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The Silent Epidemic: Sleep Disturbances Associated with Traumatic-Brain Injury

Research Question

The researchers in this study were interested in the relationship between the presence of sleep disturbances and certain characteristics of traumatic brain injuries.  The research questions sought to better understand this relationship; the questions established by the researchers were: What factors are related to the presence of sleep disturbances in individuals diagnosed with TBI?  Additionally, what are the different types of sleep disturbances and how often do they occur for TBI patients?

Background of Research Question

Past research has indicated that among the symptoms for TBI, sleep disturbance is common among patients, with 30% to 80% of individuals reporting issues with their sleep across time after their diagnosis (Ouellet, Beaulieu-Bonneau, & Morin, 2006).  In addition to these sleep disturbances, other issues may begin to occur in relation to poor sleep such as feelings of anxiety, depression, irritability, and fatigue (Fictenberg, Millis, Mann, Zafonte, & Miller, 2000).  Some research highlights that less severe TBI incidents may be related to higher complaints of sleep disturbances due to the patients’ inability to cope with their injury and restore their previous ways of life before the injury occurred.  Other studies establish that a milder diagnosis of TBI does not significantly predict issues related to sleep disruption (Verma, Anand, & Verma, 2007).

Very few studies have been able to accurately depict what areas in the brain need to be impaired by the injury in order for it to directly have an effect on an individual’s sleep.  Current studies related to sleep issues occur mostly with patients recruited from rehabilitation centers.  Research completed on these rehabilitated patients is often less than satisfactory due to issues related to neuroimaging when attempting to pinpoint certain areas of the brain.   Because of these setbacks, it is difficult to determine how characteristics of TBI, such as an imbalance of neurotransmitter systems and damage to certain structures, have a negative impact on sleep behaviors.

Hypothesis and Methods

The hypothesis of this study is that certain characteristics of TBI have a direct impact on the presence of sleep disturbances in individuals and that there are certain factors that are related to the common issue of sleep troubles in TBI populations.  98 patients (72 males, 26 females, aged between 18-70) were recruited from Changzheng hospital, Pudong New Area People’s hospital, and Fengxian Central hospital following a traumatic brain injury.  The criteria to be included in the study included being an adult patient experiencing their first ever mild traumatic brain injury diagnosis with positive cranial CT scans.

Participants had an initial screening when first admitted into the hospital to determine overall severity of the injury using the Glasgow Coma Scale (GCS).  Scores obtained on the GCS ranked the injury as either severe (a score less than 9), moderate (a score of 9-12), or mild (a score of 13-15).  Patients were also asked to recount whether they had lost consciousness after the incident occurred.

In a follow-up telephone assessment that occurred six months after their injury, participants were given three questionnaires to discuss their sleep habits since the accident.  These questionnaires were the Pittsburgh Sleep Quality Index (PSQI), the Epworth Sleepiness Scale (ESS), and the Hospital Anxiety and Depression scale (HADS).  Participants were also asked structured questions related to other symptoms such as frequent headaches or dizziness, cognitive behavior, and changes in personality or behavior.  The PSQI was utilized to measure overall quality of sleep and the ESS was used to identify incidents of daytime sleepiness.  Insomnia in this study was defined as sleep latency of 30 minutes or more, nocturnal awakenings of 30 minutes or more, presence of insomnia symptoms at least three times a week, less than six hours of sleep despite the opportunity to get more sleep, an insomnia duration of at least one month, and negative mood or impaired functioning in the daytime.


Participants in the study were separated into three different groups: TBI with hypersomnia, TBI with insomnia, and TBI without sleep disturbances.  Researchers analyzed the results of the assessments using the Kruskal-Wallis tests for univariate analyses as well as group comparisons using a Chi-square, ANOVAs, and ANCOVAs.  Analyses of the results were identified using a logistic regression model.

Demographic characteristics of the participants revealed that the main cause of their brain injuries was from motor vehicle accidents.  69 of the participants were identified to have a mild TBI, 15 were identified to have moderate TBI, and 14 were identified to have severe TBI.  Out of all of the participants, 38% reported sleep disturbances following their TBI.  Higher rates of insomnia as well as a higher frequency of sleep disturbances were found in individuals who had moderate to severe diagnoses compared to individuals with mild TBI.  On the PSQI questionnaire, the TBI insomnia group reported poorer sleep quality than the TBI hypersomnia group and the TBI without sleep disturbance group.  Analysis of the HADS scale found that TBI insomnia patients have more anxiety and depression symptoms compared to the two other groups of participants.  Frequent headaches and dizziness were also associated with sleep disturbances after TBI diagnosis.  Individuals with hypersomnia reported the highest scores on the ESS scale, which measures daytime sleepiness; individuals in the insomnia group also had high scores on the ESS scale, but were not as severe as the hypersomnia group.  Based on the CT scans taken when first admitted into the hospital, no significant association was found between sleep disturbances and location of the brain impacted by the injury.

Discussion and Implications

The results of this study found similar findings of past studies which indicate that a portion of TBI patients will experience some type of sleep disturbance following their TBI.  Several different factors were identified to have a potential impact on sleep disturbances such as anxiety, depression, headaches, dizziness and that these factors may impact daytime cognitive and behavioral functions.  Researchers highlighted potential limitations of the study since the measures were self-report and no laboratory tests during sleep sessions were conducted.  This means that participants could overestimate or underestimate the amount of sleep disturbances they experience over time without having physiological data to back up their personal report.  Future studies could attempt to combine these self-report measures with laboratory data to create a better understanding of how these individuals perceive their quality of sleep in addition to observing disruptive sleep behaviors.


Article Summary #2

Mantua, J., Henry, O., Garskovas, N., & Spencer, R. (2017). Mild Traumatic Brain Injury Chronically Impairs Sleep- and Wake-Dependent Emotional Processing. Sleep, 40(6)1-10. doi: 10.1093/sleep/zsx062

Research Question

The researchers in the study were interested in the relationship between sleep disturbances in individuals with mild, chronic TBI and emotional processing such as sleep-dependent memory consolidation and sleep-dependent emotion generation.  The research question is: Do disrupted sleep-dependent processes impact or maintain mood disturbances in TBI populations?  Furthermore, is sleep-dependent emotional processing intact in individuals with mild TBI?

Background of Research Question

Past research has indicated that an estimated 1.4 to 3 million people experience mild traumatic brain injury every year in the United States (Rutland-Brown, Langlois, Thomas, & Xi, 2003).  After injury, it is common for diagnosed individuals to experience emotional as well as sleep related disturbances.  In fact, the onset of depressive symptoms and elevated rates of depression have been reported six years after the injury occurred (Konrad et al., 2011).  The risk of suicide is also elevated ten years post-injury, even if no suicidal ideation was present before the injury (Fralick, Thiruchelvam, Tien, & Redelmeier, 2016).

Recordings of sleep activity via polysomnography post-injury indicate levels of decreased efficiency of sleep such as time spent in bed versus time asleep, an increased number of awakenings during the night, and increased symptoms of hypersomnia.  A recent meta-analysis of nine studies demonstrated that individuals diagnosed with TBI have less REM cycles during sleep than individuals with no experience of a TBI (Grima, Ponsford, Rajaratnam, Mansfield, & Pase, (2016).  Studies have identified an association between sleep and mood states, with the present study focusing on sleep-dependent memory consolidation as well as wake-dependent emotional processing.  Sleep dependent-memory consolidation supports the idea that the better sleep an individual gets, the stronger their emotional memories will be (Jones, Schultz, Adams, Baran, & Spencer, 2016).  This process may even have an impact on the individual’s mood when they wake up the next day.

Hypothesis and Methods

The hypothesis of this study is to test whether sleep-dependent memory consolidation is disrupted in individuals with chronic TBI based on the assumption that a disruption in this process could cause mood disturbances in the TBI population.  Additionally, a second hypothesis was established to test if sleep-dependent emotion generation is disrupted in chronic TBI patients.  81 individuals (59 females and 22 males, aged between 18 and 30) were recruited from the University of Massachusetts and received course credit for their participation.  Recruited participants had normal or corrected-to-normal vision and reported no history of any sleep disorders, psychological disorders, neurological disorders, and were not taking sleep medications.

Participants were divided into two groups for the experiment: TBI and non-TBI group.  Once divided, they were separated into either the Sleep condition or the Wake condition.  To be included in the TBI group, participants had to have experienced a concussion more than a year before the study.  Of those in the TBI group, 66% reported one concussion, 19% reported two concussions, 5.3% reported three concussions, and 10.4% reported four concussions.  Individuals in the mild TBI group must have reported at least one symptom that altered their brain functioning.

Materials used in the study consisted of 90 emotionally negative and 90 emotionally neutral pictures, the majority of which were obtained from the International Affective Picture System.  Based on normative data obtained from the lab, the emotionally negative pictures were rated moderate to high in levels of arousal whereas the neutral pictures were rated low in arousal.  In this between-subjects design,  each condition (Sleep or Wake) consisted of two sessions.  In the Sleep condition, participants had an encoding session between 8:00 pm and 10:00 pm and a recognition session  that occurred 12 hours later in the morning.  In the Wake condition, participants had an encoding session between 8:00 am and 10:00 am and the recognition session 12 hours later in the evening.  In session one, all participants completed the Pittsburgh Sleep Quality Index (PSQI), the Morningness-Eveningness Questionnaire (MEQ), the Epworth Sleepiness Scale (ESS), and the Stanford Sleepiness Scale (SSS).  The SSS was also completed in session 2.  Participants also completed a working memory task (digit span) to confirm similar coding abilities between the two groups.  The TBI group was given an additional assessment to determine the severity of their TBI and symptoms they have experienced.

In the encoding session, each participant viewed 30 neutral and 30 negative target stimuli on a computer screen for 1000 ms followed by a interstimulus interval.  After viewing each picture, participants were asked to rate the image they saw on a valence scale from 1-9 (1 = negative, 5 = neutral, 9 = positive) and an arousal scale (1 = no arousal, 9 = highly arousing).  In the recognition session (12 hours later), participants were shown 180 images for 1000ms, 60 of which were from the encoding session mixed with 120 foil images (60 negative and 60 neutral).  The images were rated again on their valence and level of arousal as well as whether the image was recalled from the encoding session.

Participants in the Sleep condition were recorded using a polysomnography system overnight.  Electrodes were placed on the participant after the encoding session, which included two electrooculogram, two chin electromyogram, and six cortical electroencephalogram (O1, O2, C3, C4, F3, F4).  Due to user error or equipment malfunction, sleep results were utilized from 14 non-TBI participants and 16 TBI participants.


Statistical analyses of the obtained data was completed using the SPSS 22 software.  Target images were categorized based on the encoding phase and foil images were categorized based on ratings in the recognition phase.  Negative images were defined and 1-3 and neutral images were defined as 4-6.  Hit rate in the study was defined as the percentage of target pictures that were correctly identified as being previously seen in the encoding session and False Alarms were defined as the percentage of foil images that were incorrectly identified as being seen in the encoding session.  Changes in valence and arousal ratings were calculated for negative and neutral target pictures separately based on differences observed in sessions one and two.  For the TBI group, head-injury factors (ex. number of TBIs) and sleep factors (ex. percent of night in non-REM sleep) were added to the analysis.

On the sleep assessment scales, TBI and non-TBI participants did not differ significantly on the MEQ, ESS, SSS1, or SSS2 scores.  However, the TBI group had higher scores on the PSQI compared to the non-TBI group; the major significant difference was found in the time it takes to fall asleep every night component of the scale.  Participants in the Wake condition (the morning session) reported being more tired than the individuals who were in the Sleep condition (the evening session).  Head-injury characteristics indicated that the majority of concussions sustained by individuals were from a sport-related injury (68%), a fall (17%), car accident (8%, or other (6%).  All participants in the TBI sample were reported as being on the minor end of the severity of TBI spectrum.  For sleep characteristics, there was no significant differences between the two groups for total time asleep or sleep efficiency.  The major difference resulted from sleep latency, where the TBI group had longer sleep latency than the TBI-group.  Additionally, the TBI group had longer REM latency and less REM sleep than the non-TBI group.

For memory performance and neutral stimuli, a main effect was indicated for condition, meaning that the Sleep condition had higher memory performance rates than the Wake condition.  There was no interaction found for injury and condition suggesting that the TBI group did not have a distinguishable deficit in sleep-dependent memory consolidation related to neutral stimuli. For negative stimuli, there were no main effects found for condition or injury group, but there was a significant interaction found for these factors.  Between the non-TBI Sleep condition and the non-TBI Wake condition, the non-TBI Sleep participants performed significantly better than the non-TBI Wake condition.  No difference was found between the TBI Sleep condition and the TBI Wake condition.  The TBI Sleep condition had significantly reduced memory performance than the non-TBI Sleep condition indicated by the TBI sleep group having higher false alarms than the non-TBI Sleep condition.  The TBI Wake condition had lower rates of false alarms than the non-TBI Wake condition.

For valence of negative images, a main effect was found for the injury group meaning the non-TBI group presented a higher change toward neutrality than the TBI group at session 2.  A significant effect was also found between injury group and condition in that the non-TBI Wake condition significantly became more neutral than the non-TBI Sleep condition at session 2.  In assessing emotional processing deficits, it was demonstrated that the number of TBIs sustained, sleep characteristics, or number of symptoms did not predict memory consolidation.  Head-injury factors did not predict the number of possible false alarms, but number of TBIs was a significant predictor of false alarms, suggesting that more TBIs resulted in a higher rate of reported false alarms.  Results also indicate that a single concussion or TBI can produce emotional deficits, with multiple injuries worsening these deficits.

Discussion and Implications

Results of the study demonstrated similar findings to past research which suggest that sleep quality and characteristics change after sustaining a TBI, such as longer sleep latency and less time spent in REM sleep.  It was also established that chronic TBI and sleep disturbances  have an impact on emotional memory consolidation and emotional processing indicated by false alarms in the recognition phase of the study.  Researchers highlighted potential limitations to the study including the lack of use of clinical measures to assess depression and anxiety symptoms.  Without these measures, the researchers were limited to the conclusions they could make related to how chronic TBIs can contribute to negative mental health conditions and if sleep and wake dependent emotional processes are impacted by poor mental states.  Future studies could attempt to implement these types of clinical measures to better assess mood states and levels of emotional processing and memory consolidation in patients with TBI.

Article Summary #3

Ponsford, J., Parcell, D., Sinclair, K., Roper, M., & Rajaratnam, S. (2013). Changes in Sleep Patterns Following Traumatic Brain Injury: A Controlled Study. Neurorehabilitation and Neural Repair, 27(7), 613-21. doi: 10.1177/1545968313481283

Research Question

The researchers in this study were interested in the relationship between traumatic brain injury and subjective sleep changes.  The research question is: How does sleep quality of individuals with TBI differ from non-injured individuals of a similar age and sex?  Additionally, what impact do secondary factors like anxiety, pain, and depression hold on the perception of overall sleep quality in TBI individuals?

Background of Research Question

Past research on this topic has indicated a vast variability in the types of sleep disturbances  reported by TBI patients.  These disturbances include nightmares, delayed onset of sleep, early awakening periods, poor sleep efficiency, excessive daytime sleepiness, as well as a  variety of sleep disorders such as sleep apnea and hypersomnia (Mathis & Alvaro, 2012).  While the cause of these sleep problems remains a mystery, past studies have suggested that they stem from damage to certain areas of the brain and systems connected to neurotransmitters that regulate sleep pathways, such as the hypothalamus and the midbrain (Baumann, Werth, Stocker, Ludwig, & Bassetti, 2007).  Some studies have also suggested that secondary symptoms such as anxiety, depression, or fatigue may be associated with poor sleep patterns post-injury.

Hypothesis and Methods

The hypothesis of the study is that individuals with TBI would report higher incidences of sleep changes than non-injured age and sex matched controls as well as other changes in sleep such as poorer quality of sleep, increased sleep latency, more awakenings throughout the night, and increased daytime sleepiness.  Additionally, it was hypothesized that these changes would be associated with secondary factors such as depression, anxiety, and pain.

Participants (aged 16-65) were recruited from the Epworth Hospital in Melbourne, Australia, and were required to have experienced a mild to severe TBI.  These participants were age and sex matched with non-injured individuals from the general population.  All participants were screened to ensure they had no previous sleep disorders and were not taking medications to assist with falling asleep.  Injury characteristics such as time since injury and reason for injury were obtained and scores from the Glasgow Coma index (GCS) were obtained from medical records.  Individuals in the TBI group (n = 153) and non-TBI group (n = 128) were asked to complete several self-report questionnaires about their sleep and were asked to keep a diary for seven days that detailed their sleep patterns.  Measures and questionnaires completed by the participants included the Epworth Sleepiness Scale (ESS), Pittsburgh Sleep Quality Index (PSQI), General Sleep Questionnaire (GSQ), Hospital Anxiety and Depression Scale (HADS), and Brief Pain Inventory (BPI).  The sleep-diary contained information related to sleep patterns such as bedtime, sleep onset, wake time, number of awakening during the night, number of daytime naps, and  caffeine and alcohol consumption.


Data analysis was completed using SPSS version 20 and consisted of between-group comparisons using independent t-tests and

x2tests.  Demographic results determined that the TBI group was more likely to be taking medication, were less likely to be employed, and were more likely to be experiencing pain symptoms.  Injury characteristics of the TBI group indicated a small percentage had a mild TBI injury (4%), 22% had a moderate injury, 49% had a severe injury, and 25% had a very severe injury (based on analysis of posttraumatic amnesia PTA).  Causes of injury included car accidents, pedestrian accidents, assaults, and falls.  In the TBI group, participants indicated abnormalities in the brain in the frontal lobe (40%), temporal lobe (24%), parietal lobe (21%), occipital lobe (12%),  and medial/limbic regions in (11%).  The TBI group scored significantly higher on the HADS scales than the control group.  Anxiety was reported to increase with time post-injury, but time since injury was not found to be related to increased symptoms of depression.

For sleep symptoms, the TBI group reported significantly poorer sleep quality when compared to the control group.  TBI patients also reported significantly more symptoms related to insomnia.  Responses on the GSQ asking about how “rested” participants felt upon waking up in the morning were significantly poorer in the TBI group compared to controls.  Factors identified to have an impact on sleep for the TBI group included pain, worries, and work/chores.  The non-injured group also reported work/chores, but identified children and light as other potential factors.  Daytime sleepiness was rated higher in TBI participants and they also reported higher levels of excessive daytime sleepiness in comparison with the non-injured participants.  A high proportion of TBI participants (80%) reported a notable change in their sleep post-injury.  Additionally, they reported longer time to fall asleep, poorer efficiency of sleep, longer daytime naps, and a higher total sleep duration.

For secondary factors, it was found that increased time since injury was associated with poorer sleep quality and higher reports of daytime sleepiness.  The more severe the injury, as determined by the GCS and PTA scores, the average sleep duration was observed to increase**.  Being employed was reported as a factor associated with less daytime naps, shorter daytime nap duration, and an increased overall sleep quality.  For TBI participants, higher levels of pain severity were associated with poorer sleep quality as well as higher levels of depression and anxiety.  In the non-injured group. there was no association found between sleep quality related to pain, anxiety, or depression.  Increased levels of anxiety and depression were associated with increased daytime sleepiness, poorer sleep quality, and a higher average number of naps per day in the TBI group.  Based on this information, it was predicted that pain, depression, and anxiety were significant factors related to sleep quality.  Upon further analysis, pain and anxiety, not depression, were found to account for variations in overall sleep quality in the TBI participants.

Discussion and Limitations

The study demonstrated that individuals who have experienced a TBI have a higher chance of experiencing and reporting sleep changes than age and sex matched non-injured individuals.  This study also highlighted how secondary factors, such as pain and anxiety, could be potential predictors of these sleep disturbances in TBI populations.  A limitation suggested by the researchers indicated the use of self-report measures used in the study.  Individuals may have a difficult time accurately describing their quality of sleep which may impact how they answer questions on self-report measures.  This is why self-report measures used in conjunction with objective recording tools, such as polysomnography, can create a more detailed account for sleep disturbances experienced by TBI patients.

Article Summary #4

Shekleton, J. A., Parcell, D. L., Redman, J. R., Phipps-Nelson, J., Ponsford, J. L., & Rajaratnam, S. M. W. (2010). Sleep disturbance and melatonin levels following traumatic brain injury. Neurology74(21), 1732–1738. doi: 10.1212/WNL.0b013e3181e0438b

Research Question

The researchers in this study were interested in the relationship between sleep-wake disturbances and a traumatic brain injury.  The research question is: How do the physiological mechanisms related to sleep such as melatonin levels and circadian rhythms change when an individual suffers a TBI?

Background of Research Question

Past research on this topic suggest that individuals who have suffered a TBI report issues related to their sleep patterns such as insomnia, hypersomnia, and altered sleep-wake states (Orff, Ayalon, Drummond, 2009.)  Studies based around sleep architecture have also identified potential changes to REM patterns in TBI patients such as increased slow wave sleep and reduced levels of REM sleep (Parcell, Ponsford, Redman, & Rajaratnam, 2008).  Additionally, researchers have indicated that TBIs may impact circadian rhythms or even delay circadian rhythms post-injury  (Ayalon, Borodkin, Dishon, Kanety, & Dagan, 2007).   This delay may be associated with a disturbance of melatonin levels that regulate sleep-wake cycles (Rajaratnam, Cohen, & Rogers, 2009).

Hypothesis and Methods

The hypothesis of the study aimed to characterize sleep-wake disturbances following a TBI and they predicted that these changes could be assessed by observing polysomnographic sleep, melatonin rhythms, and mood states.   23 participants were recruited from the Epworth Hospital in Melbourne, Australia where they had received treatment for TBI; these 23 participants were age and gender matched with healthy volunteers.  Participants completed the Pittsburgh Sleep Quality Index (PSQI), the Epworth Sleepiness Scale (ESS), the Morning-Eveningness Questionnaire (MEQ), and the Hospital Anxiety and Depression Scale (HADS).

The participants attended two separate overnight visits at the Monash University Sleep Laboratory seven days apart.  On the first visit, participants arrived at 5 p.m., were placed in a dimly lit room, had a sensor placed on their forehead, and were given instructions to control their food intake and activity level.  At 7:00 p.m., both groups of participants were fitted with face and scalp electrodes to record polysomnographic information, however, this information was not recorded on the first visit.  From 6 p.m. to 12:30 a.m., participants were asked to provide a sample of saliva every half hour.  The sample were frozen and were analyzed for their melatonin concentration at the Department of Obstetrics and Gynaecology in Adelaide, Australia.  This first visit was considered a trial run in order for the participants to become accustomed to the sleep laboratory environment.  One the second visit, participants arrived two hours before their normal sleep time (as determined by personal sleep-wake diaries) to complete polysomnographic monitoring using EEG, EOG, and EMG analysis.  Participants got into bed 15 minutes before
a scheduled lights out time and were instructed to stay in bed for eight hours.


Analysis of sleep recordings consisted of measurements of total sleep time, non-REM stages, REM sleep, wake after sleep, sleep efficiency, and sleep latency.  In this study, sleep efficiency was defined as total sleep time divided by time in bed.  On the self-report measures, the TBI group scored higher on the PSQI and the HADS, indicating poorer sleep quality and more symptoms of anxiety and depression than the healthy controls.  The groups scores were not significantly different for either the ESS or the MEQ assessments.  From the melatonin samples gathered from all participants, it was observed that at dim light onset, the control group had higher levels of  melatonin production than the TBI group.

From the analyses of the polysomnographic data, the TBI group had lower levels of sleep efficiency and took longer to fall asleep than the control group.  The TBI group also had less REM sleep cycles throughout the night and higher levels of slow-wave sleep when compared to the control group.  An association was found between injury severity and time it takes to fall asleep.  Individuals who had experienced a more severe TBI took longer to fall asleep than others who experienced a mild TBI.  When considering symptoms of anxiety and depression related to sleep, depression and anxiety were associated with longer periods of waiting to fall asleep, but only anxiety was found to relate to sleep efficiency.  Melatonin levels were not observed to be associated with sleep efficiency, the time it took to fall asleep, anxiety, or depression.  However, there was an association for melatonin levels and REM and non-REM sleep stages.

Discussion and Implications

The current study demonstrated that TBI is associated with sleep disturbances as observed from self-report measures as well as objective sleep data. TBI patients were observed to have more trouble falling asleep in addition to poorer sleep efficiency when compared to age-and-gender matched controls.  TBI group participants were also observed to have higher reports of anxiety and depressive symptoms as well as significantly lower melatonin production than the control group.  A limitation suggested by the researchers is that they did not obtain enough data to fully understand how lower melatonin levels present in TBI individuals impacts REM sleep which then impacts overall sleep efficiency.  Future studies would benefit from focusing strictly on REM cycles of TBI individuals and how these cycles impact their overall sleep quality.

General Synopsis

Learning Impact


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Ayalon, L., Borodkin, K., Dishon, L., Kanety, H., & Dagan, Y. (2007). Circadian rhythm sleep disorders following mild traumatic brain injury. Neurology, 68(14), 1136-1140. doi: 10.1212/01.wnl.0000258672.52836.30

Baumann, C., Werth, E., Stocker, R., Ludwig, S., & Bassetti, C. (2007). Sleep–wake disturbances 6 months after traumatic brain injury: A prospective study.Brain, 130(7), 1873-1883. doi: 10.1093/brain/awm109

Fichtenberg, N.L., Millis, S.R., Mann, N.R., Zafonte, R.D. & Millard, A.E. (2000) Factors associated with insomnia among post-acute traumatic brain injury survivors. Brain Injury, 14(7), 659-667. doi: 10.1080/02699050050044015

Fralick, M., Thiruchelvam, D., Tien, H., & Redelmeier, D. (2016). Risk of suicide after a concussion. Canadian Medical Association Journal, 188(7), 497-504. doi: 10.1503/cmaj.150790

Grima, N., Ponsford, J., Rajaratnam, S., Mansfield, D., & Pase, M. (2016). Sleep Disturbances in Traumatic Brain Injury: A Meta-Analysis. Journal of Clinical Sleep Medicine, 12(3), 419-28. doi: 10.5664/jcsm.5598

Hou, L., Han, X., Sheng, P., Tong, W., Li, Z., Xu, D., Yu, M., Huang, L., Zhao, Z., Lu, Y., & Dong, Y. (2013). Risk factors associated with sleep disturbance following traumatic brain injury: Clinical findings and questionnaire based study. PLoS One, 8(10), 1-8. doi: 10.1371/journal.pone.0076087

Konrad, C., Geburek, A.J.,  Rist, F.,  Blumenroth, H., Fischer, B.,  Husstedt, I., Arolt, V., Schiffbauer, H., & Lohmann, H. (2011). Long-term cognitive and emotional consequences of mild traumatic brain injury. Psychological Medicine, 41(6), 1197-211. doi: 10.1017/S0033291710001728

Mantua, J., Henry, O., Garskovas, N., & Spencer, R. (2017). Mild traumatic brain injury chronically impairs sleep- and wake- dependent emotional processing. Sleep, 40(6)1-10. doi: 10.1093/sleep/zsx062

Mathias, J.L.& Alvaro, P.K. (2012). Prevalence of sleep disturbances, disorders, and problems following traumatic brain injury: A meta-analysis. Sleep Medicine, 13(7), 898-905. doi: 10.1016/j.sleep.2012.04.006

Orff, H.J., Ayalon, L.,  & Drummond, S.P. (2009). Traumatic Brain Injury and Sleep Disturbance: A Review of Current Research. Journal of Head Trauma Rehabilitation 24(3), 155-165. doi: 10.1097/HTR.0b013e3181a0b281.

Ouellet, M.C.,  Beaulieu-Bonneau, S., & Morin, C. (2006). Insomnia in patients with traumatic brain injury: frequency, characteristics, and risk factors.  Journal of Head Trauma Rehabilitation. 21(3), 199-212. doi: 10.1097/00001199-200605000-00001.

Parcell, D. L., Ponsford, J. L., Redman, J. R., & Rajaratnam, S. M. W. (2008). Poor sleep quality and changes in objectively recorded sleep after traumatic brain injury: A preliminary study. Archives of Physical Medicine and Rehabilitation89(5), 843-850. doi: 10.1016/j.apmr.2007.09.057

Ponsford, J., Parcell, D., Sinclair, K., Roper, M., & Rajaratnam, S. (2013). Changes in Sleep Patterns Following Traumatic Brain Injury: A Controlled Study. Neurorehabilitation and Neural Repair, 27(7), 613-621. doi: 10.1177/1545968313481283

Rajaratnam, S.W.,  Cohen, D.A.,  & Rogers, N.L. (2009). Melatonin and Melatonin Analogues. Sleep Medicine Clinics, 4(2) 179–193. doi: 10.1016/j.jsmc.2009.02.007.

Rutland-Brown, W., Langlois J.A., Thomas, K.E., Xi, Y.L. (2003). Incidence of traumatic brain injury in the United States.  Journal of Head Trauma Rehabilitation, 21(6), 544-548. Retrieved from:

Shekleton, J. A., Parcell, D. L., Redman, J. R., Phipps-Nelson, J., Ponsford, J. L., & Rajaratnam, S. M. W. (2010). Sleep disturbance and melatonin levels following traumatic brain injury. Neurology74(21), 1732–1738. doi: 10.1212/WNL.0b013e3181e0438b

Verma, A., Anand, V., & Verma, N.P. (2007). Sleep disorders in chronic traumatic brain injury. Journal of Clinical Sleep

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