Evolution of severe sleep-wake cycle disturbances following traumatic brain injury: a case study in both acute and subacute phases post-injury
BMC Neurology volume 16, Article number: 186 (2016)
Sleep-wake disturbances are frequently reported following traumatic brain injury (TBI), but they remain poorly documented in the acute stage of injury. Little is known about their origin and evolution.
This study presents the case of a patient in the acute phase of a severe TBI. The patient was injured at work when falling 12 m into a mine and was hospitalized in the regular wards of a level I trauma centre. From days 31 to 45 post-injury, once he had reached a level of medical stability and continuous analgosedation had been ceased, his sleep-wake cycle was monitored using actigraphy. Results showed significant sleep-wake disturbances and severe sleep deprivation. Indeed, the patient had an average nighttime sleep efficiency of 32.7 ± 15.4 %, and only an average of 4.8 ± 1.3 h of sleep per 24-h period. After hospital discharge to the rehabilitation centre, where he remained for 5 days, the patient was readmitted to the same neurological unit for paranoid delusions. During his second hospital stay, actigraphy recordings resumed from days 69 to 75 post-injury. A major improvement in his sleep-wake cycle was observed during this second stay, with an average nighttime sleep efficiency of 96.3 ± 0.9 % and an average of 14.1 ± 0.9 h of sleep per 24-h period.
This study is the first to extensively document sleep-wake disturbances in both the acute and subacute phases of severe TBI. Results show that prolonged sleep deprivation can be observed after TBI, and suggest that the hospital environment only partially contributes to sleep-wake disturbances. Continuous actigraphic monitoring may prove to be a useful clinical tool in the monitoring of patients hospitalized after severe TBI in order to detect severe sleep deprivation requiring intervention. The direct impact of sleep-wake disturbances on physiological and cognitive recovery is not well understood within this population, but is worth investigating and improving.
Chronic sleep-wake disturbances, such as insomnia and hypersomnia, are among the most widely-reported sequelea following traumatic brain injury (TBI), and have been documented across all levels of TBI severity, until several years post-injury . Less attention has been paid to sleep-wake disturbances that occur in the first weeks post-injury. This might be explained by the challenges of performing sleep studies in an acute care setting, where most patients are confused and are not able to evaluate their own sleep quality.
A first group of studies that aimed at documenting sleep disturbances in post-acute TBI used nurse observations in individuals admitted to rehabilitation centres. One study found that of 31 patients, 21 (68 %) had two or more hours awake during the night . Similarly, a second study showed that mild to severe sleep disturbances were present among 84 % of TBI patients upon rehabilitation admission, and persisted for 66 % of patients one month post-injury . This research group used item one of the Delirium Rating Scale-Revised-98 to classify the severity of sleep-wake cycle disturbances as none, mild, moderate, or severe.
With the aim of using more objective methods to document the sleep-wake cycle of patients in the acute and post-acute phases of moderate-severe TBI, a second group of studies used actigraphy, which measures physical motion over time, to derive a rest-activity pattern. It has been shown that the rest-activity cycle measured with actigraphy strongly correlates with the sleep-wake cycle ; consequently, the rest-activity cycle derived from actigraphy is often referred to as the sleep-wake cycle. Within this context, a study carried out during early rehabilitation found that 11 of 14 moderate-severe TBI patients had an average sleep efficiency lower than 63 %, pointing to pervasive sleep-wake disturbances . More recently, Gardani and colleagues evaluated 30 patients with chronic severe TBI in an inpatient rehabilitation setting, using actigraphy and self-report measures . The authors found that 67 % of patients had sleep-wake cycle disturbances, 50 % of which met diagnostic criteria for a sleep disorder. Additionally, we recently used 10-day actigraphy recordings with 16 TBI patients hospitalized in a level I trauma centre in order to quantify the clustering of activity during the daytime and of rest during the nighttime as an estimate of their sleep-wake cycle consolidation. We found that patients had a poor sleep-wake cycle consolidation, which gradually improved over time . However, using a threshold of ≥80 % of all 24-h activity occurring in the daytime, only half of the patients reached an acceptable sleep-wake cycle consolidation during the recording period. Patients who reached an acceptable sleep-wake cycle consolidation were more likely to emerge from posttraumatic amnesia (PTA) and to have lower disability at hospital discharge.
Despite the high prevalence of acute and subacute sleep-wake disturbances in TBI patients, their aetiology is not well understood. Furthermore, no study has yet documented the sleep-wake cycle during both the acute and subacute phases of TBI, while the patient was hospitalized in the same environment, which is of interest given that the hospital environment itself may be a contributing factor to disturbed sleep and wake. The aim of this article is to document the case of one of our TBI patients from the abovementioned study , who suffered severe sleep-wake cycle disturbances during his acute hospital stay. Since this patient was readmitted 5 days post-discharge and wore the actigraph during his second hospital stay, his case enables us to document the evolution of his sleep-wake cycle over time and to juxtapose the sleep-wake cycle recorded during two different hospital stays in a similar environment, during the acute (measured days 31–45 days post-injury, starting 4 days following discharge from the intensive care unit (ICU)) and subacute (measured days 69–75 post-injury) phases.
LC is a 43-year-old right-handed Caucasian male, who resides with his spouse and two teenage daughters. Prior to his injury, LC was in good physical health, had no previous history of TBI, chronic disease, drug or alcohol abuse, or psychiatric, neurological or sleep disorders.
LC suffered a severe TBI when falling 12 m into a well of a mine during work hours. LC lost consciousness, had an initial Glasgow Coma Scale (GCS) score of 6 , and was immediately transported by ambulance to the nearest hospital, located approximately 160 km from the site of injury. Upon arrival at the regional hospital, his GCS score was 8. Following clinical evaluation, he was immediately transferred by ambulance to a level I trauma centre located over 500 km from the site of injury. A level I trauma centre provides the highest level of surgical and specialized care to trauma patients, is comprised of a full range of equipment and specialists dedicated to the care of patients having suffered TBI or orthopaedic injuries, and generally receives the most severe cases within a large geographical area.
LC was admitted to the trauma centre approximately 15 h after injury. His GCS score was three (intubated) upon admission to the emergency room, and he was taken to the ICU. A computed tomography (CT) scan revealed diffuse subarachnoid haemorrhage in the left hemisphere, left parieto-occipital subdural hematoma, right temporal intraparenchymal hematoma (3 cm), intrapeduncular, left intrapontine and temporal petechiae, as well as left frontal and right parieto-occipital contusions (see Fig. 1). His Marshall score was two , and his Rotterdam score was also two . LC also suffered multiple facial fractures, a C4 cervical fracture, D6, D8 and D12 thoracic fractures, a fracture of the left 9th rib, a spleen laceration, a pseudo-aneurysm of the aorta (4 mm), and a left pneumothorax.
LC was hospitalized in the ICU for 27 days. Overall, he was under continuous sedation for 16 days, during which time he received an average daily dose of 4.79 ± 2.33 g of propofol, and 6.2 ± 2.2 mg of fentanyl. During 11 of those 16 days of continuous sedation, LC also received an average daily dose of 0.55 ± 0.25 mg of midazolam. He was intubated 25 days, had elevated intracranial pressure (≥20 mmHg) during 13 days with a peak at 46.3 ± 14 mmHg, and had on average 7.3 ± 14 episodes of elevated intracranial pressure per day.
LC began responding to simple orders 15 days post-injury, when sedation was interrupted briefly to assess his level of response, and he opened his eyes 16 days post-injury. Subsequent to ICU discharge (27 days post-injury), LC was transferred to a six-patient room in the neurological ward. LC suffered akinetic mutism and moderate-severe oropharyngeal dysphagia throughout the first 46 days post-injury, and he then began to whisper, reaching a normal voice level 2 days prior to hospital discharge. At this point, he could walk unassisted and was fully functional in all bed and chair transfers.
LC was discharged from the trauma centre 55 days post-injury and admitted to a 200-bed inpatient rehabilitation centre, specialized in the care of TBI, orthopaedic injuries and neurology. Within the 72 h prior to hospital discharge, LC had a score of 10 out of 29 on the Disability Rating Scale , reflecting confused communication ability, partial cognitive disability for grooming, a markedly dependent level of functioning (mental, emotional, or social), and a non-competitive level of employability. The neurological examination carried out 8 days prior to hospital discharge (47 days post-injury) yielded a score of 5 on the Neurological Outcome Scale for Traumatic Brain Injury without the supplemental items . Deficits arose when LC was asked the current month and his age, which he both answered incorrectly, as well as when asked to identify odours or name objects for stimulus cards. This could either be the result of mild to moderate aphasia, or PTA, which would account for an inability to recall the words associated to various stimuli. Due to persistent akinetic mutism throughout most of the hospitalization period, neuropsychological evaluations were only carried out during the second hospital stay.
Five days after his admission to the inpatient rehabilitation centre, LC was readmitted to the trauma centre by ambulance for persecutory paranoid delusion, as per clinical observations at the inpatient rehabilitation centre, and remained hospitalized for 43 days in a two-patient room of the same neurological ward on which he had previously been hospitalized.
During this second hospital stay, LC continuously suffered retrograde and anterograde memory deficits with confabulations, severe temporal and spatial disorientation, verbal desinhibition, distrusting and suspicious behaviour, paranoia, and anosognosia. LC’s condition was attributed the diagnosis of post-TBI psychotic disorder. Neuropsychological evaluation carried out on days 87 and 89 post-injury showed severe dysfunctions in all cognitive domains (see Table 1).
LC was discharged 43 days after this second admission (102 days post-injury), and was readmitted to the inpatient rehabilitation centre. The occupational therapy report from LC’s final evaluation, carried out one week prior to this second discharge, described him as completely dependent for domestic activities of daily living (for timeline of injury and hospital stays, see Fig. 2).
Given his lengthy second admission, his psychiatric complications and persistent cognitive and functional sequelea, LC’s case does not represent one of typical post-TBI recovery, but rather depicts a slower and complexified recovery process.
LC was recruited as part of a larger longitudinal study taking place at Hôpital du Sacré-Coeur de Montréal, which was approved by the hospital ethics committee. Consent for participation was obtained from LC’s spouse, since he was unable to provide informed consent on his own.
LC wore a wrist actigraph on his non-dominant (left) arm during his first and second hospital stays (Actiwatch-2 during the first stay, and Actiwatch Spectrum during the second stay; MiniMitter Philips Healthcare, Andover, MA, USA). The actigraph is a small, watch-like device that contains an accelerometer, which records physical motion in all directions with a sensitivity of 0.05 g. Motion is then converted to an electric signal, which is digitally integrated to derive an activity count per one-min epoch. During the first hospital stay, the actigraphy recording began 31 days following the injury, 4 days after discharge from the ICU. Continuous intravenous or subcutaneous administration of a sedative drug was ceased 11 days prior to the start of actigraphic recording. LC was no longer intubated and had reached a level of medical stability defined by the absence of elevated intracranial pressure, of hemodynamic instability, and of fever or active infections. When the actigraph was installed, LC had also reached a score of IV on the Rancho Los Amigos Levels of Cognitive Functioning Scale, indicative of a confused/agitated state . LC could follow simple commands for motor action inconsistently and with delay, would turn his head when his name was called. Data was acquired for 15 days during hospitalization in the regular unit, during which time he received no sedatives or analgesics. Approximately every three days, data were uploaded into dedicated software (Actiware 5.0).
During the second hospital stay, LC wore the actigraph for 7 days, beginning 69 days post-injury. During this recording period, LC received a daily dose of 3 mg of lorazepam (1 mg at 8:30 h, 17:00 h, and 22:00 h).
For each day the actigraph was worn, each minute of recording was scored as “sleep” or “wake” using the automatic scoring system of the dedicated software (Actiware 5.0). A particular one-min epoch was scored as wake by comparing the activity counts of this epoch to those immediately surrounding it. The threshold chosen to score a one-min epoch as wake was > 20 activity counts per minute. A smaller number yielded a score of sleep. For each epoch the actigraph was not worn, due to the removal of the actigraph for data downloads or bathing, the epoch was scored as wake since the patient was awake in both contexts.
A sleep bout was defined as a period of five or more consecutive epochs scored as sleep by Actiware 5.0. To reduce the artificial fragmentation of rest periods, isolated one-min epochs scored as wake were manually converted to sleep, similar to the smoothing method suggested by Sitnick et al. .
Sleep efficiency was calculated for the nocturnal period (22:00 h to 6:59 h), and was defined as [(number of epochs scored as sleep / total number of nocturnal epochs)*100].
Sleep-wake cycle consolidation, or the clustering of activity during the daytime and of rest during the nighttime, was estimated with the ratio of daytime activity to total 24-h activity, as previously described . Briefly, for each 24-h period, the activity counts were summed separately for daytime (07:00 h −21:59 h) and nighttime (22:00 h - 6:59 h) periods. Total 24-h activity (07:00 h - 06:59 h) was the sum of the daytime and nighttime periods. The percentage of total 24-h activity occurring in the daytime was calculated to obtain the daytime activity ratio [daytime activity ratio = (daytime activity/24-h activity) x100].
Descriptive statistics (means and standard deviations) were computed for the total quantity of sleep per 24-h period, mean duration of daytime and nighttime sleep bouts (“sleep bout duration”), the nocturnal sleep efficiency, and the daytime activity ratio. Student’s t-tests were carried out to assess differences in these results between the first and second hospital stays.
The actigraphy recordings for the first and second hospital stays are presented in Fig. 3. During the first hospital stay, high levels of activity were dispersed throughout 24-h periods for most of the 15 days of recording, and very brief periods of sleep are observed. As for the second hospital stay, prolonged periods of sleep are observed, mostly during nighttime.
Total quantity of sleep per 24-h period
During the actigraphy recording of the first hospital stay, LC had an average of 4.8 ± 1.3 h of sleep per 24-h period, which significantly increased to 14.1 ± 0.9 h during the second hospital stay (t(20) = −16.8, p < 0.001) (see Fig. 3).
Duration of sleep bouts
During the first hospital stay, sleep bouts had an average duration of 14.9 ± 11.9 min and the longest sleep bout over the 15 days of actigraphy was 97 min (occurring at 22:39 h on day 41 post-injury). During the second stay, sleep bouts were on average 38.4 ± 59.0 min, which represents a significant improvement compared to the first hospital stay (t(400) = −6.2, p < 0.001). The longest sleep bout started at 21:16 h on day 72 post-injury and was of 342 min in duration. During the night, averaged sleep bout was significantly longer during the second hospital stay, increasing from 16.6 ± 13.7 min in the first stay to 90.1 ± 88.6 min in the second stay (t(192) = −9.9, p < 0.001). The average duration of daytime sleep bouts also increased from the first to the second hospital stay, from 12.5 ± 8.3 min to 17.9 ± 17.3 min (t(206) = −2.9, p = 0.005).
Nocturnal sleep efficiency increased significantly from the first to the second hospital stay (32.7 ± 15.4 % vs. 96.3 ± 0.9 %, t(20) = −10.27, p < 0.001).
Rest-activity cycle consolidation
When all days of recording were considered for each hospital stay, daytime activity ratio was 67.8 ± 9.8 % during the first hospital stay, and 96.2 ± 1.0 % during the second hospital stay, which represents a significant improvement in sleep-wake cycle consolidation (t20) = −7.53, p < 0.001)).
We presented the case of a 43-year old male, who suffered significant sleep-wake disturbances in the first 3 months post-TBI. LC’s first hospital stay was marked by an average of only 4.8 ± 1.3 h of sleep per 24-h for the 15 days of recording. Importantly, this short sleep duration measured with actigraphy probably overestimates the quantity of sleep LC actually experienced. In fact, actigraphy is known to underestimate wakefulness [15–18], particularly when individuals lie in bed immobile but awake , and especially among a critically ill population . On the other hand, it is not impossible that LC may have slept during periods of motor activity. However, the recorded levels of activity were very high (see Fig. 3), suggesting that if sleep did occur, it was agitated and most likely not restful. Taken together, our results suggest severe and persistent sleep deprivation during the first hospital stay.
Aside from sleep deprivation, this study also suggests that LC suffered severe sleep fragmentation. The patient was not able to stay asleep for a long period of time (mean nighttime sleep bout duration of 16.6 ± 13.7 min), and the mean sleep efficiency of 32.7 % measured during the first hospital stay was well below the 85 % mark that is generally considered pathological . Altogether, these results demonstrate that sleep was highly disturbed during the first hospital stay. Such a pattern of sleep is most likely incompatible with the deeper sleep stages associated with recovery, although this cannot be confirmed with actigraphy measures alone.
When LC’s sleep-wake cycle was re-evaluated during the second hospital stay, LC was able to have significantly longer periods of continuous bouts of sleep, especially during the night. Sleep efficiency improved significantly, increasing from 32.7 ± 15.4 % to 96.3 ± 0.9 %. Total quantity of sleep per 24-h period also increased from 4.8 ± 1.3 h during the first stay to 14.1 ± 0.9 h during the second stay. Moreover, periods of activity were mainly concentrated during the daytime (daytime activity ratio of 96.2 ± 1.0 %), suggesting the presence of a well-consolidated sleep-wake cycle. During the second hospital stay, LC’s sleep pattern may be more closely aligned with hypersomnia, which is reported in approximately 10-30 % of TBI patients in the post-acute and chronic phases of injury [1, 22].
During the actigraphy recording of his first hospital stay, LC was hospitalized in the neurological ward, in a room of 6 patients, and was re-hospitalized in the same ward during his second hospital stay, in a two-patient room. In this ward, hallway lights are generally turned on from 7:00 h to 22:00 h, and the hospital personnel attempts to keep noise and light levels as low as possible between 22:00 h and 7:00 h. Considering the significant improvement in sleep-wake cycle consolidation during the second hospital stay, despite LC being hospitalized in the same ward, this case study suggests that the hospital environment cannot entirely account for the sleep deprivation and sleep disturbances occurring in patients with TBI.
Being under the effects of sedatives, analgesics, narcotics, anticonvulsants and antipsychotics may also influence sleep characteristics during acute hospitalization following TBI . Furthermore, withdrawal from such medications may also influence sleep and wake. As LC was discharged from the ICU only 4 days prior to the start of actigraphy, the sleep-wake cycle measured during his first hospital stay may have been influenced by withdrawal from the sedatives and analgesics administered while he was in the ICU. Conversely, improvements in sleep-wake cycle consolidation during the second hospital stay, including longer nighttime sleep periods, could partially be due to the effect of lorazepam, as LC was not taking analgosedative medication during the 15 days of actigraphy recording of his first stay. However, since equal (1 mg) doses were administered three times daily (8:30 h, 17:00 h, 22:00 h) during the second stay, and not exclusively prior to bedtime, LC’s consolidated daytime wakefulness and nighttime sleep cannot be due solely to the effect of medication.
Pain may also be an important contributing factor to sleep disturbances following TBI. LC had multiple fractures, which most likely generated significant pain. In the chronic phase of TBI (all severities), pain is known to negatively influence sleep [24–27], as early as the post-acute period . Among ICU patients without TBI, pain has also been associated to sleep disturbances [29–31]. The influence of pain on LC’s sleep may have been stronger during the first hospital stay, as pain may have gradually subsided with time, though no pain evaluations were systematically carried out due to akinetic mutism.
This case report is the first to extensively document sleep-wake disturbances in both the acute and subacute phases of severe TBI. Indeed, this was the only case we encountered of a patient being readmitted shortly after discharge, providing us with a unique opportunity to follow-up on our actigraphy measures. This successive monitoring of LC’s sleep-wake cycle, while in the same hospital ward, distinguishes the present study from previously published TBI sleep studies [2, 3, 5, 6], including our own . Results revealed the presence of severe sleep deprivation and the absence of normal 24-h sleep-wake organisation during the acute phase after a severe TBI. Severe sleep deprivation is bound to have negative consequences on physical, psychological and cognitive recovery following TBI. Indeed, post-TBI sleep disturbances have been shown to heighten cognitive, mood and communication impairments, in addition to intensifying pain and compromising recovery [32, 33]. In a more general manner, partial or chronic sleep deprivation has been shown to negatively impact cognitive, behavioural, immune, inflammatory, cardiovascular, endocrine and metabolic functions [34–38]. In the case of LC, severe and persistent sleep deprivation and fragmentation, as well as the severe disturbance of the sleep-wake cycle in the first hospital stay, may have contributed to the psychiatric condition having led to his second hospital admission. Indeed, sleep and circadian disturbances are associated to mental health and psychiatric symptoms and disorders [39–41], while sleep deprivation has been associated with psychotic symptomatology .
The sleep deprivation experienced by LC was much more severe and prolonged and than that of other moderate-severe TBI evaluated within our larger study . Interestingly, the case of LC differs from previously observed cases of TBI patients for whom improved sleep and wake seem to coincide with improved cognitive functions in the weeks following injury [5, 7, 43] Rather, LC had persistent PTA, cognitive deficits and psychiatric symptoms, despite significant improvement of sleep-wake cycle consolidation from the first to the second hospital stay. This may suggest that severe and prolonged sleep deprivation in acute TBI could possibly exacerbate cerebral damage and have persistent effects on cognitive sequelea and recovery.
No sleep medication was given to LC during the actigraphy recording period of the first hospital stay, during which he was suffering from severe sleep deprivation, probably because he was not able to communicate his sleep problem. Systematic monitoring of sleep by observation are difficult to conduct and quite time-consuming. It is therefore rarely included in the nursing care, especially in patients in such severe medical conditions. Actigraphy may be particularly useful among patients with confusion or communication deficits, as it objectively identifies sleep patterns and may contribute to providing timely and adequate treatment if sleep disturbances arise. The sleep disturbances experienced by LC could probably have been attenuated, though the means through which sleep can be facilitated within this population still need to be further investigated.
This report highlights the importance of monitoring the sleep-wake cycle in acute care, as it may inform or influence patient recovery, though more studies are needed to define this relationship and determine whether it is causal or bidirectional. Even though actigraphy cannot distinguish rest from sleep, it remains a useful tool for the prolonged measurement of sleep-wake disturbances in a hospital setting, even among patients who may lack the cognitive capacity to identify and/or report sleep-wake problems to healthcare personnel.
One limitation to this study is that no magnetic resonance imaging was performed. Given its superior spatial resolution compared with CT , magnetic resonance imaging would have enabled a more precise detection of alterations in cortical and subcortical structures and networks involved in the regulation of sleep and wake. However, with the CT scan at admission, we were still able to detect petechiae within the pons, which is a region highly involved in sleep-wake regulation [45, 46].
Glasgow coma scale
Intensive care unit
Traumatic brain injury
Duclos C, Dumont M, Wiseman-Hakes C, Arbour C, Mongrain V, Gaudreault PO, Khoury S, Lavigne G, Desautels A, Gosselin N. Sleep and wake disturbances following traumatic brain injury. Pathol Biol (Paris). 2014;62(5):252–61.
Makley MJ, English JB, Drubach DA, Kreuz AJ, Celnik PA, Tarwater PM. Prevalence of sleep disturbance in closed head injury patients in a rehabilitation unit. Neurorehabil Neural Repair. 2008;22(4):341–7.
Nakase-Richardson R, Sherer M, Barnett SD, Yablon SA, Evans CC, Kretzmer T, Schwartz DJ, Modarres M. Prospective evaluation of the nature, course, and impact of acute sleep abnormality after traumatic brain injury. Arch Phys Med Rehabil. 2013;94(5):875–82.
Martin JL, Hakim AD. Wrist actigraphy. Chest. 2011;139(6):1514–27.
Makley MJ, Johnson-Greene L, Tarwater PM, Kreuz AJ, Spiro J, Rao V, Celnik PA. Return of memory and sleep efficiency following moderate to severe closed head injury. Neurorehabil Neural Repair. 2009;23(4):320–6.
Gardani M, Morfiri E, Thomson A, O’Neill B, McMillan TM. Evaluation of sleep disorders in patients with severe traumatic brain injury during rehabilitation. Arch Phys Med Rehabil. 2015;96(9):1691–7. e1693.
Duclos C, Dumont M, Blais H, Paquet J, Laflamme E, de Beaumont L, Wiseman-Hakes C, Menon DK, Bernard F, Gosselin N. Rest-activity cycle disturbances in the acute phase of moderate to severe traumatic brain injury. Neurorehabil Neural Repair. 2013;28(5):472–82.
Teasdale G, Jennett B. Assessment of coma and impaired consciousness. A practical scale. Lancet. 1974;2(7872):81–4.
Marshall LF, Marshall SB, Klauber MR, Van Berkum CM, Eisenberg H, Jane JA, Luerssen TG, Marmarou A, Foulkes MA. The diagnosis of head injury requires a classification based on computed axial tomography. J Neurotrauma. 1992;9 Suppl 1:S287–92.
Maas AIR, Hukkelhoven CW, Marshall LF, Steyerberg EW. Prediction of outcome in traumatic brain injury with computed tomographic characteristics: a comparison between the computed tomographic classification and combinations of computed tomographic predictors. Neurosurgery. 2005;57(6):1173–82. discussion 1173–1182.
Rappaport M, Hall KM, Hopkins K, Belleza T, Cope DN. Disability rating scale for severe head trauma: coma to community. Arch Phys Med Rehabil. 1982;63(3):118–23.
Wilde EA, McCauley SR, Kelly TM, Weyand AM, Pedroza C, Levin HS, Clifton GL, Schnelle KP, Shah MV, Moretti P. The Neurological Outcome Scale for Traumatic Brain Injury (NOS-TBI): I. Construct validity. J Neurotrauma. 2010;27(6):983–9.
Hagen C, Malkmus D, Durham P. Rancho Los Amigos Levels of Cognitive Functioning Scale. Downey: Professional Staff Association; 1972.
Sitnick SL, Goodlin-Jones BL, Anders TF. The use of actigraphy to study sleep disorders in preschoolers: some concerns about detection of nighttime awakenings. Sleep. 2008;31(3):395–401.
Paquet J, Kawinska A, Carrier J. Wake detection capacity of actigraphy during sleep. Sleep. 2007;30(10):1362–9.
Blood ML, Sack RL, Percy DC, Pen JC. A comparison of sleep detection by wrist actigraphy, behavioral response, and polysomnography. Sleep. 1997;20(6):388–95.
de Souza L, Benedito-Silva AA, Pires MLN, Poyares D, Tufik S, Calil HM. Further validation of actigraphy for sleep studies. Sleep. 2003;26(1):81–5.
Kushida CA, Chang A, Gadkary C, Guilleminault C, Carrillo O, Dement WC. Comparison of actigraphic, polysomnographic, and subjective assessment of sleep parameters in sleep-disordered patients. Sleep Med. 2001;2(5):389–96.
Acebo C, LeBourgeois MK. Actigraphy. Respir Care Clin N Am. 2006;12(1):23–30. viii.
Beecroft JM, Ward M, Younes M, Crombach S, Smith O, Hanly PJ. Sleep monitoring in the intensive care unit: comparison of nurse assessment, actigraphy and polysomnography. Intensive Care Med. 2008;34(11):2076–83.
Edinger JD, Bonnet MH, Bootzin RR, Doghramji K, Dorsey CM, Espie CA, Jamieson AO, McCall WV, Morin CM, Stepanski EJ. Derivation of research diagnostic criteria for insomnia: report of an American Academy of Sleep Medicine Work Group. Sleep. 2004;27(8):1567–96.
Ouellet MC, Beaulieu-Bonneau S, Morin CM. Sleep-wake disturbances after traumatic brain injury. Lancet Neurol. 2015;14(7):746–57.
Dispersyn G, Pain L, Challet E, Touitou Y. General anesthetics effects on circadian temporal structure: an update. Chronobiol Int. 2008;25(6):835–50.
Ponsford JL, Parcell DL, Sinclair KL, Roper M, Rajaratnam SM. Changes in sleep patterns following traumatic brain injury: a controlled study. Neurorehabil Neural Repair. 2013.
Khoury S, Chouchou F, Amzica F, Giguere JF, Denis R, Rouleau GA, Lavigne GJ. Rapid EEG activity during sleep dominates in mild traumatic brain injury patients with acute pain. J Neurotrauma. 2013;30(8):633–41.
Fogelberg DJ, Hoffman JM, Dikmen S, Temkin NR, Bell KR. Association of sleep and co-occurring psychological conditions at 1 year after traumatic brain injury. Arch Phys Med Rehabil. 2012;93(8):1313–8.
Beetar JT, Guilmette TJ, Sparadeo FR. Sleep and pain complaints in symptomatic traumatic brain injury and neurologic populations. Arch Phys Med Rehabil. 1996;77(12):1298–302.
Fichtenberg NL, Millis SR, Mann NR, Zafonte RD, Millard AE. Factors associated with insomnia among post-acute traumatic brain injury survivors. Brain Inj. 2000;14(7):659–67.
Raymond I, Nielsen TA, Lavigne G, Manzini C, Choiniere M. Quality of sleep and its daily relationship to pain intensity in hospitalized adult burn patients. Pain. 2001;92(3):381–8.
Raymond I, Ancoli-Israel S, Choiniere M. Sleep disturbances, pain and analgesia in adults hospitalized for burn injuries. Sleep Med. 2004;5(6):551–9.
Manian FA, Manian CJ. Sleep quality in adult hospitalized patients with infection: an observational study. Am J Med Sci. 2015;349(1):56–60.
Wiseman-Hakes C, Murray B, Moineddin R, Rochon E, Cullen N, Gargaro J, Colantonio A. Evaluating the impact of treatment for sleep/wake disorders on recovery of cognition and communication in adults with chronic TBI. Brain Inj. 2013;27(12):1364–76.
Wiseman-Hakes C, Victor JC, Brandys C, Murray BJ. Impact of post-traumatic hypersomnia on functional recovery of cognition and communication. Brain Inj. 2011;25(12):1256–65.
Goel N, Rao H, Durmer JS, Dinges DF. Neurocognitive consequences of sleep deprivation. Semin Neurol. 2009;29(4):320–39.
Shamsuzzaman AS, Winnicki M, Lanfranchi P, Wolk R, Kara T, Accurso V, Somers VK. Elevated C-reactive protein in patients with obstructive sleep apnea. Circulation. 2002;105(21):2462–4.
Spiegel K, Leproult R, Van Cauter E. Impact of sleep debt on metabolic and endocrine function. Lancet. 1999;354(9188):1435–9.
Mullington JM, Haack M, Toth M, Serrador JM, Meier-Ewert HK. Cardiovascular, inflammatory, and metabolic consequences of sleep deprivation. Prog Cardiovasc Dis. 2009;51(4):294–302.
Spiegel K, Sheridan JF, Van Cauter E. Effect of sleep deprivation on response to immunization. JAMA. 2002;288(12):1471–2.
Barczi S, Teodorescu M. Medical and Psychiatric Disorders and the Medications Used to Treat Them. In: Kryger M, Roth T, Dement W, editors. Principles and Practice of Sleep Medicine. 5th ed. St. Louis: Elsevier; 2011. p. 1524–35.
Soehner AM, Kaplan KA, Harvey AG. Insomnia comorbid to severe psychiatric illness. Sleep medicine clinics. 2013;8(3):361–71.
Sutton EL. Psychiatric disorders and sleep issues. Med Clin North Am. 2014;98(5):1123–43.
Gulevich G, Dement W, Johnson L. Psychiatric and EEG observations on a case of prolonged (264 hours) wakefulness. Arch Gen Psychiatry. 1966;15(1):29–35.
Holcomb EM, Towns S, Kamper JE, Barnett SD, Sherer M, Evans C, Nakase-Richardson R. The relationship between sleep-wake cycle disturbance and trajectory of cognitive recovery during acute traumatic brain injury. J Head Trauma Rehabil. 2015.
Coles JP. Imaging after brain injury. Br J Anaesth. 2007;99(1):49–60.
Peplow M. Structure: the anatomy of sleep. Nature. 2013;497(7450):S2–3.
Espana RA, Scammell TE. Sleep neurobiology from a clinical perspective. Sleep. 2011;34(7):845–58.
We would like to thank LC and his family for their cooperation during LC’s first and second hospital stays at Hôpital du Sacré-Coeur de Montréal.
The research was supported by the Canadian Institutes of Health Research (CIHR), by the Fonds de la recherche du Québec, Santé (FRQS), which both provided funding for materials, data collection and research assistants. Studentship to CD was also provided by the CIHR, University of Montréal, by the Fondation Neurotrauma Marie-Robert, and by the J. A. De Sève foundation.
Availability of data and materials
CD recruited the patient, acquired the data, participated in the analysis and interpretation of the data, drafted and critically revised the manuscript. MD contributed to the conception and design of the study, contributed to interpreting the data, drafting and critically revising the manuscript. MJP acquired data, participated in the interpretation of data, and critically revised the manuscript. AD contributed to the conception of the study, data acquisition, interpretation of data, and critically revised the manuscript. DG contributed to the interpretation of data and critically revised the manuscript. DKM contributed to the conception and design of the study, interpretation of data, and critically revised the manuscript. FB contributed to the conception and design of the study, interpretation of data, and critically revised the manuscript. NG led the conception and design of the study, obtained funding for the study, contributed to analysis and interpretation of data, and was involved in drafting and critically revising the manuscript. All authors have given final approval of the version to be published and have agreed to be accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved.
The authors declare that they have no competing interests.
Consent for publication
Written informed consent was obtained from the patient for publication of this Case report and any accompanying images. A copy of the written consent is available for review by the Editor of this journal.
Ethics approval and consent to participate
This study was approved by the ethics committee of Hôpital du Sacré-Cœur de Montréal, named Comité d’éthique de la recherche et de l’évaluation des technologies de la santé (protocol no. 2011–690).
Written and informed consent for study participation was provided by the patient’s wife. A copy of the written consent is available for review by the Editor of this journal.
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Duclos, C., Dumont, M., Potvin, MJ. et al. Evolution of severe sleep-wake cycle disturbances following traumatic brain injury: a case study in both acute and subacute phases post-injury. BMC Neurol 16, 186 (2016). https://doi.org/10.1186/s12883-016-0709-x