ICD ed. 10- Classifies it as having 2+ neg symptoms & recognises 3 Pos symptoms (extra experiences beyond u
subtypes: Paranoid (pos), Hebephrenic (neg), Catatonic (movement Hallucinations- Unusual sensory experienc
issues). DSM ed. 5- For diagnosis, 1+ pos symptoms are present related to environment) e.g. voices that tal
sufferer, distorted facial expressions. Delus
An effective diagnosis system must possess reliability (consistency
beliefs resistant to the truth e.g. being hist
between the psychiatrists rating patients) & validity (assesses
figure, persecuted by gov/aliens, under ext
what it claims to be). Key issues; Co morbidity- Occurrence of 2
illnesses together, confuses diagnosis & treatment. Symptom
overlap- When 2+ conds share symptoms, questions val Neg symptoms (loss of usual abilities & expe
Diagnosis & Avolition- Difficulty to begin or keep up w/ g
Serious condition that affects 1%, has a cluster of classification activity due to reduced motivation e.g. Andr
unrelated symptoms. Onset occurs in mid to late of schiz are (1982) poor hygiene & grooming, lack of
adolescence. Interferes w/ daily tasks, may end up homeless persistence in work. Speech Poverty- Reducti
or hospitalised. Type 1: Acute form- Pos symptoms & & quality of speech e.g. delayed verbal respo
response to meds. Type 2: Chronic type- Neg & unresponsive disorganisation (topic change mid sentence
Supported by research- Rosenhan (1973) asked Gender & cultural bias- M are more freq diagnosed than F due t
E
8 confeds to be pseudopatients in 12 hospitals better (able to work, manage family relations, mask symptoms
v
by complaining about hearing voices saying case). Afro Americans are more freq diagnosed in the west than
a
empty, hollow & thud. Once admitted, they origin (hearing voices can be seen as being connected to ancest
l
behaved normally yet staff diagnosed 11 w/ generalisability since others may not function in the same way-
u
schiz & 1 w/ bipoliar (detected the sane Co morbidity- A review found that ½ schiz patients also had a
a
behaviours as insane- decreases val of claim depression (50%) or substance abuse (47%)- decreases val &
t
about diagnoses since none of the patients met tools cant differentiate illnesses e.g. severe depression=schiz
i Symptom overlap- Both schiz & bipolar disorder involve pos
the criteria so the diagnostic tool was
o
unsuccessful- therefore… diagnostic tools of the delusions) & neg symptoms (e.g. avolition)- decreases val & r
n ICD might diagnose a patient as schiz but DSM might say bip
DSM/ICD are an effective classification of schiz
,Gottesman (1991) summarised 40 twin studies, found 2)Dop High levels or activity of dopamine (Hyperd
a concordance rate of 48% for MZ (identical) twins & amine the subcortex- Excess dopamine receptors
17% for DZ. Family studies- Found that both parents hypothesis (speech reproduction) may be linked w/ po
w/ schiz= 46% chance of developing it, 16% chance if & auditory hallucinations. Goldman Rakic (
1 parent has & 1% if no one has. Candidate genes- levels of dop (Hypodopaminergia) in the pr
Linked to risk of inheritance. Schiz is polygenic, Biological (decision making) plays a role in neg sympt
requires a no. of factors to work in combo not just 1 explanation
gene. It’s also aetiologically heterogenous, different for schiz 3)Neural Measurements of brains s
combo of factors can lead to it 1)Genetic correlates function that correlate w/
basis Motivation= Anticipation of reward & certain brain regions. Ju
Tiernari studied 112 adopted kids who’d been found Ventral Striatum activity & neg symptoms (e.g. avolition
separated from schiz mum & 135 who didn’t have correlated. Allen (2007) scanned schiz brains whilst spotting r
schiz mum. By adulthood, 10.3% of those w/ schiz as theirs or others, control group made less errors. Found Sup
mum developed it & 1.1% of those w/o Gryus and Anterior Cingulate & auditory hallucinations to be
1) Role of mutation- Brown (2002) found pos correlation 3) Only shows a correlation- There may be other fa
between paternal age (old=high risk of DNA mutation) & risk contributing w/ neural correlations in schiz sympto
E
of schiz, 0.7% w/ fathers under 25 & over 2% in over 50’s. be that neg symptoms cause less info to pass throu
v
Sper can mutate via radiation, poison or viral infections- (results in reduced activity), abnormal neural activi
a
increases val since schiz can take place in the absence of the initial trigger- decreases val since we can't infer
l
family history yet still be caused by genetics- therefore… effect so it doesn’t provide a complete explanation
u 1) Supported by research- Gottesman shows how 2) Contradictory research- Current research attention h
a genetic similarity and shared risk of schiz are related, the role of the neurotransmitter glutamate for causing
t Tiernari shows how kids of schiz sufferers are still at production isnt the only factor (Moghaddam & Jaitt, 20
i risk of schiz if adopted into families with no history of val of the claim about the importance of genetics/dopa
o it- increases val since genetic factors make some more activity since it doesn’t provide a complete (holistic) ex
n vulnerable to developing schiz than others- therefore… therefore… biology is an effective explanation of schizo
subtypes: Paranoid (pos), Hebephrenic (neg), Catatonic (movement Hallucinations- Unusual sensory experienc
issues). DSM ed. 5- For diagnosis, 1+ pos symptoms are present related to environment) e.g. voices that tal
sufferer, distorted facial expressions. Delus
An effective diagnosis system must possess reliability (consistency
beliefs resistant to the truth e.g. being hist
between the psychiatrists rating patients) & validity (assesses
figure, persecuted by gov/aliens, under ext
what it claims to be). Key issues; Co morbidity- Occurrence of 2
illnesses together, confuses diagnosis & treatment. Symptom
overlap- When 2+ conds share symptoms, questions val Neg symptoms (loss of usual abilities & expe
Diagnosis & Avolition- Difficulty to begin or keep up w/ g
Serious condition that affects 1%, has a cluster of classification activity due to reduced motivation e.g. Andr
unrelated symptoms. Onset occurs in mid to late of schiz are (1982) poor hygiene & grooming, lack of
adolescence. Interferes w/ daily tasks, may end up homeless persistence in work. Speech Poverty- Reducti
or hospitalised. Type 1: Acute form- Pos symptoms & & quality of speech e.g. delayed verbal respo
response to meds. Type 2: Chronic type- Neg & unresponsive disorganisation (topic change mid sentence
Supported by research- Rosenhan (1973) asked Gender & cultural bias- M are more freq diagnosed than F due t
E
8 confeds to be pseudopatients in 12 hospitals better (able to work, manage family relations, mask symptoms
v
by complaining about hearing voices saying case). Afro Americans are more freq diagnosed in the west than
a
empty, hollow & thud. Once admitted, they origin (hearing voices can be seen as being connected to ancest
l
behaved normally yet staff diagnosed 11 w/ generalisability since others may not function in the same way-
u
schiz & 1 w/ bipoliar (detected the sane Co morbidity- A review found that ½ schiz patients also had a
a
behaviours as insane- decreases val of claim depression (50%) or substance abuse (47%)- decreases val &
t
about diagnoses since none of the patients met tools cant differentiate illnesses e.g. severe depression=schiz
i Symptom overlap- Both schiz & bipolar disorder involve pos
the criteria so the diagnostic tool was
o
unsuccessful- therefore… diagnostic tools of the delusions) & neg symptoms (e.g. avolition)- decreases val & r
n ICD might diagnose a patient as schiz but DSM might say bip
DSM/ICD are an effective classification of schiz
,Gottesman (1991) summarised 40 twin studies, found 2)Dop High levels or activity of dopamine (Hyperd
a concordance rate of 48% for MZ (identical) twins & amine the subcortex- Excess dopamine receptors
17% for DZ. Family studies- Found that both parents hypothesis (speech reproduction) may be linked w/ po
w/ schiz= 46% chance of developing it, 16% chance if & auditory hallucinations. Goldman Rakic (
1 parent has & 1% if no one has. Candidate genes- levels of dop (Hypodopaminergia) in the pr
Linked to risk of inheritance. Schiz is polygenic, Biological (decision making) plays a role in neg sympt
requires a no. of factors to work in combo not just 1 explanation
gene. It’s also aetiologically heterogenous, different for schiz 3)Neural Measurements of brains s
combo of factors can lead to it 1)Genetic correlates function that correlate w/
basis Motivation= Anticipation of reward & certain brain regions. Ju
Tiernari studied 112 adopted kids who’d been found Ventral Striatum activity & neg symptoms (e.g. avolition
separated from schiz mum & 135 who didn’t have correlated. Allen (2007) scanned schiz brains whilst spotting r
schiz mum. By adulthood, 10.3% of those w/ schiz as theirs or others, control group made less errors. Found Sup
mum developed it & 1.1% of those w/o Gryus and Anterior Cingulate & auditory hallucinations to be
1) Role of mutation- Brown (2002) found pos correlation 3) Only shows a correlation- There may be other fa
between paternal age (old=high risk of DNA mutation) & risk contributing w/ neural correlations in schiz sympto
E
of schiz, 0.7% w/ fathers under 25 & over 2% in over 50’s. be that neg symptoms cause less info to pass throu
v
Sper can mutate via radiation, poison or viral infections- (results in reduced activity), abnormal neural activi
a
increases val since schiz can take place in the absence of the initial trigger- decreases val since we can't infer
l
family history yet still be caused by genetics- therefore… effect so it doesn’t provide a complete explanation
u 1) Supported by research- Gottesman shows how 2) Contradictory research- Current research attention h
a genetic similarity and shared risk of schiz are related, the role of the neurotransmitter glutamate for causing
t Tiernari shows how kids of schiz sufferers are still at production isnt the only factor (Moghaddam & Jaitt, 20
i risk of schiz if adopted into families with no history of val of the claim about the importance of genetics/dopa
o it- increases val since genetic factors make some more activity since it doesn’t provide a complete (holistic) ex
n vulnerable to developing schiz than others- therefore… therefore… biology is an effective explanation of schizo
