Persisting Insomnia Following Traumatic Brain Injury

Tobe, Edward H.; Schneider, Jay S.; Mrozik, Thaddeus; Lidsky, T.I.

doi:10.1176/jnp.11.4.504

Cited by 10 publications

(5 citation statements)

References 8 publications

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“…Despite the widely accepted hypothesis that damage to the cerebral structures regulating sleep might result in sleep disturbance in TBI patients, no convincing neuroimaging evidence has been obtained. Some studies found no structural abnormalities on cerebral imaging (CT or MRI scans) despite significant sleep disturbance [33,34]. Others failed to illustrate relationship between location of injury on CT scan and presence of sleep disturbance [14].…”

Section: Discussionmentioning

confidence: 99%

Risk Factors Associated with Sleep Disturbance following Traumatic Brain Injury: Clinical Findings and Questionnaire Based Study

et al. 2013

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BackgroundSleep disturbance is very common following traumatic brain injury (TBI), which may initiate or exacerbate a variety of co-morbidities and negatively impact rehabilitative treatments. To date, there are paradoxical reports regarding the associations between inherent characteristics of TBI and sleep disturbance in TBI population. The current study was designed to explore the relationship between the presence of sleep disturbance and characteristics of TBI and identify the factors which are closely related to the presence of sleep disturbance in TBI population.Methods98 TBI patients (72 males, mean age ± SD, 47 ± 13 years, range 18-70) were recruited. Severity of TBI was evaluated based on Glasgow Coma Scale (GCS). All participants performed cranial computed tomography and were examined on self-reported sleep quality, anxiety, and depression.ResultsTBI was mild in 69 (70%), moderate in 15 (15%) and severe in 14 (15%) patients. 37 of 98 patients (38%) reported sleep disturbance following TBI. Insomnia was diagnosed in 28 patients (29%) and post-traumatic hypersomnia in 9 patients (9%). In TBI with insomnia group, 5 patients (18%) complained of difficulty falling asleep only, 8 patients (29%) had difficulty maintaining sleep without difficulty in initial sleep and 15 patients (53%) presented both difficulty falling asleep and difficulty maintaining sleep. Risk factors associated with insomnia were headache and/or dizziness and more symptoms of anxiety and depression rather than GCS. In contrast, GCS was independently associated with the presence of hypersomnia following TBI. Furthermore, there was no evidence of an association between locations of brain injury and the presence of sleep disturbance after TBI.ConclusionOur data support and contribute to a growing body of evidence which indicates that TBI patients with insomnia are prone to suffer from concomitant headache and/or dizziness, report more symptoms of anxiety and depression and severe TBI patients are likely to experience hypersomnia.

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Section: Discussionmentioning

confidence: 99%

Risk Factors Associated with Sleep Disturbance following Traumatic Brain Injury: Clinical Findings and Questionnaire Based Study

et al. 2013

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“…As a consequence, if FPI and secondary hypoxemia reduced the motivational value of food, then food intake would be reduced much less in the light than in the dark, which sustained the largest reductions in accuracy. A second explanation might be that rat's sleep in the light was more fragmented by FPI and secondary hypoxemia than by FPI alone (Tobe et al, 1999). As a consequence, rats in the FPI-hypoxia group were perhaps more likely to commit errors during the dark, which is the photoperiod during which rats were most actively executing the visual discrimination.…”

Section: Light/dark Cyclementioning

confidence: 99%

Secondary Hypoxemia Exacerbates the Reduction of Visual Discrimination Accuracy and Neuronal Cell Density in the Dorsal Lateral Geniculate Nucleus Resulting from Fluid Percussion Injury

Bauman

Widholm

Petras

et al. 2000

Journal of Neurotrauma

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The purpose of this study was to determine the impact of secondary hypoxemia on visual discrimination accuracy after parasagittal fluid percussion injury (FPI). Rats lived singly in test cages, where they were trained to repeatedly execute a flicker-frequency visual discrimination for food. After learning was complete, all rats were surgically prepared and then retested over the following 4-5 days to ensure recovery to presurgery levels of performance. Rats were then assigned to one of three groups [FPI + Hypoxia (IH), FPI + Normoxia (IN), or Sham Injury + Hypoxia (SH)] and were anesthetized with halothane delivered by compressed air. Immediately after injury or sham injury, rats in groups IH and SH were switched to a 13% O2 source to continue halothane anesthesia for 30 min before being returned to their test cages. Anesthesia for rats in group IN was maintained using compressed air for 30 min after injury. FPI significantly reduced visual discrimination accuracy and food intake, and increased incorrect choices. Thirty minutes of immediate posttraumatic hypoxemia significantly (1) exacerbated the FPI-induced reductions of visual discrimination accuracy and food intake, (2) further increased numbers of incorrect choices, and (3) delayed the progressive recovery of visual discrimination accuracy. Thionine stains of midbrain coronal sections revealed that, in addition to the loss of neurons seen in several thalamic nuclei following FPI, cell loss in the ipsilateral dorsal lateral geniculate nucleus (dLG) was significantly greater after FPI and hypoxemia than after FPI alone. In contrast, neuropathological changes were not evident following hypoxemia alone. These results show that, although hypoxemia alone was without effect, posttraumatic hypoxemia exacerbates FPI-induced reductions in visual discrimination accuracy and secondary hypoxemia interferes with control of the rat's choices by flicker frequency, perhaps in part as a result of neuronal loss and fiber degeneration in the dLG. These results additionally confirm the utility of this visual discrimination procedure as a sensitive, noninvasive means of assessing behavioral function after experimental traumatic brain injury.

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“…Reduced sleep efficiency 8 and increased sleep fragmentation post-TBI [9][10][11] have been reported. Some studies have shown increased sleep onset latency (SOL), 8,12 while others have reported no difference. 9,10,13 Findings regarding sleep architecture are also inconsistent, with studies reporting no changes in patients with TBI, 8 increased slow wave sleep, 11 reduced REM sleep, 11,13 increased REM in the second half of the night, 14 no change to REM, 8 or decreased REM onset latency.…”

mentioning

confidence: 99%

“…Several studies (some single case) report no structural abnormalities on cerebral imaging (MRI or CT) despite significant sleep disturbance. 12,17,38 Others have been unable to show associations between location of injury on CT or MRI scan with reports of sleep disturbance. 3 Our own study indicates that cerebral damage associated with TBI may disrupt the neural structures regulating sleep-wakefulness, including synthesis of melatonin by the pineal gland, which may not reliably be revealed with nonfunctional imaging.…”

mentioning

confidence: 99%

Sleep disturbance and melatonin levels following traumatic brain injury

Shekleton¹,

Parcell²,

Redman³

et al. 2010

Neurology

224

156

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Objectives: Sleep disturbances commonly follow traumatic brain injury (TBI) and contribute to ongoing disability. However, there are no conclusive findings regarding specific changes to sleep quality and sleep architecture measured using polysomnography. Possible causes of the sleep disturbances include disruption of circadian regulation of sleep-wakefulness, psychological distress, and a neuronal response to injury. We investigated sleep-wake disturbances and their underlying mechanisms in a TBI patient sample. Methods:This was an observational study comparing 23 patients with TBI (429.7 Ϯ 287.6 days post injury) and 23 age-and gender-matched healthy volunteers on polysomnographic sleep measures, salivary dim light melatonin onset (DLMO) time, and self-reported sleep quality, anxiety, and depression.Results: Patients with TBI reported higher anxiety and depressive symptoms and sleep disturbance than controls. Patients with TBI showed decreased sleep efficiency (SE) and increased wake after sleep onset (WASO). Although no significant group differences were found in sleep architecture, when anxiety and depression scores were controlled, patients with TBI showed higher amount of slow wave sleep. No differences in self-reported sleep timing or salivary DLMO time were found. However, patients with TBI showed significantly lower levels of evening melatonin production. Melatonin level was significantly correlated with REM sleep but not SE or WASO. Conclusions:Reduced evening melatonin production may indicate disruption to circadian regulation of melatonin synthesis. The results suggest that there are at least 2 factors contributing to sleep disturbances in patients with traumatic brain injury. We propose that elevated depression is associated with reduced sleep quality, and increased slow wave sleep is attributed to the effects of mechanical brain damage. Neurology ® 2010;74:1732-1738 GLOSSARY AUC ϭ area under the curve; DLMO ϭ dim light melatonin onset; EOG ϭ electrooculogram; ESS ϭ Epworth Sleepiness Scale; HADS ϭ Hospital Anxiety and Depression Scale; MEQ ϭ Morningness Eveningness Questionnaire; NREM ϭ non-REM; PSQI ϭ Pittsburgh Sleep Quality Index; PTA ϭ posttraumatic amnesia; SE ϭ sleep efficiency; SOL ϭ sleep onset latency; SWS ϭ slow wave sleep; TBI ϭ traumatic brain injury; WASO ϭ wake after sleep onset.Sleep disturbances are common following traumatic brain injury (TBI), reported by 30%-75% of individuals and contributing to ongoing disability.

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Persisting Insomnia Following Traumatic Brain Injury

Abstract: Persisting insomnia secondary to traumatic brain injury, rarely reported and documented, is described in an adult male following head injury. The neuronal mechanisms underlying this sleep disorder as well as the neuropsychological concomitants and therapeutic approaches are discussed.

Cited by 10 publications

References 8 publications

Risk Factors Associated with Sleep Disturbance following Traumatic Brain Injury: Clinical Findings and Questionnaire Based Study

Risk Factors Associated with Sleep Disturbance following Traumatic Brain Injury: Clinical Findings and Questionnaire Based Study

Secondary Hypoxemia Exacerbates the Reduction of Visual Discrimination Accuracy and Neuronal Cell Density in the Dorsal Lateral Geniculate Nucleus Resulting from Fluid Percussion Injury

Sleep disturbance and melatonin levels following traumatic brain injury

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