Introduction

On the night of May 23, 1987, Kenneth Parks rose from his bed, wandered out of his house, and drove 14 miles to his mother- and father-in-law’s house in the neighboring town [1]. He beat his mother-in-law to death with a tire iron and choked his father-in-law. Now a bloody mess, he drove to a nearby police station. In a confused manner, he told the police that he “thought” he killed someone. Though disoriented, he identified his in-laws and murmured that it was “all his fault.” Eventually, Parks was tried for one charge of murder and one charge of attempted murder. His defense claimed that, during the entire episode, he was sleepwalking [1].

This case presents an extreme media play of sleepwalking, scientifically known as Somnambulism, where we involuntarily and subconsciously engage in activities while still asleep. The range of sleepwalking actions varies dramatically. When thinking of sleepwalking, the image that most often springs to mind is that of a person rising from their bed and walking around like a zombie. But the potential implications are a lot larger than this. For instance, while one person may just mutter words, there are other cases like Kenneth Parks’ where violence and murder enter the playing field.

Characteristics of Sleepwalking

To fully understand the range of sleepwalking, we must first understand how sleep functions. Every night, sleep cycles through two main physiological stages: Rapid Eye Movement (REM) and non-Rapid Eye Movement (NREM) sleep [2]. REM sleep is characterized by brain waves similar to when we are awake, and this is also where we do most of our dreaming. NREM starts with NREM 1, where light sleep occurs for less than 10 minutes. NREM 2 consists of deeper sleep compared to NREM 1 and is indicated by a decline in body temperature and heart rate. NREM 3 is the deepest stage of sleep, during which our body often undergoes repair and restoration. NREM 3 is characterized by very slow, synchronous brain waves that look markedly different from wakefulness and REM sleep. This trait is referred to as Slow Wave Sleep. This is also the stage in which sleepwalking occurs [2].

Sleepwalking is associated with partial arousal during NREM sleep, specifically the slow wave sleep that occurs during these stages [2]. This partial arousal can be determined by a variety of factors. In the short term, stress, sleep deprivation, and medication all have effects on sleepwalking. Genetics and family history also play an important role in its development [3].

The amount of slow wave sleep declines as we age and can be a determining factor for sleepwalking [3]. This may explain why children are the majority of the population affected by sleepwalking. A 2016 meta-analysis estimated that 5% of children are affected by somnambulism, compared to 1.5% of adults [4].

Influences on Sleepwalking

Sleepwalking physiology in the brain is influenced by interactions between partial arousal during NREM 3 and cerebellum and brainstem activity during sleep [2]. Complex thinking in humans is made possible by structures in the brain called the cerebrum and cerebral cortex. Early research into the brain suggested that the cerebrum was in charge of muscle memory and motor control [5]. However, it was later shown that the brainstem and cerebellum are more involved with these functions, while the cerebrum and cerebral cortex are associated with higher thinking and intelligence [6]. We also see that the cerebral cortex is associated with consciousness. This further suggested that sleepwalking had less to do with cerebral cortex function, hence the partial consciousness in sleepwalkers, and more to do with cerebellum and brainstem activity, causing motor activity. This is also why this disturbance in slow wave sleep does not lead to a sleepwalking person waking up [2].

Sleepwalking is among several other disorders involving partial arousal and unusual behavior during sleep, such as night terrors and sleep paralysis, which are together called "parasomnias.” Sleepwalking can be distinguished from other parasomnias by a lack of memory of the events that occurred while sleepwalking, as well as the stage of sleep in which it occurs. These two characteristics of sleepwalking help us confirm when someone is suffering from somnambulism and not a related parasomnia [5]. The fact that Kenneth Parks had no memories of the events is what led some researchers to suggest that he was genuinely sleepwalking when he committed the acts of violence [1].

It is well known that some medications can cause or exacerbate sleepwalking. In 62 research studies on this topic, it was found that 29 drugs were shown to be a possible trigger for sleepwalking [7]. The main types of medication that were associated with increased levels of sleepwalking were drugs that affect neurotransmitters in the brain. These drugs even have the potential to trigger sleepwalking in those who have never sleepwalked before, along with those who have previously sleepwalked [7]. Serotonergic agents and antipsychotics, for example, were identified as possible triggers [8]. Side effects of these drugs, which can include muscle relaxation and sedation, disturb slow wave sleep. As sleepwalking is mainly caused by disturbances in slow wave sleep, drugs that induce this can also induce sleepwalking [8].

Zolpidem appears to have the largest correlation with inducing sleepwalking [7]. Zolpidem is a drug that helps those with insomnia and other sleep related issues. This occurs through altering the effectiveness of Gamma Amino Butyric Acid, or GABA. GABA is a very important neurotransmitter that plays a role in anxiety, stress, fear, and most importantly, sleep. GABA calms the neuron it goes into by reducing its ability to communicate with the rest of the brain. Zolpidem boosts the action of GABA in the brain, creating a calming effect and allowing for easier sleep. Research into the topic is still relatively young. So, despite knowing that drugs impact sleepwalking, right now we can mostly only theorize about the mechanism in which Zolpidem affects sleepwalking [7]. The main theory has to do with Zolpidem possibly causing the characteristic partial arousal we see in sleepwalking during NREM 3 [9]. This may be due to GABA’s effects of calming the brain, which is somewhat similar to the sedative state caused by other drugs that also disturb slow wave sleep. Although sleepwalking is an unwanted side effect of these drugs, this association allows us to gain insight into how sleepwalking works and potentially find ways to solve neurotransmitter dysregulation in sleepwalking.

Conclusion

Research into sleepwalking remains quite young compared to other fields. Difficulties in this field include the logistical aspects of requiring human participants to sleep in the lab, the unpredictability of sleepwalking symptoms, and the inability to control when sleepwalking occurs. As a result, many studies rely on personal experience and the accounts of those who witness the event, but relying on the memory of a subject is often flawed. Studies conducted only with people who slept with a partner had less variability than those who reported their own dreams and sleep habits [4]. However, new research methodologies could yield promising results. Electroencephalograms (EEGs) and sleep studies incorporating modern medicine offer a path into further study by being able to document exactly what state the brain is in while also monitoring other vitals. With these breakthroughs, we will understand this unique behavioral disorder much better.

References

[1] Supreme Court of Canada. (2019). R. V. Parks - SCC Cases (Lexum). Lexum.com, 2019, scc-csc.lexum.com/scc-csc/scc-csc/en/item/907/index.do

[2] Popat, S., & Winslade, W. (2015). While You Were Sleepwalking: Science and Neurobiology of Sleep Disorders & the Enigma of Legal Responsibility of Violence During Parasomnia. Neuroethics, 8(2), 203–214. https://doi.org/10.1007/s12152-015-9229-4

[3] Colrain, I. M., & Baker, F. C. (2011). Changes in sleep as a function of adolescent development. Neuropsychology review, 21(1), 5–21. https://doi.org/10.1007/s11065-010-9155-5

[4] Stallman, H. M., & Kohler, M. (2016). Prevalence of Sleepwalking: A Systematic Review and Meta-Analysis. PloS one, 11(11), e0164769. https://doi.org/10.1371/journal.pone.0164769

[5] Mahowald, M., Bornemann, M.A.C., & Schenck, C.H. (2011). State Dissociation: Implications for Sleep and Wakefulness, Consciousness, and Culpability. Sleep Medicine Clinics. 6. 393-400. https://doi.org/10.1016/j.jsmc.2011.08.002.

[6] Tononi, G., & Koch, C. (2015). Consciousness: here, there and everywhere?. Philosophical transactions of the Royal Society of London. Series B, Biological sciences, 370(1668), 20140167. https://doi.org/10.1098/rstb.2014.0167

[7] Stallman, H. M., Kohler, M., & White, J. (2018). Medication induced sleepwalking: A systematic review. Sleep medicine reviews, 37, 105–113. https://doi.org/10.1016/j.smrv.2017.01.005

[8] Ferrándiz-Santos, J. A., & Mataix-Sanjuan, A. L. (2000). Amitriptyline and somnambulism. The Annals of pharmacotherapy, 34(10), 1208. https://doi.org/10.1345/aph.10073

[9] Hoque, R., & Chesson, A. L., Jr (2009). Zolpidem-induced sleepwalking, sleep related eating disorder, and sleep-driving: fluorine-18-flourodeoxyglucose positron emission tomography analysis, and a literature review of other unexpected clinical effects of zolpidem. Journal of clinical sleep medicine : JCSM : official publication of the American Academy of Sleep Medicine, 5(5), 471–476.