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Sleep-wake disorders in patients with traumatic brain injury
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Sleep-wake disorders in patients with traumatic brain injury
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Nov 2017. | This topic last updated: May 30, 2017.

INTRODUCTION — Sleep-wake disturbances are among the most prevalent and persistent sequelae of traumatic brain injury (TBI) [1-3]. Patients suffering from TBI of any severity, in both the acute and chronic phases, commonly report excessive daytime sleepiness, increased sleep need, insomnia, and sleep fragmentation [4-6]. Identification and treatment of sleep disorders in patients with TBI is important and can complement other efforts to promote maximum functional recovery.

The clinical features, evaluation, and treatment of sleep-wake disorders in patients with TBI are discussed here. The classification of TBI and management of other complications of head injury, including the postconcussion syndrome, are reviewed separately. (See "Traumatic brain injury: Epidemiology, classification, and pathophysiology" and "Acute mild traumatic brain injury (concussion) in adults" and "Postconcussion syndrome" and "Management of acute severe traumatic brain injury".)

EPIDEMIOLOGY — In the acute and subacute phases after mild TBI, sleep-wake complaints of any kind are reported by approximately one-third of patients within the first 10 days after injury and up to 50 percent at six weeks post-injury [7-9]. The prevalence is even higher among individuals with severe TBI [10,11]. In a prospective study of 205 patients admitted to an acute rehabilitation hospital after severe TBI, 84 percent had sleep-wake disturbances upon admission and 66 percent continued to have disturbances at one month post-injury [11].

Sleep-wake disturbances are also common in the chronic phase after injury. In a meta-analysis of 1706 survivors of TBI across 21 studies, the most common sleep disturbances were [12]:

Insomnia (50 percent)

Difficulty maintaining sleep (50 percent)

Poor sleep efficiency on polysomnography (PSG) (49 percent)

Early morning awakenings (38 percent)

Nightmares (27 percent)

A limitation of many of the studies in the meta-analysis is that insomnia was measured subjectively and not objectively using electrophysiological testing [12]. In at least one study, brain-injured patients tended to overestimate insomnia when subjective and objective measures were compared [13].

Smaller studies using actigraphy, PSG, and multiple sleep latency testing have found a similar trend across a broader range of sleep symptoms [5,14]. In a prospective study of 65 patients with TBI of all ranges of severity, sleep-wake disturbances were reported by 72 percent of patients six months post-injury; the most common abnormalities on formal testing were excessive daytime sleepiness (28 percent) and increased sleep need (22 percent) [14]. In the same cohort (n = 51), two-thirds of patients had persistent sleep-wake disturbances at three years post-injury [15].

Sleep-related breathing and movement disorders are also prevalent in the chronic phases of TBI. The reported prevalence of obstructive sleep apnea ranges from 25 to 35 percent [5,16].

PATHOPHYSIOLOGY — The pathophysiology and neuropathology of sleep-wake disturbances after TBI are under investigation in both animal models and humans [3].

Given the prominence of excessive daytime sleepiness and nighttime sleep fragmentation in patients with TBI, several studies have focused on the neuropeptide orexin (also known as hypocretin), which is deficient in human narcolepsy type 1 (narcolepsy with cataplexy). Orexin neurons in the posterior hypothalamus excite several downstream wake-promoting monoaminergic and cholinergic systems and therefore possess a strong wake-promoting effect [17].

Measured orexin levels in the cerebrospinal fluid (CSF) were low in 95 percent of 44 patients within the first four days of moderate to severe TBI [18]. A small study of four patients who died 7 to 42 days after severe TBI showed a 27 percent reduction in the number of orexin neurons compared with non-TBI controls [19]. Likewise, studies using mouse models of mild and moderate TBI show decreased brain orexin levels and decreased orexin neuron activation during wakefulness after brain injury [20,21].

Deficits in orexin signaling are unlikely to explain all sleep-wake abnormalities, however, especially in the chronic phase of TBI when CSF orexin levels for the most part return to baseline [14]. Although there are several other wake-promoting brain regions (eg, ventral periaqueductal gray, locus coeruleus, basal forebrain, and tuberomammillary nucleus), their roles in TBI have not yet been studied. A postmortem human study in 12 patients with severe TBI showed a 41 percent loss of histaminergic neurons in the tuberomammillary nucleus compared with 16 matched control subjects [22].

Structural brain changes may also play a role in some patients. Abnormal neuroimaging is only found in 5 to 10 percent of patients with mild TBI, although it is likely to miss more subtle brain damage such as diffuse axonal injury or microhemorrhages, which may affect sleep-wake and circadian circuits. In an electrophysiological and imaging study, intracranial hemorrhage was associated with increased sleep need, but this was not influenced by the extent and location of the intracranial hemorrhage [23].


Symptom spectrum — The most common manifestations of sleep-wake disorders after TBI are excessive daytime sleepiness, increased sleep need, and insomnia. Less commonly, patients experience circadian rhythm disturbances and abnormal movements or behaviors during sleep, such as sleep talking, bruxism, and dream enactment.

Excessive daytime sleepiness — Excessive daytime sleepiness, distinct from fatigue, is a prominent symptom after TBI. The reported frequency in patients with TBI ranges from approximately 50 to 80 percent, compared with an expected rate in the general population of 10 to 25 percent [16,24-26].

Excessive daytime sleepiness refers to the inability to maintain wakefulness and alertness during the major waking episodes of the day, with sleep occurring unintentionally or at inappropriate times [27]. Sleepiness manifests mainly during sedentary activities, in contrast with fatigue, which typically affects pursuit of more active goals. (See "Approach to the patient with excessive daytime sleepiness", section on 'Definitions'.)

Some individuals with excessive daytime sleepiness after TBI describe daytime sleep attacks, similar to those experienced by patients with narcolepsy. However, additional symptoms of narcolepsy, such as cataplexy and sleep paralysis, are uncommon and have been described only in rare case reports [28]. No patient has been reported with the complete syndrome of post-traumatic hypocretin-deficient narcolepsy with cataplexy.

Excessive daytime sleepiness is often but not always accompanied by a short time to fall asleep on the multiple sleep latency test (MSLT). A mean sleep latency of ≤8 minutes is generally considered to be abnormal. In addition to a reduced mean sleep latency, some patients have two or more sleep-onset rapid eye movement (REM) periods (SOREMPs) during the MSLT, fulfilling electrophysiological criteria for narcolepsy type 2 (narcolepsy without cataplexy). However, before diagnosing narcolepsy after TBI, insufficient sleep syndrome must be ruled out, as chronic sleep deprivation can produce increased REM sleep pressure. (See "Clinical features and diagnosis of narcolepsy in adults", section on 'Diagnostic criteria'.)

In one prospective study of 65 patients six months after TBI, 28 percent had post-traumatic sleepiness and 3 percent met criteria for narcolepsy type 2 [14]. A similar study found that 6 percent of patients met MSLT criteria for narcolepsy type 2 at a mean of 64 months after TBI, a marked increase compared with the prevalence in the general population (<0.1 percent) [5,29]. Other studies have also found that sleepiness persists long term in many patients [30]. (See 'Natural history' below.)

Increased sleep need (pleiosomnia) — Increased sleep need is common after TBI. Since the term hypersomnia is often used for both excessive daytime sleepiness and increased sleep need, the term pleiosomnia has been proposed to denote an increased need for sleep per 24 hours compared with the patient's pre-TBI baseline [31].

In a prospective electrophysiological study of 65 patients who were studied six months after TBI, 22 percent reported that they needed at least two more hours of sleep in a 24-hour period than before the injury [14]. This general pattern was confirmed in a prospective case control study that included 42 patients with TBI studied six months after injury, in which post-TBI patients slept 1.2 hours more than matched controls [23]. This pattern persisted at 18 months [30]. (See 'Natural history' below.)

In both of these studies, patients with TBI underestimated both excessive daytime sleepiness and pleiosomnia [14,23]. In addition, daytime sleepiness was more pronounced in TBI patients with shorter sleep duration, suggesting that sleepiness might constitute an epiphenomenon of insufficient sleep in subjects needing more sleep than usual.

Insomnia — Insomnia (ie, difficulty falling asleep or sleeping through the night with daytime consequences such as fatigue or irritability) has been widely documented among patients in the chronic phases after TBI. Unlike most other sleep disturbances after TBI, insomnia complaints are more prevalent in mild TBI compared with moderate or severe TBI [32].

Symptoms of insomnia include difficulty initiating sleep, sleep fragmentation, and early morning awakenings [6]. The spectrum of insomnia symptoms after TBI is demonstrated in the following studies:

A retrospective study of 202 patients with TBI (37 percent with moderate to severe TBI) at a mean of two years post-injury found that 65 percent of patients with mild TBI complained of insomnia, compared with 41 percent of patients with moderate to severe TBI [32]. Approximately one-quarter of patients with mild TBI continued to complain of insomnia five years post-injury.

In another retrospective study, 75 percent of 145 patients with mild TBI reported insomnia after injury; the most common manifestation was waking up too early [33].

Among military personnel, the incidence of insomnia appears to increase in a dose-dependent fashion with the number of head injuries incurred, ranging from 6 percent in those with no history of TBI, 20 percent after a single TBI, and 50 percent in those with multiple episodes [34].

The presence of insomnia correlates with decreased satisfaction in life, anxiety, and depression [35]. (See "Overview of insomnia in adults".)

Circadian rhythm disturbances — There is preliminary evidence that circadian rhythm disorders, including delayed sleep phase or irregular sleep-wake type, occur with increased frequency in patients with TBI.

Symptoms of a circadian rhythm disorder are easy to overlook and are often misattributed to insomnia. In one study, 36 percent of individuals who complained of insomnia after mild TBI instead met criteria for a circadian rhythm disorder [36,37]. The distinction is important, since treatment approaches differ. (See 'Treatment' below.)

Patients with delayed sleep-wake phase syndrome typically go to bed late and wake up late relative to the general population. They may complain of difficulty falling asleep at usual bed times, and difficulty getting up at standard wake times. This may be confused with insomnia, in which patients have difficulty falling asleep or staying asleep regardless of bed time. (See "Delayed sleep-wake phase disorder", section on 'Clinical features'.)

Patients with an irregular sleep-wake rhythm lack a clearly defined circadian rhythm of sleep and wakefulness, such that sleep and wake patterns appear somewhat random across days to weeks. They may complain of both difficulty sleeping at the desired time and excessive daytime sleepiness and naps. Although insomnia can be accompanied by complaints of excessive daytime sleepiness, it is more commonly associated with difficulty napping or sleeping during the day. (See "Overview of circadian sleep-wake rhythm disorders".)

In the acute phase after TBI, circadian rhythm disturbances may be particularly prominent, although more studies are needed. Actigraphy recordings in 16 patients with moderate to severe TBI within the first 10 days post-injury revealed severe fragmentation of the rest-activity cycle, reflecting severe sleep-wake fragmentation and possibly consistent with an irregular sleep-wake type circadian rhythm disorder [38]. Nevertheless, it is difficult to exclude the confounding effects of pain and anxiety in the acute phase of TBI.

Abnormal movements or behaviors during sleep — Small studies have suggested that parasomnias and sleep-related movement disorders may occur with increased frequency after TBI in both the acute and chronic phases.

Symptoms include dream reenactment behaviors characteristic of rapid eye movement (REM) sleep behavior disorder (RBD), somniloquy (sleep talking), sleep-related enuresis, and sleep-related bruxism (teeth grinding).

In a case control study of 19 adolescents with a history of mild TBI three years before, the following symptoms were more common in patients with TBI compared with controls: somniloquy (42 versus 19 percent), bruxism (42 versus 6 percent), and enuresis (21 versus 0 percent) [39]. Rates of somnambulism were similar (16 versus 19 percent).

In another study, parasomnias accounted for 25 percent of the presenting sleep-related complaints among 60 adults being evaluated at least three months post-TBI [40].

Sleep-disordered breathing — Sleep-related breathing disorders, including obstructive sleep apnea (OSA) and central sleep apnea (CSA), may occur with increased frequency after TBI, although data are relatively sparse. Small studies have found an OSA prevalence ranging from 25 to 35 percent in TBI survivors, which is higher than rates in most general population-based studies [5,41,42]. (See "Overview of obstructive sleep apnea in adults", section on 'Epidemiology'.)

Many symptoms of OSA overlap with those of TBI as well as other sleep-wake disorders. The most common symptoms of OSA in the general population are daytime sleepiness and loud snoring. Additional symptoms include waking up gasping or choking, morning headaches, nocturia, moodiness or irritability, lack of concentration, and memory impairment. On physical examination, patients are often obese and may have evidence of a crowded oropharynx and increased neck circumference. Clinical features of CSA are similar, except that obesity is less likely to be present. (See "Clinical presentation and diagnosis of obstructive sleep apnea in adults", section on 'Clinical features'.)

Important comorbidities — Psychiatric disorders and chronic pain commonly co-occur in patients with TBI. These comorbidities are important to recognize, since they may cause or exacerbate a wide range of sleep-wake disturbances.

Depression and anxiety – Patients with TBI have high rates of depression and anxiety. In some, depression and anxiety are premorbid conditions that may be exacerbated after TBI; in others, depression or anxiety emerges after TBI [43,44].

Nearly 75 percent of adults with depression report sleep difficulties, including insomnia, excessive daytime sleepiness, increased sleep need, early morning awakenings, and sleep fragmentation [45]. TBI may exacerbate sleep-wake disturbances in patients with comorbid depression and anxiety [46,47]. Conversely, untreated depression or anxiety may prevent successful treatment of sleep disturbances in patients with TBI.

Post-traumatic stress disorder – TBI and post-traumatic stress disorder (PTSD) commonly co-occur, especially in the military population, rendering a much higher incidence of PTSD-related nightmare disorder and dream enactment compared with the non-TBI population [48,49]. TBI may increase vulnerability to PTSD by damaging autonomic networks in the central nervous system [50].

Chronic pain – Patients with TBI report more difficulty managing pain [51]. In a systematic review of 23 studies and over 4000 patients with TBI, chronic pain affected 52 percent of patients [52]. Chronic pain affects sleep quality by fragmenting sleep and reducing slow-wave sleep [53].

Electrophysiologic changes — Electrophysiologic changes in sleep are apparent in both the acute and chronic stages of TBI and vary according to the severity of the injury.

In the acute stage after mild TBI, patients may show longer sleep latency and lower sleep efficiency, along with lower delta power (but higher alpha and beta power) during non-REM (NREM) sleep [54,55]. This electroencephalogram (EEG) pattern of fast frequencies intruding into deep NREM sleep has been described in insomnia patients and may represent a deficit in turning off arousal [56].

EEG patterns in the acute stage after severe TBI may have prognostic implications. A retrospective study of 64 adults with severe TBI admitted to the intensive care unit found that sleep features seen on continuous EEG monitoring were associated with significantly better functional outcomes, including improved modified Rankin Scale scores and discharge to home or acute rehabilitation after hospitalization [57]. In animal models, enhancing deep sleep acutely after TBI decreases the burden of diffuse axonal injury and spares cognitive function [58].

Chronic changes in sleep architecture have also been described after TBI across of range of severities.

A review of 105 polysomnograms in patients with severe chronic brain injuries identified lack of deep sleep and increased sleep fragmentation in those more severely affected [59].

In a case control study that included 26 adults with chronic (one year or more), mild TBI, PSG revealed more stage N2 sleep compared with deeper stages of sleep and less REM sleep [60].

PSG at six months in patients with TBI of any severity enrolled in a prospective case control study showed consolidated (ie, less fragmented) NREM sleep and a trend towards a higher amount of delta power compared with controls [23].

Compared with controls, PSG in 20 adults with mild TBI showed longer durations between spontaneous K-complexes and fewer evoked K-complexes in response to stimuli, which is thought to reflect inhibition of information processing during sleep [61-63].

Natural history — Many of the sleep-wake disturbances described above appear to persist long term after TBI. This was illustrated by a prospective case-control study in which 31 out of 60 patients with TBI of any severity were evaluated at 18 months after injury [30]. Key findings included the following:

Pleiosomnia persisted at 18 months, independent of the severity of TBI and other clinical characteristics. Compared with healthy controls, patients with TBI required significantly more sleep per 24 hours at both six months (8.3 versus 7.1 hours) [23] and 18 months after injury (8.1 versus 7.1 hours) [30].

Two-thirds of patients with TBI had objective evidence of excessive daytime sleepiness on MSLT at 18 months, and symptoms were largely unrecognized by patients.

As in the earlier phases of injury, patients underestimated their degree of sleepiness and sleep need on sleep logs and questionnaires.

Cross-sectional studies indicate that insomnia is also very common in patients with a history of TBI, although prospective studies are needed to better understand the natural history of this symptom in the months and years following injury. (See 'Insomnia' above.)

EVALUATION — Sleep-wake disorders are common after TBI and should be suspected in patients presenting with a broad range of sleep complaints. The goals of the evaluation are to define the sleep complaint, diagnose specific treatable sleep disorders, and identify any additional medical and psychiatric comorbidities that may be contributing to the sleep disturbances.

Most sleep-wake disorders are diagnosed using a combination of both subjective and objective screening tools in the clinic [64]. Subjective tools include a sleep history and questionnaires completed by patients, while objective tools include actigraphy, polysomnography (PSG), multiple sleep latency test (MSLT), and the maintenance of wakefulness test (MWT).

Patients with TBI may overestimate insomnia complaints, whereas they underestimate excessive daytime sleepiness and sleep need [13,23,24,30,65,66]. These observations stress the importance of objective sleep testing in patients with TBI.

History — The goals of the history are to refine the sleep complaint and identify potential causes. Questions should target multiple sleep domains, including perceived sleep quality, sleep latency, sleep duration, sleep disturbances (including abnormal movements or behaviors during sleep), sleep medication use, daytime dysfunction, and daytime sleepiness. The Pittsburgh Sleep Quality Index (PSQI) (table 1 and table 2) is a clinical questionnaire encompassing multiple sleep domains that can be useful to guide a structured interview [67] and has been partially validated in the TBI population [24,68,69].

For patients who complain predominantly of excessive daytime sleepiness, the history should attempt to differentiate sleepiness from other common complaints such as fatigue, lack of energy, or weakness. The Epworth Sleepiness Scale (ESS) (table 3) (calculator 1) is a widely used instrument for quantifying subjective sleepiness that has also been partially validated in patients with TBI [24,68,69]. Scores of 10 or more points are generally considered abnormal and support the complaint of excessive daytime sleepiness. As with other measures, ESS scores should be used in combination with other tools, as patients with TBI may underestimate their degree of daytime impairment [24]. (See "Quantifying sleepiness", section on 'Epworth Sleepiness Scale (ESS)'.)

In patients whose predominant complaint is insomnia, the history should elicit a detailed description of sleep habits over a 24-hour period and trends over time. This includes questions about sleep quantity and quality, quality of the sleep environment, and daytime symptoms. A sleep diary or log, to be completed by the patient in advance or following the initial evaluation, can be particularly helpful to supplement the history (table 4 and table 5).

Sleep diaries have the advantage of assessing sleep quality, sleep quantity, and circadian patterns over many days or weeks. Review of a sleep diary can provide clues to circadian rhythm disturbances, which are often mistaken for insomnia (see 'Circadian rhythm disturbances' above). To more objectively assess circadian rhythm disorders, actigraphy recordings for two to three weeks are very useful. (See 'Actigraphy' below.)

Collateral information from family members and bed partners should be obtained if possible. In particular, bed partners are a more reliable source than the patient for information about snoring, periodic limb movements, acting out of dreams, sleep walking, and other parasomnias. Loud or habitual snoring and witnessed apneas can suggest a diagnosis of obstructive apnea and should prompt PSG, especially if the presenting complaint is daytime sleepiness. (See 'Polysomnography' below.)

Given the frequent comorbidity of psychiatric disorders in patients with TBI and their implications for treatment, the history should also probe for symptoms of depression, anxiety, and post-traumatic stress disorder (PTSD). Patients can be screened for depression by asking about depressed mood, loss of interest or pleasure in activities, change in appetite or weight, psychomotor retardation or agitation, low energy, poor concentration, thoughts of worthlessness or guilt, and recurrent thoughts of death or suicide. A two- or nine-item screening tool such as the PHQ-9 is easy to use, reliable, and valid in primary care settings (table 6). (See "Screening for depression in adults".)

The medication list should be reviewed in all patients to identify potentially contributing agents. A wide variety of medications used in the management of acute complications of TBI may contribute to daytime sleepiness, including antiepileptic drugs, opioid analgesics, benzodiazepines, antipsychotics, and certain antidepressants. The list is similarly long for drugs that may cause or aggravate insomnia (eg, glucocorticoids, bronchodilators, and central nervous system stimulants). Alcohol use and substance abuse are also relevant.

Laboratory studies — Basic laboratories are likely to be of low yield in the evaluation of sleep-wake disorders. Serum thyroid stimulating hormone (TSH) and ferritin may be useful in ruling out sleep-wake disturbances secondary to thyroid disorders and iron insufficiency. (See "Clinical features and diagnosis of restless legs syndrome/Willis-Ekbom disease and periodic limb movement disorder in adults", section on 'Low iron stores'.)

Cerebrospinal (CSF) markers and saliva melatonin measurements are not currently used clinically but may hold promise in the future.

Actigraphy — Actigraphy records rest-activity patterns using an accelerometer to detect motion, often combined with a light detector, usually worn on the nondominant wrist or waist. Actigraphy results are an objective counterpart to data obtained from a sleep diary. (See "Overview of actigraphy".)

Although not widely available for clinical purposes in the United States and moderately expensive, actigraphy can be useful as an objective measure of sleep-wake patterns in patients with a complaint of excessive daytime sleepiness. It also has the advantage over PSG of recording activity patterns over long periods of time (ie, weeks to months). An actigraphy pattern showing much longer sleep times on weekends than weekdays supports a diagnosis of insufficient sleep syndrome in patients with a complaint of daytime sleepiness.

Actigraphy has been used in many studies of adult patients with TBI [10,14,31,38,70,71], though caution should be exercised regarding using activity as a surrogate for sleep in patients with locomotor limitations including spasticity, paresis, depression, and/or agitation.

Polysomnography — PSG is not necessary in all patients with sleep-wake complaints but should be obtained in selected patients, based on the history. Given the higher prevalence of sleep-wake disorders in patients with TBI, there should be a low threshold to obtain PSG for any sleep history or complaint that is suspicious for sleep apnea (eg, excessive daytime sleepiness, snoring, comorbid obesity) or hypersomnia.

In-laboratory PSG is the gold standard for diagnosing certain clinical sleep-wake disorders, including sleep-related breathing disorders and periodic limb movement disorder, and provides information on sleep architecture, sleep efficiency, and physiologic parameters during sleep. The electroencephalography (EEG) collected during in-laboratory PSG allows comprehensive assessment of sleep staging and arousals. If obstructive sleep apnea is the overriding suspicion based on the history, home sleep apnea testing is an alternative to in-laboratory PSG. (See "Home sleep apnea testing for obstructive sleep apnea in adults".)

By contrast, clinical history alone may suffice in patients whose primary complaint is insomnia or circadian rhythm disturbance.

Multiple sleep latency test — The multiple sleep latency test (MSLT) is a daytime test using electrophysiological recordings, including EEG, and is a validated objective measure used to quantify daytime sleepiness [72]. The MSLT is performed the day after nocturnal PSG. For results to be reliable, individuals must have had sufficient sleep the night before the test and must not have been sleep-deprived recently. (See "Quantifying sleepiness", section on 'Multiple sleep latency test (MSLT)'.)

Like PSG, the MSLT is not necessary in all patients with sleep-wake complaints but is suggested in selected patients, particularly those with a chief complaint of excessive daytime sleepiness who have had sleep apnea ruled out by PSG.

A mean sleep latency less than eight minutes is generally considered to be objective evidence of excessive daytime sleepiness. Several specific sleep disorders can also be diagnosed in the appropriate clinical setting. Examples include the following:

If excessive daytime sleepiness persists for three months after TBI with a mean sleep-onset latency of less than eight minutes and with fewer than two sleep-onset rapid eye movement (REM) periods, then the diagnosis is "hypersomnia caused by medical condition," or "post-traumatic hypersomnia" [73].

In the case of a short mean sleep-onset latency and the occurrence of multiple sleep-onset REM periods, "post-traumatic narcolepsy" or "narcolepsy caused by medical condition" should be distinguished from insufficient sleep syndrome (ie, chronic sleep deprivation), which can also present with enhanced REM sleep pressure [74].

TREATMENT — Behavioral and pharmacologic treatments are available for the majority of sleep-wake disorders in patients with TBI. Treatment varies according to the dominant symptom or specific sleep disorder as well as relevant comorbidities. Beyond symptomatic improvement, the potential benefits of successful treatment of sleep-wake disorders in the TBI population include improvement in functional outcomes and quality of life [10,75,76].

Symptom-directed therapy

Excessive daytime sleepiness — Excessive daytime sleepiness in patients with TBI is multifactorial in many patients. Any underlying conditions identified during the evaluation that may contribute to daytime sleepiness should be addressed and treated. This may include treatment of depression, initiation of positive airway pressure (PAP) therapy for obstructive sleep apnea (OSA), treatment of any underlying circadian rhythm disturbances, treatment of restless legs syndrome, and/or elimination of offending medications if safe and feasible. Also, insufficient sleep syndrome should be treated with extended sleep times.

For patients with persistent symptoms or no other identifiable causes, pharmacologic treatment options include wakefulness-promoting agents (modafinil, armodafinil) and stimulants such as methylphenidate. Of these, we suggest modafinil or armodafinil as first-line therapy, based on supporting data in case reports and two small randomized trials in patients with TBI, as well as indirect data from larger randomized trials in patients with narcolepsy [77,78]. (See "Treatment of narcolepsy in adults", section on 'Modafinil'.)

In a randomized, placebo-controlled, multicenter trial of 117 adults with a history of TBI, baseline Epworth Sleepiness Scale (ESS) score ≥10, and sleep latency less than eight minutes on a multiple sleep latency test (MSLT), patients treated with armodafinil 250 mg daily for 12 weeks showed significant improvement in sleep latency compared with placebo (+7.2 versus +2.4 minutes) [77]. Subjective sleepiness was improved on some measures but not others at various doses of armodafinil (50, 150, or 250 mg/day). Similar results were reported in a smaller randomized trial of modafinil [78]. Modafinil and armodafinil were well tolerated in both trials; headache is the most common side effect of both drugs.

Modafinil is typically started at a dose of 100 mg twice daily (first dose upon awakening, second dose at mid-day) and can be titrated up to 200 mg twice daily as needed by symptomatic benefit. Armodafinil has a longer half-life and is typically dosed at 50, 150, or 250 mg once daily in the morning.

Methylphenidate is an alternative to modafinil and armodafinil that is less well studied in patients with TBI [79,80].

Morning bright light therapy has been studied as a nonpharmacologic treatment option in post-traumatic fatigue and may also have some benefit for daytime sleepiness, although data are limited. In a small randomized trial of 30 patients with TBI and persistent fatigue, patients treated with home-based short wavelength (blue) light therapy showed reduced fatigue and daytime sleepiness after four weeks compared with lower-intensity yellow light therapy and no treatment [81].

Other novel treatments being studied include dietary supplementation with branched chain amino acids, which improved wakefulness in an animal model of mild to moderate TBI [20].

Insomnia — Pharmacologic and behavioral approaches for insomnia in patients with a history of TBI are generally similar to those in the general population. (See "Treatment of insomnia in adults".)

In patients with TBI, special consideration should be paid to cognitive impairment, which may increase the risk of side effects from sedative/hypnotic medications, and comorbid affective disorders, which are common in patients with TBI and may require additional therapy.

With all pharmacologic therapies for insomnia, patients should be treated with the lowest effective dose and for the shortest time period possible [82,83]. Limited data in patients with TBI suggest that benzodiazepine and nonbenzodiazepine receptor agonists are similarly effective [84].

Behavioral approaches that have been studied in the TBI population include cognitive-behavioral therapy for insomnia (CBTi) and acupuncture [85,86]. In one small randomized study, acupuncture did not affect objective measures of sleep by actigraphy but did improve subjective sleep quality, cognitive function, and the ability to taper sleep medication use [86].

Pleiosomnia — There are no specific therapies for increased sleep need after TBI, and more research is needed to understand its pathophysiology. Nonetheless, the symptom can be quite disturbing to patients, particularly those with a sleep need of 12 hours per day or more.

One possibility is that increased sleep need represents a necessary physiologic response to the injured brain; if this is the case, curtailing sleep could counteract a necessary healing response. On the other hand, pleiosomnia might be solely due to damage to wake-maintaining systems. In this case, tailored treatment strategies may emerge in the future.

Specific disorders

Circadian rhythm disorders — Therapeutic approaches to circadian sleep-wake rhythm disorders in the general population include behavioral modifications, light therapy, and melatonin. (See "Delayed sleep-wake phase disorder", section on 'Management'.)

These approaches have been used with some success in patients with TBI in cases reports and small studies [87,88]. In one case report, delayed sleep-wake phase syndrome after TBI in a 15-year-old girl was successfully treated with evening melatonin (5 mg) [87]. Melatonin (5 mg) and amitriptyline (25 mg) were examined in a pilot randomized, placebo-controlled crossover study of seven patients with post-TBI chronic sleep disturbances [88]. While there were no significant differences in sleep latency, duration, quality, or daytime alertness for either drug compared with baseline, there were some encouraging trends, in that patients on melatonin reported improved daytime alertness, and patients on amitriptyline reported increased sleep duration.

Parasomnias — Non-rapid eye movement (NREM) parasomnias are more common in children than adults, but in some cases symptoms persist or arise in adulthood. Patients with TBI often have comorbid post-traumatic stress disorder (PTSD), which can result in nightmares and other NREM parasomnias.

All parasomnias are exacerbated by sleep deprivation or sleep fragmentation, and therefore the first-line approach to treatment is to identify and treat causes of poor sleep quality (ie, improve sleep hygiene, avoid alcohol, treat sleep apnea and restless legs syndrome). PTSD-related nightmares can be effectively treated with prazosin and/or image-rehearsal therapy with or without cognitive behavioral therapy for insomnia [89]. If parasomnias persist despite treatment of secondary causes, and are bothersome to the patient, low-dose clonazepam is often helpful (ie, 0.5 to 2 mg nightly). (See "Pharmacotherapy for posttraumatic stress disorder in adults".)

In patients with REM sleep behavior disorder, which can result in violent dream enactment, establishing a safe sleeping environment is the primary goal of treatment. This can be achieved through modification of the sleep environment and pharmacotherapy, if necessary. Medications known to cause or exacerbate REM sleep behavior disorder, such as serotonin reuptake inhibitors, serotonin-norepinephrine reuptake inhibitors, and tricyclic antidepressants, should be discontinued or avoided if possible. Low-dose clonazepam and high-dose melatonin are effective therapies in patients with frequent, disruptive or injurious behaviors. (See "Rapid eye movement sleep behavior disorder", section on 'Treatment'.)

Obstructive sleep apnea — Behavioral modifications, including weight loss, and positive airway pressure therapy are the cornerstones of therapy for OSA. Both have been shown to improve outcomes in the general population in randomized trials [90-92], and their effects may be additive [93]. (See "Management of obstructive sleep apnea in adults", section on 'General approach'.)

Individuals with OSA in the post-TBI setting should be treated similarly, although literature in this specific patient population is sparse. In the one study that examined continuous PAP (CPAP) therapy in patients with TBI, CPAP therapy was associated with a decreased apnea hypopnea index (AHI) and improved sleep quality three months after administration, but it did not improve excessive daytime sleepiness as measured by the MSLT [94]. CPAP adherence and medication side effects were not taken into account, however, which could explain the lack of improvement in daytime sleepiness.

The potential consequences of untreated OSA in patients with TBI were illustrated by a small case control study that included 19 TBI patients with OSA and 16 TBI patients without OSA on nocturnal polysomnography [95]. Patients with OSA performed significantly worse than those without OSA on tasks of sustained attention and memory.


Sleep-wake disturbances are some of the most common sequelae of traumatic brain injury (TBI), reported by approximately one-third of patients in the acute phase after mild injury and approximately half of patients in the chronic phase. (See 'Epidemiology' above.)

The pathophysiology of post-traumatic sleep-wake disturbances is not well understood. Reductions in wake-promoting neurotransmitters such as orexin and histamine have been implicated in small studies, but they are unlikely to account for the full spectrum of abnormalities, particularly in the chronic phase. (See 'Pathophysiology' above.)

The most common manifestations of sleep-wake disorders after TBI are excessive daytime sleepiness, increased sleep need, and insomnia. Less commonly, patients experience circadian rhythm disturbances; abnormal movements or behaviors during sleep, such as sleep talking, bruxism, and dream enactment; and sleep-disordered breathing. (See 'Symptom spectrum' above.)

Sleep-wake disorders are diagnosed by history, supplemented by objective sleep testing in selected patients. The goals of the evaluation are to refine the sleep complaint, diagnose specific treatable sleep disorders, and identify any additional medical and psychiatric comorbidities that may be contributing to the sleep disturbances. (See 'History' above.)

Treatment varies according to the dominant symptom or specific sleep disorder as well as relevant comorbidities. Treatment strategies in patients with a history of TBI are generally similar to those in the general population. (See 'Symptom-directed therapy' above and 'Specific disorders' above.)

In patients with TBI who have persistent and bothersome excessive daytime sleepiness that cannot be explained by other causes or comorbidities, we suggest treatment modafinil or armodafinil (Grade 2B). (See 'Excessive daytime sleepiness' above.)

Pharmacologic and behavioral approaches for insomnia in patients with a history of TBI are generally similar to those in the general population. Special consideration should be paid to cognitive impairment, which may increase the risk of side effects from sedative/hypnotic medications, and comorbid affective disorders, which are common in patients with TBI and may require additional therapy. (See 'Insomnia' above.)

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