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2010-B5 Schizuc

tuesdayshuffle


Published on December 2, 2014

 ‐ • Mor holo ical   chan es –brain   as mmetr   with   decreased   cortical/hippocampal   size   and   increased   ventricular   size • Neurotransmitter   changes The   theories   were   largely   derived   from   observations   of   pharmacological   observations,   unfortunately   not   on   detail   understanding   to   the   neurochemistry   of   particular   neutronasmitter   system – Dopamine   theory –central   and   most   important   one,   it   will   be   discussed   urther   in   detail – Glutamate   theory   –comes   from   psychotic   symptoms   induced   by   administrations   o   NMDA ‐ antagon sts   etamine   an   p encyc i ine ,   toget er   wit   o servations   from   post ‐ mortem   examination   • It   was   proposed   that   reduced   glutamatergic and   increased   dopaminergic neurotransmissions   may   impair   the   gating   function   of   GABA ‐ ergic   neurons   projecting   themselves   into   the   thalamus   –which   cause   deteriorations   of   the   SENSORY   „GATE“. – Serotonine   theory –schizophrenia ‐ like   symptoms   induced   by   LSD ,   many   atypical   antipsychotics   block   also   5 ‐ HT   receptors 7 Dopamine   theory: dopaminergic   systems   in   CNS • Schema   of   dopamine   pathways   in   the   brain Please   se   Ran ‐ Dale   .   495   Fi .   34.3 8 Dopamine   theory   of   schizophrenia • ymp oms   o   sc zop ren a   ar se   rom   yperac v y   o   opam nerg cpa ways   n   mesolimbic/mesocorticalsystem • It   was   based   on   observation   that   psychotic   symptoms   and   related   behavioural       – Induced by • Drugs   causing   dopamine   release   – e.g.,   amphetamines • ‐ agon s s e.g.,   romocryp ne   an   opam ne   precursors   e   ‐ – Inhibited by   • Drugs   blocking   dopamine   storage   (e.g.,   reserpine ) • D ‐ antagonists   • Dopamine   receptors – D 1 type (D 1 and   D 5 )   and   D 2 ‐ type (D 2 ,   D 3 ,   D 4 ) • D 2 ‐ receptors – Are   evidently   involved – There   is   a   strong   correlation   between   D 2 ‐ antagonistic   effects   and   antipsychotic   action – Clinical   response   is   reached   when   80%   of   D 2 receptors   is   occupied • Involvement   of   other   D ‐ receptors   ???   D 4 –specific   antagonists   are   ineffective • Some   theories   suggest   that   the   key   issue   may   be   the   overactivationof   D 2 receptors   in   subsorticalregions (positive   symptoms)   while   activation   of   D 1 receptors   can   be   deficient (negative   symptoms) 9       • Positive   symptoms     ,       – Hallucinations (usually   hearing   of   voices,   typically   spurring) – Incoherent   thought: disconnection  ‐ loosing   of   associations,   inability   of   lo ical   anal sis   of   the   situation   ambivalence   –contradictor   thou hts Suspiciousness,   hostility   and   potentially   agressvity – Disorganised   speech – Stereotype/abnormal   movements • Negative   symptomes – Affective   flattening –poor   emotional   experience n e on a – oss   o   e   capac y   o   exper ence   p easure – Avolition ‐ lack   of   desire,   drive,   or   motivation   to   pursue   goals – Withdrawal   from   social   contacts • Cognitive   symptomes – Impaired   attention,   working   memory   and   executive   function • Clinical   picture   may   vary   considerably,   especially   according   to   the   positive/negative   symptoms   balance 10 11 • Positive   symptoms • Negative   symptoms – Hallucinations – Delusions – Social   withdrawal – Emotional   withdrawal – Disordered   thinking – Disorganized   speech – Lack   of   motivation – Poverty   of   speech – Combativeness – Agitation – Blunted   affect – Poor   insight – Paranoia – Poor   judgement – Poor   self ‐ care 12