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May 24, 2016; 86 (21) Editorial

Bringing posttraumatic sleep–wake disorders out of the dark

Brian L. Edlow, Gert Jan Lammers
First published April 27, 2016, DOI: https://doi.org/10.1212/WNL.0000000000002710
Brian L. Edlow
From the Department of Neurology (B.L.E.), Massachusetts General Hospital, Boston; Athinoula A. Martinos Center for Biomedical Imaging (B.L.E.), Massachusetts General Hospital, Charlestown, MA; Department of Neurology and Clinical Neurophysiology (G.J.L.), Leiden University Medical Center; and SleepWake Center SEIN (G.J.L.), Heemstede, the Netherlands.
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Gert Jan Lammers
From the Department of Neurology (B.L.E.), Massachusetts General Hospital, Boston; Athinoula A. Martinos Center for Biomedical Imaging (B.L.E.), Massachusetts General Hospital, Charlestown, MA; Department of Neurology and Clinical Neurophysiology (G.J.L.), Leiden University Medical Center; and SleepWake Center SEIN (G.J.L.), Heemstede, the Netherlands.
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Bringing posttraumatic sleep–wake disorders out of the dark
Brian L. Edlow, Gert Jan Lammers
Neurology May 2016, 86 (21) 1934-1935; DOI: 10.1212/WNL.0000000000002710

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The restorative effects of sleep on the brain are widely known. We have all observed how attention, memory, and even executive function can be affected by the quality and duration of the prior night's sleep. The physiologic mechanisms underlying this association between cognitive performance and sleep have yet to be fully elucidated, but sleep may have an important role in promoting the clearance of neuronal waste products such as β-amyloid via interstitial spaces in the brain.1 For patients with traumatic brain injury (TBI), sleep may be necessary for brain healing, as sleep is involved in a broad spectrum of recovery mechanisms including synaptic plasticity.2 However, despite the role of sleep in facilitating recovery after TBI, a growing body of evidence suggests that many patients with TBI have long-term sleep–wake disturbances. For these patients, the homeostatic sleep–wake circuits that are critical to recovery are themselves disrupted.

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  • © 2016 American Academy of Neurology
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