ScZ Flashcards

ScZ revision

1
Q

What are the diagnostic symptoms of ScZ according to the DSM 5?

A

Two or more of the following, each present for much of the time during a one-month period (unless symptoms are remitted)

  • Delusions
  • Hallucinations
  • Disorganised Speech
  • Grossly disorganised behaviour
  • Negative Symptoms
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2
Q

What is the Etiology of ScZ (Sullivan, 2005)?

A
  • Social stressors in urban settings
  • Cannabis abuse
  • Miswiring of the brain during development
  • Perinatal hypoxia
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3
Q

What are the genetic risks (percentage) for ScZ?

A

Parents: 6%
Dizygotic twins: 17%
Monozygotic: 49%
non-twin siblings: 9%

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4
Q
  • ScZ patients have less synapses in cortical regions & enlarged ventricles
  • Cortical vol reduction is due to neuronal size and reduced neuropil
  • Pathophysiology reflects an abnormal activity in the PFC, hippocampus and subcortical structures. (????)
A

Harrison, (1999)

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5
Q

Severity of disease depends on age of onset (????)

A

Rajji and colleagues (2009)

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6
Q

What did Dierks and colleagues (1999) find?

A

fMRI study found

- BOLD singal in Herschls gyrus during auditory hallucinations

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7
Q

What did Chen and colleagues (2015) find?

A

Severity of auditory hallucinations was correlated with the degree of reduction in the right Herschls gyrus

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8
Q
  • deficits of white and gray matter in left MTL (LMTL) and left STG (LSTG)
  • other regions did tend to be implicated for ScZ
  • 2 key regions for structural differences in ScZ compared to HCs
  • suggests changes of gray matter in ScZ could be regionally specific (????)
A

Honea and colleagues (2005)

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9
Q
  • ScZ have significant gray matter volume loss in left STG
  • suggests that changes of gray matter in Scz could be regionally and temporally specific
  • but findings could be due to pharmacological and neuroradiological variables (e.g. anti-psychotics) (????)
A

(Vita et al., 2012)

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10
Q

Using a phenomenological approach and interviewing ScZ’s could give a deeper understanding into the experiences of symptoms in ScZ (????)

A

(Ulhaas et al., 2007)

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11
Q

Define cognitive deficits

A

Cognitive deficits is the dysfunction of connectivity and communication between areas of the brain.

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12
Q

Uhlhaas & Singer, (2010) review find?

A
  • Evidence suggests abnormalities in the synchronicity of oscillations may have central role in pathophysiology of ScZ
  • Oscillations are fundamental for temporal relationships between neuronal responses which is relevant for memory, perception and consciousness
  • beta and gamma frequency abnormalities are related to cog dysfunctions and core symptoms of ScZ
  • Developmentally oscillations are involved in maturation of cortical networks
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13
Q

Should we only focus on gamma/beta or alpha/theta bands or should we focus on the full spectrum and their potential dysfunctional interactions. (????)

A

Moran & Hong, (2011)

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14
Q

Found a reduction in fronto-temporal activity may contribute to the attribution of self-generated events and non-self generated events. (????)

A

(Ford et al., 2002)

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15
Q

What did Grent-‘t-Jong et al., (2016) find?

A

study measured high-frequency oscillations, using MEG (a robust and reliable tool) of 16 HC’s and 16 ScZ’s. They engaged in a visual task, and found whilst undertaking the task reduced gamma-band activity in ventral regions of the visual cortex.

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16
Q

Side effects of anti-psychotics

A

loss of brain tissue, weight gain, diabetes, blurred vision, constipation, sexual problems due to hormone changes and more. (rethink.org, 2019)

17
Q

Ho and colleagues (2011) conducted a longitudinal study with secondary data and found

A

that progressive brain vol changes in ScZ aren’t due to the disease but may be due to long-term antipsychotic use. And so would need to re assess the risk-benefit of anti-psychotic treatment in terms of duration and dosage.

18
Q
  • Clozapine is the only effective medication for treatment-resistant ScZ
  • Side effects of cardiometabolic dysfunction
  • small efficacy, but no first-line treatment suitable for all patients (????)
A

Lally and MacCabe (2015)

19
Q

ScZ affects 1% of world pop and leading cause of chronic disability in young adults (????)

A

Murray and colleagues (1996)

20
Q
  • Anti-psychotics have more efficacy for treating +ve symptoms but not -ve
  • Agents stimulating NMDARs have received attention but more clinical trials need to be researched
A

(Yang and Tsai, 2017)

21
Q

Cella and colleagues (2017) found

A

A small to moderate effect for Cognitive Remediation for negative symptoms, and negative symptoms were still reduced at follow-up.

22
Q

Wykes et al., (2011)

A

Cognitive remediation has desriable effects on global cognition and functioning, however symptom reduction was small.

23
Q

provides support for the hypothesis that hallucinations (positive symtoms) are related to cortical hyperexcitability. Which is manifested by an increase in gamma and beta band oscillations in modality-specific brain regions (????)

A

(Spencer et al., 2008)

24
Q

disorganization and negative symptoms have been related to both enhanced and reduced high-frequency oscillations (????;????)

A

(Spencer at al., 2004; Tillmann et al., 2008)

25
Bowie and colleagues (2014)
- examined the efficacy and effectiveness of cognitive remediation in early-course and long-term schizophrenia. - found CR treatment of cognitive impairments is feasible in both early-course and chronic schizophrenia - better for treating cognitive functions when delivered early - cognitive remediation should be considered a tool for early intervention in schizophrenia.
26
Researched into the efficacy of anti-psychotics and found most patients discontinued their assigned treatment due to side effects, inefficacy and other reasons (????)
(Lieberman et al., 2005)
27
What is the synaptic pruning hypothesis?
a big part of the reorganisaitn of the brain take place during adolescence. Improper synaptic pruning in this developmental period may lead to the onset of ScZ.
28
Nature (2014) conducted a GWAS
ScZ have a variation of C4 within chromosome 6. C4 is responsible for the development and synaptic pruning. Which gives evidence for the synaptic pruning hypothesis of ScZ.
29
Zuardi and colleagues (2012) conducted research into CBD
- found that CBD was as effective as an antipsychotic. | - suggests that CBD could be a therapeutic alternative for psychosis and idvs who have ScZ
30
- Impairments in working memory (WM) and other cognitive functions are cardinal neuropsychological symptoms in ScZ. The PFC is important for mediating and executing these functions. - the review suggests that abnormal prefrontal gamma band responses may contribute to WM and other cognitive deficits in ScZ. (????)
(Senkowski & Gallinat, 2015)
31
- Hypo functioning of NMDA receptor has been known to implicate the pathophysiology of ScZ. Tested effects of ketamine on rest state in heathy participants - Gamma power increased while beta band activity decreased (gamma power was within the thalamus, hippo, frontal and temporal cortex) Inhibition on NMDA-R = dysregulation of high-freq oscillations - Ketamine induced neuronal dysregulation in the thalamo-coritcol areas, which could give understand of ScZ as a disinhibition of neural circuits
(Rivolta et al., 2015)
32
- CRT is beneficial for chronic and severe ScZ Significant improvements in memory, attention, social cognition, independent living skills - Development of CRT is promising as pharmacological treatments fail to bring changes in cognition and socio-affective processing
(Tripathi et al., 2018)