ORIGINAL ARTICLE Poor Sleep Quality and Changes in Objectively Recorded Sleep After Traumatic Brain Injury: A Preliminary Study Diane L. Parcell, DPsych, Jennie L. Ponsford, PhD, Jennifer R. Redman, PhD, Shantha M. Rajaratnam, PhD ABSTRACT. Parcell DL, Ponsford JL, Redman JR, Rajarat- nam SM. Poor sleep quality and changes in objectively re- corded sleep after traumatic brain injury: a preliminary study. Arch Phys Med Rehabil 2008;89:843-50. Objectives: To evaluate changes in sleep quality and objec- tively assessed sleep parameters after traumatic brain injury (TBI) and to investigate the relationship between such changes and mood state and injury characteristics. Design: Survey and laboratory-based nocturnal polysomnog- raphy. Setting: Sleep laboratory. Participants: Ten community-based subjects with moderate to very severe TBI and 10 age- and sex-matched controls from the general community. Interventions: Not applicable. Main Outcome Measures: Pittsburgh Sleep Quality Index for self-report sleep quality, nocturnal polysomnography for objective sleep recording, and Hospital Anxiety and Depres- sion Scales. Results: Compared with controls, TBI patients reported significantly poorer sleep quality and higher levels of anxiety and depression. Objective sleep recording showed that TBI patients showed an increase in deep (slow wave) sleep, a reduction in rapid eye movement sleep, and more frequent nighttime awakenings. No significant relationship was ob- served between these changes in sleep and injury severity or time since injury. Anxiety and depression covaried with the observed changes in sleep. Conclusions: The findings contribute to the growing body of evidence that sleep is involved in the physiologic processes underlying neural recovery. The association between anxiety and depression and the observed changes in sleep in TBI patients warrants further examination to determine whether a causative relationship exists. Key Words: Anxiety; Brain injuries; Depression; Recovery of function; Rehabilitation; Sleep. © 2008 by the American Congress of Rehabilitation Medi- cine and the American Academy of Physical Medicine and Rehabilitation S LEEP CHANGES ARE reported by the majority of survi- vors of traumatic brain injury (TBI). 1-3 Despite this, there have been few objective studies investigating sleep changes after TBI and the small number of polysomnographic investi- gations reported have yielded mixed results. 4-7 In view of the deleterious effects of poor sleep quality and reduced sleep quantity on physical and mental health, 8 the development of appropriate treatments for sleep complaints in TBI patients is warranted. Investigation of the nature and etiology of such sleep complaints is a first step in developing appropriate treat- ments. There are many possible causes of sleep change after TBI, and identification of such causes has proved difficult even in relatively large samples. 9 TBI may damage structures involved in the generation and maintenance of sleep, including the reticular activating system, hypothalamus, basal forebrain and pontine nuclei and their connections, 10 or the circadian system, notably the suprachiasmatic nuclei of the anterior hypothala- mus and its connections. Damage to hypothalamic structures may result in physiologic change, with a secondary impact on the biochemical regulation of sleep. Growth hormone defi- ciency and altered cortisol levels are known to have specific effects on sleep architecture, as do some other forms of endo- crine dysfunction. 11 Hypopituitarism, leading to altered levels of growth hormone and pituitary hormone production, has been shown to occur in approximately 40% of people after TBI. 12 Compared with a sample of healthy controls, TBI patients in the acute phase showed reduced levels of hypocretin-1, a hypothalamic neuropeptide involved in sleep-wake regula- tion. 9,13 Finally, sleep changes may stem from concomitant changes in mood, lifestyle, and medication use after TBI. There is significantly increased incidence of anxiety and depression in the TBI population. 14,15 Anxiety and depression are associated with alterations in sleep architecture, 16,17 although a recent study reported no association between depression ratings and the pres- ence or severity of post-traumatic sleep-wake disturbances. 9 Changes in employment status and other lifestyle factors may contribute to low or anxious mood and/or alter the person’s daily activity schedule, such as the need to wake for work. Some medications taken after TBI, such as antidepressants and anticon- vulsants, may also affect sleep architecture. 16,18 Polysomnography is regarded as the criterion standard for ob- jective recording of sleep. Relatively few studies have investigated sleep in TBI patients using polysomnography. The most fre- quently reported change to sleep architecture after TBI is an alteration in the proportion of rapid eye movement (REM) sleep. Ron et al 6 found an overall decrease in the amount of REM sleep as well as fewer eye movements in REM in TBI patients (n=9) compared with controls. Conversely, Frieboes et al 5 reported an increase in REM sleep in the second half of the night, as well as a tendency toward REM sleep disinhibition in the postacute stages of TBI. Busek and Faber 4 reported both increases and decreases in the proportion of REM sleep, and concluded that REM sleep is the sleep stage most vulnerable to TBI. A recent study 7 reported no significant difference in the proportion of REM sleep between TBI patients and healthy controls. From the School of Psychology, Psychiatry and Psychological Medicine, Monash University, Melbourne, Australia (Parcell, Ponsford, Redman, Rajaratnam); and the Monash-Epworth Rehabilitation Research Centre, Epworth Hospital, Melbourne, Australia (Ponsford). Presented in part to the Fatigue and Sleep Symposium of the International Neuro- psychological Society, July 2006, Zurich, Switzerland. Supported in part by the National Health and Medical Research Council (project no. 334002). No commercial party having a direct financial interest in the results of the research supporting this article has or will confer a benefit upon the authors or upon any organization with which the authors are associated. Reprint requests to Shantha M. Rajaratnam, PhD, School of Psychology, Psychiatry and Psychological Medicine, Monash University, Bldg 17, Victoria 3800, Australia, e-mail: shantha.rajaratnam@med.monash.edu.au. 0003-9993/08/8905-00281$34.00/0 doi:10.1016/j.apmr.2007.09.057 843 Arch Phys Med Rehabil Vol 89, May 2008