An Introduction to Schizophrenia Flashcards

1
Q

What does “Folie Circulaire” mean (Falvet, 1851)?

A

Cycling insanity

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2
Q

What term did Hecker coin in 1871, and what does it mean?

A

“hebephrenia”; a form of unusual and inappropriate youth.

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3
Q

Who combined the symptoms into a single disease?

A

Kraeplin (1878) was the first to describe Sz as a form of disease; “dementia Praecox”

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4
Q

In 1908, who defined schizophrenia as a split between affect and thought?

A

Bleuler

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5
Q

What did Schneider define in 1959?

A

First rank symptoms.

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6
Q

According to Kraeplin (1898), what is dementia praecox?

A

“Dementia” described the global disruption of perceptual and cognitive processes; “praecox” described the early adulthood onset. Kraeplin was the first to describe Sz as progressive, with no return to premorbid functioning.

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7
Q

What did Bleuler (1911) do?

A

He reformulated dementia praecox; coined the term Sz - “schizo” = split , “phrene” = mind. He characterised fragmented thinking as a breakdown of integrated functions that co-ordinate thought affect and behaviour.

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8
Q

Describe the positive vs negative dichotomy (Crow, 1980).

A

(Type I) Positive symptoms (symptoms which are present but shouldn’t be)
(Type II) Negative symptoms (symptoms which aren’t present, but should be)

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9
Q

What are positive symptoms of Sz?

A

Delusions, Hallucinations, Thought disorders

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10
Q

What are negative symptoms of Sz?

A

Anhedonia, flattened affect - limited range of emotions

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11
Q

Name some cognitive symptoms of Sz.

A

Avolition (lack of motivation), alogia (unable to speak), problems with working memory/planning/learning

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12
Q

What did Liddle (1987) do?

A

Re-examined the pos/neg dichotomy. Factor analytic study with 40 patients with chronic Sz. He confirmed the pos/neg dichotomy, but he also included a third factor called “disorganisation syndrome”, attributable to the positive dimension.

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13
Q

What syndrome categories did Liddle (1987, 2002) identify?

A

1) psychomotor poverty (poverty of speech/movement; blunted affect); 2) Reality distortion; 3) Disorganisation syndrome (inappropriate affect, thought disturbances). In 2002 Liddle added two more factors: 4) Psychomotor excitation; 5) Anxiety/depression

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14
Q

What did Fletcher & Frith (2009) do?

A

Gave examples of symptoms such as delusional perception, thought insertion. Just one symptom would be enough to diagnose a patient with Sz.

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15
Q

What did Weinberger find?

A

After MRI scans of discordant twins’ brains, a difference in ventricular size was found such that those with Sz have larger ventricles in the brain.

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16
Q

What is the percentage of concordance of developing Sz for identical twins?

17
Q

What did Ward find?

A

Lower activity in frontal cortex even when behaviour is comparable between patients and controls. Decreased brain activity in Sz subjects compared with normal controls in an fMRI study examining cognitive functioning.

18
Q

What approaches are there to investigating the neurochemistry of Sz?

A

Post mortem studies; peripheral markers; mechanism of action of antipsychotic drugs - animal and human studies; in vivo receptor binding (PET)

19
Q

Briefly, what is the dopamine hypothesis?

A

Sz results from overactivity in brain dopamine transmission. Hyperactivity in mesolimbic dopamine gives rise to positive symptoms, while hypoactivity in the frontal cortex results in negative symptoms.

20
Q

What is the effects of neuroleptics?

A

Clinical potency of effective neuroleptics parallels their pharmacological potency in blocking dopamine binding. Parkinsonian side-effects of neuroleptics; amphetamine which releases dopamine induces psychosis that responds to neuroleptics.

21
Q

What have receptor affinity studies found?

A

They have found increased D2 but not D1 receptors in the striatum.

22
Q

What did Seeman (1993) find?

A

6 fold elevation of D4 receptors. Yet other studies have found no D4 receptors - even in controls.

23
Q

What did Howes (2009) find?

A

Elevated striatal dopamine function linked to prodomal signs of Sz. There was a significant difference in Ki (influx rate constants) values at the group level for the whole striatum and for the associative striatum

24
Q

What have metabolite measurements (peripheral markers) found?

A

Brain DA turnover can be reflected by plasma Homovanillic acid concentrations. Chronic antipsychotic treatment lowers plasma HVA which relates to good treatment outcomes.

25
What have in vivo methods in animal studies found?
- Mesolimbic dopamine systems implicated in animal models of disrupted selective attention in Sz. - latent inhibition and pre-pulse inhibition found. - chronic neuroleptic decrease DA firing in A9(nucleus accumbenns) and A10 (striatum). - chronic atypical antipsychotics decrease firing in A10 only.
26
What have in vivo methods in patients found?
- In vivo measurement of D2 receptor affinity in humans using PET - Some studies find increase in D2 binding (Wong et al 1986) but no change found in other studies (Pilowsky, 1994) - possible reasons for discrepancies: specificity of ligands, patient populations
27
What role does glutamate play in Sz during treatment?
Drugs that block glutamate receptors such as PCP produce psychosis.
28
What role does serotonin play in Sz during treatment?
Atypical antipsychotic drugs have high affinity for 5-HT2 receptor. Could be via modulatory role on DA function, like that of GABA which plays a modulatory role on DA function.