900s → hyperactive children (damage from encephalitis) → hyperactivity syndrome
- 1960’s → heterogenous group → poor coordination, LD & emotional liability but without specific Neuro
Disorder
Symptoms - Hysteric
- Tiptoeing
- Sensitive to loud noises
- Delayed speech development
- Ignoring dangers
- Rejecting cuddles
- Build toys in one line
- Avoiding eye contact
- Playing alone
Clinical - Hyperactivity
features - Attention deficient (short attention span, distractibility, preservation, failure to finish tasks, inattention,
poor concentration)
- Impulsivity (action before thought, abrupt shifts, lack of organisation, jumping)
- Memory and thinking deficits
- SLD
- Speech and hearing deficits
Comorbidity - Communication disorders & learning disorders → hamper acquisition and retention
- Display of knowledge complicates the course of ADHD
Diagnosis
(Synopsis of DSM-5 ICD-10
psychiatry)
Name - Attention-deficit/hyperactivity disorder Hyperkinetic disorder, disturbance of
activity and attention
Course In partial remission: last months. Symptoms continue but are less than required for diagnosis.
specifiers
DSM-5 - Reading disorder, mathematics disorder, disorder of written expression and learning disorder →
DSM4
- In DSM5 they are designated using specifiers (impairment in; reading, written expression,
mathematics) (mild. Moderate, severe)
aetiology/Etiology - data from cognitive, neuroimaging and genetic studies suggest that reading impairment is a
neurobiological disorder with a significant genetic contribution
- It reflects a deficiency in processing sounds of speech sounds, and thus, spoken language
- As it is related to language deficit, the left brain is the anatomical site of this dysfunction
- The planum temporale is [the cortical area just posterior to the auditory cortex(heschl’s gyrus)] in
the left brain and shows less symmetry than the same site in the right brain in children with both
language disorders and SLD
- Cell analysis studies suggest that in reading-impaired individuals, the visual magnocellular system
(which typically contains large cells) contains more disorganised and smaller cell bodies than
expected.
- Studies indicate that 35-40% of the first-degree relatives of children with reading deficits also have
reading disability.
- Ability to identify single words mapped to chromosome 15
- Chromosome 6 maps to phonological awareness
- Locus on chromosome 18 has a strong influence on single-word reading and phoneme awareness
cognitive factors diverse hypotheses exist for underlying cognitive deficits in reading disorders
→ phonological theory
- Left hemisphere perisylvian
- Double-deficit → phonological + naming speed
- Triple-deficit → “ + orthographic (recalling written words)
→ Rapid auditory processing theory
- perform poorly on auditory tasks
- Exhibit abnormal neurophysiological responses to various auditory stimuli
- Perceptual deficits → acoustic structure → level of the syllable - rhythm detection
- Detection of modulation of the speech waveform
→ Cerebellar theory
→ Visual/magnocellular theory
Aetiology Neurological Factors: Often linked to abnormal brain areas related to language and motor skills (e.g., left
parietal lobe, cerebellum). It may also have a genetic component.
Developmental Factors: Common in childhood and often associated with developmental coordination
disorder (DCD).
Cognitive and Perceptual Factors: Includes visual-perceptual challenges and working memory deficits
that affect writing accuracy.
Motor Coordination Problems: Difficulties with fine motor and hand-eye coordination make writing
challenging.
Psychological and Environmental Factors: Stress or lack of classroom support can worsen symptoms.
Acquired dysgraphia may result from brain injury or stroke.
Treatment Occupational Therapy: Strengthening fine motor skills and improving handwriting techniques.
Educational Interventions: Individualised support plans (IEP/504), multisensory teaching, and assistive
technology.
Cognitive and Behavioural Strategies: Working memory training and self-regulation skills.
Physical Exercises: Activities that enhance overall motor skills and repetitive handwriting practice.
Parent and Teacher Education: Training for consistent support at school and home.
Dyscalculia - Trouble with understanding and manipulating numbers and mathematical concepts
- Impairment in mathematics
Symptoms - Difficulty with number sense, memorisation of arithmetic facts and performing calculations
- Problems with mathematical reasoning and problem-solving
- Trouble with concepts like time, measurement and spatial reasoning
Aetiology Neurological Factors: Linked to abnormal development in brain areas for numerical processing (e.g., intraparietal
sulcus, left angular gyrus).
Cognitive Deficits: Includes issues with working memory, spatial processing, and understanding numerical concepts.
Developmental and Environmental Influences: May co-occur with other disorders (e.g., ADHD, dyslexia);
inadequate maths education and socioeconomic factors can worsen symptoms.
Psychological Factors: Maths anxiety and low self-esteem can further impact learning.
Treatment Educational Interventions: Includes individualised education plans (IEPs), specialised maths instruction, and
tutoring.
Cognitive and Behavioural Strategies: Cognitive-behavioural therapy (CBT) and metacognitive techniques for
managing anxiety and enhancing problem-solving.
Assistive Technology: Tools such as maths software, calculators, and speech-to-text support.
Occupational Therapy: Aims to improve fine motor skills for writing numbers and using maths tools.
Parental and Teacher Support: Training and collaboration for consistent support and progress monitoring.
History - The early 1900s → hyperactive children (damage from encephalitis) → hyperactivity syndrome
- 1960’s → heterogenous group → poor coordination, LD & emotional liability but without specific Neuro
Disorder
Symptoms - Hysteric
- Tiptoeing
- Sensitive to loud noises
- Delayed speech development
- Ignoring dangers
- Rejecting cuddles
- Build toys in one line
- Avoiding eye contact
- Playing alone
Clinical - Hyperactivity
features - Attention deficient (short attention span, distractibility, preservation, failure to finish tasks, inattention,
poor concentration)
- Impulsivity (action before thought, abrupt shifts, lack of organisation, jumping)
- Memory and thinking deficits
- SLD
- Speech and hearing deficits
Diagnosis
(Synopsis of DSM-5 ICD-10
psychiatry)
Name - Attention-deficit/hyperactivity disorder Hyperkinetic disorder, disturbance of
activity and attention
Course In partial remission: last months. Symptoms continue but are less than required for diagnosis.
specifiers
Prevalence General Population: Approximately 4-6% of adults are affected, based on studies in Europe and North America.
Primary Care Settings: Prevalence is higher, estimated at 10-20% over 12 months, with even higher rates (40-60%)
in clinics specialising in psychosomatic or functional disorders.
Gender Differences: Women are more likely to experience and report somatic symptoms than men, leading to
higher prevalence among women.
Comorbidity - Anxiety and depression are common, each affecting up to 50% of cases and significantly worsening
functional impairment and quality of life.
- PTSD, OCD, and, in men, sexual dysfunction are also linked.
- In individuals with medical conditions, somatic symptom disorder amplifies impairment, reduces
treatment adherence, and worsens health outcomes, leading to higher healthcare use and lower quality of
life.
Illness anxiety disorder
Diagnostic A. Preoccupation with having or acquiring a serious illness.
Criteria B. Somatic symptoms are not present or, if present, are only mild in intensity. If another medical condition is
present or there is a high risk of developing a medical condition (e.g., a strong family history is present), the
preoccupation is excessive or disproportionate.
C. There is a high level of health anxiety, and the individual is easily alarmed about their personal health status.
D. The individual performs excessive health-related behaviours (e.g., repeatedly checks his or her body for
signs of illness) or exhibits maladaptive avoidance (e.g., avoids doctor appointments and hospitals).
E. Illness preoccupation has been present for at least 6 months, but the specific illness that is feared may
change over that period.
F. The illness-related preoccupation is not better explained by another mental disorder, such as somatic
symptom disorder, panic disorder, generalised anxiety disorder, body dysmorphic disorder,
obsessive-compulsive disorder, or delusional disorder, somatic type.
Specify whether:
- Care-seeking type: Medical care, including physician visits or undergoing tests and procedures, is frequently
used.
- Care-avoidant type: Medical care is rarely used.
Prevalence - based on health anxiety or hypochondriasis prevalence data, affects 1.3% to 10% of the general population
in high-income countries,
- with 6-month to 1-year rates in medical settings ranging from 2.2% to 8%.
- Speciality clinics report higher rates, with about 20% of patients experiencing illness anxiety.
- Prevalence is similar between men and women.
Factitious Disorder
Factitious Disorder A. Falsification of physical or psychological signs or symptoms, or induction of injury or disease,
Imposed on Self associated with identified deception.
B. The individual presents himself or herself to others as ill, impaired, or injured.
C. The deceptive behaviour is evident even in the absence of obvious external rewards.
D. The behaviour is not better explained by another mental disorder, such as delusional disorder or
another psychotic disorder.
Specify:
- Single episode
- Recurrent episodes (two or more events of falsification of illness and/or induction of injury)
Factitious Disorder A. Falsification of physical or psychological signs or symptoms, or induction of injury or disease, in
Imposed on another, associated with identified deception.
Another B. The individual presents another individual (victim) to others as ill, impaired, or injured.
(Previously C. The deceptive behaviour is evident even in the absence of obvious external rewards.
Factitious Disorder D. The behaviour is not better explained by another mental disorder, such as delusional disorder or
by Proxy) another psychotic disorder.
Note: The perpetrator, not the victim, receives this diagnosis.
Specify:
Single episode
- Recurrent episodes (two or more events of falsification of illness and/or induction of injury)
Dissociative disorders-Depersonalization/Derealization disorder
Diagnostic criteria A. Disruption of identity is characterised by two or more distinct personality states, which may be
described in some cultures as an experience of possession. The disruption in identity involves marked
discontinuity in the sense of self and sense of agency, accompanied by related alterations in affect,
behaviour, consciousness, memory, perception, cognition, and/or sensory-motor functioning. These
signs and symptoms may be observed by others or reported by the individual.
B. Recurrent gaps in the recall of everyday events, important personal information, and/or traumatic
events that are inconsistent with ordinary forgetting.
C. The symptoms cause clinically significant distress or impairment in social, occupational, or other
important areas of functioning.
D. The disturbance is not a normal part of a broadly accepted cultural or religious practice.
Note: In children, the symptoms are not better explained by imaginary playmates or other fantasy play.
E. The symptoms are not attributable to the physiological effects of a substance (e.g., blackouts or
chaotic behaviour during alcohol intoxication) or another medical condition (e.g., complex partial
seizures).
Biological Genetic Predisposition: Although no specific gene has been linked to DID, there may be a hereditary component,
causal factors as individuals with DID often have close relatives with other mental health conditions, such as mood disorders or
PTSD.
Neurobiological Differences:
- Brain Structure: Research suggests that individuals with DID may have structural differences in areas of the
brain involved in memory, emotional regulation, and self-awareness, such as the hippocampus, amygdala,
and prefrontal cortex.
- Brain Function: Functional brain imaging studies show variations in brain activity patterns when different
identities or "alters" are present. Differences have been observed in the areas linked to emotional processing
and stress response.
Stress Response and Cortisol Levels: Chronic trauma, often a precursor to DID, may alter the body's stress
response system. People with DID sometimes show irregularities in cortisol production and response, which could
contribute to dissociative states and identity fragmentation.
Neurodevelopmental Factors: Early childhood trauma or neglect can interfere with normal neurodevelopment,
potentially leading to issues with emotional regulation, memory, and the development of a cohesive sense of self.
This may increase the likelihood of dissociation as a coping mechanism, leading to DID in those predisposed to the
disorder.
Abnormal Integration of Consciousness: There may be a biological susceptibility that impairs the integration of
consciousness, memory, and identity under stress. This can result in fragmented identities or personalities,
especially in response to trauma during early development.
Psychological Severe Childhood DID is often linked to chronic and severe trauma, particularly in early childhood, such as
Causal factors Trauma: physical, sexual, or emotional abuse. This can lead to dissociation as a coping mechanism,
where the mind creates separate identities to "compartmentalise" traumatic memories and
emotions.
Attachment Issues Children who lack a stable, secure attachment with caregivers may develop dissociative
and Insecure tendencies. When primary caregivers are neglectful, abusive, or inconsistent, children may be
Attachment: unable to form a cohesive sense of self.
Dissociation can serve as a protective mechanism, helping children detach from frightening or
harmful situations by creating separate identities.
Fantasy Proneness Some individuals with DID have a high tendency toward fantasy and imagination. This trait,
and Suggestibility: along with suggestibility (an increased likelihood of being influenced by external cues), may
make it easier for the mind to create alternate identities.
Individuals with a high capacity for fantasy may find it easier to dissociate as a way to cope
with trauma, creating separate personas that can handle different aspects of reality.
Disrupted Early trauma interferes with the normal development of self-identity. In healthy development,
Development of children integrate various aspects of their personality over time. However, trauma can
Self-Identity: interrupt this process, leading to a fractured sense of self.
Dissociation may act as a defence mechanism, with different identities emerging to handle
specific emotions, memories, or social roles, ultimately resulting in DID.
Emotion People with DID often have trouble regulating intense emotions due to disrupted
Regulation development. Dissociation allows them to "escape" from overwhelming emotions, creating
Difficulties: alters that can experience or hold emotions the individual feels they cannot handle as a single
identity.
Over time, these fragmented parts may solidify into separate identities as a way to
compartmentalise unmanageable emotions.
Repetitive Repeated dissociation during trauma can reinforce the habit of dissociating when stressed,
Reinforcement: eventually leading to identity fragmentation. In severe cases, separate identities become
established as a coping strategy, triggered not only by traumatic events but by other stressors
as well.
Unit 5
Obsessive-compulsive and related disorders
Obsessive-compulsive disorder
Obsessive Compulsive Disorder:
DSM Persistent and recurrent intrusive thoughts, images, or impulses that are experienced as disturbing, inappropriate and
uncontrollable
People → actively try to resist or suppress them or to neutralise them with some other thought or action.
Over repetitive behaviour → lengthy rituals
More covert mental rituals
The diagnosis requires that obsessions and compulsions must take at least 1 hour a day.
Severe cases → Most of a person’s waking hours
Prevalence - 90% of people with OCD who seek treatment have obs & comp
- Divorced & unemployed people → overrepresented among people with OCD
- Little or no gender difference in adults
- Early adolescent → more common in boys → ↑ severity, ↑ heritability
- Gradual onset → once serious → tends to be chronic → severity → wax and wane over time
Psychological Maladaptive Overestimation of threat: Believing that bad things are more likely to happen and have severe
causes Thought Patterns consequences.
and Beliefs Inflated responsibility: Feeling overly responsible for preventing harm or bad events.
Perfectionism: A need for things to feel "just right," which can drive repetitive behaviours
Cognitive Catastrophizing: Assuming the worst possible outcome will occur if a ritual or compulsion is
Distortions not performed.
Thought-action fusion: Believing that simply having a thought about something (e.g.,
harming someone) is equivalent to acting on it or increasing the likelihood it will happen.
Magical thinking: The belief that certain thoughts, words, or actions can influence outcomes
in unrealistic ways, leading to superstitious or ritualistic behaviours.
Biological Genetical OCD tends to run in families, suggesting a genetic component. Studies indicate that people
causes with a first-degree relative with OCD are at a higher risk of developing the disorder. Specific
genes related to serotonin, glutamate, and dopamine pathways are thought to increase
susceptibility to OCD, although the exact genetic mechanisms are complex and not fully
understood.
Neurotransmitters Serotonin: Low levels of serotonin, a neurotransmitter associated with mood regulation, are
strongly implicated in OCD. This link is supported by the effectiveness of selective serotonin
reuptake inhibitors (SSRIs) in reducing OCD symptoms.
Glutamate: High levels of glutamate, an excitatory neurotransmitter, have also been associated
with OCD. Excessive glutamate activity may contribute to the overactivity of certain brain
circuits seen in OCD.
Dopamine: Dysregulation of dopamine, which plays a role in reward and motivation, is also
thought to contribute to the disorder, especially in compulsive behaviours.
Brain structure Cortico-Striato-Thalamo-Cortical (CSTC) Circuit: The CSTC loop, involving the
orbitofrontal cortex, striatum, and thalamus, is hyperactive in individuals with OCD. This
circuit is responsible for regulating thoughts, emotions, and behaviours, and its overactivity is
associated with obsessive thoughts and compulsive behaviours.
Anterior Cingulate Cortex (ACC): The ACC is involved in error detection and conflict
monitoring. Overactivity in the ACC can contribute to heightened feelings of doubt and
anxiety, potentially triggering compulsive behaviours as a way to reduce perceived errors.
Basal Ganglia: This structure, especially the caudate nucleus, plays a role in habit formation
and procedural learning. Dysregulation in the basal ganglia is linked to repetitive, ritualistic
behaviours, which are characteristic of OCD
Prevalence Adults in the US are 2.4% (2.5% in women and 2.2% in men).
Germany shows similar prevalence rates of 1.7%–2.9%, with a similar gender distribution.
Globally
- 11%–13% of dermatology patients
- 13%–15% of general cosmetic surgery patients
- 20% of rhinoplasty patients
- 11% of adult jaw correction surgery patients
- 5%–10% in adult orthodontia or cosmetic dentistry patients.
Among adolescents and college students, prevalence rates are notably higher in girls and young women than in boys
and young men.
Comorbidity Major depressive disorder → onset usually after that of body dysmorphic disorder. Comorbid social anxiety disorder,
OCD, and substance-related disorders (including the use of anabolic-androgenic steroids in the muscle dysmorphia
form of body dysmorphic disorder) are also common.
Hoarding disorder
Diagnostic A. Persistent difficulty discarding or parting with possessions, regardless of their actual value.
criteria B. This difficulty is due to a perceived need to save the items and to distress associated with discarding them.
C. The difficulty of discarding possessions results in the accumulation of possessions that congest and clutter
active living areas and substantially compromise their intended use. If living areas are uncluttered, it is only
because of the interventions of third parties (e.g., family members, cleaners, authorities).
D. The hoarding causes clinically significant distress or impairment in social, occupational, or other important
areas of functioning (including maintaining a safe environment for self and others).
E. The hoarding is not attributable to another medical condition (e.g., brain injury, cerebrovascular disease,
Prader-Willi syndrome).
F. The hoarding is not better explained by the symptoms of another mental disorder (e.g., obsessions in
obsessive-compulsive disorder, decreased energy in major depressive disorder, delusions in schizophrenia or
another psychotic disorder, cognitive deficits in major neurocognitive disorder, restricted interests in autism
spectrum disorder).
Specify if:
- With excessive acquisition: If difficulty discarding possessions is accompanied by excessive acquisition of
items that are not needed or for which there is no available space.
Specify if:
- With good or fair insight: The individual recognizes that hoarding-related beliefs and behaviours (about
difficulty discarding items, clutter, or excessive acquisition) are problematic.
- With poor insight: The individual is mostly convinced that hoarding-related beliefs and behaviours (about
difficulty discarding items, clutter, or excessive acquisition) are not problematic despite evidence to the
contrary.
- With absent insight/delusional beliefs: The individual is completely convinced that hoarding-related beliefs
and behaviours (about difficulty discarding items, clutter, or excessive acquisition) are not problematic
despite evidence to the contrary.
Prevalence - 1.5% to 6% in the U.S. and Europe, with a meta-analysis indicating a prevalence of 2.5% across high-income
countries.
- symptoms are nearly three times more common in adults over 65 compared to younger adults (ages 30–40).
Hair-pulling disorder(Trichotillomania).
Diagnostic A. Recurrent pulling out of one’s hair, resulting in hair loss.
criteria B. Repeated attempts to decrease or stop hair pulling.
C. The hair pulling causes clinically significant distress or impairment in social, occupational, or other
important areas of functioning.
D. The hair pulling or hair loss is not attributable to another medical condition (e.g., a dermatological
condition).
E. The hair pulling is not better explained by the symptoms of another mental disorder (e.g., attempts to
improve a perceived defect or flaw in appearance in body dysmorphic disorder).
Biological Genetic factors OCD and related disorders often run in families, suggesting a hereditary component. Twin studies show a
causal factors moderate genetic influence, especially in childhood-onset OCD
Certain gene variations related to serotonin and glutamate regulation may contribute to OCD risk.
Brain Structure Neuroimaging studies have found abnormalities in brain circuits involving the orbitofrontal cortex, anterior
and Function: cingulate cortex, and basal ganglia.
These areas are associated with habit formation, error detection, and emotional regulation.
Increased activity in these regions is often observed in individuals with OCD, with symptoms often
improving alongside the normalisation of these brain patterns after successful treatment.
Neurotransmitter Dysfunctional serotonin pathways play a key role in OCD, as well as potential dysregulation of dopamine
Imbalance: and glutamate systems.
SSRIs (selective serotonin reuptake inhibitors), which increase serotonin levels, are often effective in
reducing OCD symptoms, supporting the role of neurotransmitter imbalances.
Psychological Cognitive People with OCD may have maladaptive thought patterns, such as an inflated sense of responsibility,
causal factors Factors intolerance of uncertainty, and a heightened need for control
These beliefs often lead to compulsive behaviours to prevent or "undo" perceived threats, reinforcing the
OCD cycle.
Behavioural Compulsions and rituals are reinforced through a cycle of relief from anxiety, which strengthens the
Factors: behaviour over time (negative reinforcement).
Avoidance behaviours reduce immediate distress but prevent individuals from learning that their fears are
irrational, maintaining the disorder.
Stress and Stressful life events or trauma may trigger the onset of OCD symptoms, particularly in individuals with a
Trauma: genetic predisposition.
Treatment Pharmacological SSRIs: These are the first line of treatment and are effective for many individuals with OCD and related
and Outcome Treatments: disorders, helping to reduce symptoms.
Antipsychotics: In cases where SSRIs are ineffective, low doses of antipsychotic medications may be added
to target symptoms resistant to SSRIs alone.
Glutamate Modulators: Research is exploring medications that influence glutamate to target specific
neurochemical dysfunctions in OCD.
Psychotherapy: Cognitive Behavioral Therapy (CBT): CBT, particularly Exposure and Response Prevention (ERP), is
highly effective for OCD. ERP helps individuals face their fears without engaging in compulsive
behaviours, gradually reducing anxiety.
Cognitive Therapy: Focuses on challenging maladaptive beliefs and cognitive distortions, which helps to
reduce compulsive responses to obsessive thoughts.
Acceptance and Commitment Therapy (ACT): Used in conjunction with CBT, ACT helps individuals accept
distressing thoughts without reacting compulsively.
Lifestyle and Family Therapy: Helps families support individuals with OCD without enabling their compulsions, reducing
Supportive conflict and stress.
Therapies:
Support Groups and Education: Group therapy and psychoeducation help individuals feel less isolated and
provide additional coping strategies.
Outcomes While many patients experience significant symptom reduction with treatment, complete remission is rare.
Treatment effectiveness varies, with about 40-60% of individuals responding well to CBT and/or
medication.
For treatment-resistant OCD, deep brain stimulation or transcranial magnetic stimulation are sometimes
considered.
Unit 6
Types of personality disorders-
A- Paranoid, Schizoid and Schizotypal personality disorders;
Details Paranoid Schizoid Schizotypal
Pervasive & excessive Exaggerated sense of Violate and show disregard Pattern of instability of
emotionality & self-importance, for the rights of others interpersonal relationships,
attention-seeking preoccupational with being through deceitful, aggressive, self-image, affects, marked
behaviour. admired, and a lack of or antisocial behaviour, impulsivity
Early adulthood → variety empathy for the feelings of typically without remorse.
of context others Inability to conform to the
social norms that ordinarily
govern many aspects of a
person’s adolescent and adult
behaviour.
- Hostile towards
others
- Impulsive
- Disregard for rules
- Feeling of superior
- Manipulating others
- Not accepting
responsibilities.
C- Avoidant, Dependent and Obsessive-Compulsive Personality Disorder.
Domains Avoidant OCPD Dependent
Symptoms - Choosing isolation over social - Excessive doubt and - Trouble making decisions
- Fear of emnarrasment indecisiveness without reassurance
- Hyper sesenstive - Being unwilling to - Fear that they cant take care of
compromise themselves
- Being unwilling to throw out - Trouble expressing
broken or worthless object disagreement
- Perfectionism that interferes - Difficulty being alone
with completing tasks
- Becoming overly fixated on
a single task or belief
- Difficulty coping with
criticism
Sexual Variants and Sexual Abuse - The Paraphilias, Gender dysphoria, Sexual abuse - Childhood sexual abuse, Pedophilic disorder.