Bipolar I disorder is characterized by one or more manic episodes, with or without major depressive episodes. The lifetime prevalence is 0.4-1.6% and is highly genetic, with a 90% prevalence in monozygotic twins of patients. Diagnosis requires a manic episode lasting at least one week with inflated self-esteem and decreased need for sleep, plus additional symptoms. Treatment involves hospitalization, psychopharmacotherapy including mood stabilizers like lithium, and psychotherapy.

1. Bipolar I disorder
Dr. Mohamed Abdelghani
M.B.B.Ch., M.Sc., M.D. Psych.

2. Epidemiology
 The lifetime prevalence is 0.4-1.6%.
 The lifetime prevalence in monozygotic
twin of patients is up to 90%.
 Male to Female ratio 1:1.
 Manic episode: more in males.
 Depressive episode: more in females.

3. Diagnosis
 Presence of one or more manic episodes with or without
presence of major depressive episodes.
 Manic episode:
 Elated mood or irritable mood for one week or more.
 If mood is elated (3) or more of the following must be present but
if mood is irritable (4) or more of the following must be present:
 Inflated self-esteem or grandiosity.
 Decreased need for sleep.
 More talkative than usual.
 Flight of ideas.
 Distractability.
 psychomotor agitation.
 Loss of normal social and sexual inhibition.
 Excessive involvement in pleasurable activities that have a high potential for
painful consequences.
 Not substance-induced or not due to general medical condition.
 Significant impairment of occupational and social functioning.

4. Aetiology
1) Neurotransmitter hypothesis: increased activity of biogenic
amines serotonin, norepinephrine, and dopamine.
2) Genetic theory:
 Increase the incidence of bipolar I disorder in subjects related to
an affected person.
 Associations between bipolar I disorder and genetic markers
have been reported for chromosomes 5, 11, X.
3) Brain structure theory:
 Some patients showed enlarged cerebral ventricles.
 Magnetic resonance spectroscopy showed abnormal regulation
of membrane phospholipid metabolism.
4) Psychosocial theory:
o Feeling of inadequacy and worthlessness are converted by
means of denial, reaction formation and projection to grandiose
delusions.

5. Differential diagnosis
1. Bipolar II disorder:
 Major depressive episodes with hypomanic episodes.
2. Cyclothymic disorder:
 Numerous episodes of hypomania and numerous
episodes of depressive symptoms for at least 2 years.
 The symptoms are not sufficient to diagnose manic
episodes or major depressive episodes.
 Significant social and occupational impairment.
3. Secondary mood disorder:
 Substance-induced mood disorder.
 Mood disorder due to general medical condition.

6. Treatment
I. Hospitalization
II. Psychopharmacotherapy
III. E.C.T.
IV. Psychotherapy

7. Psychopharmacotherapy
A. For manic episodes: “Mood stabilizers”
1)Lithium:
 It is the standard treatment of bipolar disorder.
 Therapeutic blood level is 0.8-1.2 mEq/litre.
 Toxic levels start after 1.5 mEq/litre.
2)Anti-convulsants:
 Valproate, Carbamazepine, oxacarbazepine,....
3)Atypical antipsychotics:
 All except Clozapine.

8. B. For major depressive episode:
 Lamotrigine
 Olanzapine plus Flouxetine “Symbyax”
 Quetiapine
 Antidepressant drugs should be used with
caution to avoid switching to mania.

9. Electroconvulsive therapy
 At least equal to lithium in the treatment of acute and
severe manic episodes.
 Limited to:
1. Acute suicide.
2. Severe mania with psychotic symptoms.
3. Catatonia.
4. Failure of medical ttt “Resistent Bipolar”.

10. Psychotherapy
1) Cognitive therapy: to increase compliance with
pharmacotherapy.
2) Supportive therapy: with chronic patients who
may have significant interepisodic residual
symptoms and social dysfunction.
3) Family therapy: if patient’s disorder is disrupting
the family stability, and because the disorder is
strongly familial.

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