area 2- mental Health Flashcards
what is meant biochemical explanation
abnormal levels of neurotransmitters
what is the medical model
biochemical explanation, genetic explanation, brain abnormality explanation.
what is meant by exitarcy and inhibitory neurotransmitters
exitarcy- causes next neuron to be activated (over stimulated)
inhibitory- prevents action of the next neurone
what is the monoamine hypothesis of depression
low serotonin in the brain because serotonin reuptakes at pre-synaptic neuron failing to bind to post synaptic neuron
what does noradrenaline do
hypothalamus and hippocampus is largely responsible for heart rate
what evidence is their to support the monoamine hypothesis of depression
Meyer (2006)- 17 depressed patients who hadn’t taken antidepressants for 5 months, used PET scans and compared with 17 normal patients - found depressed patient had high levels of monoamine oxidase which breaks down the monoamines to quickly
what is the dopamine hypothesis of schizophrenia
excess dopamine at the D2 receptors which means more dopamine is absorbed at the post- synaptic neuron, overstimulating it.
what evidence is their to support the dopamine hypothesis
Seeman (1987)
drugs with high levels of dopamine increase some positive symptoms (hallucinations)
antipsychotics decrease symptoms
post mortems- schizophrenic brains have increased density of D2 receptors than normal
what is the GABA explanation of phobias
GABA counterbalances glutamate neurotransmitter which is responsible for panic/ anxiety
people with phobias have decreased levels of GABA so neurons in glutamate pathway is increased leading to phobias
what is evidence to support the GABA explanation
Pande (1999) 69 patients with social phobia took drug with high levels of GABA which reduced anxiety
genetic explanation of depression
family studies- Gottesman shows increased risk that children have of developing bipolar if parents have it or another disorder
Twin studies- major depression concordance rates between monozygotic twins is between 30-50%, dizygotic twins is 12%
adoption studies- few studies are conducted so less consistent support
genetic explanation of schizophrenia
family studies- 1% prevalence i world but risk is x10 greater if your 1st degree relatives have schizophrenia
Twin studies- concordance rates for MZ twins is 50%, DZ is 15%
adoption- Finnish adoption study-biological parents has schizophrenia Childs risk to 9.4%, unaffected parent 1.2%
genetic explanation for phobias
twin studies- animal type specific phobias was 26% for MZ twins and 11% for DZ twins , no difference for situation specific situation.
what brain abnormality is associated with depression
amygdala: increases in activity when presented to negative stimuli
hippocampus: smaller in patients with depression - more severe - more loss of grey matter
what is evidence that brain abnormality is associated with depression
Sheline- gave FRMI scans of 11 patients and showed amygdala was active in those with depression when shown emotional images
what is the brain abnormality associated with schizophrenia
enlarged ventricles-reduced grey matter
temporal lobes-loss grey matter- hallucinations
frontal lobes-loss grey matter- disturbed speech/disorganised speech
thalamus- loss of grey matter- auditory/verbal hallucinations
what evidence is their to support brain abnormalities in schizophrenia
pol- 159 schizophrenic individuals, found up to 30% increase size in ventricles- less grey matter- less functionality
how does brain abnormalities explain phobias
pre-frontal cortex- supresses fear to stimuli if not functioning it fails to supress urge
amygdala - detects/respond to threats - disruption to structure means they can’t control fearful response
hippocampus- learned associations- reduced functioning- person only recalls link between stimulus and previous fearful experience rather than neutral/positive feelings
what evidence is their to support that brain abnormality is associated with phobias
Ahs et al (2009)- PET scans measure cerebral blood flow in amygdala and prefrontal cortex of patients with fear of spiders/snakes
found increased activity in amygdala, reduced pre-frontal cortex - phobias are emotional
what is the background of Gottesman
past research has been done showing the increased risk of psychological disorders when parent(s) have disorders. This can be useful in genetic counselling
what is the Aim of Gottesman
to investigate the likelihood of offspring having schizophrenia or bipolar if one or both parents suffer from one of the disorders
what is the sample of Gottesman
2.7 million people born in Denmark between 1968 and 1967
what is the research design of Gottesman
secondary data from civil registration
what is the procedure of Gottesman
used civil registration to identify parents. then each child and parents was checked to see if they were on the psychiatric register and if so what specific diagnosis. Data on each offspring was then linked with parents psychiatric history so likelihood of disorder could be calculated.
what are the results of Gottesman
risk of developing schizophrenia by age 52= both parents with diagnosis: 27% same diagnosis, 67% other diagnosis
1 parent- 7%
risk of developing bipolar by age 52=
both parents with diagnosis: 24% same diagnosis, 44% other diagnosis
1 parent- 4%
what is a conclusion of Gottesman
If both parents have schizophrenia, there is an increased risk of offspring developing schizophrenia
if only one parent has disorder there is an increased chance of offspring developing the disorder but not as much as both parents
supports genetic approach that if 1st degree relatives have disorder it is an increased chance for individual
explain drug therapy for depression
anti-depressants specifically SSRI’s which are a tablet that stop the reuptake of serotonin so the post synaptic can absorb increased amounts of serotonin to improve the individuals mood.
explain drug therapy for schizophrenia
anti-psychotics specifically atypical which treat both negative and positive symptoms by giving a tablet which blocks the D2 receptors so they don’t overstimulate the post-synaptic neurone reducing the amount of times an individual will experience
explain how electroconvulsive therapy works
treat depression by patients going to the hospital to have electrodes placed either bilaterally on both temples or unilaterally on one temple. small waves of electricity will pass through the brain giving the patients a small seizure to reline their brain waves as depression is said to be caused by low level of serotonin as it is being reuptake, so waves stimulate serotonin, leading to increased mood.
what are some strengths and weaknesses of electroconvulsive therapy
+- instant- good for people at high risk
-standardised procedure- trained to administer in the same way
- give consent - but can they give consent when their at high risk? are they good head space?
– have to go out to hospital
- risky side effects- distress
- is it open to everyone (epilepsy- as it gives people a seizure)
