Bipolar disorder
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Transcript of Bipolar disorder
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