Schizophrenia

Classification- process of organising symptoms into catagoriez based on which symptoms cluster together in sufferers

Positive symptoms- additional experiences beyond those of ordinary existance eg. hallucionations

• hallucinations, unusual sensory experiences 
• delusions, irrational beliefs
  

Negative symptoms- involves loss of usual experiences

• avolition, finding it difficult to begin or keep up with goal related activity. Reduced motivation to carry on (eg. poor hygiene, lack of persisitance in work or education and lack of energy)
• povery of speech, changes in patterns of speech, includes disorganisation through change of topic mid sentence

Evaluation

• Shows weakness in diagnosis through reliability, using intre-rater reliability shows the extent which assessors agree on their assessment. Used in diagnosis for the extent to which two or more health professionals arrive at the same diagnosis. Inter-rater reliability was shown to be poor where 2 psychiatrists independently diagnosed 100 patients using DSM criteria; one dianosed 26 with schizophrenia and the other diagnosed 13. 

• Validity is poor, one way to assess validity of diagnosis is criterion validity - do different assessment systems reach the same diagnosis for the same patient. Above research suggest one over-diagnosed or the other under-diagnosed.  Either way, this is poor validity.

• Co-morbility, The phenomenon where two or more conditions occur together. Schizophrenia is commonly diagnosed with other conditions such as depression and post traumatic stress disorder. This poses a challenge for both classification and diagnosis of schizophrenia.

Genetic basis of schizophrenia

• Schizophrenia runs in the family. It has been noted but this is quite weak evidence for a genetic link as family members share genes but also aspects of their environment.

• However, twin studies can illustrate the likelihood of genetics influencing schizophrenia as identical twin shares 100% of the same DNA. If your identical twin has schizophrenia, you have a 48% chance of developing it compared to fraternal twins - 17%.

• Candidate genes. Individual genes are believed to be associated with the risk of developing schizophrenia. Schizophrenia is polygenic - requires a number of factors to work in combination.

The dopamine hypothesis

• Neurotransmitters - The brain’s chemical messengers appear to work differently in the brain of a patient with schizophrenia. Dopamine is believed to be involved - it is important in the functioning of several brain system that are implicated in the symptoms of schizophrenia.

• Hyperdopamineragia in the subcortex - original version of hypothesis focused on the possible role of high levels or activity of dopamine in the subcortex (central areas of the brain). E.g excess dopamine receptors in Broca’s area may be associated with poverty of speech or auditory hallucinations.

• Hyperdopamineragia in the cortex - more recent version of hypothesis have focused on abnormal dopamine systems in the brain’s cortex. Psychologists have identified a role for low levels of dopamine in the prefrontal cortex in the negative symptoms of schizophrenia.

Neural correlates of schizophrenia

• Measurements of the structure or function of the brain that correlate with an experience. Both positive and negative symptoms have neural correlates.
• Neural correlates of Negative symptoms: one negative symptom is avolition - loss of motivation. Motivation involves loss of anticipation of reward. Ventral striatum is particularly involved in anticipation.
• Neural correlates of positive symptoms: reduced activity in superior temporal gyrus and anterior cingulate gyrus is a neural correlate of auditory hallucinations.

Drug therapies

• Most common treatment for schizophrenia involves the use of antipsychotic drugs. Taken as tablets or form of syrup. Also available in injections.

• Could be for long term or short term use.

Typical antipsychotics: traditional

• Includes Chlorpromazine (taken as tablets, syrup or injections). If taken orally, it can be administered up to 1000mg although initial doses are much smaller and for most patients, the dosage is gradually increased to a max of 400 to 800.

• There is a strong association between the use of typical antipsychotic drugs like Chlorpromazine and the dopamine hypothesis. It works as an antagonists, a chemical which reduce the action of a neurotransmitter. It blocks dopamine receptors in the synapses of the brain, reducing action of dopamine.

• It initially increases its level but then its production is decreased. It normalises neurotransmission in key areas of brain thus reducing symptoms. It is also an effective sedative. It calms patients.

Atypical antipsychotics

Aim of developing newer drugs was to maintain or improve upon the effectiveness of drugs in suppressing the symptoms of psychosis and minimise side effects. There are a range of atypical drugs and they don’t all work the same way.

Clozapine - was withdrawing as some patients developed agranulocytosis (blood condition) but brought back as treatment for S. It binds to dopamine receptors but acts on serotonin and glutamate receptors. This helps improve mood and reduce depression.

Not available as an injection due to side effects. Dosage 300 to 450mg a day.

Risperidone - Binds to dopamine and serotonin receptors. Binds stronger than clozapine and is therefore effective in much smaller doses. Leads to fewer side effects.

Injection, tablets and syrup - 4-8mg , max 12mg.