CNS Disorders - Schizophrenia Flashcards
what are the positive symptoms of schizophrenia
hallucination - mainly auditory
though disorder
stereotyped behaviours
what are the negative symptoms of schizophrenia
poverty of affect
temporal disorientation
cognitive impairment
what is the evidence for a genetic cause of schizophrenia
high concordance in monozygotic twins of 48%
what are potential psychosocial causes of schizophrenia
adolescent onset
stress
emotionally charged home environment
blunted cortisol responses
what is the evidence to suggest that schizophrenia is not caused by structural brain damage
CAT/MRI scans show ventricular enlargement and decreased volume of temporal lobe
but no gliosis - so not neurodegenerative
what are the cytoarchitectural abnormalities in a schizophrenic patient
decreased number of small neurones in superficial layer
increased number of large neurones in deeper layers
what is the evidence for viral infection being a cause for schizophrenia
higher incidence of patients born in winter/spring
exposure of mother to virus during second trimester increases child’s risk to schizophrenia
what are the sites of brain dysfunction during auditory hallucinations
decreased size of temporal lobes and enlarged ventricles
in normal brains the left side of the brain has increased activity during verbal tasks - how is this affected by schizophrenia
this lateralisation is disrupted
dysfunction of dominant cerebral hemishpere
what does diffusor tensor imaging of schizophrenia show
hypo-functionality of dorsal-lateral pre-frontal cortex
what is the site of anti-psychotics and is also a brain dysfunction in schizophrenia
basal ganglia
what is the dopamine hypothesis for symptoms of schizophrenia and what is the evidence for this
due to excess dopamine neurotransmission in the mesolimbic and mesocortical regions
no consistent evidence for this hypothesis
chronic treatment of antipsychotics to rats was done to anaesthetise and record DA activity in rats, where specifically where they measuring DA activity
substantia nigra - SN
ventral tegmental area - VTA
before any antipsychotic treatment outline the activity of VTA neurones compared to SN
VTA neurone activity is greater than SN neurone activity
how did acute antipsychotic treatment affect the rats
increase in mesolimbic activity of VTA neurones
no change in mesocortical neurone activity
how did chronic antipsychotic treatment affect the rats
mesolimbic VTA neurones become silent
still no change in mesocortical neurone activity
so how does the study treating rats with antipsychotics explain the delayed onset effect of antipsychotics - chlorpromazine
blocks autoreceptor feedback which increases pre-synaptic activity - release of dopamine
but after a while this causes a depolarizing block in the neurone
what is the effect of DA releasing neurones entering depolarizing block in the mesolimbic region
since there is no change in neurone activity in the mesocortical neurones from antipsychotic treatment - there is a relative increase in DA activity in the mesocortical region
what are the typical antipsychotics
phenothiazines
thioxanthenes
butyrophenones
what are the common side-effects of typical antipsychotics
weight gain
sedation
postural hypotension
atropine-like side-effects
hyperprolactinaemia
what is the weight gain and sedation side-effects from antipsychotic use caused by
blockade of histamine receptors - antihistamines
what is the postural hypotension side-effect from antipsychotic use caused by
blockade of alpha-adrenoceptors
what is the hyperprolactinaemia side-effect of antipsychotic use caused by
blockade of D2 receptors
what is a rare but lethal side-effect of antipsychotics
neuroleptic malignant syndrome
