By Daniel A. Barone, MD, FAASM
Assistant Professor of Neurology, Weill Cornell Medical College
Dr. Barone reports no financial relationships relevant to this field of study.
SYNOPSIS: Traumatic brain injury may induce a chronic state of altered sleep with impaired memory consolidation and mood disorders.
SOURCE: Mantua J, et al. Mild traumatic brain injury chronically impairs sleep- and wake-dependent emotional processing. Sleep 2017;40(6).
A single traumatic brain injury (TBI), even when mild (a concussion, for example), can result in lasting consequences. More than 1 million mild TBIs occur each year in the United States, and individuals with a history of chronic (> 1-year prior) mild TBI are at an increased risk of suffering with mood disturbances (i.e., depression, suicide) as well as poor sleep quality and changes in sleep stage proportions.
Mantua et al hypothesized that sleep-dependent memory consolidation would be altered in individuals with chronic mild TBI, the rationale being that disrupted sleep causes or maintains mood disturbances. Additionally, given the known reduction in rapid eye movement (REM) sleep following a mild TBI, a second hypothesis was that sleep’s preservation of emotionality might be disrupted in individuals with chronic TBI.
To prove these hypotheses, the authors compared individuals with more than one mild TBI (3.7 ± 2.9 years post injury) against an uninjured population. The TBI group consisted of 40 participants, with an average age of 19.87 years and 75.6% women; the non-TBI group consisted of 41 participants with an average age of 20.15 years and 70.0% women.
Participants viewed negative and neutral images both before and after a 12-hour period containing sleep (“sleep” sub-group) or an equivalent period spent awake (“wake” sub-group). Participants then rated images for valence, which is a psychological term for “goodness,” and arousal at both sessions. The memory recognition of these images was tested at session two for both groups. Additional testing included nocturnal polysomnogram (PSG), which was recorded in participants’ homes using an ambulatory system.
Those in the TBI group had less REM sleep, longer REM latency, and more sleep complaints than the non-TBI group. There were no differences between the TBI and non-TBI sleep groups for total sleep time, sleep efficiency, or time spent awake after sleep onset, nor were there significant differences between the percent of the night spent in other sleep stages.
Sleep-dependent memory consolidation of non-emotional images was present in all participants, but consolidation of negative images was present only in the non-TBI group. The authors noted that sleep-dependent consolidation is optimized when both non-REM and REM sleep are present and sequential, and the negative effects on REM sleep in the TBI group may have hindered consolidation by reducing such REM/non-REM interactions.
Both the TBI sleep and the TBI wake groups found the negative images to be persistently negative at the second presentation. The authors noted that these results are compatible with current theories of depression, which purport that depressive thoughts arise and are perpetuated when an individual is unable to use proper emotional regulation strategies, such as suppression or reappraisal, to habituate when emotional experiences occur.
Multiple TBIs resulted in poorer sleep-dependent memory consolidation and a greater preservation of valence. The authors concluded that individuals who sustain multiple concussions have poorer emotional processing during sleep, during a waking period, and overall, which is consistent with literature on military and athletic activities.
COMMENTARY
Disrupted sleep- and wake-dependent emotional processing may contribute to poor emotional outcomes following mild TBI. There are far-reaching implications from this study as roughly one-third of the U.S. population will sustain a mild TBI during their lifetime.
Some issues should be pointed out that were not otherwise mentioned. The PSG testing, while conducted in the participants’ homes, could have altered sleep of their own accord (the so-called “first night effect”); it has been shown that objective and subjective sleep measurements seen in depressed insomniacs may be influenced by the monitoring setting. Additionally, the authors mentioned that some participants in both groups used over-the-counter sleep aides. While antihistamines were mentioned, exogenous melatonin was not. This is significant in that melatonin has been shown to increase REM sleep.
On a side note, medical literature is rife with studies demonstrating the complex interplay between neurologic, psychiatric, and sleep disorders. For example, it has been shown that the prevention of sleep following a traumatic event can reduce the formation of traumatic memories and, thus, the development of post-traumatic stress disorder. The information garnered from this study sheds more light on this fascinating interplay and should prompt further investigation. Determining definitively whether TBIs are predictive of emotional dysfunction and whether sleep intervention can repair or rescue sleep-dependent alterations would be a priority.
Traumatic brain injury may induce a chronic state of altered sleep with impaired memory consolidation and mood disorders.
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