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Biological Explanation of S.Z


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Auditory Hallucination
a symptom of S.Z in which one hears voices in their mind.
Cognitive Explanation of Delusions
the degree of conviction in the belief, and the extent of reoccupation with that belief. Strauss (1969)
Disordered Thinking
a symptom of S.Z in which one feels as though their thoughts have been inserted or withdrawn from their mind.
Control
a symptom of S.Z in which one experiences lack of self-control/ under the control of an alien power.
Emotional and Volitional Changes
a symptom of S.Z in which one has "flat" emotions/ little initiative/ no energy.
Wing (1992)
outlined a distinction between Primary Impairment and Secondary Impairment of S.Z.
Type I S.Z
Positive symptoms of S.Z/ Hallucination + Delusions/ Responsive to drugs/ Limbic abnormalities.
Type II S.Z
Negative symptoms of S.Z/ Less responsive to drugs/ Abnormalities in the Frontal Lobe and Enlarged ventricles.
Paranoid
Sub-type of Schizophrenia in the DSM/ Frequent auditory hallucination and preoccupation with delusions.
Catatonic
Sub-type of Schizophrenia in the DSM/ at least two of the following are present: immobility; excessive motor activity; extreme negativism; prominent mannerisms; ECHOLALIA or ECHOPRAXIA.
Disorganized
Sub-type of Schizophrenia in the DSM/ all are present: disorganised speech and behavior; flat affect.
Echolalia
repetition of a word or phrase.
Echopraxia
the repeating of gestures made by others.
Biological Explanations of S.Z
the approach sees mental disorders as having physical causes. Such as Brain abnormality or genetic.
1%
the risk of S.Z in the general population.
5.6% risk of S.Z (Gottesman and Shields 1982)
the lifetime risk of S.Z in Parents.
10.1% risk of S.Z (Gottesman and Shields 1982)
the lifetime risk of S.Z in Siblings.
12.9% risk of S.Z (Gottesman and Shields 1982)
the lifetime risk of S.Z in Siblings one parent with S.Z.
46.3% risk of S.Z (Gottesman and Shields 1982)
the lifetime risk of S.Z in Child with two parent with S.Z.
3.7% risk of S.Z (Gottesman and Shields 1982)
the lifetime risk of S.Z in Grandchildren.
Twin risk of S.Z 46% (Gottesman and Shields)
M.Z risk of S.Z
Twin risk of S.Z 14% (Gottesman and Shields 1982)
D.Z risk of S.Z
Heston (1966)
adoption study of 47 mothers, children adopted within days/ Result; 16% risk of S.Z in their children.
Lytton (1977)
suggested that M.Z twins are reared in a similar environment than D.Z, thus nurture could explain the higher concordance rate found for M.Z twins.
Dopamine hypothesis
S.Z is due to the increased level of the neurotransmitter Dopamine.
Pearlson et al (1993)
PET Scans Studies have reported a substantial increase in D2 receptors in the brains of people with S.Z.
Seeman et al (1993)
PET Scan Study that found six times the density of D4 receptors in patients with S.Z.
Neuroanatomical Explanation of S.Z
S.Z is due to Abnormal Brain structures.
Jernigan et al (1991)
Imaging studies showing that S.Z is due to the abnormalities in the Limbic System.
The Limbic System
A complex system of nerves and networks in the brain that controls the basic emotions and drives.
Nasrallah et al (1986)
study showing that the gender differences in the thickness of the Corpus Callusum in normal brains are reversed in S.Z patients.
Corpus Callusum
a broad band of nerve fibers joining the two hemispheres of the brain.
Abnormal Early Brain Development
S.Z may be due to prenatal abnormal brain development.
Raz and Raz (1990)
meta-analysis: studies comparing ventricular volume in people in people with S.Z and controls reported a significant increase in size in over half the samples and an overall effect size of 0.6.
Suddath et al (1990)
found that 14 out of 15 M.Z twins pairs (one of which had S.Z) had different brain structures, the one with S.Z had a smaller bilateral hippocampus then the other and had less brain tissue.
Lewis (1990)
meta-analysis in which he found no significant links between enlarged ventricles and negative symptoms associated with schizophrenia.