Close to 25% of patients with TBI develop some form of psychopathological or psychiatric disorder, including posttraumatic stress disorder, physical, cognitive-memory, and behavioral complications, such as sleep disturbances (Frieboes et al.,
1999). Insomnia is a prevalent condition after TBI, although most reports rely on self-administered questionnaires rather than laboratory data (Steele, Rajaratnam, Redman, and Ponsford 2005). Sleep disruption is a defining feature of anxiety and is associated with increased arousal at nighttime leading to disrupted sleep. However, it is difficult to ascertain the direction of the relation between anxiety and sleep complaints, because anxiety may be both a cause and a consequence of sleep disorder.
A recent study showed that higher anxiety is associated with longer time since injury and milder injury severity in TBI (Parcell, Ponsford, Rajaratnam, and Redman 2006). In this study, the TBI subjects showed increased nighttime awakenings and longer sleep onset latency, especially in patients with milder injury severity. Increased symptoms of anxiety and depression were associated with increased reporting of sleep changes.
Sleep disorders after TBI require more clinical and scientific attention as they may have important repercussions on rehabilitation. Altered circadian rhythms and sleep disorders and the role played by HPA hormones and proinflammatory cytokines in sleep deprivation and insomnia that we previously described (Vgontzas et al. 1999; Vgontzas et al. 2001; Vgontzas et al. 2005; Prolo, Iribarren, Neagos, and Chiappelli 2006) can certainly be transposed to TBI as well.
As a matter of fact, the elevation of secreted interleukin (IL)-6 and possibly its flattened circadian rhythm is a common feature of brain injury (Shafer, McNulty, and Young 2002). However, some issues arise when the same invasive methods used in our studies on insomnia (24-h continuous blood drawing, sleep lab setting, sleep deprivation) are applied to subjects recovering after TBI.
A convenient way of measuring sleep-wake cycles is by using continuous wrist activity recording. Actigraphy is a method used to study sleep-wake patterns and circadian rhythms by assessing movement, most commonly of the wrist (Littner et al. 2002). Actigraphy provides a means for clinicians and researchers to measure sleep and wake periods in a noninvasive, ambulatory way, thus not requiring that the subject be confined in a hospital room (i.e., sleep lab).
This approach is very convenient when the focus is on subjects that are outpatients, and are following a strict rehabilitation program. TBI subjects supposedly spend more time in bed, have more disrupted nighttime sleep, sleep more during the day, and have less robust circadian rhythms of activity.
Telemetric recording of spontaneous activity is, therefore, a reliable indicator of the circadian sleep-wake cycle. A graph obtained by continuous monitoring of a healthy individual is shown in Fig. 17.2.
Taken together, circadian rhythm alterations in sleep disorders include diminished amplitude, phase shifts, period changes, and erratic peaks and troughs in endocrine, metabolic, immunological, and rest-activity cycles.
In TBI, the common understanding is that there is a deviation of the rhythm period from 24 h so that the rhythms found in these patients are free-running, meaning that head injured patients are not synchronized with their surroundings (Kropyvnytskyy, Saunders, Pols, and Zarowski 2001), similar to a situation of long-lasting jetlag. Given the high incidence of sleep disturbances in patients with TBI, including insomnia, excessive daytime somnolence and alteration of the sleep-wake schedule (Frieboes et al. 1999; Mahmood et al. 2004; Rao and Rollings 2002), we expect that TBI subjects will show less robust circadian rhythms of activity than normal subjects.
Since sleep disorders are associated with cognitive deficits even in healthy adults, these alterations may be particularly disruptive to patients who have sustained a TBI. Sleep disturbance may disproportionately affect cognitive functioning among patients with TBI. According to several studies (Ron, Algom, Harry, and Cohen 1980; Cohen, Oksenberg, Snir, Stern, and Groswasser 1992; Fichtenberg, Zafonte, Putnam, Mann, and Millard 2002), the time elapsed since injury is inversely related to the severity of cognitive deficits and is an important factor in influencing the nature of sleep complaints in patients with TBI. Although variables such as independence and locomotion improved at rates that were not correlated with sleep measures, rapid eye movement (REM) sleep frequency and cognition seemed to improve concurrently. In contrast, other researchers found that patients with severe brain injuries are less likely than those with mild brain injuries to complain of sleep problems (Beetar, Guilmette, and Sparadeo 1996). One explanation for this finding is that patients with severe head injuries may underreport sleep disturbance because of a lack of awareness or limited memory, while subjects with mild brain injuries might be more easily accessible to fill in self reported questionnaires. Thus, there is likely to be a discrepancy between subjective reports and objective measures of sleep disturbance in TBI.
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