Sleep Disturbances

Felise S. Zollman and Eric B. Larson

BACKGROUND

What Is a Sleep Disturbance?

• Dyssomnias—disorders that result in insomnia (e.g., sleep apnea)

• Parasomnias—disorders of arousal or sleep stage transition (e.g., nightmares, sleep-walking)

• Sleep disorders caused by medical or psychiatric illness (e.g., traumatic brain injury [TBI], stroke, depression, chronic pain)

The focus of this chapter will be on the most common type of post-TBI sleep disturbance—insomnia. Another common problem often associated with sleep disturbances, fatigue, is addressed in Chapter 13. Although some authors have proposed an association between TBI and other sleep disorders such as sleep apnea, periodic limb movements, and narcolepsy, it is not clear to what extent these conditions may have been present prior to (and perhaps even contributed to the occurrence of) TBI [1]. Detailed discussion of these conditions is beyond the scope of this chapter.

Sleep Architecture

• Five stages—stages I to IV and rapid eye movement (REM) sleep.

• Non-REM sleep—stages I to IV. Stage I is lightest; Stage IV is deep sleep.

• REM sleep—approximately 20% to 25% of total sleep time. During REM sleep, the brain exhibits heightened activity. This is associated with dreaming and with actively maintaining an atonic state, which is mediated by signaling between the pons and the medulla.

Neurophysiology of Sleep and Wakefulness

• Sleep and wakefulness are regulated by interaction between the ventrolateral preoptic nucleus (VLPO) of the hypothalamus and arousal centers in the hypothalamus and brainstem.

• Melatonin-producing cells in the suprachiasmatic nucleus (SCN) of the hypothalamus induce sleep and regulate circadian rhythms.

• Serotonin and norepinephrine pathways promote wakefulness and are thought to play a role in regulating the stages of non-REM sleep.

• Acetylcholine helps maintain arousal and plays a role in REM sleep.

Neuropharmacology and Sleep

• Stimulants (e.g., catecholaminergic medications like methylphenidate) increase wakefulness and decrease REM sleep.

• Caffeine shortens REM latency and decreases non-REM sleep time.

• Antihistamines (e.g., diphenhydramine) increase non-REM sleep via blocking a descending activating histaminergic pathway from the hypothalamus to the tegmentum.

• GABA-ergic drugs (e.g., benzodiazepines) decrease time to sleep onset and increase total sleep time, but this is at the expense of deep (Stages III and IV) sleep and perhaps also REM sleep.

• Melatonin agonists (e.g., ramelteon) decrease sleep onset latency and regulate circadian rhythms.

INSOMNIA

Definition

Insomnia can be clinically defined as the occurrence of trouble sleeping characterized by difficulty falling asleep (i.e., requiring more than 30 minutes to get to sleep), and/or difficulty maintaining sleep (i.e., more than 30 minutes of nocturnal awakening), which occurs at least three nights per week, and results in impairment in daytime functioning [2].

Epidemiology

The widely accepted prevalence figure for insomnia in the general population is 30%.

Diagnosis [2]

• Subjective means include self-report and clinician rating scales such as the Insomnia Severity Index, the Epworth Sleepiness Scale, or the Pittsburgh Sleep Quality Index.

• Objective means of quantifying sleep or insomnia include sleep logs (for inpatients), actigraphy, and polysomnography (PSG).

Sleep log—typically completed by a nurse on an inpatient unit. Patient is briefly observed on an hourly basis and notation of sleep versus wake status is noted for each hour. Drawback—report is typically based observations of 5 minutes or less per hour. Such a limited sample can result in inaccurate data.

Actigraphy—uses a small motion-sensing device; activity level is sampled every tenth of a second and aggregated at a constant interval, referred to as an epoch. A computerized algorithm translates this data into a representation of time awake versus asleep. Drawback—accurate measurement requires (a) that the device be worn continuously during the period of interest and (b) that the individual have little or no motor impairment, the presence of which can compromise accurate reading of movement as a surrogate for awake time.

PSG—gold standard for measurement of sleep. PSG monitors many body functions through electroencephalogram (EEG), electro-oculogram (EOG), electromyogram (EMG), and electrocardiogram (ECG) during sleep. Drawback—because of the complexity of the equipment required, PSG is costly, labor intensive, and not convenient for routine use.

INSOMNIA AND TBI

• Insomnia may occur immediately following injury and may continue for several years thereafter.

• Incidence is reported to range from 36% to 81% [3–7]. The wide variability is in part due to variability in operational definitions of insomnia and due to challenges in accurately applying assessment technology. A recent meta-analysis of 21 studies using both objective and self-report measures estimated the prevalence of insomnia in TBI at 50% [8].

Mechanism

• Acutely, insomnia results from diffuse disruption of cerebral functioning because of both direct physical damage to deep brain structures (including the hypothalamus and/or brainstem) and because of secondary neuropathological events, which may cause damage because of cerebral pathways essential for the maintenance of normal sleep architecture.

• In moderate-to-severe TBI, these acute processes result in severe fragmentation of the rest-activity cycle, which is worse with greater injury severity. An earlier return to consolidated rest-activity cycle is associated with a shorter duration of posttraumatic amnesia and lower disability at discharge [9].

• Melatonin deficiency also appears to play a role, having been demonstrated in TBI patients in the ICU setting [10]. This observation raises the prospect that use of a melatonin agonist may be of specific benefit in this population.

• Chronically, behavioral and affective factors also come into play.

Clinical Presentation

TBI patients present with a variety of symptoms, which may be a direct result of their injuries or may be secondary to insomnia, including [5]:

• Fatigue

• Irritability

• Cognitive deficits

• Pain

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