Schizophrenia Flashcards
When is the common onset of Schizophrenia?
- Late adolescence
- Early adulthood
(acute onset over 2 - 3 weeks)
What is the median age of onset?
Median age of onset:
M: 23 years
F: 28 years
Is there a greater prevalence of Schizophrenia in one gender? Why could this be so?
- More prevalent in males than females
- Oestrogen has a role in regulating dopamine receptor sensitivity, hence increased prevalence in males.
What is the environmental aetiology (cause) of Schizophrenia?
- Males in urban areas are prone to schizophrenia
- More prevalent in countries further from equator (cold weather; affects mothers e.g. viral infection, affects foetus)
- Perinatal complications: severe malnutrition, exposure to stressful events, birth complications, altered brain development in early life
- Early cannabis use
- Advancing paternal age; germ cell (sperm) mutations increase risk of Schizophrenia in child.
What is the genetic aetiology of Schizophrenia?
- Family history
- Twin studies validates a genetic contribution; 50% chance other monozygotic twin has it if the other does
Susceptibility genes
- Neuregulin & Dysbindin
- Influence neurodevelopment and synaptic functioning
- Can lead to Schizophrenia
What are the positive symptoms of Schizophrenia? How do they present?
Acute presentation:
- Thought insertion
- 3rd person auditory hallucinations
- Thought disorder (e.g. cutting out mid-sentence, not knowing what’s happened after)
- Delusional perception
Duration criteria:
- Symptoms persist for > 1 month
What are the exclusion criterion for positive symptom presentation of Schizophrenia?
- Not secondary to mood disorder (exclude bipolar disorder e.g. ramblings)
- No organic disease
What are the negative symptoms of Schizophrenia? How do they present?
Chronic presentation: - Flattened mood - Indifference and loss of drive - Social isolation >>> (Similar to depression) - Poor self-care - Poverty of speech
Negative symptoms are relatively nonspecific; could be passed off as ‘teenage years’ etc.
What else presents for Schizophrenia apart from positive and negative symptoms?
Cognitive impairment:
- Affects attention, working and semantic memory (long-term memory not drawn from personal experience)
- Link to dementia in elderly schizophrenic patients?
Define: working memory.
Working memory (can affect academia):
- Temporary storage and manipulation of information
- Necessary for tasks such as language comprehension, learning and reasoning
Define: semantic memory.
- Long term memory that processes ideas and concepts
- Inclusive of common knowledge: colours, sounds of letters etc.
What sub syndromes of Schizophrenia are there?
- Paranoid schizophrenia
- Disorganised schizophrenia
- Catatonic schizophrenia
What is paranoid schizophrenia?
Auditory delusions and hallucinations
What is disorganised schizophrenia?
- Thought disorder
- Odd behaviour
- Inappropriate mood
What is catatonic schizophrenia?
- Due to treatment of the condition (schizophrenia)
- Rare form
- Debilitating condition
Symptoms:
- Unable to move or speak
- Person stares
- Holds body rigidly
- Unaware of surroundings
How is schizophrenia diagnosed?
One or more of (if clear cut:
- Delusions
- Hallucinations
Two of:
- Delusions
- Hallucinations
- Disorganised speech
- Catatonic behaviour
- Negative symptoms; flattened mood, inability to speak, general lack of drive
What is the dopamine theory of schizophrenia origin?
- Excess dopamine
- Excess dopamine receptors
(Parkinson’s = opposite; depletion of DA)
What is the evidence to support the dopamine theory of schizophrenia?
- Antipsychotic drugs = D2 receptor antagonists (too much DA)
- DA agonists such as amphetamines, levodopa cause paranoid psychosis
- CSF and brain studies of patients; abnormal levels of DA, its metabolites, enzymes or receptors
What is the evidence that DA is not the sole contributor to schizophrenia?
- DA changes Glu transmission downstream
- Signalling via NMDA is implicated
- NMDA receptor antagonists e.g. ketamine, phencyclidine (PCP) produce schizophrenia-like syndrome
- Thus depletion of Glu = schizophrenia symptoms
What other theories aside from the DA/Glu theory are there for the cause of schizophrenia?
Functional imaging studies:
- Abnormalities in cerebral blood flow and metabolism - impairment of neuronal circuits
- Specific impairment in frontal cortex, hippocampus, thalamus and cerebellum (hence delusions)
Structural brain changes:
- Enlargement of lateral ventricles
- Slight decrease in size of brain
- Histology; altered neuronal and synaptic organisation, affected white matter, no gliosis (absence of neurodegenerative process) THUS
»> schizophrenia = neurodevelopmental, not neurodegenerative.
What is the management strategy for schizophrenia?
Based on stage of illness: Intervention: - Physical (pharmacological therapy) - Psychological - Social (family, care home)
Initial assessment:
- Compulsory admission required (upon initial psychiatric event)
- Drug free if possible; might have to give benzodiazepine to calm them down
How is schizophrenia managed? How long do antipsychotics take to take effect? What do they combat?
- Antipsychotics effective against most positive symptoms
- Gradual onset of therapeutic effect (2-3 weeks(
- Investigate context; substance misuse (cannabis) may contravene treatment
- Family support is key
»> Early intervention; CBT, antipsychotics
What is the mechanism of action for antipsychotics?
- Inhibit D2 receptors
- Reverse excess DA activity in mesolimbic system; site for psychosis symptoms
How long is antipsychotic treatment continued for after initial psychosis? How does treatment change over time?
- 12-24 months; after ONE single episode.
- Tail off medication if improvement noted; tardive dyskinesia and other S/Es.
