T8: Schizophrenia Flashcards
Explain the classification systems of schizophrenia
- Schizophrenia is significant mental disorder- distorted perception, bouts of normal/abnormal, 1% population
- 4 subtypes
- Paranoid: delusion (greater self/ sense of being attacked)
- Cationic: muscle disturbances (random movement), motor disturbance
- Disorganised: withdrawal, can’t adapt, not very responsive, indifference/ flat
- Undifferentiated: mixture
- New model:
- T1: Positive (behaviour)- delusion
- T2: Negative: less emotion -> withdrawal
Symptoms of schizophrenia
- T1: positive (addition, not there typically)- Hallucination, delusion, disorganised speech/behaviour, disorganised thought pattern, beyond normal (FBI take you away)
- T2 negative (subtract emotion): disorganised thought pattern, no proper speech/thought/ sleep, no right conclusion or decision making, no proper memory (taken away from normal)
We tx + and - symptoms separately.
- 16 dancer, increased self conscious, more withdrawn, delusion people out to get her. Hospitalised for hallucination (voices), 45 (dinosaurs)
- Can cycle lucidity, understand not normal but cannot control, have to live with
Name disorder:
- Paranoid schizophrenia
Discuss the biological basis of schizophrenia:
- Brain Changes
- Frontal lobe: Small, less neurons (prefrontal cortex + thinner parahippocampal gyri), scattered pyramidal neurons (not organised) @ hippocampi
- Temporal lobe: Big lateral ventricles, Cortex in middle temporal area is thinned, weird dendrite shape @ dorsal prefrontal area + hippocampus
- Small level: Myelin sheath abnormal, neurons clustered, change in synapse + nt systems
- Less neurons and harder for info to transmit.
- DA Hypothesis & schizophrenia
- Associated schizophrenia with DA by looking at Amphetamines bc it induces psychotic episodes by flooding brain with DA -> releases DA-> psychotic episodes similar to Schizophrenia. Neuroleptics ,slop D2 receptors, reducing these episodes.
- Give DA block= effective
- Lots of receptor sites = more nt => psychosis (high catecholamine) + psychotic episode (high DA activated receptors)
- Glutamate hypothesis & schizophrenia
- Less NMDA receptors (due to phencyclidine -PCP- intoxication ) -> +/- symptoms
- Biochemical Changes in schizophrenia
- DA not broken down in CSF
- Higher D2 receptors in striatum
- High production of D3 & D4 mRNA in relevant cortex
- Less glutamate in cortex
- Less glu uptake in cingulate cortex
- Less mRNA to make GABA in prefrontal cortex
- More GABAA binding regions in cingulate cortex
Discuss and explain the utilization of conventional and atypical neuroleptics and their differences.
- Tx for drug & support psychosocial
- General neuroleptics (chlorpromazine & haloperidol) acts on D2 receptors
- Less +
- SE: blocks receptors @ striatum ~ parkinsons disease + rigidity, tremor, hard to move
- Chronic dose-> tardive dyskinesia, unexpected lip + jaw movements
-
Atypical neuroleptics (clozapine + risperidone)
- Less SE because doesn’t act striatums DA receptors
- More powerful against ( - ) symptoms
- Research: higher NMDA receptors + less D2 receptor activation = reduce symptoms
- Transcranial Magnetic Stim:
- Across scalp = magnetic field applied on local brain regions to stimulate deficits or excessive DA signalling areas.
- Targets:
- Frontal lobe: voice hallucination @ auditory cortex
- Prefrontal cortex= less negative symptoms
- ~20min TMS daily = less hallucination
What are the four main biological perspectives of schizophrenia discussed in the
1) Genetic Theory Evidence- methods to identify genetic component:
2) Environmental /life stress - poor maternal nutrition - difficult pregnancy - environmental stressors throughout life - drugs
3) Biochemical a. Protein abnormalities- Factor in blood serum of schizophrenics which disturbed neural functioning in the brain b. Transmethylation theory- methylated amines produced by body act as hallucinogens c. Influence of endorphins- Released from neurons in brain in response to Stress. Explains schizophrenic patients withdrawn behaviour. d. Dopamine Hypothesis- excessive dopamine receptors, excessive neurotransmitter produced, too many messages sent hence odd and peculiar behaviour. e. Glutamate Hypothesis- diminished activation of N-methyl-D-aspartate (NMDA) receptors (a type of glutamate receptor) in the brain
4) viral - e.g. syphillis involved
e symptoms of schizophrenia? Categorise into positive and negative symptoms.
Symptoms of Schizophrenia (Pinel, 2000)
*Bizarre delusions of being controlled, of being persecuted, of grandeur
*Inappropriate affect- failure to react with an appropriate level of emotionality to positive or negative events
*Hallucinations- imaginary voices telling the person what to do or commenting negatively *Incoherent thought- illogical thinking, peculiar associations, belief in supernatural forces *
*Odd behaviour- lack personal hygiene, avoid social interaction, talk in rhymes
Type I schizophrenia: characterized by positive symptoms: behavioural excesses such as: - delusions - hallucinations - disorganized speech - disorganized behaviour - agitated movement Likely to be due to a dopaminergic dysfunction.
Type II schizophrenia: characterized by negative symptoms: behavioural deficits: - reduced emotional expression - poverty of speech - difficulty in goal directed behaviour Associated with enlarged ventricles, cortical atrophy, particularly in the frontal cortex.
List some neuroanatomical correlates of schizophrenia apart from some already discussed
Even though results vary the following have been found:
Frontal lobes - Schizophrenic brains have smaller frontal lobes or at least a reduction in the number of neurons in the prefrontal cortex and thinner parahippocampal gyri. - Kovelman & Scheibel, 1984- orientation of pyramidal neurons in the hippocampi of schizophrenics are highly disorganised. Instead of the consistently parallel orientation of neurons in this region characteristic of normal brains, schizophrenic brains have a more haphazard organization.
Temporal lobe and speech areas and ventricles - Researchers have found abnormalities in the auditory regions of the temporal lobe and in Broca’s area among patients with auditory hallucinations (McGuire et al, 1993). - Structural abnormalities have been found in Wernicke’s area in patients with thought disorders (Shenton et al., 1992) - Schizophrenic brain generally has large ventricles and thinner cortex in the medial temporal regions and dendritic fields of cells in the dorsal prefrontal regions and hippocampus are abnormal (Cho Gilbert & Lewis, 2004). These regions are associated with memory. Deficit in verbal and spatial memory in schizophrenics is most likely to be correlated with these medial temporal abnormalities.
Discuss treatments for schizophrenia.
Drugs- that block the dopamine receptors. These agents (chlorpromazine) are called antipsychotics or neuroleptics- and act at D2 receptors. Antipsychotic drugs require several weeks to control the symptoms of schizophrenia and most patients require maintenance treatment for many years. Relapses common even in drug maintained patients. Neuroleptics also block dopamine receptors in the basal ganglia often producing movement disorders. Many neuroleptics also block muscarinic receptors (causing dry mouth, blurred vision and constipation), αadrenoceptors (postural hypotension) and histamine H1 receptors (sedation). Some newer drugs have a reduced tendency to cause movement disorders because they do not act directly on the dopamine receptors in the striatum e.g., clozapine, resperidone. Drug research: focus is the N-methyl-D- aspartate (NMDA) receptor. The hope is to increase NMDA receptor responsiveness, perhaps in combination with decreasing D2 receptor activation, will further alleviate symptoms of schizophrenia.
