bipolar disorder

1. BIPOLAR DISORDER
DR BIBEK RAJ PARAJULI
NMC NO 18693
MBBS (KU)

2. 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

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

10.  Bipolar I Disorder, Most Recent Episode
_______
A) Currently in a ________ Episode
B) At least one Manic, Major Depressed, or Mixed
Episode
C) 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.

11.  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.

12.  Cyclothymic Disorder
 Milder symptoms
 Considered a chronic condition
 Symptoms more consistent
 Clients with only depressive symptoms should
not be diagnosed with Cyclothymic Disorder

13.  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 Disorder
5. When the clinician believes Bipolar Disorder is present but
is unable to determine rule out medical condition or
substance

20. CAUSES
 Genetic
 Physiological
 Environmental
 Neurological
 Neuroendocrinological

21. GENETIC

22. 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

23. 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

24. 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

25. 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

32. DIFFERENTIAL DIAGNOSIS
 Schizophrenia, Schizoaffective disorder
 Substance Abuse – Stimulants
 Pseudo-Unipolar Disorder
 Steroids, Ginseng, Valerian root
 Syphilis, Hyperparathyroidism
 Borderline, Narcissistic and Histrionic
Personality disorder

33. 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?

36. MANIA

37. 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

38. 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.

39. 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

40. 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

41. 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

42. DISTRACTABILITY
 Were you having trouble thinking or
concentrating?
 Was this because things around you or even
your thoughts were getting you off track?

43. 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?

44. 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?

45. 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?

46. ACTIVITY INCREASE
 During that period, were you more active
than usual?
 Were you constantly starting new projects
and hobbies, working into the night?

47. 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?

48. 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

49. CORROBORATION
 Denial and lack of insight rule the day

50. TREATMENT

51. 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

53. 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

55. LITHIUM
Lithium 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”

56. CARBAMAZEPINE
 400 – 1000 mg/d
 Most effective for mixed states, rapid cycling
 SE’s – sedation, ataxia, aplastic anemia,
agranulocytosis

57. 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

58. 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

59. 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

60. 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

61. NEVER GIVE UP
It will help patient to be
inspired by us, rather than the
other way around

62. THANK YOU