BIPOLAR DISORDER

DR BIBEK RAJ PARAJULINMC NO 18693MBBS (KU)

F31 BIPOLAR DISORDER Bipolar disorder, also known

as bipolar affective disorder or manic depression, is a mental disorder characterized by periods of elevated mood and periods of depression.[1][2] The elevated mood is significant and is known as mania or hypomania depending on the severity or whether there is psychosis

German psychiatrist Emil Kraepelin first distinguished between manic–depressive illness and "dementia praecox" (now known as schizophrenia) in the late 19th century

Bipolar I Disorder, Most Recent Episode _______A) Currently in a ________ EpisodeB)At least one Manic, Major Depressed, or Mixed

EpisodeC) Symptoms cause significant distress or impairment

in social, occupational, or other functioning.D)The symptoms are not better accounted for by

Schizoaffective Disorder, Schizophrenia, Schizophreniform Disorder, Delusional Disorder, or Psychotic Disorder NOS.

E) The Symptoms are not better accounted for by a substance or general medical condition.

Bipolar II Disorder Manic or Mixed Episode rules out this disorder Presence of a Hypomanic Episode defferinates

between the two conditions. Symptoms must cause impairment

Sometimes hypomanic symptoms may not cause impairment

More common in women Women with the disorder are at risk for

developing episodes during postpartum.

Cyclothymic Disorder Milder symptoms Considered a chronic condition Symptoms more consistent Clients with only depressive symptoms

should not be diagnosed with Cyclothymic Disorder

Bipolar Disorder Not Otherwise Specified Disorders with bipolar features not meeting criteria

Examples: 1. Rapid alternation (over days) between manic and depressive

symptoms that meet symptom criteria but not minimal duration for Manic, Hympmanic or Major Depressive Episodes.

2. Recurrent Hypomanic Episodes without depressive symptoms.3. A Manic or Mixed Episode superimposed on Delusional

Disorder, residual Schizophrenia, or Psychotic Disorder NOS.4. Hypomanic Episodes, along with chronic depressive symptoms,

that are too infrequent for Cyclothymic Disorder5. When the clinician believes Bipolar Disorder is present but is

unable to determine rule out medical condition or substance

CAUSES

Genetic Physiological Environmental Neurological Neuroendocrinological

GENETIC

PHYSIOLOGICAL

According to the "kindling" hypothesis, when people who are genetically predisposed toward bipolar disorder experience stressful events, the stress threshold at which mood changes occur becomes progressively lower, until the episodes eventually start (and recur) spontaneously. There is evidence supporting an association between early-life stress and dysfunction of the hypothalamic-pituitary-adrenal axis (HPA axis) leading to its over activation, which may play a role in the pathogenesis of bipolar disorder

ENVIRONMENTAL

Evidence suggests that environmental factors play a significant role in the development and course of bipolar disorder, and that individual psychosocial variables may interact with genetic dispositions

NEUROLOGICAL

Less commonly bipolar disorder or a bipolar-like disorder may occur as a result of or in association with a neurological condition or injury. Such conditions and injuries include (but are not limited to) stroke, traumatic brain injury, HIV infection,multiple sclerosis, porphyria, and rarely temporal lobe epilepsy

NEUROENDOCRINOLOGICAL

 The dopamine hypothesis states that the increase in dopamine results in secondary homeostatic down regulation of key systems and receptors such as an increase in dopamine mediated G protein-coupled receptors. This results in decreased dopamine transmission characteristic of the depressive phase.The depressive phase ends with homeostatic up regulation potentially restarting the cycle over again.

Glutamate is significantly increased within the left dorsolateral prefrontal cortex during the manic phase of bipolar disorder, and returns to normal levels once the phase is over.[54] The increase in GABA is possibly caused by a disturbance in early development causing a disturbance of cell migration and the formation of normal lamination, the layering of brain structures commonly associated with the cerebral cortex

DIFFERENTIAL DIAGNOSIS Schizophrenia, Schizoaffective disorder Substance Abuse – Stimulants Pseudo-Unipolar Disorder

Steroids, Ginseng, Valerian root

Syphilis, Hyperparathyroidism Borderline, Narcissistic and Histrionic

Personality disorder

SCREENING QUESTIONS Have you ever had a period of a week or

so when you felt so happy and energetic that your friends told you that you were talking too fast or that you were behaving differently and strangely?

Has there been a period when you were so hyper and irritable that you got into arguments with people?

Has anyone ever called you manic before?

MANIA

F30 MANIC EPISODE A manic episodes is typically

characterized by the following features

Which should last for at least one week and

Cause disruption to occupation and social activities

HYPOMANIA F30.0 Hypomania is a lowered state of mania that does little

to impair function or decrease quality of life.  It may, in fact, increase productivity and creativity. In

hypomania, there is less need for sleep and both goal-motivated behaviour and metabolism increase. Though the elevated mood and energy level typical of hypomania could be seen as a benefit,

mania itself generally has many undesirable consequences including suicidal tendencies, and hypomania can, if the prominent mood is irritable rather than euphoric, be a rather unpleasant experience.

STAGES 1. Euphoria : mild elevation of mood 2. Elation: moderate elevation of

mood 3. Exaltation: severe elevation of

mood 4.Ecstasy: very severe elevation of

mood

CAUSES The biological mechanism by which mania occurs is not yet known. Based on

the mechanism of action of antimanic agents (such as antipsychotics, valproate, tamoxifen, lithium, carbamazepine, etc.) and abnormalities seen in patients experiencing a manic episode the following is theorised to be involved in the pathophysiology of mania:

Dopamine D2 receptor overactivity (which is a pharmacologic mechanism of antipsychotics in mania)

GSK-3 overactivity Protein kinase C overactivity Inositol monophosphatase overactivity Increased arachidonic acid turnover Increased cytokine synthesis Imaging studies have shown that the left amygdala is more active in

women who are manic and the orbitofrontal cortex is less active.Pachygyria may be associated with mania also

SYMPTOMS OF MANIA— DIG FAST

Distractibility Insomnia (↓ need for sleep) Grandiosity (↑ selfesteem)/more Goal

directed Flight of ideas (or racing thoughts) Activities/psychomotor Agitation Sexual indiscretions/ othepleasurable

activities Talkativeness/pressured speech

DISTRACTABILITY Were you having trouble thinking or

concentrating? Was this because things around you or

even your thoughts were getting you off track?

INDISCRETION During the period we were talking about,

how were you spending your time? Were you doing things that caused trouble

for you or your family? Were you doing things that showed a lack

of judgment, such as driving too fast, running red lights, or spending too much?

Were you doing sexual things during this this period that was unusual for you?

GRANDIOUSITY During this period did you feel so

confidant that you felt you could conquer the world?

What was your best idea when you felt that way?

Did you feel that you had special powers or abilities?

Did you feel more religious than normal for you?

FLIGHT OF IDEAS During this period did you have so

many thoughts, or were they so fast, that you could barely keep up to them?

Did it feel like your thoughts were racing?

ACTIVITY INCREASE During that period, were you more

active than usual? Were you constantly starting new

projects and hobbies, working into the night?

SLEEP DEFICIT During that period, did you need less

sleep? Did you ever stay up all night doing all

kinds of things, like working on projects or phoning people?

Did your sleep duration become reduced and still you had lots of energy?

TALKATIVENESS During this period, were you talking

more than usual for you? Were you talking so much that people

had to interrupt you to speak to you? Were you using the phone more than

usual for you

CORROBORATION Denial and lack of insight rule the day

TREATMENT

TREATMENT OPTIONS Hospitalization for mania, severe

depression Mood stabilizers, antipsychotics and

antidepressants

ECT – most effective treatment

Supportive psychotherapy and CBT

Lifestyle change

Substance abuse treatment

PSYCHOSOCIAL

Psychotherapy is aimed at alleviating core symptoms, recognizing episode triggers, reducing negative expressed emotion in relationships, recognizing prodromal symptoms before full-blown recurrence, and, practicing the factors that lead to maintenance of remission 

Cognitive behavioral therapy, family-focused therapy, and psychoeducation have the most evidence for efficacy in regard to relapse prevention, while interpersonal and social rhythm therapy and cognitive-behavioral therapy appear the most effective in regard to residual depressive symptoms. Most studies have been based only on bipolar I, however, and treatment during the acute phase can be a particular challenge. Some clinicians emphasize the need to talk with individuals experiencing mania, to develop a therapeutic alliance in support of recovery

LITHIUMLithium reduces manic episodes and aggression

900 – 1500 mg/d .8-1.3 mEq/L Most effective medication SE’s include teratogenicity, tremor, renal dysfunction,

acne, hypothyroidism, gastric upset, cardiac conduction problems, cognitive impairment

Serum TSH, Cr, EKG, electrolytes pre and TSH, Cr q6mo. Mogen Schou rule, “Always treat SE’s”

CARBAMAZEPINE 400 – 1000 mg/d Most effective for mixed states, rapid

cycling

SE’s – sedation, ataxia, aplastic anemia, agranulocytosis

VALPROATE 500 – 2000 mg/d; Highest blood level

for effect. Highest dose is 60 mg/kg/d SE’s – GI upset, weight gain, alopecia,

teratogenicity, liver problems

Best for mixed states, rapid cycling, secondary mania. Ineffective for depression

Selenium for hair loss

LAMOTRIGINE Anticonvulsant, best for Bipolar

depression Improved cognition, excellent

tolerance, serious autoimmune rash Valproate interaction 12.5 to 25 mg/wk increments. Dose

range of 75 to 300mg/d

GABAPENTIN May cause persistent sedation Excreted by kidneys only, no drug

interaction 1200 to 4000 mg/dAnticonvulsant,

least effective new drug Most helpful with anxiety, insomnia,

pain

ATYPICAL ANTIPSYCHOTICS Olanzepine – 2.5-20 mg/d; very

effective; significant wt gain and lipid problems in some

Risperdal - .5-4.0 mg/d; more EPS and increased prolactin in some

Clozapine - For truly refractory patient, but can be remarkably effective. Slow response, serious SE profile and significant wt gain

NEVER GIVE UP

It will help patient to be inspired by us, rather than the other way around

THANK YOU