Psychopathology Flashcards
Mental illnesses and psychological disorders
MDD, BPD, schizophrenia etc
Neurological disorders
Don’t need a cognitive component
e.g. chronic numbness, MS
Brain dysfunctions
Brain damage that leads to symptoms
should psych disorders, neurological disorders, and brain dysfunctions be considered separately?**
No, they all have a biological basis and some interconnectedness
principles of psych disorders
- developmental in nature
- represent multiple disorders categorized together by symptoms
- biological predisposition interacts with environment (diathesis stress model)
- represent extreme ends of normal spectrum of NS functioning, not fundamentally different
PDs relation to crime
not any more likely to commit crimes, more likely to be a victim of crime
psychosis is not…
Dissociative identity disorder
psychopathy
what type of assessment is psychopathy?
forensic, not psychological
types of symptoms related to schizophrenia
positive
negative
cognitive
mood
positive symptoms (schiz)
hallucinations (auditory), delusions, and disorganized thought/speech/behaviour
similar symptoms associated with drug use (hallucinations are more likely somatosensory)
negative symptoms (schiz)
decrease in emotional range, poverty of speech, difficulty manifesting motivation
what symptoms do schizophrenic drugs usually target?
positive symptoms
cognitive symptoms (schiz)
deficit in working memory, attention, executive functioning
mood symptoms
extremely sad or cheerful when they shouldn’t be. general mood disorder component
schizoaffective disorder
aspects of schizophrenia and MDD
prevalence/onset of schizophrenia
0.5-1.5%, slightly more in men
teens to early 30s, can see atypical behaviour in childhood processes
risks with schizophrenia
unemployment, poverty, homelessness (1:2 ratio)
Causes of schizophrenia
big role of genetics
marijuana as big of a risk factor as urbanicity or maternal prenatal infection
brain changes in schizophrenia (structural)
reduced grey matter, reduces as time passes. results in large ventricles
abnormal connectivity of white matter, disorganized
hippocampus; atypical layering structure and neuronal shape
PFC: fewer dendritic spines and GABAergic interneurons
brain changes in schizophrenia (functional)
hypoactive frontal and temporal lobes (executive functioning and theory of mind)
dysfunctional dopamine neurotransmission
brain difference in schizophrenia show us the illness is most likely….
neurodevelopmental
pharmacological treatments (schiz)
antipsychotic drugs for positive symptoms
no successful treatment of negative symptoms because a psychostimulant would increase positive symptoms
dopamine theory of schizophrenia
schizophrenia is caused by too much activity at the receptors for the NT dopamine
findings that support dopamine theory (schiz)
- brains with Parkinson’s disease have dopamine depletions in the substantia nigra, antipsychotic drugs produce symptoms similar to Parkinson’s
- drugs that increase dopamine levels produce symptoms of schizophrenia
- efficient antipsychotic drugs correlates with degree to which it blocks activity at dopamine receptors
- individuals with schizophrenia have hypersensitive dopamine release
what was the study showing that people with schizophrenia have hypersensitive dopamine release
administered amphetamine to 15 control and 15 experimental people and measured dopamine receptor availability before and after administration
there was decreased receptor availability in exp. group
problems with dopamine theory**
- newer antipsychotic drugs were just as good as traditional antipsychotics (both D2 antagonists)
- it takes 2-3 weeks for drugs to work yet their effect on dopamine receptor activity is immediate (downstream instead?)
- no improvements after first antipsychotic given
glutamate hypofunction theory
Dysfunction in glutamate NMDA receptors on GABAergic interneurons leads to decreased GABA especially in the PFC
lost inhibition meant for synchrony and organized thought
support for glutamate theory
- brains show fewer glutamate receptors
- glutamate antagonists (PCP, ketamine) can mimic symptoms and cog problems of schizophrenia
- NMDAR co-agonists provide small improvements
- activating cannabis receptor has inhibitory effects that cause CB1-NMDA receptors to internalize**
- chronic NMDAR antagonism changes dopamine transmission
problems with glutamate theory
- positive symptoms don’t respond to glutamatergic medication
- previous support has confounds such as studies not only targeting NMDA receptors, but others simultaneously
support for schizophrenia being an autoimmune disorder
bone marrow transplants between individuals with and without schizophrenia seemed to “transfer” the schizophrenic symptoms
autoimmune disorders are more prevalent in schizophrenia therefore hypothesize bone marrow transplants restores microglia functions
Auto immune disorders also target NMDA receptors
“success” of psychopaths
how well psychopaths go about society without being noticed
