One explanation of sleepwalking is down to incomplete arousal. EEG recordings made during sleep walking, show a mixture of delta waves which are typical of slow wave sleep

by crossey (student)

Sleepwalking

One explanation of sleepwalking is down to incomplete arousal. EEG recordings made during sleep walking, show a mixture of delta waves which are typical of slow wave sleep (SWS), plus the higher frequency beta waves which are characteristic of the “awake” state. It looks as if sleep walking occurs when a person in SWS is awakened, but the arousal of the brain is incomplete.

Oliviero (2008) discovered that inhibition of the brain’s motor system does not just occur in REM sleep, but also occurs in NREM sleep. This inhibition is regulated by a neurotransmitter called GABA: Oliviero argues that the system that produces GABA is more likely to be underdeveloped in children than in adults, and that this is why sleepwalking is much more common in children. In most children, the system eventually does develop normally, and hence sleepwalking disappears. In other children, though, the system fails to develop normally and so sleepwalking continues into adulthood

Oliviero also speculates that the GABA system can be affected by environmental influences. These include physical factors (e.g. drugs like alcohol, or a fever) and psychological factors (e.g. stress). This would explain why sleepwalking is more common following a night’s drinking or when we have to revise for exams.

However, remember that these are speculations. There is no evidence that physical/psychological factors do affect the GABA system, nor any convincing reason why the brain would issue commands for movement during NREM sleep, when dreaming is much less likely to occur. It is also difficult to explain why there is a ...

This is a preview of the whole essay

One environmental factor that has been clearly linked to sleepwalking is sleep deprivation. Research conducted by Zadra, et al. (2008) showed that sleepwalkers deprived of sleep for 25 hours and then allowed to sleep normally were significantly more likely to sleepwalk compared with when they slept not having been sleep deprived. Presumably, sleep deprivation also somehow interferes with the GABA system. In children, sleepwalking typically begins around the age of 4, when children stop taking daytime naps. It could be that they are, in a sense, also sleep-deprived, and hence more likely to sleepwalk.

If GABA is the important neurotransmitter, then the question is what causes the GABA system to malfunction. Interestingly, sleepwalking runs in families, and a person is ten times more likely to display the condition if a first degree relative is a sufferer. There is also a higher Concordance Rate for sleepwalking in MZ than DZ twins. Therefore, sleepwalking might be a genetic condition. Research has identified a specific genetic marker (a gene called HLA DQB1*5) which is more likely to be present in sleepwalkers than non-sleepwalkers.

This gene is involved in producing proteins called HLA, which play a role in the regulation of the immune system. Presumably, if this is the gene involved, it somehow exerts an effect on the GABA system and leads to sleepwalking occurring. However, the view that a simple single gene is involved is weakened by the fact that the gene is present in some non-sleepwalkers, and is not present in some sleepwalkers. Note, too, that most examples of genetic research are plagued by the problem of small sample sizes (making any findings difficult to interpret) and that sleepwalkers who volunteer for this kind of research may not be representative of sleepwalkers in general (i.e. those who don’t volunteer).