Lecture notes for Schizophrenia lecture in Neuroscience and Behaviour module (C82NAB)
First class
With three pages of extra reading / research
Includes information on symptoms, causes, neurotransmitters, genetics and treatment.
C82NAB: Schizophrenia
Kraeplin (1898) found SZ was a progressive disorder like dementia. Kraeplin was the first to
combine into a single disease with early adult onset (“Praecox”). “Dementia Praecox”
Bleuler (1908) termed Schizophrenia – “split mind”. Characterised fragmented thinking.
“disturbances of association are the primary symptoms of SZ.”
Schneider (1959) first ranked symptoms.
Peak at adolescence, further peak in females at menopause.
Symptoms
Tim Crow(1980) talked about SZ having positive and negative symptoms.
Type 1 – Positive Symptoms
Type 2 – Negative Symptoms
The positive symptoms are more easily dealt with and controlled by medication.
Anhedonia = inability to feel pleasure
Alogia = unable to speak.
Avolition = unable to begin tasks, lack of motivation.
Peter Liddle (1987) rethought the positive and negative dichotomy, studied 40 SZ patients and
found 3rd element – “disorganisation syndrome” – found different blood flow in association cortex in
positive/negative/disorganisation symptoms.
Later Liddle (2002) added Psychomotor excitation and anxiety/depression.
BRAIN CHANGES
STRUCTURAL CHANGES – enlarged ventricles, gray matter volume losses, minor physical
abnormalities, eye movement control problems.
Gray matter deficits: early and late, dorsal lateral prefrontal cortex (planning, working memory)
Ventricle size: large range in chronic SZ, in general SZ larger than controls. Large ventricles are
not specific to SZ, but also seen in Parkinson’s for example.
Gradual decrease in gray matter with age is normal, but slope is much faster in SZ and occurs at
an earlier age.
Schizophrenics have a different ability to track movement – more irregular eye movements.
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