Traumatic Brain Injury – Can Deep Sleep Be Neuroprotective?




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From all the injuries our body can sustain, damage to the brain is the most likely to cause death or permanent disabilities. Traumatic brain injury is a highly incident condition: it is estimated that up to 60 million people worldwide may suffer any type of traumatic brain injuries each year, including mild injuries, mainly due to motor vehicle accidents, falls or aggressions.

Brain injuries can have severe consequences, both physical and cognitive, and there’s a huge need for good therapeutic solutions.

The consequences of traumatic brain injury

Traumatic brain injury entails much more than just its immediate effects. There are many long-term consequences that are most likely due to progressive injury of neurons and axons triggered by the initial traumatic insult.

One of the most detrimental consequences of brain trauma is diffuse axonal injury. Whereas trauma is a direct result of an impact to the brain, diffuse axonal injury is the result of shearing forces that are caused by fast back-and-forth movements of the brain in the skull due to sudden acceleration or deceleration, or to rotational forces. This happens in most cases of severe head trauma.

Diffuse axonal injury can cause the release of harmful chemical mediators, the disruption of axons, neuronal cell death, and swelling, which in turn increases pressure in the brain and decreases blood flow, leading to additional injury. The initial trauma can therefore act as a trigger for a cascade of detrimental events that can cause severe disabilities. Diffuse axonal injury is regarded as a key contributor to post-traumatic cognitive impairment, which is one of the most common consequences of traumatic brain injury, occurring in almost 80% of patients.

The effect of sleep in diffuse axonal injury

A few recent studies have proposed that sleep may help in the recovery from brain injury. Sleep is well-known to be fundamental for the maintenance of health: sleep deprivation is associated with an increased prevalence of a number of diseases, including type II diabetes, obesity, hypertension, cardiovascular diseases, and stroke itself. Sleep dysfunctions are often observed after traumatic brain injury, potentially contributing to the deterioration of health. But can sleep be used as a therapy?

Increased slow-wave, or deep sleep has shown beneficial effects in stroke, traumatic brain injury and Alzheimer’s disease patients. Now, a new study published in the Journal of Neuroscience reinforces the therapeutic potential of sleep. This experimental study, conducted in an animal model of traumatic brain injury, aimed at assessing whether increasing slow-wave sleep immediately after trauma could reduce diffuse axonal damage and the consequent cognitive deficits.

The results showed that increasing deep sleep led to a significant reduction in the post-traumatic levels of amyloid precursor protein, which is a cellular marker of diffuse axonal injury. The development of cognitive deficits was also prevented in the experimental group whose slow-wave sleep was increased, whereas the group whose sleep was not modulated showed clear signs of cognitive impairment.

Interestingly, this study also revealed that sleep restriction could also prevent diffuse axonal injury and the development of cognitive impairment. Even though this seems contradictory, the mechanism underlying both circumstances is actually the same: temporary sleep deprivation leads to an increase in slow-wave activity in the subsequent, rebound sleep.

Can deep sleep be a therapy for traumatic brain injury?

The findings of this work stand in line with results from studies in stroke patients which have shown that sleep deprivation before the occurrence of the stroke episode may have a neuroprotective effect, most likely due to increased deep sleep after stroke.

Also, Alzheimer’s patients whose slow-wave sleep is compromised show a higher toxic accumulation of the amyloid-beta protein in the brain. Given that slow-wave sleep seems to be associated with a more effective removal of cellular waste products, and neurotoxic agents, this buildup of A-beta may be due to a reduced capacity to remove waste products due to impaired deep sleep.

Likewise, waste product and toxic agents released as a consequence of brain injury may be more effectively removed by increasing slow-wave sleep, consequently stopping the cascade of post-traumatic harmful events, including the effects of diffuse axonal injury.

Slow-wave sleep may therefore contribute to increased neuroprotection and functional recovery after traumatic brain injury in humans, making sleep modulation a potential therapeutic approach for traumatic brain injury.

References

Baumann, C. (2016). Sleep and Traumatic Brain Injury Sleep Medicine Clinics, 11 (1), 19-23 DOI: 10.1016/j.jsmc.2015.10.004

Maas, A., & Menon, D. (2012). Traumatic brain injury: rethinking ideas and approaches The Lancet Neurology, 11 (1), 12-13 DOI: 10.1016/S1474-4422(11)70267-8

Maas, A., Stocchetti, N., & Bullock, R. (2008). Moderate and severe traumatic brain injury in adults The Lancet Neurology, 7 (8), 728-741 DOI: 10.1016/S1474-4422(08)70164-9

Morawska, M., Buchele, F., Moreira, C., Imbach, L., Noain, D., & Baumann, C. (2016). Sleep Modulation Alleviates Axonal Damage and Cognitive Decline after Rodent Traumatic Brain Injury Journal of Neuroscience, 36 (12), 3422-3429 DOI: 10.1523/JNEUROSCI.3274-15.2016

Pace, M., Baracchi, F., Gao, B., & Bassetti, C. (2015). Identification of Sleep-Modulated Pathways Involved in Neuroprotection from Stroke SLEEP, 38 (11), 1707-1718 DOI: 10.5665/sleep.5148

Roozenbeek, B., Maas, A., & Menon, D. (2013). Changing patterns in the epidemiology of traumatic brain injury Nature Reviews Neurology, 9 (4), 231-236 DOI: 10.1038/nrneurol.2013.22

Turner, R., Lucke-Wold, B., Lucke-Wold, N., Elliott, A., Logsdon, A., Rosen, C., & Huber, J. (2013). Neuroprotection for Ischemic Stroke: Moving Past Shortcomings and Identifying Promising Directions International Journal of Molecular Sciences, 14 (1), 1890-1917 DOI: 10.3390/ijms14011890

Image via Riccardo Piccinini / Shutterstock.

Sara Adaes, PhD

Sara Adaes, PhD, has been a researcher in neuroscience for over a decade. She studied biochemistry and did her first research studies in neuropharmacology. She has since been investigating the neurobiological mechanisms of pain at the Faculty of Medicine of the University of Porto, in Portugal. Follow her on Twitter @saradaes
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