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Brain and Behaviour Year 2 > Schizophrenia > Flashcards

Schizophrenia Flashcards

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1
Q

what is the definition of schizophrenia

A
  • Schizophrenia is a chronic mental disorder characterised by a triad of core symptoms
  • These are positive, negative and cognitive
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2
Q

What is the onset of schizophrenia

A
  • Tends to emerge between ages of 16 and 30, women tend to have a later onset
  • Persists throughout a patient’s lifetime
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3
Q

what are the three types of symptoms in schizophrenia

A
  • positive
  • negative
  • cognitive
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4
Q

describe examples of the three types of symptoms in schizophrenia

A

Positive symptoms
- Hallucinations, delusions, agitations, disorganised thinking = gain of function
Negative symptoms
- Introversion, apathy, low self-esteem, personal neglect = loss of function
Cognitive symptoms
- Poor memory (working memory is particularly affected – e.g. remembering a sequence of instructions), attention deficit, executive dysfunction

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5
Q

How do you diagnose schizophrenia

A

• At least two of the following (per DSM-5):
o Delusions.
o Hallucinations.
o Disorganized Speech.
o Disorganized/catatonic behavior.
 Catatonic = a variety of abnormal motor postures.
o Negative symptoms (flat effect = inappropriate response, avolition = decreased motivation).
• At least one must be delusions, hallucinations or disorganized speech.

  • Continuous signs of disturbance must persist for 6 months, where the patients must experience at least 1 months of active symptoms with deterioration problems occurring over a significant time.
  • must be without substance misuse or mood disorder
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6
Q

define catatonic behaviour

A

= a variety of abnormal motor postures.

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7
Q

describe genetics and schizophrenia

A
  • not entire determined by genes
  • concordance rates occur higher in MZ twins
  • the more closely related you are to a patient with schizophrenia the more likely you are to have it
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8
Q

What is the biggest risk factor to do with schizophrenia

A

genetics

- having a close relativee with it

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9
Q

name some examples of genes that are associated with schizophrenia

A
  • Dysbindin: may affect D2 receptors levels/glutamate and GABA transmission
  • Neuregulin: neuroplasticity.
  • DISC 1: neurodevelopment and signalling in Corticolimbic areas.
  • DAOA: glutamatergic transmission
  • COMT: dopaminergic transmission.
  • BDNF: neurotrophic factor
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10
Q

there is a genetic continuum between….

A

There is a genetic continuum between protypical schizophrenia and protypical mood disorders.
- there is considerable overlap between typical schizophrenia and psychological mood disorder

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11
Q

what is the most important predictor of prognosis of someone with schizophrenia

A

cognitive dysfunction

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12
Q

How can you test for frontal cortical dysfunction

A

Wisconsin card sorting test

– patient won’t be able to adapt as they cannot focus, cant concentrate and cannot make decision in the change of rules

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13
Q

describe the structural changes that occur in schizophrenia

A
  • increased rate of grey matter loss this leads to larger ventricles and smaller medial temporal lobes
  • hypofrotnality - decreased frontal lobe activation during cognitive task
  • overal brain volume loss
  • when measuring event related potentials in schizophrenic patients the reaction to stimulation is increased
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14
Q

what happens to schizophrenic patients in terms of event related potentials

A
  • there reaction to stimulation is increased

- they have increased salience

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15
Q

what is the krapelinian definition of poor outcome for patients with schizophrenia

A
  • this is when the disease follows a progressive deteriorating course and is associated with poor outcome
  • this type of schizophrenia is a form of neurodegeneration
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16
Q

when does schizophrenia start

A

• Associated with decreased synaptic spines/decreased dendritic complexity in the cortex.
o This creates abnormalities in formation/maturation of brain circuits.

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17
Q

Name and describe some explanations for the psychotic symptoms of schizophrenia

A

Corticolimbic Circuits and Dopaminergic Systems
• Hypofrontality leads to excessive striatal dopamine release.

Altered brain Connectivity
• Mainly of the default brain network.
o Increased synchrony of DBN when subjects rest/allow mind to wander in SD.
 Possible explanation for psychotic symptoms.

18
Q

name some environmental reasons as to why schizophrenia can start

A
  • viral infections
  • cannabis use
  • drug abuse
  • increased maternal age
  • urban environment which is associated more with stress
  • winter birth
19
Q

when does schizophrenia start in the males versus in the females

A

starts mid 20s in males and later in females

20
Q

describe the link between synaptic maturation and the onset of schizophrenia

A
  • there is a critical time around the onset of schizophrenia where there is an change in the transcription of genes in the brain
  • this is called the transcriptome trajectory turning point
  • these genes that change at this time are associated with synapses and gives an indication that schizophrenia is linked to a deficit in the maturation of synapse
21
Q

describe how the dopaminergic pathway is associated with schizophrenia

A
  • hyperactivity in the mesolimbic pathway

- hypo activity int he mesocortical pathway

22
Q

what are the target of the main pharmacological drugs used to treat schizophrenia

A

dopamine D2 receptors

- drugs that act on dopamine D2 receptors are antagonists

23
Q

name some typical antipsychotics

A
  • Chlorpromazine – first neuroleptic
  • Thioridazine
  • Fluphenzine
  • Haloperidol
  • Flupenthizol
24
Q

How do typical antipsychotics work

A
  • Block dopamine receptors as well as acting as antagonists at other receptors (e.g. muscarinic cholinergic, histamine H1 and alpha2-adrenergic receptors).
  • Lack of selectivity of action
25
Q

what factor of typical antipsychotics can help schizophrenia in the community

A

• Some drugs can be given as depot slow release preparation (makes chronic SD manageable in community).
o Also, useful in non-compliance.

26
Q

name the adverse effects of typical antipsychotics

A 
•	More extrapyramidal effects vs atypical (normally reversible) *
o	Tardive dyskinesia
o	Dystonia
o	Parkinsonism
o	Bradykinesia
o	Tremor
  • Weight gain
  • Postural hypotension
  • Blurred vision
  • Dry mouth (muscarinic)
  • Hypothermia
  • QT interval prolongation
  • Sudden death
  • Hyperprolactinaemia
27
Q

why does hyperprolactinaemia occur

A

this is because dopamine usually inhibits the release of prolactin from the pituitary gland but cannot do this if it is inhibited

28
Q

Define and describe the symptoms of extrapyramidal side effects

A
  • Dystonia: continuous spasms and muscle contractions
  • Akathisia (restlessness)
  • Parkinsonism (rigidity)
  • Bradykinesia
29
Q

name some examples of atypical antipsychotics

A
  • Risperidone
  • Olanzapine
  • Clozapine
  • Quetiapine
  • Paliperidone
  • Aripiprazole
30
Q

describe the mechanism of action of atypical antipsychotics

A

• Acts as antagonists at D2 receptors as well as antagonists 5-HT2 receptors

31
Q

what Is the atypical antipsychotics clozapine used for

A

• Clozapine is used in patients that are drug resistant (30% of SD patients do not respond to treatment).

32
Q

describe the adverse effects of atypical antipsychotics

A
  • Less prone to give extrapyramidal effects.
  • Improve negative effects/cognitive dysfunction
  • Significant weight gain
  • Dyslipidaemia
  • T2D (insulin resistance)
33
Q

describe what is meant by tardive dyskinesia

A

involuntary movements of the lips, jaw, face; grimacing, constant chewing, tongue thrusting)

  • Associated mainly with typical antipsychotics, taken for longer than a few months/years
  • Often difficult to return to normal
34
Q

what is neuroleptic malignant syndrome

A 
•	Rare but potentially lethal complication.
•	It is a medical emergency
•	Characterized by:
o	Hyperpyrexia (high fever)
o	Tremor
35
Q

what antipsychotics can be used for slow release

A
  • fluphenazine and haloperidol can be offered in intramuscular infections for slow release
36
Q

what side effect can come with clozapine

A
  • There is a risk of agranulocytosis – therefore blood monitoring is essential
37
Q

what are the non pharmacological approaches to schizophrenia

A
  • CBT
  • Family therapy
  • These do not replace the pharmacological treatment
38
Q

what are the aims of treatment for schizophrenia

A

full symptom control, return to pre-morbid functioning, patient safety

39
Q

what is a new alternative treatment for schizophrenia

A

NMDA glutmate receptor

  • schizophrenia is associated with decreased glutmatergic transmission
  • therefore it may be possible to potentiate the activity of the NMDA glutmate receptor
  • Modulation of glutamatergic transmission based on metabotropic mGluR may have the potential to alleviate positive and negative symptoms
  • The reported effectiveness in the first trial was comparable to olanzapine, but with no weight gain, increased prolactin or extrapyramidal effects
40
Q

describe how schizophrenia is linked to inflammation

A
  • increased levels of cytokines during pregnancy can increase the risk of schizophrenia in the offspring
  • proinflammaotry cytokines are elevated in the pre-frontal cortex of SCH patients
  • increased loss of cortical grey matter in SCH patients with high levels of cytokines
  • • SCH patients with high levels of cytokines display signs of greater immune cell migration into the brain
    • Activated microglia are present in the brains of SCH patients within a few years of the disease onset
    • Might have an inflammatory status, cytokines in the blood are higher for inflammatory cytokines and in the post mortem there is activation of microglia, this is the state of neuroinflammation
41
Q

describe how schizophrenia is linked to white matter and myelination

A
  • Reduced oligodendrocyte density in SCH
  • Key molecules regulating myelination are differentially expressed in SCH (e.g. neuregulin 1)
  • Inflammation and immune activation may lead to oligodendrocyte damage

Brain and Behaviour Year 2 (36 decks)

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