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
Q

Bowie and colleagues (2014)

A
  • 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
Q

Researched into the efficacy of anti-psychotics and found most patients discontinued their assigned treatment due to side effects, inefficacy and other reasons (????)

A

(Lieberman et al., 2005)

27
Q

What is the synaptic pruning hypothesis?

A

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
Q

Nature (2014) conducted a GWAS

A

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
Q

Zuardi and colleagues (2012) conducted research into CBD

A
  • 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
Q
  • 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. (????)
A

(Senkowski & Gallinat, 2015)

31
Q
  • 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
A

(Rivolta et al., 2015)

32
Q
  • 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
A

(Tripathi et al., 2018)