schizophrenia Flashcards
what is schizophrenia who created the term and when
Eugen Bleuler in 1908. ‘the term schizophrenia refers to a break from reality’
how much of worlds population is effected by schizophrenia
1%
what did Insel say about schizophrenia and when
in 2010, ‘a collection of signs and symptoms of unknown aetiology (cause)’
what are the three MAIN symptoms of schizophrenia
positive, negative and cognitive
how do the symptoms of schizophrenia work, what time period, what age
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
positive symptoms
includes thought disorders, delusions and hallucinations.
what are the 3 different types of delusions
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
what are hallucinations
perceptions of stimuli that aren’t actually present
what are the negative symptoms
flattened emotional response, lack of initiative, anhedonia, social withdrawal
what are some of the cognitive symptoms
difficulty sustaining attention, low psychomotor speed (ability to rapidly perform fluent movements of fingers and hands)
what are neurocognitive deficits associated with Schizophrenia. who suggested it
the hypofunction of the frontal lobe. Weinberger 1988
how do people with schizophrenia perform on stoop task. And Wisconsin card sort test
schizophrenics are usually slower and less accurate. in non-schizophrenic there is an increase in retinal blood flow to PFC (FMRI)
what are sensory-motor-gating deficits. who studied in 1987
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
how is oculomotor function affected by schizophrenia
the eye movement of schizophrenics is not smooth compared to control patients
what are the structural differences in schizophrenic patients. who studied it
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.
how do genes and heritability effect SH
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
the mutation of what gene is thought to increase likelihood of SH. what is it involved in
DISC1 gene and its presence appears to increase chances by factor of 50. involved in regulation of neurogenesis and neuronal migration
how does parental age affect schizophrenia and why
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.
what have twin studies found. by who?
MZ twins especially those that were monochorionic (shared same placenta) are found to around double the chance of developing SH (60%). Davis & Phelps 1995
name the 3 neurodevelopmental theories of SH
- the early neurodevelopment theory 2. the late neurodevelopment model. 3. the two-hit model
what is the early neurodevelopment model. who suggested it
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
explain the late neurodveleopment theory. who suggested it?
SH may rest from an abnormality or deviation in adolescent when synaptic pruning takes place. Feinberg 1982;1983
Explain the ‘two-hit’ Model. who suggested it
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
explain the dopamine hypothesis (DA)
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.
