Ocd santhosh final

Editor's Notes

• #2: 4th most common psychiatric condition(phobias,substance use, mdd) prevalance1.9%-3.3%(~1.6)
• #4: Dd-gad, bdd,hoardind,hair pilling,skin pricking,stereotypic movement disorder,eating disorder,addictive disorder,illness anxiety disorder,paraphilias,impulse control disorder,schiz,asd, ocpd
• #6: the Thalmus processes sensory images coming to the brain from the rest of the body, while the Caudate Nucleus, part of the Basal Gangli in the centre of the brain controls and sorts sensory information and does thought filtering.  When these messages are being misinterpreted, ‘misfiring’, the thinking part of the brain is naturally confused and is responding chemically to a threat perceived by the primitive, non-reasoning part of the brain with rational doubt of the threat’s danger, but a major need to response as if the danger is real. In effect, the Caudate Nucleus is letting unnecessary thoughts and impulses through to the Cortex where the thoughts and emotions combine; and an over active Cingulate Nucleus at the brain’s centre, which helps shift attention from one thought or behaviour to another, becomes over active and gets stuck on certain behaviours, thoughts or ideas. The Cingulate is that part of the brain which tells the OCD sufferer that something terrible will happen if the compulsions are not carried out.
• #7: In ocd cd losts the filtering functions;allows unnecessary thoughts n urges works as a poor doorman There is a convergence of evidence implicating the corticostriatothalamocortical (CSTC) loop involving orbitofrontal (OFC) cortex, anterior cingulated cortex (ACC) and basal ganglia as central to the pathophysiology of OCD.[4–6] Two distinct routes are conceptualized from the striatum to the thalamus; the so-called “direct” and “indirect” pathways. The direct pathway projects from the cortex to the striatum to the internal segment of globus pallidus and substantia nigra to the thalamus and then back to the cortex. The indirect pathway is similar from the cortex to the striatum but then projects to the external segment of the globus pallidus to the subthalamic nucleus, before returning to the internal segment of the the globus pallidus/substantia nigra, there joining the direct pathway to the thalamus and projecting back to the cortex. Impulses transmitted via the direct pathway disinhibit the thalamus, presumably resulting in a release of behaviors as necessary for an adaptive function. Activity in the indirect pathway inhibits the thalamus, resulting in the cessation of ongoing behavioral routine. The prevailing theory on OCD suggests that a hitherto unknown primary striatal pathologic process underlies a relative imbalance favoring striatothalamic inhibition leading to hyperactivity within OFC and ACC, the caudate nucleus (CN) and the thalamus
• #8: Ofc tells us when something is wrong an when something should be avoided like an early warning system In ocd it does overtime In ocd cg becomes overactive
• #10: Volume reduction proportionate to severity of illness
• #12: Ht7 antagonism results in decreased oc syptoms
• #13: Glu regulators are topiramate,riluzole n d-cycloserine
• #15: seretonin transporter gene(5httlpr)
• #21: When the initial treatment is unsatisfactory, several factors may be contributing to the lack of improvement: interference by concomitant conditions, inadequate patient adherence to the treatment plan, the presence of psychosocial stressors, the family's degree of accommodation for the patient's symptoms, and the patient's inability to tolerate psychotherapy or medication.
• #24: CMI was first used in 1968 by Reynghe de voxrie
• #27: should all be considered when deciding which medication to use Y-BOCs, Maudsley oc inventory, brown assessment of beliefs, Responsibility attitude scale, CGI scale
• #28: Some patients may need to start at one half of this dosage or less to minimize undesired side effects such as nausea or to accommodate anxiety about taking medication. CMI less than 150mg subtherapeutic These dosages are sometimes used for rapid metabolizers or for patients with no or mild side effects and inadequate therapeutic response after eight weeks or more at the usual maximal dosage. Combined plasma levels of clomipramine plus desmethylclomipramine 12 hours after dosing should be kept below 500 ng per mL to minimize risk of seizures and cardiac conduction delay. Sertraline is better absorbed with food
• #30: Trd defined by thase n rush treat,ment guidelines for trd fleck and horwath- optimization of dose,switching to another first line approach,augmentation,combination
• #33: One study had shon 76% benefit in ssri non-responsers But if the pt not responded to paroxetine then venlaf not useful
• #35: Relapse rate of 83% with in first 2 months after stoppinh augmentation;so better to continue with primary drug
• #36: Aim for clomipramine levels of 225-350 ng/ml and combined clomipramine and desmethylclomipramine levels of < or = to 500 ng/ml in blood samples drawn about 12 hours after a dose; steady state takes two to three weeks to achieve
• #37: Massachusetts irt study administered for 3 months 30% improvement in ybocs score
• #41: They applied rTMS (80% motor threshold, 20 Hz for 2 s/min) for 20 min to 12 patients with OCD and found significantly decreased compulsive urges for 8 h after stimulation
• #42: The SMA was chosen as a useful target for rTMS because it has extensive connections with regions implicated in cognitive processes and motor control
• #44: ECT has occasionally been used for the treatment of anxiety disorders and currently no existing guideline considers anxiety disorders as a primary indication for ECT
• #47: Kumud Chawla Gamma Knife Centre in India :The 1st Centre of Gamma Knife Radiosurgery In India