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Summary Biopsychology of Psychiatric Disorders
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Talks about many disorders in depth in reltion to their causes and neuroanatomical mechanisms
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Biopsychology of psychiatric disordersDiagnosis depends on symptomatic profile from the patients. Diagnoses must be reviewed regularly
to understand if the symptoms have worsened, gotten better, or if new symptoms have appeared
which can change the diagnosis.
Schizophrenia
Patients can suffer a variety of symptoms. Hallucinations, delusions, catatonia, delirium, wax
flexibility (moving in place of people’s touch), disorganised speech, echolalia, and paranoia. These
symptoms are diverse and overlap into personality disorders and neurodivergent disorders.
Positive symptoms include something happening to the person which interferes with their thought
and behaviour, like hallucinations, delusions, inappropriate affect, odd behaviour, and disorganised
speech.
Negative symptoms include the absence of something that is normal, so having a flat affect, social
withdrawal, and catatonia (LACK OF expression and mobility).
These symptoms must last at least a month and must cause severe impairment.
Causal factors in schizophrenia:
- Genetics: close relatives can risk passing the disorder on. 10% chance of schizophrenic
parent passing it to child even if the child is later adopted. Monozygotic twins concordance
rate is 45-50% compared to dizygotic twins, where the rate is 10-17%. Some studies say that
people inherit it, but environmental experiences trigger the symptoms to come through. It is
a heterogenous disorder, with not one single gene interaction causing the disorder.
- Environment: birth complications, maternal stress, prenatal infections, socioeconomic
status, and childhood adversity are risk factors of schizophrenia.
Discovery of the first antipsychotics: Chlorpromazine was the first AP discovered, and it was found
by accident. Antihistamines were meant to be developed, but they ended up creating APs. It was
found to have a calming effect on patient with psychosis. Emotionally blunt (negative symptom)
patients were awakened, and hyperactive, delirious patients were calmed by them. Reserpine was
also used but discontinued after the dose needed for treatment caused low blood pressure. Shows
how far we have come. The symptoms calm after two weeks of administration, and muscles become
rigid, like in Parkinson’s. This suggests that APs affect dopamine, since low dopamine causes
Parkinson’s.
Dopamine theory of schizophrenia
The striatum, which contains projected dopaminergic nuclei from the substantia nigra, had been
depleted in Parkinson’s patients. If APs caused muscle rigidity, symptoms of Parkinson’s, then APs
must be related to dopamine. Since APs are related to lowering dopamine, then schizophrenia must
be related to too much dopamine. APs break down dopamine synaptic vesicles, so less could be
stored. Cocaine can increase the level of dopamine in the brain and taking too much can cause
schizophrenia like symptoms.
Chlorpromazine is an antagonist, it works not by depleting dopamine, but by sitting at receptors and
not activating them, which then prevents dopamine transmission. The amount of dopamine was not
changed, but rather the reuptake was changed. There were more metabolites at receptor sites, but
less the amount of dopamine was the same, the receptors were simply inactive. The metabolites are
, needed, and with inefficient metabolism, there can be issues oxidation, which can increase
neurotoxicity. Excess dopamine can cause excess metabolism or inefficient metabolism, which
causes toxicity and brain degeneration.
There is not a change in the amount of dopamine, but rather there is a lot of activity at the
receptors.
There are many dopamine receptor sub-types, which was identified when an antipsychotic
haloperidol had a low affinity when it came to reducing dopamine number at the receptors. It did
not bind very well to receptors, but it could still reduce schizophrenic symptoms very well. Most APs
bind to receptor 1 and 2, but haloperidol could only bind to receptor 2.
Haloperidol is a butyrophenone, and chlorpromazine is a phenothiazine.
Schizophrenia was then reconsidered in terms of the dopamine theory. Instead of dopamine,
researchers figured that receptor D2 had an excess amount of dopamine, since haloperidol only
tackled this receptor, and it did very well at treating the disorder. The most potent AP is spiroperidol.
It is also a butyrophenone.
APs treat positive symptoms effectively, not negative symptoms. Typical antipsychotics, which affect
the dopaminergic system, suppress schizophrenia symptoms, but patients do not feel therapeutic
effects after weeks of dosing, suggesting they do not improve mood or well-being instantly even
though the drugs are active within hours.
Schizophrenia: current research and treatment
- Atypical APs: They are second generation APs. They effectively treat schizo, but do not bind
to the D2 receptor. Clozapine is an atypical AP, having high affinity for D1 D4 and histamine
receptors. They do not differ much from typical antipsychotics, even if people claim they
produce less Parkinson like symptoms or don’t block the D2 receptors. These drugs do
slightly antagonise D2 receptors, but affinity is low. Drugs that block glutamate are coming
into actions, preliminary testing shows that they reduce symptoms of schizo.
- Hallucinogenic drugs interest: Lysergic acid diethylamide, was discovered in the 1950s. It
causes alterations in perception, emotion, and cognition. It’s a psychedelic. Other
psychedelics include dissociate hallucinogens and cannabinoids. These drugs are used to
model positive symptoms of schizophrenia. It is now difficult to research using these drugs.
LSD mimics positive schizophrenia like symptoms by acting as an agonist on serotonin
receptors. This meant there was heightened arousal due to block of reuptake. Dissociative
hallucinogens, like ketamine, mimic the negative symptoms of schizophrenia, by acting as
antagonists on the glutamate receptors, which causes inhibitions.
- Mechanisms of schizophrenia relates genes: Each genes have slight contributions to onset
of schizo. Some schizo related genes disrupt proliferation and migration at the neural plates.
Proliferation is the abundance of newly emerging neurons whilst migration is the alignment
of these neurons to help produce new cells which become specialised. Schizo genes also
disrupt myelination of emerging neurons, and it speeds up transmission at glutamatergic
synapses whilst decreasing activity at GABAergic synapses.
- Schizophrenia and brain structure changes: Large ventricles and fissures in brains,
suggesting lower brain volume. Nucleus accumbens, amygdala, hippocampus, and thalamus
were much smaller in schizo patients. Lower grey and white matter in temporal lobe. Areas
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