MOOD DISORDERS
RIBKA BIRHANU, MD, Psychiatrist
Department of Psychiatry, AAU, CHS
Learning Objectives
• Introduction
• Clinical Descriptions and Epidemiology of Mood
Disorders
• Etiology of Mood Disorders
• Treatment of Mood Disorders
I wish to inform you that I have received the cake. Many
thanks, but I am not worthy. You sent it on the
anniversary of my child’s death, for I am not worthy of
my birthday; I must weep myself to death; I cannot live
and I cannot die, because I have failed so much, I shall
bring my husband and children to hell. We are all lost; we
won’t see each other any more; I shall go to the convict
prison and my two girls as well, if they do not make away
with themselves because they were born in my body.
A patient of Emil Kraepelin (1905)
• Feeling a positive or negative reaction to some experience
or event and is the subjective experience of emotion
• Emotion refer to spontaneous and transitory experience
similar to but not identical to feeling, as it need not
incorporate the physical accompaniments of the
experience.
• Mood a pervasive and sustained emotion that colors the
person’s perception of the world
• Affect expression of emotion as judged by the external
manifestations that are associated with specific feelings
Theories of Emotion
1. James–Lange theory
• emotions are the result of self-awareness of
physical and bodily changes in the presence
of a stimulus
2. Cannon–Bard theory
• argued that emotion has temporal primacy
and that any visceral or behavioral change
follows the emotion.
• leaves no room for any cognitive aspect to
the origin of emotions.
3. two-factor theory of emotion(Schachter and
Singer’s (1962)
• influential theory
• The two relevant factors are physiological
arousal and cognition
• an individual is in a given social context, and
he responds to this situation with a
physiological arousal. The meaning attributed
to this arousal is determined by his cognitions.
Basic Emotions
• Ekman and colleagues (Ekman and Friesen,
1971)
• six basic emotions that are expressed in the
face: anger, disgust, fear, happiness, sadness
and surprise
• expressions of emotion are universal.
• but not universal in every regard.
Communication of Mood
• ‘No man is an Island, entire of
itself’(JohnDonne,1571–1631),and in no area of
life is this more true than that of feelings.
– Mirror neurons
– Emotions are communicated nonverbally by different
parts of the body,
– for example by the face (especially the eyes), gesture,
posture, tone of voice and general appearance,
especially the choice of clothes
– While assessing another’s affective response, the
assessor in part influences it by his own behavior and
disposition.
Classification of pathology of emotion
• no consensus on how to classify abnormalities
of the experience and display of emotions
• Cutting (1997) provides a viable framework
• Abnormalities of basic emotions
• ■ Intensity of emotions
• ■ Duration, time and quality of experience
• ■ Expression of emotion
• ■ Appropriateness to object
• Abnormality of physiological arousal
• ■ Alexithymia
• Abnormalities of evaluation of social context
• ■ Negative cognitive schemas
• ■ Prosopoaffective agnosia
• ■ Receptive vocal dysprosody
• Diminution of intensity
• Experienced as loss of feeling, affecting emotions
including sadness, joy, anger, fear etc..
• Patient suffers greatly, feels guilty about this
feeling
• It is a subjective experience rather than
objectively observed absence
• Occurs in Depressive psychosis occasionally with
personality disorders, schizophrenia
• depersonalization
Anhedonia
• specifically refers to a loss of the capacity to
experience joy and pleasure.
• a total inability to enjoy anything in life or even
get the accustomed satisfaction from everyday
events or objects; a ‘loss of ability to experience
pleasure’ (Snaith, 1993).
• considered to be a prominent symptom of
depressive illness by Klein (1974)
• the best clinical marker, predicts the response to
treatment.
It was the autumn of 1826. I was in a dull state of nerves,
such as everybody is occasionally liable to; unsusceptible to
enjoyment or pleasurable excitement; one of these moods
when what is pleasure at other times, becomes insipid or
indifferent … In this frame of mind it occurred to me to put
the question directly to myself, ‘suppose that all your
objects in life were realized; that all the changes in
institutions and opinions which you are looking forward to,
could be completely effected at this very instant: would this
be a great joy and happiness to you?’ And an irrepressible
self-consciousness distinctly answered, ‘
No!’ At this my heart sank within me. (Mill, 1873)
• Exacerbation of emotion
• Intensification of sadness or joy
• In sadness this may present as feeling of sadness
and gloom, despondency, despair or
hopelessness
• Depression
• Refers to an emotional state characterized by
grief or mild periods of sadness or being down
• It also refers to a clinical condition characterized
by depressed mood
I was feeling in my mind a sensation close to, but
indescribably different from actual pain.
(William Styron, 1990)
It is a positive and active anguish, a sort of
psychical neuralgia wholly unknown to normal
life. (William James, 1902)
• Melancholia’ would appear to be a far more apt and
evocative word for the blacker forms of the disorder,
but it was usurped by a noun with a bland tonality and
lacking any magisterial presence, used indifferently to
describe an economic decline or a rut in the ground, a
true wimp of a word for such a major illness …
Nevertheless, for 75 years the word has slithered
innocuously through the language like a slug, leaving
little trace of its intrinsic malevolence and preventing,
by its insipidity, a general awareness of the horrible
intensity of the disease when out of control.
• Intensification of joy or pleasure
• Euphoria – state of unreasonable excessive
cheerfulness
• Intense elation often associated with feeling
of grandeur
• Classically occur in mania and hypomania
• can also be seen in organic states and in
schizophrenia
• When you’re high it’s tremendous. The ideas and
feelings are fast and frequent like shooting stars and
you follow them until you find better and brighter
ones. Shyness goes; the right words and gestures are
suddenly there, the power to captivate others a felt
certainty. There are interests found in uninteresting
people. Sensuality is pervasive and the desire to seduce
and be seduced is irresistible … But somewhere this
changes … Everything previously moving with the grain
is now against – you are irritable, angry, frightened,
uncontrollable, and enmeshed in the blackest caves of
the mind
• Ecstasy an exalted state of feeling
• state of extreme well-being associated with a
feeling of rapture, bliss and grace.
• can occur in the healthy population at times of
profound religious experience or occasions of
deep emotion , schizophrenia, lysergic acid
diethylamide misuse and epilepsy
• abnormal ? self-neglect or neglect of others is
present, or when it is prolonged.
• Unlike elation, no over activity or flight of ideas.
• Sometimes it may be associated with
grandiose delusions
• example, a patient with schizophrenia sat
smiling to himself and when asked why
declared that he was the King of Israel and
was about to marry the Queen of Heaven.
• Changes in timing, duration, quality of
experience
1.Pathological grief- delayed or prolonged
2. Lability of mood involves intensification of
emotions accompanied by an instability in the
persistence of emotions
• communicates itself to the observer as an
inappropriateness to the social context
• a sign of brain damage and is seen following
frontal lobe injury or cerebrovascular
accident.
3-Pathological laughter or crying is usually an
unprovoked emotion that does not have an
apparent object
• occurs in epilepsy( gelastic) , acquired brain
injury, focal brain injury
• ABNORMALITIES OF EXPRESSION AND
APPROPRIATENESS TO OBJECT
• Blunting and Flattening of Feeling
• unchanging facial expression, decreased spontaneous
movements, poverty of expressive gesture, poor eye
contact, affective unresponsivity and lack of vocal
inflection (Andreasen, 1979).
• Blunting implies a lack of emotional sensitivity
• Flattening is a limitation of the usual range of emotion
expressed usually by facial but also bodily gestures.
• Both blunting and flattening occur in schizophrenia.
• Free-Floating Emotion
• A powerful affect seems to have no goal and is
associated with no object.
• Eg- a patient describes himself as feeling
generally anxious, not anxious about anything in
particular but just anxious.
• This free-floating anxiety has somatic and
psychological concomitants.
• It may seem to be localized physically in certain
areas of the body.
• Abnormality of Experience and Physiological Activity
• alexithymia
• a specific disturbance in psychic functioning characterized by
difficulties in the capacity to verbalize affect and elaborate
fantasies.
• difficulty in recognizing and describing their own feelings and in
discriminating between emotional states and bodily sensations.
• They show a stiff, robot-like existence, ‘almost as if they are
following an instruction book’;
• there may be stiffness of posture and lack of facial expression.
• psychosomatic disorders, somatoform disorders, psychogenic pain
disorders, substance abuse disorders, post-traumatic stress
disorder
• Abnormalities of Evaluation
• cognitive schemas - assumptions about the
self, the world and the future, that developed
from previous experiences and that habitually
influenced how events in the world were
appraised and these could induce mood
change, either directly or via disruption in self-
esteem.
• There are also abnormalities of appraisal of the
facial or vocal expression of emotions in others
• Prosopoaffective agnosia refers to the selective
deficiency in appreciating the emotional
expression displayed in the face of others.
• prosopagnosia recognition of familiar faces is
impaired.
• acquired brain disease and frontotemporal dementia.
• Prosodic aspects of speech such as pitch,
duration and amplitude are part of the
nonverbal cues that modify the meaning of
the spoken word and indicate the emotional
value of an utterance and the intention of the
speaker (Mitchell and Ross, 2013).
• Expressive emotional prosody - refers to
the generation of affect in speech.
• Receptive emotional dysprosody refers
to the selective deficit in recognizing the
emotional tone in speech.
• expressive emotional dysprosody the
impairment of the production of emotional
tone in speech.
– Parkinson’s disease
Mood Disorders
Loss of sense of control and a subjective
experience of great distress
Result in impaired interpersonal, social,
and occupational functioning
Mood Disorders
• depressive disorders:
– Major depressive disorder
– Dysthymia
– Mixed anxiety/depressive disorder
– Premenstrual dysphoric disorder
– Disruptive mood dysregulation disorder
• Bipolar Disorders:
– Bipolar I disorder
– Bipolar II disorder
– Cyclothymia
DSM 5 Depressive Disorders
• Disruptive mood dysregulation disorder
• Major depressive disorder
• Persistent depressive disorder
• Premenstrual dysphoric disorder
• Substance/medication-induced depressive disorder
• Depressive disorder due to another medical
condition
• Other specified depressive disorder
• Unspecified depressive disorder
Depressive Disorder
Inter-episode recovery
Normal
N mood
Depressive episodes
Clinical presentation of Depressive
episodes
• Depressed mood and a Loss of interest
– may say that they feel sad, depressed, blue,
hopeless, in the dumps, discouraged or worthless
– distinct quality from the normal emotion of
sadness or grief
• agonizing emotional pain
• being unable to cry
Clinical presentation of Depressive
episodes
• Depressed mood and a Loss of interest
– may say that they feel sad, depressed, blue,
hopeless, in the dumps, discouraged or worthless
– distinct quality from the normal emotion of
sadness or grief
• agonizing emotional pain
• being unable to cry
Depressed mood
Depressed mood, most of the day,
nearly every day,
As indicated by subjective report (e.g.
feels sad, hopeless or empty)
OR observation made by others e.g.
appears tearful
In children & adolescents can be
irritable mood
Depressive episode cont’
• 2/3 contemplate suicide
• 10 - 15 % commit suicide
• Withdrawal from family, friends, and activities
that previously were interesting
• Decreased energy (97%)
• Difficulty finishing tasks (thinking, concentration)
• Impaired at school and work, and have less
motivation to undertake new projects
Depressive episode cont’
• Trouble sleeping (80%)
• Decreased appetite and weight loss
• Anxiety (90%)
• Decreased libido
• Somatic complaints
• Worsening of coexisting medical illnesses
• Alcohol abuse
Depressive episode - MSE
• General appearance
– Generalized psychomotor retardation
– Psychomotor agitation
• hand-wringing and hair-pulling
– Stooped posture, no spontaneous movements,
and a downcast, averted gaze
– Catatonic
Depressive episode – MSE cont’
• Mood, Affect, and Feelings
– Depression is the key symptom
• 50 % deny depressive feelings and do not appear to be
depressed.
• Speech
– Decreased rate and volume of speech
• respond to questions with single words
• exhibit delayed responses to questions
Depressive episode – MSE cont’
• Perceptual Disturbances
– Hallucinations
• Thought
– Negative views of the world and of themselves
– Non-delusional ruminations about loss, guilt,
suicide, and death
– Thought blocking and profound poverty of content
– Delusions
• Mood-congruent delusions in a depressed person
include those of guilt, sinfulness, worthlessness,
poverty, failure, persecution, and terminal somatic
illnesses
Depressive episode – MSE cont’
• Cognition
– insufficient energy or interest to answer questions
– impaired concentration & forgetfulness (50-75%)
• Reliability
– overemphasize the bad and minimize the good
Diagnosis
• DSM 5 Criteria
DSM-V:
Major Depressive Episode
5 total of:
Depressed mood and / or
Loss of interest or pleasure
+
Significant weight loss / decrease or increase in
appetite
Insomnia / hypersomnia
Psychomotor retardation / agitation
Fatigue / Loss of energy
Worthlessness or excessive /inappropriate guilt
Poor concentration / indecisiveness
Recurrent thoughts of death / suicidal ideation
DSM-V criteria
2 weeks
Change from previous functioning
Clinically significant distress /
impaired functioning
Not due to medical condition
Not due to substance
Major Depressive Disorder (MDD)
• Episodic
– Symptoms tend to dissipate over time
• Recurrent
– Once depression occurs, future episodes likely
• Average number of episodes is 4
• Subclinical depression
– Sadness plus 3 other symptoms for 10 days
– Significant impairments in functioning even though full
diagnostic criteria are not met
Course - MDD
• Onset
– About 50 % of patients having their first episode
exhibited significant depressive symptoms before the
first identified episode
– usually no premorbid personality disorder
• Duration
– An untreated depressive episode lasts 6 to 13 months
– Treated episodes last about 3 months
– As the course of the disorder progresses, patients
tend to have more frequent episodes that last longer
Course – MDD cont’
• Development of Manic Episodes
– About 5 -10% of patients with an initial diagnosis
of MDD have a manic episode 6-10 years after the
first depressive episode
– Mean age for this switch is 32
– Often occurs after 2 to 4 depressive episodes.
– Often depression characterized by
• hypersomnia, psychomotor retardation, psychotic
symptoms, a history of postpartum episodes, a family
history of bipolar I disorder, and a history of
antidepressant-induced hypomania, mixed feature
specifier, onset in adolescence
Prognosis - MDD
• Good prognostic indicators
– Mild episodes, the absence of psychotic
symptoms, and a short hospital stay
– History of solid friendships during adolescence,
stable family functioning, and generally sound
social functioning for the 5 years preceding the
illness
– Absence of a comorbid psychiatric disorder and of
a personality disorder, no more than one previous
hospitalization for major depressive disorder, and
an advanced age of onset
Prognosis - MDD cont’
• Poor prognostic indicators
– coexisting dysthymic disorder, abuse of alcohol
and other substances, anxiety disorder symptoms,
and a history of more than one previous
depressive episode
Epidemiology
• Lifetime prevalence of MDE range between 5 -
17%, average 12
• Sex ratio of MDD M:F= 1:2
• Age of onset of MDD
– Mean = 40 years
– 50 % have an onset between the ages of 20 – 50
– can begin in childhood or in old age
– increasing among people younger than 20 years of
age
Epidemiology cont’
• Comorbidity
– alcohol abuse or dependence, panic disorder,
obsessive - compulsive disorder (OCD), and
social anxiety disorder
• Men
– Substance use disorders
• Women
– Eating disorder
– Anxiety disorder
Why do people become
depressed?
Etiology/Risk factors
• Biopsychosocial….
– Temperament: neuroticism (negative affectivity)
– Personality factors
– Adverse childhood experience
– Stressful life events
– Genetic: family history
– Biological abnormalities
• Biogenic amines
• Alterations in hormonal regulation
Etiology of depression
o Biological
Amines- ↓ NE, ↓ 5HT
(Serotonin), ↓ DA
Alteration of hormonal
regulation- ↑ HPA activity-
hypercortisolemia- ↑ CRH
( dexa-non-suppression test)
Thyroid dysfunction
Chronic medical conditions-
Chronic pain, HIV, TB, DM,
Seizure d/o
Differential Diagnosis
• Medical/neurological disorders
• Substance induced disorders
• Other mental disorders
• Bereavement
Depression in Ethiopia –
how the community sees it
100 Key informants from Butajira
(traditional healers / religious leaders
/ officials)
7 vignettes
Severe Depression ranked as least
common* and less serious than all
except mania / neurotic depression
*Compared to epilepsy, schizophrenia, acute psychosis, mental
retardation, neurosis and mania
Alem et al. 1999
Why is depression
important?
1. Depression is common
Prevalence = % of people with a disorder
• over a specified period of time.
12 month prevalence of depression = 4-5%
Lifetime prevalence = 10-17%
2. Depression causes high
disease burden
Burden = disability
Global
Currently ranked 4th; projected to be
2nd in 10 years
Ethiopia
7th
3. Depression increases
risk of premature death
• Mortality
• A twofold increase in general risk Mortality
from suicide—12-19%
• Similar findings from Ethiopia (except
• for suicide mortality)
4. Depression is costly
Personal distress
In Ethiopia—involves family cost
Lost productivity—efficiency; absence
from work
Increased use of health services
due to somatic symptoms
Expense related to treatment
5. Depression affects
physical health
WHO, 2012; based on data from 70 countries
How could maternal depression affect child
health?
Maternal Forgetful
Depression
No energy
Low
motivation
Hopelessness
Tired
Difficulty with
•Maintaining hygiene
Poor •Following health advice
concentration •Seeking help on time
Child Illness &
Undernutrition
Treatment
•Bio-psycho-social
•Immediate, intermediate, long term
•Safety, symptom control, recovery
Treatment approach
Psychoeducation
Reduce stress & strengthen social supports
Consider antidepressants
If available, consider referral for
Interpersonal therapy (IPT), cognitive
behavioural therapy (CBT), behaviour
activation and problem solving
DO NOT manage the symptoms with
ineffective treatments, e.g. vitamin injections.
Offer regular follow-up.
Consider antidepressants
Should be moderate-severe
depression
3 treatment phases
Acute: treatment to induce remission
Continuation: treatment for 4-6
months post-remission to prevent
relapse
Maintenance: long-term treatment to
prevent recurrence
Main medication options
in Ethiopia
SSRIs=Selective Serotonin Reuptake
Inhibitors (fluoxetine, sertraline)
Tricyclic antidepressants
(amitriptyline, imipramine,
clomipramine)
Start low and go slow
SSRI: Fluoxetine
Dosing fluoxetine in healthy adults
» Initiate treatment with 20 mg every day and
increase
» If no response in 4 – 6 weeks or partial
response in 6 weeks, increase dose by 20 mg
(maximum dose 60 mg) according to
tolerability and symptom response.
Fluoxetine in adolescents
Try psychosocial approaches first
» Initiate treatment with 20 mg every
other day and increase to 20 mg if the
medication is tolerated.
» If no response in 6 weeks, increase
dose by 20 mg (maximum dose 40 mg)
» Monitor weekly for increase in suicidal
thoughts
Tricyclic antidepressants
(TCAs; e.g. amitriptyline)
Dosing amitriptyline in healthy adults
» Initiate treatment with 25 mg at
bedtime.
» Increase by 25 to 50 mg every 1 – 2
weeks, aiming for 100 – 150 mg by 4
– 6 weeks depending on response
and tolerability
Amitriptyline
Time to response after initiation of
adequate dose
» 4 – 6 weeks (pain and sleep
symptoms tend to improve in a few
days).
Side effects of TCAs
Serious side-effects (these are rare)
» cardiac arrhythmia.
Common side-effects
» (most side-effects diminish after a few
days; none are permanent)
» orthostatic hypotension (fall risk), dry
mouth, constipation, difficulty urinating,
dizziness, blurred vision and sedation.
Other physical therapies
Electro-convulsive therapy (ECT)
Vagus Nerve Stimulation (VNS)
Deep Brain Stimulation (DBT)
Magnetic Seizure Therapy (MST)
Transcranial Magnetic Stimulation
(TMS)
Bipolar Disorder
Manic episodes
Normal
mood
N
Inter-episode recovery Depressive episodes
Bipolar Disorder: mania
• Occurrence of
mania is the
essential
feature of
bipolar disorder
Clinical manifestations
DIGFAST
• Distractibility
• Indiscretion
• Grandiosity
• Flight of ideas
• Activity
• Sleep- decreased need
• Talkativeness
Clinical manifestations
• Core:
– Elated or irritable mood
– Hyperactivity
• Other symptoms
– Inflated self-esteem or grandiosity.
– Decreased need for sleep
– More talkative than usual or pressure to keep talking.
Clinical manifestations
• Flight of ideas or subjective experience that
thoughts are racing.
• Distractibility
• Increase in goal-directed activity
• Excessive involvement in activities that have a high
potential for painful consequences
Marked impairment in occupational or social function
Duration of at least 1 week
Bipolar Disorders
• Bipolar I
– At least one episode or mania
• Bipolar II
– At least one major depressive episode with at least one
episode of hypomania
• Cyclothymic disorder (Cyclothymia)
– Milder, chronic form of bipolar disorder
• Lasts at least 2 years in adults, 1 year in children/adolescents
– Numerous periods with hypomanic and depressive
symptoms
• Does not meet criteria for mania or major depressive episode
• Symptoms do not clear for more than 2 months at a time
© 2012 John Wiley & Sons, Inc. All
rights reserved.
Bipolar Disorder
• Distinguished from unipolar disorder
• Concept is only 50 year old
• Often subsumed under psychosis
Bipolar disorder
• But severe condition
• Significant level of burden
• Risks from the depressive and manic phases of
illness
DSM 5 criteria
Bipolar disorder-clinical features
• Lack of judgement may cause irresponsible,
impulsive acts
• Irritability leads to verbal and even physical
aggression
• Hypomania is the milder form of mania
• DIGFAST
Causes of Bipolar d/o
• Genetics and environment: 60% heritability;
40% environmental effects
• May follow psychological stress, surgery or
infection
• May follow childbirth, the use of
antidepressants, ECT or other drugs
Causes
• Corticosteroids, psycostimulants,
dopaminergic drugs (L-dopa, bromocriptine)
or anabolic steroids
• Discontinuation of drugs, especially lithium
• Sometimes episodes are seasonal
Other potential organic causes
• Organic brain damage, particularly in the right
frontal or temporal lobes from causes such as
– head injury,
– stoke,
– HIV infection,
– multiple sclerosis,
– epilepsy
– cerebral tumour
Diagnosis
• Bipolar I disorder at least one manic
episode.
• May present with
– Manic episode
– Major depressive episode
– Hypomanic episode
– Manic or major depressive episode with mixed
features
Diagnosis
• Bipolar II disorder Major depression +
hypomania
• May present with
– Hypomanic episode
– Major depressive episode
– Hypomanic or major depressive episode with
mixed features
Epidemiology
• Life time prevalence
– Bipolar I - 0-2.4%
– Bipolar II – 0.3- 4.8%
• M=W,
– W- rapid cycling, mixed
Course
• Mania is very rare before puberty
• Mean age of onset is 21
• Onset after 60 likely to be associated with
organic causes
• First episode likely to be triggered by life
events
Course
• Manic episodes may develop slowly over
some days, or rapidly over a few hours
• They may start from a normal state or follow a
depressive illness
• May last few days but often lasts several
weeks to months
Course
• Duration:
– untreated depression: 6‐12 months;
– mania 3‐6 months
• Recurrent in about 90%
• Unipolar mania is uncommon(5-10% of cases)
• Risk of suicide 15%‐20%
Pathophysiology
• Over activity of dopamine pathways
• Abnormal G‐protein and second messenger
function
• Abnormal biological clocks (Circadian
pacemakers)
TREATMENT PRINCIPLES
General guidance for Mania Tx
• Manage patient—do not argue; attempt to
establish rapport by discussing some of the
recent difficulties; calm, friendly handling
• Psychoeducation—patient and family
• Consider the need for admission
• Exclude potential causes
General guidance
• Acute versus maintenance treatment
• First task-deal with acute episode; manage
risk with patient and family
• Invariably require medication
• Antipsychotics and benzodiazpeines effective
in the short term
Medication Treatment
• Discontinue all antidepressants ASAP
• Short term treatment-any antipsychotics can
be used, but atypicals preferred;
• Benzodiazepines-clonazepam, lorazepam,
haloperidol
• Lithium can also be used to treat acute mania
Medication treatment
4 groups of medications
– Mood stabilisers
– Antipsychotics
– Benzodiazepines
– Antidepressants (very limited evidence of benefit
in bipolar disorder)
Mood stabilizer Treatment
• Lithium has slower onset of action
• Valproate-more rapid onset of action; good
for mixed episodes and rapid cycling
• Carbamazepine- 2nd/3rd line option
Maintenance treatment
• Not always easy decision
• Depends on history of illness and risk
• First episode only if significant risk
• 3 episodes in 5 years is generally an indication
for maintenance treatment
Choices
• Antipsychotics—not good choice in terms of
side effect profile; atypicals can be used
• Mostly mood stabilisers preferred
• These include lithium (primary choice),
sodium valproate and carbamazepine
Mood stabilisers
• Avoid sodium valproate in women of child
bearing age
Lithium
• No standard dose
• Dose guided by serum level (therapeutic range
0.4 mmol/L to 1.2 mmol/L)
• Higher level for acute episodes of mania
• Lower level for depression and maintenance
Lithium--investigations
• Before starting, do essential investigations
– FBC
– RFT
– LFT
– TFT (TSH +- Free T4)
– ECG if elderly
Lithium-investigations while on
treatment
• Serum lithium level
– 5th day after start and dose increment; once stable
level achieved, measure 3-6 monthly
– PRN if sign of toxicity
• RFT (BUN and creatinine 3-6 monthly)
• TFT-6 monthly
Lithium-dosing
• Start at 300 mg nocte or 300 mg b.i.d
(depending on patient characteristics and
preparation)
• Check level in 5 days; taper up by 300 mg
depending on level and response
• Monitor for neurotoxicity
Lithium-key risks
• Neurotoxicity
• Renal toxicity
Neurotoxicity
Mild to moderate intoxication (lithium level = 1.5 to 2.0 mEq/L)
GI Vomiting
Abdominal pain
Dryness of mouth
Neurologic
Ataxia
Dizziness
Slurred speech
Nystagmus
Lethargy or excitement
Muscle weakness
Moderate to severe intoxication (lithium level = 2.0 to 2.5 mEq/L)
GI Anorexia
Persistent nausea and vomiting
Neurologic
Blurred vision
Muscle fasciculations
Clonic limb movements
Hyperactive deep tendon reflexes
Choreoathetoid movements
Convulsions
Delirium
Syncope
Electroencephalographic changes
Stupor
Coma
Circulatory failure (lowered BP, cardiac arrhythmias, and conduction
abnormalities)
Severe lithium intoxication (lithium level >2.5 mEq/L) Generalized convulsions Oliguria and renal failure
Death
Bipolar Depression
• Optimize dose of mood stabilizers or atypical
antipsychotics
• Avoid anti depressants unless significant
suicidal risks
– Choose SSRI
– Never use w/o mood stabilizer
THANK YOU!!