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Bipolar disorder

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Mood Disorders (18.19-2-2010)

Publicada em: Saúde e medicina
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Bipolar disorder

  1. 1. ByDr. Maged Al AdrousyLecturer of psychiatry- Cairo university
  2. 2. introduction Bipolar disorder is an episodic, potentially life-long, disabling disorder that can be difficult to diagnose. known as Manic Depression, Results in pathological mood swings from mania to depression, These mood swings occur spontaneously.
  3. 3. ManiaEuthymiaDepression
  4. 4. History Bipolar Disorder  200 CE First reports  1654 Jean Pierre Falret  “folie circulaire" (circular insanity)  Familial illness  1913 Emil Kraepelin  Manic - Depressive  1930’s ECT first used  1949 Lithium first used  1950 Chlorpromazine first used  1952 Genetic link recognized  1980 Bipolar Disorder term adopted  1995 Depakote approved for BP  2003 First atypical approved for BP
  5. 5. Types of Mood Disorders 10% 2%  DSM IV 2% MDD  Major Depressive Disorder BP I  Dysthymic Disorder BP II  Bipolar Disorder Type I NOS  Bipolar Disorder Type II 86%  Cyclothymic Disorder  NOS  Mixed Phase  Rapid Cyclers 33% MDD BP I  Bipolar Spectrum (BPS) 50% BP II BPS 15% 2%
  6. 6.  Bipolar disorder is a cyclical mood disorder Abnormally elevated mood or irritability alternates with depressed mood bipolar I – at least one manic or mixed episode bipolar II – at least one major depressive episode and at least one hypomanic episode Cyclothymia = hypomania with “minor” depression “Bipolar spectrum” = Depression + other complexities  Bipolar NOS or Mood DO NOS
  7. 7. Structure of a Recurrent Illness Precipitant EpisodeUnderlying illness
  8. 8. Spectrum of Illness CourseEpisodic UnstablePurely episodic course: Radical mood instability:-interepisode stability -’interepisode’ instability-no mixed states -mixed states-infrequent episodes -frequent episodes-good recovery -incomplete recovery-low incidence of complications -high incidence of complications -early onset -stronger genetic loading? Course of illness dictates response strategies for the acute episode
  9. 9. DIAGNOSTIC CRITERIA FOR MANICEPISODES THREE TO FOUR OF THE FOLLOWING CRITERIA ARE REQUIRED DURING THE ELEVATED MOOD PERIOD Highly inflated or grandiose self-esteem Decreased need for sleep, or rested after only a few hours of sleep Pressured speech Racing thoughts and flight of ideas Easy distractibility, failure to keep attention Increased goal-directed activity High excess involvement in pleasurable activities (sex, travel, spending money)General criteria for a manic episode require a period of elevated, expansive,or irritable mood that lasts 1 week or requires hospitalization. A generalmedical condition and substance abuse must be ruled out before thesesymptoms are considered mania.
  10. 10. Manic Episode:Differential Diagnoses Differential diagnosis Consider if . . . Mood disorder due to a Major medical condition present general medical condition First episode at >50 years of age Symptoms in context of intoxication Substance-induced or withdrawal mood disorder History of treatment for depression Mood disturbance not severe Hypomanic episode enough to require hospitalization or impair functioning Mixed episode Manic episode and MDE in 1 week
  11. 11. Manic Episode:Differential Diagnoses (cont.) Differential diagnosis Consider if . . . AD/HD Early childhood mood disturbance onset Chronic rather than episodic course No clear onsets and offsets No abnormally elevated mood No psychotic features American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders (DSM-IV). 4th ed. 1994.
  12. 12. Major Depressive Episode:DSM-IV Criteria Depressed mood and/or loss of interest or pleasure ≥ 2 weeks duration Associated symptoms  Physical: insomnia/hypersomnia, appetite/weight change, decreased energy, psychomotor change  Psychological: feelings of guilt or worthlessness, poor concentration/indecisiveness, thoughts of death/suicidal intentions (SI)
  13. 13. …and ≥4 of the following symptoms Physical  Psychological  Sleep disorder  Low self  Appetite change esteem/guilt  Poor concentration/  Fatigue indecisiveness  Psychomotor  Thoughts of death/SI retardation
  14. 14. Mixed Episode: DiagnosticCriteria Criteria met for both manic episode + MDE for ≥1 week Symptoms  Are sufficient to impair functioning or  Necessitate hospitalization or  Are accompanied by psychotic features
  15. 15. Epidemiology Peak age of onset: adolescence through early 20s  Onset of first manic episode after age 40 years is “red flag” to consider substance use or general medical condition Lifetime suicide rates range from 10% to 15% Seasonal variation  Depression more common in spring and autumn  Mania more common in summer
  16. 16. Bipolar Disorders:EpidemiologyCharacteristics BPD I BPD IIPrevalence ≤1.6% 0.5%Ethnic/racialdifferential None NoneGenderdifferential M=F F›M (?)
  17. 17. Bipolar Disorders: Epidemiology Characteristics BPD I BPD II Course Recurrent in >90% Hypomanic episodes in of cases BPD II immediately precede or follow MDEs in 60% to 70% of cases First-degree First-degree relatives Familial pattern relatives have may have increased increased rates of rates of BPD I, BPD II, BPD I, BPD II, and and MDD MDD
  18. 18. Diagnostic Dilemmas:Unipolar Versus Bipolar No evidence of hypomania, Unipolar cyclothymia, hyperthymic personality, or family history of BPD ≥1 manic episode BPD I Recurrent major depression with BPD II hypomania and/or cyclothymic temperament Recurrent major depression without BPD NOS spontaneous hypomania but often with hyperthymic temperament and/or family history of BPD
  19. 19. Bipolar vs unipolar
  20. 20. BD II
  21. 21. CYCLOTHYMIC DISORDER  Cyclothymic disorder is a recurrent, chronic, mild form of bipolar disorder in which mood typically oscillates between hypomania and dysthymia.  If a manic episode or depressive episode is experienced, cyclothymic disorder is not diagnosed. http://www.allaboutdepression.com/cyclothymia/images/graph ic2.gif
  22. 22. CYCLOTHYMIC DISORDER EPIDEMIOLOGY ETIOLOGY The lifetime prevalence of Genetic and familial studies revealcyclothymic disorder is 0.4% to 1%. an association with other mood disordersThe rate appears equal in men and women, although women are usually more likely to seek treatment
  23. 23. CLINICAL MANIFESTATIONS OFCYCLOTHYMIC DISORDER Cyclothymic disorder is a milder form of bipolar disorder consisting of recurrent mood disturbances between hypomania and dysthymic mood. A single episode of hypomania is sufficient enough to diagnose cyclothymic disorder, although most individuals also have dysthymic periods. Cyclothymic disorder is never diagnosed when there is a history of mania, major depressive episode, or mixed episode.
  24. 24. Etiology
  25. 25. Heritability Evidence for heritability is much stronger for bipolar than for unipolar disorders Specific genetic association has not been consistently replicated
  26. 26. EVIDENCE FOR HERITABILITY OF BIPOLAR DISORDER Family Studies- First degree relatives are 8 to 18 times more likely to have Bipolar I 2 to 10 times to have MDD. Risk is 25% if one parent has illness, and 50% to 75% with both parents affected
  27. 27. FAMILY STUDIES The majority of individuals with bipolar disorder have a positive family history of some type of mood disorder About 50% of all bipolar I patients have at least one parent with a mood disorder
  28. 28. ADOPTION STUDIES Prevalence of bipolar disorder in adopted away offspring corresponds to rates in biological, but not adoptive relatives Twin Studies- Concordance rate in MZ twins is 33 to 90%, in DZ is 5 to 25%
  29. 29. Genetic Polymorphism A functional polymorphism is a genetic variant that appears in at least 1% of a population and alters the biological functioning of the individual Some types of polymorphisms in Mood Disorders  Serotonin transporter  Serotonin 2A receptor  MTHF reductase  Catachol -o- methyl tranferase (COMT)  Tyrosine hydroxylase  Cytochrome P450 metabolism of medications
  30. 30. Biological factors Dysregulation in levels catecholamines (++ levels of dopamine and norepinephrine). -- levels of serotonoine ?? Neuroendocrinal factors:• HPA axis (cortisol hypersecreation) may affect BDNF.• Throid dysfucntion. EEG changes (kindling model) Degenerative structural brain changes.
  31. 31. Psychosocial factors Life time events. Behavioral models . Psychological theories.
  32. 32. Impact of BD Higher rates of mortality from other medical conditions Increased substance abuse risk Lifetime suicide attempt risk (.02% in general populatio  Bipolar Disorder Type I – 17%  Bipolar Disorder Type II – 24%  90% of completed suicides can be traced back to a Mood Disorder High rates of cognitve defeicets affecting Working memory Sustained attention, Abstract reasoning, Visuomotor skills, Verbal memory, Verbal fluency, Cognitive flexibility
  33. 33. Management
  34. 34. A- psychopharmacology Mood stabilizers Atypical antipsychotics. Benzodiazepines. Channel blockers. Others Combination therapy is more effective than monotherapy
  35. 35. Mood stabilizers Lithium Conventional anti-epileptics as carbamazepine and Na valproate. New anti-epileptics lamotrigene gababentine, and topiramate
  36. 36. What Exactly Is a MoodStabilizer? • Some authorities suggest 2 out of 3 of the following properties: – Antimanic, antidepressive, prophylactic • Other experts are more stringent—requiring: – Treatment of acute mania, – Treatment of acute depression, AND – Prevention of recurrent mania and depression – Dosen’t ppt mania or depression. • Lithium remains the gold standard
  37. 37. Lithium  Widely recommended treatment for Bipolar Disorder  60-80% success in reducing acute manic and hypomanic states  However… issues in non-compliance to take medication, side effects, and relapse rate with its use are being examined in terms of being the best option
  38. 38. Pharmacokinetics:  Peak blood levels reached in 3 hrs, fully absorbed in 8 hrs  Absorbed rapidly and completely orally  Efficacy correlates with blood levels  Crosses blood-brain barrier slowly and incompletely  Usually taken as a single daily dose
  39. 39. Kinetics Cont.  Approx. 2 wks to reach a steady state within the body  ½ of oral dose excreted in 18-24 hrs,rest within 1-2 wks  Recommended 0.8-1.2 mEq/L, optimum would be 0.6-0.8 mEq/L, with 2 mEq/L displaying toxicity .  Monovalent ion not metabolized in liver, excreted by the kidney.
  40. 40. Pharmacodynamics  No psychotropic effect on non-Bipolars  Affects nerve membranes, multiple receptor systems and intracellular 2nd messenger impulse transduction systems.  Interacts with serotonin  Potential to regulate CNS gene expression, stabilizing neurons w/ associated multiple gene expression change.
  41. 41. How does a simple ion do all ofthis?  Even as a simple ion, it has complex effects on multiple transmitter systems and mood stabilizing attributes  This is due to a latter effect reducing a neuron’s response to synaptic input, and therefore stabilizing the membrane
  42. 42. Side Effects and Toxicity  Relate to plasma concentration levels, so constant monitoring is key  Higher concentrations ( 1.0 mEq/L and up produce bothersome effects, higher than 2 mEq/L can be serious or fatal  Symptoms can be neurological, gastrointestinal, enlarged thyroid, rash, weight gain, memory difficulty, kidney disfunction, cardiovascular  Not advised to take during pregnancy, affects fetal heart development
  43. 43. Side effects of Li1. GIT symptoms (diarrhea intially)2. Hypokalaemia…….cardiotoxic.3. Polyuria and D.insipius (ADH).4. Tremors.5. Epileptogenic.6. Teratogenic.7. hypothyroidism8. Li toxicity may occure (ttt?)
  44. 44. Na valproate Tab 200mg and 500 mg Dose 50-150 mg% Best for rapid-cycling and acute-mania Actions: through GABA potentiation, Ca channel blockade, Na channel blockade, glutamat antagonist.
  45. 45.  Side effects2. Hepatotoxic.3. Wt gain4. Hair loss.5. GIT symptoms.6. Tremors and sedation7. Neural tube defects
  46. 46. carbamazepine Tab 200mg 400 mg Dose 5-15 µg/L Action similar to valproate. Superior to lithium for rapid-cycling, regarded as a second-line treatment for mania Correlation between therapeutic and plasma levels (estimated between 5-10 Mg/L) Side effects:7. Agranulocytosis8. Skin reaction9. Teratogenic10.Liver enzyme induction
  47. 47. Gabapentin  Primarily an anti-convulsant, yet also “off label,” or without FDA approval for treatment of Bipolar and many other anxiety, behavioral and substance abuse problems, possibly pain disorders  GABA analogue  not bound to plasma proteins, not metabolized, few drug interactions  Half-Life is 5-7 hours  Side Effects include sleepiness,dizziness,ataxia and double vision
  48. 48. Lamotrigine  Reported effective with Bipolar, Borderline Personality, Schizoaffective, Post-Traumatic Stress Disorders  98% of administered drug reaches plasma  Half-Life is 26 hrs.  Inhibits neuronal excitability and modifies synaptic plasticity  Side Effects may include dizziness, tremor, headache, nausea, and rash
  49. 49. Topiramate and Tiagabine  Two newer anti-convulsants that have potential for use in the treatment of Bipolar disorder
  50. 50. Anticonvulsants: Efficacy in BD Probably effective:  Lamotrigine, CBZ, oxycarbazepine, valproate Possibly effective:  Gabapentin, zonisamide, phenytoin, levetiracetam Ineffective/problematic:  Topiramate, tiagabine, vigabatrin
  51. 51. Calcium Channel Blockers Modulate transmitter release & plasticity Most not consistently effective, possibly due to inconsistent uptake into brain Nimodipine reported effective in rapid-cycling, including refractory & ultra-rapid
  52. 52. Atypical Anti-psychotics  Risperidone seems more anti-depressant than anti-psychotic  Clozapine is effective, yet not readily used due to potential serious side effects  Olanzapine is approved for short-term use in acute mania  Quatiapine is now approved as a broad spectrum medication in BD esp (Bipolar depression).
  53. 53. Acetylcholinesterase Inhibitors  Potentiating the action of acetylcholine may exert relief from mania  This potentiation is the result of inhibiting the enzyme acetylcholine esterase
  54. 54. Omega-3 Fatty Acids  Obtained from plant or marine sources  Known to dampen neuronal signaling transduction systems in a variety of cell systems  Being investigated as a treatment for Bipolar Disorder
  55. 55. Three Phases of Treatment Episode Continuation Maintenance0-2 months 2-12 months IndefiniteSymptomatic Functional Stability/adaptive Each phase has specific goals Each phase has specific pharmacological and nonpharmacological rx Treatment must be harmonized across phases
  56. 56. NonpharmacologicTreatments ECT  Reports of effectiveness in mania, depression, & refractory mixed states  Bilateral generally more effective  Continuation ECT may prolong recovery; maintenance? Transcranial magnetic stimulation Psychotherapy : May include cognitive behavioral, psychodynamically oriented, family, couples, interpersonal, and self-help group therapies
  57. 57. Thank you

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