MEDI7111 Lecture Notes - Lecture 3: Fish Oil, Schizophreniform Disorder, Neuroimaging
Mental Health 3
Schizophrenia
Epidemiology
Schizophrenia has a lifetime prevalence of 0.6%, it is more common in males (1.4x) and has a modal
age of onset (M: 18-25yrs, F: 25-35yrs).
Aetiology & Risk Factors
The aetiology of schizophrenia is predominantly genetic predisposition with interplay of social and
environmental factors.
Risk Factors:
Family history of schizophrenia (massive heritable genetic component)
Cannabis use
oEspecially early/heavy use
oInteractions with COMT gene polymorphisms (up to 10% ↑risk)
Social adversity
Low social cohesion
Complications in pregnancy
oAbnormal fetal growth
oComplicated delivery
Birth in late winter (maternal vitamin D deficiency & URTI)
Offspring of migrants (combination of low vitamin D, low social cohesion & URTI)
Pathophysiology
The pathophysiological mechanism of schizophrenia is unknown. There are some studies which have
shown various random features of brain pathology in patients with schizophrenia, with a general
theme of pathology on the cellular level and smaller.
Generalised brain atrophy
oNot less cells – loss of extracellular matrix proteins & supports
oIncreased density of neurons in cortex
oLoss of dendritic and axonal branching
oCorrelated to disease severity
Altered receptors
oDopamine 2 receptor, glutamate receptor
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oMHC - ?is this an autoimmune condition
Neuroimaging findings
oOveractivity of the mesolimbic pathway is likely responsible for positive symptoms
oDysfunction of the mesocortical pathways are likely responsible for
negative/cognitive symptoms
The Dopamine Hypothesis
The positive pathology of schizophrenia (i.e. psychosis) is likely to be related to dopamine signalling.
This hypothesis is held because of the following:
Administration of stimulants (e.g. amphetamines, cocaine etc.) increases dopaminergic
activity and can cause a psychosis that resembles schizophrenia
Low doses of amphetamines can induce a psychotic reaction in schizophrenics in remission
Post synaptic DA receptor antagonism is where anti-psychotic medications target &
effectively stop psychotic symptoms
Limitations of this theory are related to the involvement of NMDA and serotonin in the process as
well as the partial effectiveness of dopamine only antagonism.
Clinical Features
Schizophrenia is defined as a severe and persistent heterogeneous syndrome caused by abnormal
brain information processing. The prodromal phase of the disease begins ~10 years before the onset
of the first psychotic episode. The clinical image of schizophrenia is comprised of positive psychotic
symptoms, negative symptoms and cognitive deficit with examples of these given below.
Positive Psychotic Symptoms Negative Symptoms Cognitive Symptoms
Hallucinations
-Perceptions which occur in the
absence of sensory stimulus
-Perceived like real sensations
(mostly auditory/visual)
Delusions
-False, unshakable beliefs
which are maintained despite
evidence to the contrary
-Out of keeping with prevailing
culture/religion
Thought disorder & disorganised
behaviour
-Inability to maintain a logical
conversation
- Amotivation
- Anhedonia
- Blunted affect (little
showing of emotions)
- Poor self-care
- Social withdrawal
Widespread cognitive deficit
- Working memory
- Executive function
- Impaired attention
*Cognitive symptoms are the
cause of severe disability
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find more resources at oneclass.com
Document Summary
Schizophrenia has a lifetime prevalence of 0. 6%, it is more common in males (1. 4x) and has a modal age of onset (m: 18-25yrs, f: 25-35yrs). The aetiology of schizophrenia is predominantly genetic predisposition with interplay of social and environmental factors. Family history of schizophrenia (massive heritable genetic component) Cannabis use: especially early/heavy use, interactions with comt gene polymorphisms (up to 10% risk) Complications in pregnancy: abnormal fetal growth, complicated delivery. Birth in late winter (maternal vitamin d deficiency & urti) Offspring of migrants (combination of low vitamin d, low social cohesion & urti) There are some studies which have shown various random features of brain pathology in patients with schizophrenia, with a general theme of pathology on the cellular level and smaller. Generalised brain atrophy: not less cells loss of extracellular matrix proteins & supports, increased density of neurons in cortex, loss of dendritic and axonal branching, correlated to disease severity.
