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schizophrenia Flashcards

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1
Q

what is schizophrenia who created the term and when

A

Eugen Bleuler in 1908. ‘the term schizophrenia refers to a break from reality’

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2
Q

how much of worlds population is effected by schizophrenia

A

1%

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3
Q

what did Insel say about schizophrenia and when

A

in 2010, ‘a collection of signs and symptoms of unknown aetiology (cause)’

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4
Q

what are the three MAIN symptoms of schizophrenia

A

positive, negative and cognitive

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5
Q

how do the symptoms of schizophrenia work, what time period, what age

A

appears gradually over 3-5 years in early adulthood. negative symptoms are usually the first to emerge follow d by cognitive symptoms, the positive symptoms emerge last

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6
Q

positive symptoms

A

includes thought disorders, delusions and hallucinations.

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7
Q

what are the 3 different types of delusions

A

persecution - false beliefs that others are plotting and conspiring against onself
grandeur - false beliefs about ones power and importance
control - related to persecution, person believed they are being controlled by someone else

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8
Q

what are hallucinations

A

perceptions of stimuli that aren’t actually present

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9
Q

what are the negative symptoms

A

flattened emotional response, lack of initiative, anhedonia, social withdrawal

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10
Q

what are some of the cognitive symptoms

A

difficulty sustaining attention, low psychomotor speed (ability to rapidly perform fluent movements of fingers and hands)

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11
Q

what are neurocognitive deficits associated with Schizophrenia. who suggested it

A

the hypofunction of the frontal lobe. Weinberger 1988

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12
Q

how do people with schizophrenia perform on stoop task. And Wisconsin card sort test

A

schizophrenics are usually slower and less accurate. in non-schizophrenic there is an increase in retinal blood flow to PFC (FMRI)

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13
Q

what are sensory-motor-gating deficits. who studied in 1987

A

a phenomenon in which the brain shows reduced evoked response to repeated stimuli. Freedman did a study were schizophrenic patients experience no change to stimuli compared to normal pps

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14
Q

how is oculomotor function affected by schizophrenia

A

the eye movement of schizophrenics is not smooth compared to control patients

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15
Q

what are the structural differences in schizophrenic patients. who studied it

A

Weinberger and Wyatt 1982, CT scans of 80 schizophrenics and 66 healthy controls of same age (29) measured lateral ventricles of pps and schizophrenics had 2x the size but they also had reduced grey matter in temporal/frontal lobes and hippocampus.

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16
Q

how do genes and heritability effect SH

A

adoption and twin studies suggest SH is heritable although it is not due to a singular gene. you can have a ‘SH gene’ that makes you more susceptible and can be triggered by environmental factors

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17
Q

the mutation of what gene is thought to increase likelihood of SH. what is it involved in

A

DISC1 gene and its presence appears to increase chances by factor of 50. involved in regulation of neurogenesis and neuronal migration

18
Q

how does parental age affect schizophrenia and why

A

children of older fathers more likely to develop SH. due to mutations in spermatocytes due to them dividing up to 540 times by the age of 35.

19
Q

what have twin studies found. by who?

A

MZ twins especially those that were monochorionic (shared same placenta) are found to around double the chance of developing SH (60%). Davis & Phelps 1995

20
Q

name the 3 neurodevelopmental theories of SH

A
  1. the early neurodevelopment theory 2. the late neurodevelopment model. 3. the two-hit model
21
Q

what is the early neurodevelopment model. who suggested it

A

events in early life (prenatal) cause deviations from normal neurodevelopment and these lie dormant until brain matures. early life events e.g. infections, obstetric complications. Murray & Lewis 1987

22
Q

explain the late neurodveleopment theory. who suggested it?

A

SH may rest from an abnormality or deviation in adolescent when synaptic pruning takes place. Feinberg 1982;1983

23
Q

Explain the ‘two-hit’ Model. who suggested it

A

atypical development in SH takes place during 2 critical time points early brain dev and adolescence. early dev insults may lead to dysfunction to neural networks. then during adolescence excessive synaptic prying and loss of plasticity may account for emergence of symptoms. Fatemi & Folsom 2009

24
Q

explain the dopamine hypothesis (DA)

A

proposes SH caused by abnormalities in DA. overactivity of DA in mesolimbic system results in positive symptoms of SH. underactivity of DA in mesocortical system results in negative and cognitive symptoms of SH.

25
Q

what is some evidence to support DA hypothesis in terms of agonists

A

DA agonists produce symptoms that resemble positive symptoms of SH. Eg. drugs like cocaine and amphetamine. symptoms caused by those drugs can be alleviated by anti-psychotic drugs. therefore so can SH

26
Q

what was the first anti-psychotic who discovered it

A

Henri Laborit surgeon who discovered drug called Chlorpromazine (CPZ) developed in 1952. it is a DA antagonist (substance that inhibits the physiological action of smiths else)

27
Q

what are the major families of DA receptors

A

D1 type family and D2 type family

28
Q

what is IBZM

A

lodobenzamine. it is a D2 receptor reversible ligand meaning it will compete with DA for binding to that receptor

29
Q

evaluate with ‘typical’ antipsychotics

A

they eliminate/diminish positive symptoms. 20-30% don’t respond though. however long-term treatment can lead to symptoms resembling Parkinson’s. and around 1/3 patients may suffer from Tardive Dyskinesia - unable to stop moving

30
Q

what can be used instead of typical antipsychotic drugs is it better?

A

atypical antipsychotics. e.g. clozapine. improves both positive and negative symptoms of SH and doesn’t novel the Parkinson like symptoms due to if not havnig an affinity for D2 receptors

31
Q

what is clozapine. side effects?

A

a atypical antipsychotic. has lower affinity for D2 receptor and higher affinity’s for D3,D4. it is the only antipsychotic to reduce suicide rates in SH. can lead to weight gain, tachycardia and hypotension

32
Q

what are the problems with the DA hypothesis

A

only explains part of SH (positive not negative symptoms) atypical antipsychotics are better than typical antipsychotics.

33
Q

what is glutamate

A

is the ‘king’ of neurotransmitters. its a major excitatory neurotransmitter. nearly 50% of neurones in brain use glutamate as their neurotransmitter. glutamate is balanced with GABA

34
Q

what is an NMDA receptor

A

is an ionotropic receptor and a glutamate subtype. at rest it is blocked by Mg2+ when it opens it allows for Ca2+ influx

35
Q

how does glutamate specifically NMDA hypofunction affect us. whats the evidence?

A

schizophrenia can be due to NMDA hypofunction. NMDA is a subtype of glutamate receptor. evidence: drug: PCP or ket are NMDA antagonists and both of them cause positive and negative symptoms of SH whereas Glutamate agonists relieve both positive and negative symptoms

36
Q

how does PCP & ket affect us. what did Jentsch 1997 find.

A

PCP & Ket cause negative cognitive symptoms due do decrease in metabolic activity of frontal lobes. study: administered PCP to monkeys found control monkeys were fine but PCP monkeys showed severe deficit in reaching task

37
Q

what is the theory of microglia being involved in the development of schizophrenia

A

microglia are immune cells of CNS. ppl with SH are thought to have hyperactive microglia these symptoms are reduced with antipsychotics or treatment with antibiotics that reduce microglial activation.

38
Q

Which chromosome is associated with the development of schizophrenia

A

chromosome 6

39
Q

what are microglia used for

A

works within the immune system but also involved in neuronal cell death and survival, synaptogenesis and synaptic pruning

40
Q

how does delayed microglial activation work

A

microglial activation isn’t instantaneous in response to infection. Microglia grow steadily thru life reaching peak In late adolescence & early adulthood. so pre/perinatal infection can prime microglia to induce long lasting changes which can lead to behavioural impairment later on in life

41
Q

what is oestrogen’s role in schizophrenia

A

oestrogen seems to play a protective role in development of schizophrenia (buffers it). If women do develop schizophrenia then their symptoms are less severe

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