Black: AO1 - Description
Blue: AO2 - Research
Red: AO3 - Evaluative points/IDAs
Sleepwalking tends to run in families, being 10 times more likely if a first-degree relative has a history of sleepwalking, and having higher concordance rates between monozygotic (genetically identical) than dizygotic (non-identical) twins. This has led to the development of a genetic explanation which suggests that sleepwalking has a genetic basis, being coded for by the presence of a certain gene.
Bassetti provided supporting evidence for the genetic explanation of sleepwalking, gene-testing 16 adult sleepwalkers to find that 50% had a gene found in only 25% of the general population - HLA-DQB1*05, partially responsible for producing HLA immune regulation proteins. The fact that HLA-DQB1*05 gene is twice as common in sleepwalkers as in non-sleepwalkers suggests that it in some way leads to the inhibition of motor control which causes sleepwalking, supporting the genetic hypothesis. However, other factors must be involved in sleepwalking, or else the gene would be present in 100% of sleepwalkers.
Lecendreux et al provide further supporting evidence for the genetic explanation of sleepwalking, finding a concordance rate of 50% in monozygotic twins compared to 17% concordance in dizygotic twins. This supports a genetic basis but not a complete explanation - it cannot be entirely genetic, or else a 100% monozygotic concordance rate would have been found.
Although the genetic explanation is well supported by research evidence, it is an overly reductionist explanation of sleepwalking, being unable to explain the condition's incidence in all sufferers. To reduce a complex syndrome down to the presence of a single gene is an oversimplification - other factors must be important, as only 50% of sleepwalkers have the gene suggested as an explanation, and there is not 100% concordance between monozygotic twins. There is research to support the role for personality factors in sleepwalking - such as Type A personalities being more likely to experience the condition - and the genetic explanation ignores these suggested personality and environmental factors and cannot fully explain sleepwalking as a result.
Additionally, the genetic explanation is overly deterministic, stating that if you possess a certain gene or combination of genes, you'll sleepwalk, while this is not necessarily the case, as 24% of people with the HLC-DQB1*05 gene do not sleepwalk. The existence of these counterexamples suggests that having the gene will not necessarily lead to sleepwalking, challenging the explanation's predictive validity. Cases of crimes comitted while sleepwalking have raised the free will versus determinism debate - in the case of Ken Parkes, who killed his family members while sleepwalking and was later acquitted for murder, the law fell on the side of determinism, claiming that he was not in control of his actions and therefore should not be held responsible.
Identical twins tend to share a very similar environment during childhood and adolescence, so the influence of nature can't be separated from the influence of nurture to determine a direct cause and effect for the genetic basis of sleepwalking. Genetically identical twins may also have shared environmental factors during upbringing such as stress, alcohol and other drug usage and sleep deprivation - due to these multiple confounding variables as aspects of nuture, sleepwalking cannot be pinned down as a result of nature through the use of concordance studies.
The psychodynamic approach explains sleepwalking as a result of repressed unconscious desires to sleep where they slept as a child, and a way of working through unconscious anxieties. During REM sleep the person is paralysed and cannot act out their dreams - once they transition to NREM and can move, this instinctive energy and desire to return to where they slept as a child is expressed through sleepwalking.
However, this explanation lacks face validity - most sleepwalkers are children rather than adults, so a desire to return to the place of childhood sleep would only explain the condition in the small proportion of sufferers that are adults. Similarly, it fails to explain the range of activities carried out by sleepwalkers - cooking food, eating - behaviours completely unrelated to returning to the place of childhood sleep.
The higher incidence rate of sleepwalking in children than in adults is likely to be explained by the fact that children spend more time in slow wave sleep, when sleepwalking takes place - so there is more opportunity for the behaviour to occur. Also, it could be explained by parts of the brain that inhibit movement in sleep not being fully developed in children - as supported by Hublin et al who found that 20% of children experience sleepwalking compared to 2 % of adults, suggesting that a lack of neurological maturation and development is the cause.
The psychodynamic explanation is also unfalsifiable and untestable, as the unconscious mind cannot be directly accessed reliably and objectively. The explanation does not treat psychology using the scientific methodology and objectivity that it should, and lacks scientific credibility as a result; unlike the genetic approach which uses quantifiable techniques such as genome sequencing and chromosome analysis to gather objective data.
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