schizophrenia

Question 1

Symptoms

Answer 1

Positive: hallucinations, illusions (e.g., distorted visual input), delusions

Negative: Avolition (lack of motivation + apathy), anhedonia, flat effect (reduces emotional range and causes poverty of speech)

cognitive: decreased verbal fluency, problem solving, memory/learning, visual processing, and social cognition.

Often see a 20-30% IQ reduction

Question 2

Genetic Causes

Answer 2

10% risk with 1 parent, 50% with 2.

108 risk associated genomic loci are involved in schizophrenia. No 1 gene causes it, combination of several mutations. Likely has a neuroinflammation basis.

Question 3

Environmental causes and neurodevelopment hypothesis

Answer 3

Birth complications, viral infection, childhood trauma, substance abuse, urban living, social isolation.

Neurodevelopment hypothesis suggests combo of genetics and environment. Those at genetic risk, who are exposed to environmental triggers get the disease.

Question 4

Mechanisms and neurobiology of schizophrenia.

Answer 4

Hyperactivity in the mesolimbic tract mediates positive symptoms.

Hypoactivity in the mesocortical tract mediates negative symptoms.

Increased DA is seen in the association and reward regions of the striatum, likely leads to defective processing in the associative region of the striatum.

Sees increased DA release and D2 receptor density in schizophrenics.

Question 5

First gen (typical) antipsychotics

Answer 5

Chlorpromazine, trifluoperazine, haloperidol

First gen effectively treat positive symptoms, but can worsen negative ones. Mechanism is DA receptor antagonism. Commonly cause extrapyramidal side effects

Question 6

Examples of antipsychotics from 2 classes

Answer 6

clozapine, risperidone, aripiprazole

Second gen have less severe extrapyramidal side effects, and can also treat negative symptoms. Have a wide range of pharmacological mechanisms, e.g., D2, D1, 5-HT1/2, a1-AR, H1, M1

Question 7

Other hypotheses

Answer 7

Glutamate hypothesis suggests altered glutamine/glutamate metabolism, leading to lower glutamatergic signalling

Neuroinflammatoion suggests hieghtened microglial activation as a leading cause.

Likely to be multifactorial as opposed to only one hypothesis