Schizophrenia Flashcards
1
Q
What is Psychosis?
A
- loss of boundaries with reality and loss of insight
- delusions, hallucinations and conceptual disorganization is a primary feature in this illness also
- a psychotic episode is deemed to be a 1 week duration of either of these symptoms at a significant severity
- often associated with some behavioural disturbance
2
Q
What are delusions?
A
- Belief held firmly but on inadequate grounds, not affected by rational argument or evidence to the contrary, and not shared by someone of similar age, educational, cultural, religious or social background.
- Types of delusion include:
- primary (delusional perception), secondary, persecutory, -of reference, grandiose, -of guilt, nihilistic, -of passivity etc.
- maybe due to error of salience of attribution
3
Q
What are hallucinations?
A
- A perception experienced in the absence of an external stimulus.
- In any sensory modality but auditory hallucinations is the most common in psychosis
- maybe due to internal perception attribution error
4
Q
What is Conceptual disorganization?
A
- confused, disorganized and disconnected thought processes: demonstrated through speech
- aka Loosening of associations | Knight’s Move | Schizophrenic thought disorder | Disorder of form of thought | Formal thought disorder
- This should be rated on the basis of integration of the verbal products of the patient and not on the patients own subjective impression their level of function
5
Q
What are Schneider First Rank Symptoms for Schizophrenia? (1946)
A
- Auditory Hallucinations:
- Thoughts spoken aloud
- Third person hallucinations
- Running commentary
- Somatic hallucinations
- Thought insertion, withdrawal or broadcast
- Passivity phenomena. Made acts/ impulses/ affect
- Delusional perception
6
Q
What is the ICD 10 Diagnosis of Schizophrenia?
A
needs to have a minimum of a-d or two of e-h for at least 1 month al in the absence of an organic disorder
- a Thought echo, insertion, withdrawal or broadcast
- b Delusion of passivity or delusional perception
- c Running commentary hallucination or 2 voices discussing the patient
- d Persistent delusions of other kinds
- e Persistent hallucinations in any modality with accompanying brief delusions
- f Breaks in thought resulting in abnormal speech (eg. incoherent, neologisms)
- g Catatonic behaviour eg. Excitement, posturing, waxy flexibility, negativism
- h Negative symptoms not due to depression or medication
7
Q
What are potential Differential Diagnose instead of Schizophrenia
A
- Affective psychosis:
- Bipolar disorder
- Depressive psychosis
- Schizoaffective disorder
- Organic psychosis: (loads)
- Epilepsy (temporal lobe)
- Infections: encephalitis, SSP, neurosyphilis, HIV
- Cerebral trauma/ Cerebrovascular disease
- Dementias
- Acute drug intoxication
- Endocrine disorders/ Metabolic disorders
- Personality disorder
8
Q
Signs of Schizophrenia
A
- Bizzare appearance or behaviour
- ‘talking to themselves’
- self-neglect, clothing
- social disturbance, posturing, perplexity
- symptoms from schizophrenia medication
non are specific to schizophrenia, no predictive tests or imaging, genetics only tract to identify a vulnerability
9
Q
What are the side effects of Schizophrenia medication?
A
- Parkinsonian symptoms: tremor, rigidity, bradykinesia
- Tardive dyskinesias including orofacial, athetosis, dystonias
- Skin discolouration
- Severe weight gain
10
Q
What would a mental state examination find in an individual who had positive symptoms of Schizophrenia
- Appearance
- Mood
- Thinking/ perception
- Insight
- Cognition
A
- Appearance: Preoccupied and withdrawn to restless and unpredictable
- Mood: Blunting of mood, disinhibition, perplexed, anxious
-
Thinking/ Perception:
- Disorder of thinking: Vague, Formal thought disorder (loosening of associations) Disorders of stream (thought block)
- Delusions: Primary, secondary
- Hallucinations: Auditory, visual, tactile (somatic), olfactory, gustatory
- Insight: Impaired
- Cognition: Normal orientation and memory (initially)
11
Q
What would a mental state examination find in an individual who had chronic syndrome Schizophrenia (negative symptoms)
- Appearance
- Movement
- Mood
- Thinking/ perception
- Insight
- Cognition
A
- Appearance and behaviour: Lack of drive and activity, Social withdrawal, Self-neglect
- Movement: Stupor, Catatonia, abnormal movements and tone
- Mood: Blunting of mood, Depression
-
Thinking/ Perception:
- Delusions and Hallucinations as in acute syndrome but maybe less evident
- Insight: Impaired as in acute syndrome
- Cognition: Normal orientation. Disturbed attention. Later cognitive decline
12
Q
Go over the epidemiology and aetiology of Schizophrenia
A
- prevalence 0.2-0.7% of population
- increasing incidence in S London - 2/10000 a year
- incidence up to 5x variation worldwide
- more prevalent in urban areas and in lower social classes (social drift)
- earlier onset in men with more negative symptoms
- male peak onset: 21-26
- female peak onset 25:32
- there is an additive/ interactive effect between the multiple susceptibility genes and environmental factors
- genes involved overlap with autism and other neurodevelopment syndromes but activation at different ages presents different neuropathy
- increased likelihood if ScZ in the family
13
Q
What is the prognosis of Schizophrenia?
A
- 20% have a complete recovery and stop treatment LIne a
- 25% have persistent symptoms after first episode or what was originally described as ‘dementia praecox’. Line b
- >50% have a relapsing-remitting illness with some functional impairment between episodes. Line c
- progressive episodes may lead to progressive decoration
- functional recovery lags behind symptom recovery
- suicide in 5-10% particularly in men within 3 years of onset
14
Q
What would indicate a good Schizophrenia prognosis?
A
- Female
- Married
- Family history of affective disorder
- Good premorbid function
- Acute onset
- Life event at onset
- Early treatment
- Affective symptoms
- Good treatment response
15
Q
What would indicate a poor Schizophrenia prognosis?
A
- Male
- Single
- Family history of schizophrenia
- Premorbidly schizoid: (looner, cold, aloof)
- Slow onset
- Long duration untreated
- Negative symptoms
- Obsessions
- High Expressed Emotion in the family
- Substance misuse
17
Q
What are the neuropathological changes seen in Schizophrenia?
A
- Ventricular enlargement
- reduced brain volume (less grey matter)
- temporal lobes, frontal lobes, subcortical structures reduced
- Cytoarchitectural differences in cortex and hippocampus (different cell structures)
- Reduction in length of the Paracingulate sulcus
- associated with hallucinations
18
Q
What does the neurodevelopmental model of schizophrenia suggest?
A
- during adolescence, grey matter is lost which may speed up in early-onset schizophrenia
- age of the first admission is just after adolescence
- Grey matter loss occurs in the parietal, frontal and temporal lobe
- could be due to synaptic pruning or increase myelination
19
Q
The Wisconsin Card Sorting Task
- what does it show?
A
- when carrying out the task there is an increase in the dlPFC activity in healthy individuals, whereas this is absent
- shows that brain damage/ lesions in the frontal cortex impaired the planning, decision making and behavioural inhibition that is supposed to be carried out
- hence the behavioural changes in those with schizophrenia
21
Q
What neurophysiological changes are seen in the brain in Schizophrenia?
A
- Auditory cortex activation during hallucinations (fMRI)
- High-frequency oscillations and synchrony emerge during the transition from adolescence to adulthood.
- in ScZ patients, there is less activation in the neural oscillations and synchrony
- Hypofrontaility
- Hyper-excitbale sensory cortex
24
Q
Explain the Glutamate psychopharmacology behind ScZ
A
- PCP (phencyclidine, angel dust)
- Causes many positive, negative and cognitive symptoms of schizophrenia
- NMDA receptor antagonist
- N-methyl-D-aspartate receptors (NMDARs) are a subclass of glutamate receptors
- reduced NMDA receptor activity results in schizophrenic-like behaviour as seen in genetically modified mice with fewer NMDA receptors
- NMDA antagonism in PFC - less glutamatergic firing to VTA GABA neurons
- Less GABAergic inhibition of VTA-NAcc DA neurons –> Greater DA release in NAcc
- Less activation of VTA-PFC DA neurons - less Glu - hypofrontality
28
Q
What are the 3 main DA pathways in the brain?
A
