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Clinical Neuroscience > Schizophrenia > Flashcards

Schizophrenia Flashcards

1
Q

What is commonly found in tissues in AD, huntington’s and a hallmark of neurodegenesis BUT absent in SCZ patients?

A

Gliosis - scarring of tissues (like a scar after injury)

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2
Q

Factors affecting SCZ

A
  1. Genes
  2. Nutrition (famine)
  3. Environment
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3
Q

Features of SCZ (dead) patients (7 points)

A
  1. Reduced Neurophil hypothesis : neurons density increase and tighter packing - due to less cell size and branching and therefore takes up less space -> loss of connectivity richness
  2. Absence of gliosis
  3. DECREASE in gray matter (with enlarged ventricles)
  4. Impaired frontal lobe
  5. DECREASE in oligodendrocytes
  6. Deficiency of GAD (of interneurons) -> less ability to express the genes -> affecting memory and coordination of PFC
  7. Arcuate Fasciculus (connection between auditory and frontal corext) is problematic

IN GENERAL ENTIRE CORTEX AFFECTED

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4
Q

When is the usual onset of SCZ?

A

late adolescence or early adulthood

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5
Q

What is the best predictor of long term outcome for SCZ?

A

Cognitive impairment

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6
Q

Which symptoms must persist for at least one month for diagnosis?

A

Delusions, hallucinations, disorganised speech (other symptoms like disorganized behaviour and negative symptoms must be briefly present for 6 months)

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7
Q

When does negative symptoms usually occur for SCZ?

A

Stable phase (last stage)

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8
Q

What are the phases for SCZ?

A

Premorbid -> prodromal -> psychotic -> Stable phase

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9
Q

There is symptomtoic and genetic overlap for which diseases?

A
  1. Affective (bipolar, MDD)

2. Neurocognitive (autism spectrum disorder)

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10
Q

SCZ - dimensional or categorical approach to diagnosis?

A

Dimensional - varying degrees of impairment (metaphor like a light switch, dim , dimmer, super dim etc)
Categorical - very seperate and distinct(e.g. pregnancy)

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11
Q

DRUGS may alter the brain and mimic mental disorder including SCZ (e.g. amphetamines/cocaine/ketamine)

A

NIL

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12
Q

What is dementia praecox? Who was the one who thought that SCZ is dementia praecox?

A

Emil Kraeplin, premature aging

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13
Q

What is the lifetime prevalance of SCZ?

A

1%

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14
Q

Sex differences in SCZ?

A

Onset for female compared to males 5 years later. Men more severe and greater negative symptoms

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15
Q

Risk factors (early childhood) for SCZ?

A
  1. Increasing age of dad
  2. maternal infectoins
  3. obsteric complications
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16
Q

Why is misdiagnosis of SCZ common?

A

Cos its a heterogenous problem

17
Q

Psychosis may not lead to SCZ (end up bipolar etc)

A

NIL

18
Q

Infection of TOXOPLASMA GONDII increase risk of SCZ 2-8 folds. Associated with bipolar, suicide, addition, depression.

A

NIL

19
Q

What is the major risk factor for SCZ?

A

Genetics (heritability 80%)

20
Q

What is two(or multi) hit hypothesis?

A

Combi of genes and env to cause SCZ

21
Q

SCZ and neurotransmitters (name and describe).

A
  1. Dopamine antagonist ( induce positive symptoms)
    2 Glutamate antagonist (induce all core symptoms)
  2. Dysfunction of GABA
  3. D2 receptors (all anti-psychotic drugs block this)
22
Q

Name positive, negative and cognitive symptoms for SCZ.

A

Positive: hallucinations, delusions
negative: amotivation, affective flatening
Cognitive: motor dys, improvised speech and language , executive functioning decline

23
Q

What are anti-psycho drugs used for?

A

SCZ, schizo-affective, dementia, delusional disorder, affective disorders.

24
Q

What are the treatments for positive symptoms?

A
  1. Antipsychotic med (1st gen med)
  2. Electroconvulsive therapy
  3. repetitive transcranial magnetic stimulation (rTMS)
25
Q

What are the treatments for negative symptoms?

A
  1. Clozapine (2nd gen med)
  2. Psychosocial interaction
  3. CBT
  4. Family therapy, social skills training
26
Q

What are the treatments for neurocognitive symptoms?

A
  1. rTMS
  2. Vocational training
  3. Cognitive remediation therapy
27
Q

What is one of the side effects of first gen med and 2nd gen med targeting D2 receptors?

A

Tardive Dyskinesia (jerky movement of face and body that u can’t control)

28
Q

Features of Clozapine.

A
  1. High affinity of 5HT (serotonin) receptors and low affinity for dopamine (weakly blocks D2)
  2. effective for patients resistant to treatment
  3. may help in negative symptoms
  4. causes weight gain
  5. causes low blood cell count (agranulocytosis)
29
Q

When is electroconvulsive therapy used (ect)?

A
  1. highly effective for positive symptoms
  2. For patients resistant to treatments (at least 2 failed treatments)
  3. Treating catatonic symptoms
  4. some effectiveness for negative symptoms
  5. causes retrograde amnesia
  6. can be good for depression in short term.
  7. Difficult to target which part of brain for treatment (usually DLPFC)
30
Q

When is Repetitive Transcranial Magnetic stimulation used?

A
  1. For negative and cognitive symptoms
  2. For patients resistant to treatments (at least 2 failed treatments)
  3. Not so effective like ECT
  4. No amnesia
    BETTER FOR DEPRESSIOn
31
Q

SCZ - results from too much Dopamine

A

NIL

32
Q

Overall side effects of drugs on SCZ?

A
  1. Block D2 but also block HT receptors

2. Symptoms suchs as: neuroleptic maglinant syndrome, fatty liver, sexual dysfunction, QT elongation

33
Q

SCZ with autism -> rep rare highly penetrant mutants (v diff to detect)
SCZ with bipolar / MDD -> common
SEE LECTURE SLIDES

A

NIL

34
Q

What is hypofrontality?

A

Cognitive impairment affecting frontal cortex

35
Q

Name one protein that is reduced in the brain of SCZ. What does it usually do?

A
  1. Reelin (Reelin DNA are more methylated)

2. Crucial for neuronal migration, axonal braching

Clinical Neuroscience (4 decks)

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