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Obsessive-compulsive disorder

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Obsessive-compulsive disorder

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    1. Obsessive-compulsive disorder Symptoms Neuropathology Treatments Causes

    2. OCD Obsessions: persistent thoughts Compulsions: persistent behaviors Individual is aware that the behavior or obsession is unreasonable or excessive

    5. Heterogeneity “folie du doute” (madness of doubt) and “delire du toucher” (delusion of touch) (Flaret, 1869) Checkers vs. washers Continuing challenge

    6. OCD ONSET males, childhood, often associated with tic disorders Females, puberty and early adulthood 3.3 million adults in the United States (2-3 %) Cross-cultural studies find symptoms are similar in various racial and ethnic groups

    7. Associated Disorders Associated Disorders: Trichotillomania Onychophagia Co-morbidity Depression Tourette’s body dysmorphic disorder Eating disorders

    8. Neuropathology Imaging studies Structural: increases or decreases in size of the orbitofrontal cortex, striatum, or thalamus Increased activity in caudate, orbitofrontal cortex, cingulate cortex Dysfunction of cortical/basal ganglia loop Huntington’s, Tourette’s, maybe Parkinson’s, Sydenham’s chorea also exhibit OCD Remember craving and compulsive drug-taking?

    9. Structural alterations

    10. Reduced left orbitofrontal cortex in OCD patients correlates with severity of symptoms

    11. Alterations in the anterior cingulate and globus pallidus

    12. Altered white matter in the anterior cingulate cortex

    13. Altered function of the cortico-striatal-thalamo-cortical loop

    14. Overactivity of prefrontal-basal ganglia loops

    15. Increased activity in the thalamus

    17. At rest: Increased activity of the orbitofrontal cortex Increased activity of the cingulate cortex Increased activity in the caudate nucleus Increased activity in the thalamus

    18. fMRI “Contaminated” items vs neutral items Handling of contaminated items exacerbated activity in the prefrontal cortical areas (anterior cingulate, orbitofrontal), the basal ganglia, and the amygdala Hyperactivity is exacerbated during symptom provocation

    19. Activation in the orbitofrontal cortex and amygdala during symptom provocation

    20. Subtypes of OCD Symmetry/ordering Hoarding Contamination/cleaning Obsessions/checking

    22. Washing

    23. Checking

    24. Hoarding

    25. There may be distinct neural pathological patterns associated with different symptom dimensions Cleaning may be more related to emotional processing Checking may be more related to dysfunction in attention and inhibitory control

    26. Injury-induced OCD

    27. Overactivity of cortico-basal ganglia Baseline During provocation of symptoms Specific pattern may depend on OCD type OCD can be caused by damage to the basal ganglia OCD occurs in other prefrontal-basal ganglia disorders

    30. Alterations in other cognitive/emotional processes

    31. Activation of the anterior cingulate when errors are committed on a cognitive task in OCD patients

    32. Cognitive Alterations Memory (working, etc) Set shifting Response inhibition (more errors of commission)

    33. Dysfunction of inhibitory processing

    34. Altered Direct/Indirect Pathway Balance Overactivity of the DIRECT LOOP

    35. Dysfunction of habit formation?

    36. Neurochemical alterations

    37. Serotonin hypothesis OCD is related to serotonin dysfunction Pharmacological treatments for OCD Clomipramine Fluoxetine (Prozac) Paroxetine (Paxil) Serotonin Antagonists exacerbate symptoms Data on serotonergic measures in OCD patients have been conflicting

    38. Serotonin modulates the prefrontal cortex, striatum, and thalamus

    39. Symptoms can be exacerbated by increasing 5-HT function

    41. Evidence of 5-HT dysfunction Increased 5-HT2A receptors in caudate which are normalized after SSRI treatment (Adams et al., 2005, Int J Neuropsychopharmacol) Alterations in serotonin transporters

    42. Increased midbrain serotonin transporter binding sites

    43. No difference in serotonin transporter binding

    44. Reduced 5-HT transporters in midbrain

    45. Dopamine Up to 40% of OCD patients do not respond to SSRIs. Dopamine agonists induce stereotyped movement in humans and animals Dopamine agonists can exacerbate OCD symptoms Co-morbidity of Tourette’s and OCD (up to 90% of individuals with Tourette’s have OCD) Adjunctive therapy with conventional antipsychotics add to reduction of OCD symptoms in individuals treated with SSRIs

    46. Increases in striatal dopamine transporter binding in OCD patients

    47. Increased striatal DA transporters in psychotropic-naďve OCD patients

    48. Alterations in striatal D2 receptors

    49. Treatments

    50. Treatments SSRIs Adjunctive antipsychotics (dopamine antagonists) Behavior therapy Psychosurgery Effective treatment, pharmacologic or behavioral therapy, normalizes activity

    51. Normalization of striatal activity with SSRI treatment

    52. Normalization of orbitofrontal cortex activation

    53. Behavioral treatment is effective

    54. PET scans of OCD patients

    55. Either drug treatment or behavioral treatment normalizes brain activity

    56. Surgical treatments Destroy connections between the frontal lobe and basal ganglia/limbic structures Cingulotomy

    57. Psychosurgeries

    59. Psychosurgery Success 27% definite improvement, 27% probably improvement, 46% no improvement (Baer et al, 1995) 32% definite improvement, 14% partial improvement, 54% no improvement (Dougherty et al, 2002)

    60. Psychosurgeries

    61. Can imaging help predict treatment efficacy?

    62. Causes Genetics Concordance rates are higher among monozygotic twins compared to dizygotic twins First-degree relatives are 3-12 times more likely to develop OCD Streptococcal infection: immune reaction

    63. Genetic targets Polymorphism in the promoter region for the serotonergic reuptake transporter 5-HT 1D receptor gene DRD4 receptor mutations

    64. PANDAs Pediatric autoimmune neuropsychiatric disorders associated with streptococcal infection

    65. Case of Frances

    66. Summary OCD is related to dysfunction of prefrontal-basal ganglia loops that lead to repetitive thoughts and actions Effective treatments normalize this activity Treatments include SSRIs, behavioral therapies and psychosurgery Causes include genetic factors and possible autoimmune reactions

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