Mild Traumatic Brain Injury Chronically Impairs Sleep- and Wake-Dependent Emotional Processing

Abstract

Study Objectives: A single traumatic brain injury (TBI), even when mild (ie, concussion), can cause lasting consequences. Individuals with a history of chronic (>1-year prior) mild TBI have an increased risk of mood disturbances (eg, depression, suicide). This population also has lingering sleep alterations, including poor sleep quality and changes in sleep stage proportions. Given these sleep deficits, we aimed to test whether sleep-dependent emotional memory consolidation is reduced in this population. We utilized a mild TBI group (3.7 ± 2.9 years post injury) and an uninjured (non-TBI) population. Methods: Participants viewed negative and neutral images both before and after a 12-hour period containing sleep ("Sleep" group) or an equivalent period of time spent awake ("Wake" group). Participants rated images for valence/arousal at both sessions, and memory recognition was tested at session two. Results: The TBI group had less rapid eye movement (REM), longer REM latency, and more sleep complaints. Sleep-dependent memory consolidation of nonemotional images was present in all participants. However, consolidation of negative images was only present in the non-TBI group. A lack of differentiation between the TBI Sleep and Wake groups was due to poor performance in the sleep group and, unexpectedly, enhanced performance in the wake group. Additionally, although the non-TBI participants habituated to negative images over a waking period, the TBI participants did not. Conclusions: We propose disrupted sleep-and wake-dependent emotional processing contributes to poor emotional outcomes following chronic, mild TBI. This work has broad implications, as roughly one-third of the US population will sustain a mild TBI during their lifetime.

Sleep, Sleep Disorders, and Circadian Health following Mild Traumatic Brain Injury in Adults: Review and Research Agenda

“…In light of the frequent occurrence and adverse consequences of sleep disturbances in mTBI, investigators have sought to identify a causal link between sleep and mood outcomes. Mantua and colleagues 71 conducted a study to examine sleep-dependent emotional processing among individuals with chronic mTBI (n = 40) and controls (n = 41). Participants viewed negative and neutral images both before and after a 12-h period including or not including sleep, and memory recognition was assessed at session two.…”

“…These results suggest sleep and wake-dependent emotional processing might underlie poor emotional outcomes associated with chronic mTBI. 71 Sleep Disorders in mTBI Sleep pathologies are described in terms of insufficient sleep quantity, altered sleep architecture, clinical sleep disorders, and circadian misalignment. Sleep and circadian disturbances are associated with numerous and potentially severe daytime consequences.…”

A Review of Chronic Pain and Cognitive, Mood, and Motor Dysfunction Following Mild Traumatic Brain Injury: Complex, Comorbid, and/or Overlapping Conditions?

“…Sleep alterations are also present in this population, which may further exacerbate emotional symptoms. Patients with mTBI have less rapid eye movement (REM), longer REM latency, and more sleep complaints [ 25 ]. Taken in context with sleep quality and quantity having a significant influence on the development and persistence of pain, mood, and movement disorders, these findings not only highlight an important consequence of mTBI but also suggest that disorders of sleep, pain, mood, and movement may have shared mechanisms and exponential effects in patients with mTBI.…”

Environmental Subconcussive Injury, Axonal Injury, and Chronic Traumatic Encephalopathy

“…Fluoride accumulation is shown to calcify bones and interestingly the pineal gland ( 63 , 64 ). The clinical relevance of calcified pineal gland has not been fully elucidated; however, it poses an interesting question given the pineal gland’s role in sleep regulation regarding a potential correlation because sleep disruption is a characteristic symptom associated with many neurodegenerative diseases, as well as acute brain trauma ( 65 – 67 ). More research seems indicated.…”