Biological explanations of schizophrenia

Just some cards I made to revise biological explanations of schizo, feel free to use :D


Biological explanations of schizophrenia

  • The biological approach is seen as the medical model
  • It views mental disorders as having a physical cause (eg, genetics/brain structure) and therefore favours the use of biological treatments such as drugs
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Genetic Explanations

  • Family studies have been conduted since the 1900's to try and identify a genetic link
  • Schizophrenia tends to run in families and studies have shown that the closer the genetic relatedness, the higher the concordanace rate. 
  • The general risk to the population is around 1%, but Kendler et al (1985) found that first-degree relatives of those with schizophrenia are 18x  more at risk than the general population
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Gottesman and Sheilds (1982)

Researched into the lifetime risk of schizophrenia in the relatives of people with schizophrenia through a meta analysis of 40 studies.

Relative----Percentage of lifetime expectancy

Parent --- 5.6


Siblings with one parent with schizophrenia --- 12.9

Siblings with both parents with schizophrenia --- 46.3

Grandchildren --- 3.7

Gottesman did further research on the concordanace rates of schizophrenia between family members and found that

MZ twins have around a 48% concordance, but can increase to 80%, whilst DZ twins have a 14% concordance and a brother or sister have a 6% concordance. This is in relation to the 1% of the general population.

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Evaluation of family studies

  • It could be psycho-social stress, or social learning (modelling) rather than the genetic factors which results in the higher incidence of schizophrenia
  • Family studies have confirmed that schizophrenia does tend to run in families, however the extent to which this is due to genetic or environmental (nature/nurture debate) influences are not clear (families tend to spend a lot of time together, could be due to environmental influences.)
  • The Gottesman and Shields study had small sample sizes, and was done 30 years ago and so lacks temporal validity. Additionally, it was done before DNA developments could distinguish whether twins were fraternal or identical, and experimenters had to guess which they were based on their appearence (not valid.) Also, nowadays, diagnosis is more strict and 30 years ago people were regularly misdiagnosed, so these percentages may not reflect the true figure.
  • Twin and adoption studies have attempted to unravel this, and to try and clarify if it is nature or nurture that causes schizophrenia.
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Twin studies

  • Monozygotic (MZ) twins --- 100% genes in common
  • Dizygotic (DZ) twins --- 50% genes in common
  • If schizophrenia is a genetic disorder, the concordanance rate should therefore be greater for MZ twins than DZ twins
  • Studies such as Gottesman and Sheilds support this (MZ-46%/DZ-14%)
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Adoption studies

  • Adoption studies are unique in their ability to seperate environment from genes. Typically the studies are of children adopted within weeks of birth, from mothers with schizophrenia. These children have no common genes with their adopted family (ie, nobody has schizophrenia, and therefore genes and environment are seperated.)
  • An early adoption study by Heston (1966) of 47 mothers with schizophrenia, whose children were adopted within days of birth by pscychiatrically well mothers, found the incidence of schizophrenia in children to be 16% (well above the 1% of the general population.)
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Evaluation of the genetic explanations of schizoph

  • Prenatal factors may also determine later functions, and therefore adoption studies may not completly exclude environmental factors.
  • The 46% concordanace rate found in MZ twins suggest a major contribution of genotype
  • Concordanace for MZ twins is about 3x that of DZ twins, neverthelessm although high, there is still a disconcordanace rate of around 40%. However, studies have shown that about half the discordant group will go on to develop a schizoid (resembles schizophrenia but doesn't have the psychotic symptoms such as a loss of reality) or similar disorder and thus, if a broader definition for 'schizophrenia' is adopted, the MZ concordanace is even higher.
  • Many of the studies are very old (over 40 years) and testing is now more rigorous and diagnosis in the past may not have been completley valid.
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Evaluation of genetic explanations (2)

  • Owing to the rare incidence of both twins and schizophrenia in the general population, twin studies have, of necessity, contained small samples.
  • Evidence from normal twin pairs (Lytton, 1977) suggest that MZ twins are reared in a more similar environment than DZ twins, and therefore nurture could explain the high concordanace rates for MZ twins.
  • Findings from adoption studies suggest that inheritence does play a part in schizophrenia and there may be a genetic predisposition to the disorder.
  • No genes have been identified by a scitentist that causes schizophrenia
  • The Diathesis-Stress model, which suggests an individual has a genetic predisposition to the disorder, but needs environmental influences to 'set it off' combines both the nature and nurture side of the debate, and may be a better explanation of schizophrenia.
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Neurochemical explanations of schizophrenia

Neurotransmitters are 'chemical messengers' that enable neurons to communicate with different parts of the brain. The investigation of these neurotransmitters have been carried out in three ways:

  • By looking for evidence of metabolites (substances produced through metabolism. Metabolism refers to the biological processes occuring in the organism that result in growth and energy production) in the urine and blood.
  • Through examination of post-mortem brain tissue
  • More recently, through the use of neuroimaging techniques, eg, positron emission tomography (PET scan.)

The activity of neurotransmitters, for example, dompamine and the enzyme responsible for it's metabolism (monoamine oxidase - MAO) has been investigated in the search for a neurochemical explanation for schizophrenia. 

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The dopamine hypothesis

It was thought that excessive dopaminergic activity in the brain was the cause of schizophrenic symptoms. Evidence for this came from three areas:

  • When taken by healthy individuals, drugs that increase dompaminergic activity in the brain, such as amphetamines, result in psychotic symptoms like those experienced by people with schizophrenia (eg, hallucinations.)
  • Such drugs also exacerbate psychotic symptoms in people with schizophrenia
  • Neuroleptic drugs that block the dopaminergic neurons reduce psychotic symptoms
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The dopamine hypothesis (2)

However, this early theory that schizophrenia was linked to an overactive dopaminergic circuit in the brian was difficult to support as:

  • Post-mortem studies did not show consistent evidence for an increased dopamine level in the brains of schizophrenics.

This led to a theory that the cause was not an increase in dopamine, rather, it was the heightened sensitivity of the receptors for dopamine in the brain that led to an abundance of the chemical which therefore caused schizophrenic symptoms. Evidence for this is found:

  • Post-mortem studies have shown there are many more dopamine (D2) receptors in the brains of people with schizophrenia than there are in normal brains.
  • Studies using PET scans have reported a substantial increase in dopamine (D2) receptors in patients with schizophrenia  who hadn't been predisposed to neuroleptic drugs (Pearlson et al 1993).
  • Seeman et al (1993), again using PET, found 6x the density of D4 receptors (receptor subtype very similar to D2) in patients with schizophrenia. 
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Evaluation of the neurochemical theory

  • Makes sense, as it has been found that too many recpetor sites/ too much dopamine results in positive symptoms like hallucinations, as weak signals get exaggerated. This can be treated by blocking recpetors with drugs.
  • Not clear whether the increase in D2 receptors found in schizophrenic people at post mortem is the cause of the pathology or an effect of the neuroleptic drugs taken
  • But the neuroimaging studies by Pearlson et al were conducted on participants who hadn't been pre-disposed to neuroleptic drugs, and thereofore this rules out the cause and effect found in post-mortem studies.
  • Thought it's accepted that the major anti-psychotic drugs block dopamine receptors, to infer from this that dopamine hyperactivity is a major cause of schizophrenia is to oversimplify. It's now clear that the neurotransmitter systems interact and the examining and mapping of these cortical pathways are only just being explored, serotonin is also thought to play a role, but this is only just being researched into.
  • A correlation can't tell the direction of cause and effect and increased dopamine may be the result of schizophrenia, rather than the cause.
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Neuroanatomical explanations of schizophrenia

  • This approach has a long history
  • Brains of people diagnosed with schizophrenia have been compared with healthy brains (controls) on sections such as anatomical structure, hemisphere differences and cell counts. 
  • Traditionally, this could only be carried out post mortem, which created the problem of cause and effect. 
  • Also neuroleptic drugs used to treat schizophrenia may have caused  the abnormality - this would then confound the result.
  • New scanning techniques such as MRI allow living brains to be investigated, and can therefore examine consistent changes in particular brain areas.
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The limbic system

  • Is a subcortial structure that includes the hippocampus and amygdala
  • Significant cell loss has been found in the structures of the limbic system in post-mortem patients with schizophrenia, and these findings have been confirmed with more recent imaging studies (Jernigan et al 1991). There's also evidence of unusual cell connections in the hippocampus.
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The corpus callosum

  • Is a large bundle of fibres that connects the two hemispheres of the brain
  • Studies have found that the gender differences in the thickening of these fibres in normal individuals are reversed in schizophrenics (Nasrallah et al 1986.)
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Abnormal early brain development

  • In the third trimester of pregnancy, when the last stage of the development of the cerebal cortex occurs, is thought to be associated with schizophrenia. 
  • It's during this prenatal stage that the disorder in the brain may occur, particularly with the development of the neuronal dendrites and the organisation of synapses in the cortex. 
  • The two hemispheres of the normal brain are asymmetrical, particularly in the tempero-parietal regieon of the cortex.
  • Both post-mortem and imaging studies have shown asymmetry is much less evident in schizophrenics.
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Brain imaging studies

  • Have found significant differences in both structure and function of the schizophrenic brain.
  • Studies have shown that people with schizophrenia have reduced brain tissue and enlarged ventricles.
  • A meta-analysis by Raz and Raz (1990) of studies comparing ventricular volume in people with schizophrenia and controls reported a significant increase in size in over half of the samples, and an overall effect size of 0.6. This is a significant effect and may be linked to major functioning abnormalities.
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Suddath et al (1990)

  • Investigated discordanant twin pairs for structural abnormalities that might account for the incidence of schizophrenia in one of each pair
  • 15 discordanant MZ twins, only one of which was diagnosed with schizophrenia were given MRI scans to determine any differences in brian structures between the them.
  • The twin with schizophrenia had a smaller bilateral hippocampus than the twin without in 14 out of 15 pairs, and the twin with schizophrenia also had larger ventricles (less brain tissue.)
  • This shows that when genotype is controlled for, there is a signficantly dimished brain volume in the twin with schizophrenia.
  • However, it is difficult to establish whether the smaller hippocampus is a cause or an effect of the schizophrenia.
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Functional studies of the schizophrenic brain

  • Imaging techniques can detect cerebral blood flow (CBF) in parts of the cortex
  • At rest, people with schizophrenia show evidence of under activity in the tepero-frontal areas of the cortex compared to controls. 
  • This has become known as 'hypofrontality' and is particularly evident in chronic patients (Liddle 1996.)
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Evaluation of the neuroanatomical theory

  • Attempts to link structural changes to particular symptoms have not yet shown consistent findings. Eg, Lewis (1990) reviewed 18 studies and found no significant link between enlarged ventricles and negative symptoms.
  • A variety of brain mechanisms seem to be implicated, but as yet, none are sufficiently understood to say that it provides a causal link. It might be the other way around (ie, changes in structure is caused by the schizophrenia.)
  • Likely that a number of environmental risk factors contribute to the onset. Perhaps it is more realistic to propose that biological factors contribute towards an individual's liablity to develop schizophrenia.
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