7. Fatigue and Sleep Disorders Post Acquired Brain Injury
Level of Evidence
|MANAGEMENT OF FATIGUE|
|Exercise||A progressive walking program may reduce fatigue in patients with TBI
There is level 2 evidence (from one randomized controlled trial; Kolakowsky-Hayner et al., 2017) that a home-based walking program may reduce fatigue up to 24 weeks following treatment compared to a nutritional counselling program in patients with TBI.
|Pacing||More research is necessary to determine the efficacy of pacing interventions for patients with ABI.
No studies to date have examined the benefits of pacing within a population with ABI.
|Cognitive Behavioural Therapy||Cognitive behavioural therapy may reduce fatigue in patients with TBI.
There is level 1b evidence (from one randomized controlled trial; Ngyuen et al., 2017) and level 4 evidence (from one pre-post test; Ouellet and Morin, 2007) that cognitive behavioural therapy may reduce fatigue compared to usual care in patients with TBI.
|Light Therapy||Blue light therapy may reduce fatigue and daytime sleepiness in patients with TBI.
There is level 1a evidence (from two randomized controlled trials; Quera Salva et al., 2020, Sinclair et al., 2014) that blue light therapy may be effective in reducing fatigue and daytime sleepiness compared to no treatment in patients with TBI.
There is level 1b evidence (from one randomized controlled trial; Sinclair et al., 2014) that yellow light therapy may not be effective in reducing fatigue and daytime sleepiness compared to control.
|Lifestyle Management Strategies||Programming focusing on lifestyle factors, adaptive coping, and goal management training may reduce fatigue and sleepiness in patients with ABI.
There is level 4 evidence (from one pre-post trial; Stubberud et al., 2017) that programming focusing on lifestyle factors, adaptive coping, and goal management training may reduce fatigue up to 3 months and sleepiness up to 9 months post intervention in patients with ABI.
|Modafinil||Modafinil has not been shown to be effective in treating fatigue post TBI.|
|Modafinil has been shown to be effective in the short-term for treating excessive daytime sleepiness, but may also cause insomnia post TBI.
There is level 1a evidence (from two randomized controlled trials; Kaiser et al., 2010, Jha et al., 2008) that modafinil may not be effective for treating fatigue compared to placebo in patients with TBI, but may be effective short-term in treating excessive daytime sleepiness post TBI.
|(-)-OSU6162||(-)-OSU6162 treatment may not be effective for reducing fatigue post TBI.
There is level 1b evidence (from one randomized controlled trial; Berginstrom et al., 2017) that (-)-OSU6162 may not be effective for treating fatigue compared to placebo in patients with TBI.
|Melatonin||Melatonin may reduce fatigue in patients post TBI.
There is level 1b evidence (from one randomized controlled trial; Grima et al., 2018) that melatonin treatment may be effective in reducing fatigue compared to a placebo group in patients post TBI.
|MANAGEMENT OF SLEEP DISORDERS|
|Relaxation Strategies||A warm footbath in the evening may improve waking after sleep onset and sleep onset latency in patients with TBI.
There is level 1b evidence (from one randomized controlled trial; Chiu et al., 2017) that a warm footbath in the evening may improve wake after sleep onset and sleep onset latency but not sleep efficiency or sleep time compared to usual care in patients with TBI.
|Lifestyle Management||Programming focusing on lifestyle factors, adaptive coping, and goal management training may reduce sleepiness, but may not improve insomnia in patients with ABI.
There is level 4 evidence (from one pre-post trial; Stubberud et al., 2017) that programming focusing on lifestyle factors, adaptive coping, and goal management training may reduce sleepiness up to 9 months post intervention, but may not improve insomnia in patients with ABI.
|Cognitive Behavioural Therapy||Cognitive behavioural therapy may improve sleep quality and reduce insomnia in patients with TBI.
There is level 1b evidence (from one randomized controlled trial; Ngyuen et al., 2017) and level 4 evidence (from one pre-post trial; Ouellet and Morin, 2007) that cognitive behavioural therapy may reduce insomnia compared to usual care in patients with TBI.
|Acupuncture||Acupuncture therapy may not improve insomnia in patients with TBI.
There is level 2 evidence (from one randomized controlled trial; Zollman et al., 2012) that acupuncture may not improve insomnia compared to instructions on good sleep habits in patients with TBI.
|Sleep Hygiene||More research is necessary to determine the efficacy of sleep hygiene interventions for patients with ABI.
There is level 2 evidence (from one randomized controlled, unblinded trial; Markley et al., 2020) that a sleep hygiene intervention is feasible in a population with moderate to severe TBI; however, more research is needed to determine its efficacy.
|Modafinil||Modafinil has been shown to be effective in the short-term for treating excessive daytime sleepiness, but may also cause insomnia post TBI.
There is level 1a evidence (from two randomized controlled trials; Kaiser et al., 2010, Jha et al., 2008) that modafinil may be effective short-term in treating excessive daytime sleepiness but may also cause insomnia in patients post TBI.
|Methylphenidate||Methylphenidate may not have an adverse effect on the sleep-wake cycle of patients post TBI.
There is level 3 evidence (from one case-control; Al-Adawi et al., 2006) that methylphenidate may not have adverse effects on the sleep-wake cycle compared to those not receiving medication post TBI.
|Lorazepam & Zopiclone||More research is necessary to determine the safety and efficacy of benzodiazepines and non-benzodiazepine hypnotics for patients with ABI.
No studies to date have examined the effects of benzodiazepines and non-benzodiazepine sleep aids within a population with ABI.
|Melatonin||Melatonin may improve sleep quality and sleep efficiency in patients post TBI.
There is level 1b evidence (from one randomized controlled trial; Grima et al., 2018) that melatonin treatment may be effective in improving sleep quality and sleep efficiency compared to a placebo group in patients post TBI.
|Melatonin may not improve sleep onset latency or daytime sleepiness.
There is level 1b evidence (from one randomized controlled trial; Grima et al., 2018) that melatonin treatment may not affect sleep onset latency or daytime sleepiness in patients post TBI.
Fatigue and sleep disorders are among the more commonly reported symptoms associated with brain injury (Cronin & O’Loughlin, 2018; Duclos et al., 2014; Elovic et al., 2005) and can exacerbate other co-morbid symptoms and negatively affect quality of life. Understanding fatigue and sleep disorders and how to manage them is therefore important for addressing the needs of persons with ABI and can be a crucial complement to other efforts to optimize recovery post ABI. Although it would seemingly make sense to link disorders of sleep with fatigue (Clinchot et al., 1998), this relationship remains inconclusive (Fellus & Elovic, 2007). Sleep disturbances can exacerbate fatigue; however, fatigue may also manifest independent of sleep disorders and not all sleep disorders may produce fatigue (Ouellet et al., 2015).
One of the major challenges in this area is the large variability in the prevalence estimates of fatigue and sleep disorders within the ABI literature, which may affect 30-73% of persons post ABI (Englander et al., 2010; Ouellet et al., 2019; Ponsford et al., 2012). Much of this variability is due to variation in how data is collected: both subjective and objective means of collecting fatigue and sleep data are available. A systematic review found 16 measures of fatigue and sleep were commonly used in TBI studies (Mollayeva et al., 2013). Subjective questionnaires are the most commonly used, but polysomnography, actigraphy, multiple sleep latency tests, and maintenance of wakefulness tests are objective measures that may also be used (Mollayeva et al., 2013). Most of these measures have not been validated in persons with ABI. Despite the significant methodologic variability, epidemiologic estimates indicate that persons with ABI more often experience disorders of fatigue and/or sleep than the general population (Ouellet et al., 2019; Rao et al., 2015; Silver et al., 2018).
There are many putative sources of fatigue and sleep dysfunction, including neuroanatomical, psychological, biochemical, endocrine, or environmental causes (Mollayeva et al., 2013). A review by Duclos et al. (2014) suggests that fatigue and sleep disturbances may be due to altered circadian rhythms, damage to the cortical and subcortical structures involved in sleep and wakefulness, endocrine dysfunction (e.g., growth hormone or cortisol levels), pain, anxiety and depression, environmental factors, or may be multifactorial, encompassing elements in each of these categories. This complex interplay between pathophysiological, psychological, social, and environmental factors complicates our ability to determine the precise etiology of fatigue or sleep dysfunction (Ouellet et al., 2015). It is therefore important to investigate potentially treatable or reversible causes of fatigue or sleep dysfunction (e.g., anemia, hypothyroidism, obstructive sleep apnea, medications that may cause insomnia or worsen fatigue, etc.) in patients with ABI. When recovering from an ABI, fatigue and sleep disorders have the ability to interfere with their ability to participate in rehabilitation programs designed to assist them in performing their activities of daily living. It also impacts their physical, cognitive, and social abilities, emphasizing the importance of addressing fatigue and sleep dysfunction.
7.1 Fatigue Post ABI
One of the greatest challenges is in properly defining fatigue, which is a subjective experience and thus is not easily assessed by objective measures (Lewis & Wessely, 1992). Individuals experiencing fatigue report it as a feeling of tiredness, weakness, or exhaustion (Rao et al., 2006). Others define fatigue as the “unconscious decreased ability for physical and or mental activity due to an imbalance in availability, utilization or the retrieval of the physiological or psychological resources required to perform the activity” p.2 (Aaronson et al., 1999). Those studying or reporting on fatigue have attempted to distinguish between physical and psychological fatigue (Aaronson et al., 1999). Physical fatigue has been defined as “the result of excessive energy consumption, depleted hormones or neurotransmitters or diminished ability of muscle cells to contract” p.2 (Jha et al., 2008). Psychological fatigue has been defined as “a state of weariness related to reduced motivation, prolonged mental fatigue or boredom” p.1 (Lee et al., 1991).
Although fatigue has been recognized as a significant problem post ABI, there are few interventional studies addressing fatigue in this population. When comparing individuals with TBI to healthy controls, those who have had a brain injury experience greater levels of fatigue (Ashman et al., 2008; Borgaro et al., 2005; Chiou et al., 2016; LaChapelle & Finlayson, 1998; Ponsford et al., 2012; Ziino & Ponsford, 2006). Between 32% and 73% of individuals reported fatigue post TBI (Englander et al., 2010; Ponsford et al., 2012; Silver et al., 2018). To better understand the severity of the problem, data is often collected through surveys, interviews, and/or questionnaires. Comparison groups in many of the studies are those without an ABI. Scales frequently used in these surveys include the Fatigue Severity Scale, the Fatigue Impact Scale, the Visual Analogue Scale-F, the Global Fatigue Index, the Barroso Fatigue Scale, and the Epworth Sleepiness Scale; however, none of these scales were designed specifically for use in patients with brain injury, but rather they were developed for patients with Human Immunodeficiency Virus or Multiple Sclerosis (Armutlu et al., 2007; Fish et al., 2007). Because fatigue is a subjective experience, there are no objective measures of fatigue severity.
Fatigue is highly associated with psychological and cognitive comorbidities frequently found in the ABI population such as difficulties with vigilance, attention, depression, anxiety, and cognition. Those who sustain a TBI often have a lower cognitive reserve and may be unable to maintain the same levels of vigilance or sustained attention as they did before their injury (Ziino & Ponsford, 2006). This may be exacerbated by mental fatigue as reported by Jonasson et al. (2018) who found after cognitive activity, those dealing with mental fatigue had impaired cognitive performance. Ponsford et al. (2015) reported on the relationship between fatigue, depression, and anxiety post TBI: fatigue strongly predicted depression and anxiety according to the Hospital Anxiety and Depression Scale. A review by Kumar et al. (2018) also found numerous studies that reported a positive correlation between post-traumatic depression and self-reported fatigue. Bay & de-Leon (2011) surveyed individuals with TBI from an outpatient clinic and reported a significant correlation between fatigue and perceived stress.
Similar to sleep disorders, fatigue can have a significant negative effect on an individual’s ability to fully participate in rehabilitation post ABI. Moreover, the often intense rehabilitation programs themselves may exacerbate fatigue. In a study by Toda et al. (2006), the investigators found that individuals who had sustained a TBI reported significantly higher levels of fatigue during their time in rehabilitation than they did at 6- or 12-months post injury. One putative explanation is that once the patient is removed from the demands of inpatient rehabilitation and has achieved a greater understanding of their deficits, the feelings of fatigue may lessen; alternatively, natural recovery may be associated with some improvements in fatigue. However, the literature shows that fatigue can persist for years post injury regardless (Bay & de-Leon, 2011; Olver et al., 1996; Ouellet & Morin, 2004; Rao et al., 2006). In addition to negatively affecting rehabilitation participation, fatigue has been associated with subjective reports of cognitive problems, difficulties with decision-making, needing to work slowly to ensure accuracy, and challenges in getting things done on time (Esbjornsson et al., 2013). Fatigue can also negatively impact relationships, as there is a tendency towards reacting too quickly in response to others among individuals suffering from fatigue (Esbjornsson et al., 2013). Additionally, one’s ability to work is often compromised when fatigue is present. Schnieders et al. (2012) found those with fatigue, compared to those without, had lower-level jobs and more non-paying jobs. Therefore, managing fatigue is imperative in helping individuals live a productive life post injury.
Management of Fatigue
Fatigue post ABI can be managed using pharmacological or non-pharmacological techniques. Although fatigue is common post ABI and can have serious negative implications for recovery and quality of life, few interventions have been studied for these conditions. Moreover, the few studies available are often hampered by small sample sizes and short duration of follow-up. Thus, the optimal management of fatigue is likely elusive, and patients may require a constellation of interventions to meet their needs.
7.2 Non-pharmacological Interventions for Fatigue
Non-pharmacological strategies for the management of fatigue include exercise, pacing, cognitive behavioural therapy, and light therapy. Diet and lifestyle may also play an important role in combating fatigue; thus, it is believed that eating a “balanced diet” and learning to balance exercise with rest may help to reduce fatigue (Elovic et al., 2005; Rao et al., 2006). In this section, we review the literature evaluating the effectiveness of each of these techniques in the ABI population.
A progressive walking program may reduce fatigue in patients with TBI.
Exercise may improve fatigue and has significant benefits for cardiovascular health, general well-being, emotional and immune system functioning.
There is level 4 evidence (from one pre-post trial; Krese et al., 2020) that yoga-based physical therapy is feasible and safe in a mixed population with TBI; however, more research is needed to determine its efficacy.
7.2.3 Cognitive Behavioural Therapy
Another study compared an education and problem-solving therapy program targeted to management of fatigue and health education and did not find any between group differences on three measures of fatigue (Raina et al., 2016). The results of this study should be interpreted with caution, as the purpose of the study was to determine the feasibility of conducting a larger trial using an internet-delivered manualized intervention.
7.2.4 Light Therapy
There is level 1b evidence (from one randomized controlled trial; Sinclair et al., 2014) that yellow light therapy may not be effective in reducing fatigue and daytime sleepiness compared to control.
7.2.5 Lifestyle Management Strategies
7.3 Pharmacological Management Strategies For Fatigue
Modafinil has been shown to be effective in the short-term for treating excessive daytime sleepiness, but may also cause insomnia post TBI.
7.4 Sleep Disorders Post ABI
Understanding how prevalent sleep disorders are post brain injury is challenging. It has been shown that individuals with ABI self-report significantly less EDS on subjective measures compared to what is observed on objective measures (Imbach et al., 2016; Imbach et al., 2015). One study found that 47% of individuals with TBI reported EDS (Castriotta et al., 2007). Based on subjective measures, approximately 50% of a TBI sample reported symptoms of insomnia; however, more than half of the individuals who reported having sleep difficulties were not being treated for the condition (Ouellet et al., 2006). Ascertaining the true prevalence of sleep dysfunction is further complicated by reports that persons with severe TBI may underreport poor sleep, while those with mild TBI may be more aware of their sleep patterns and thus more likely to report sleep changes that have occurred as a result of their injury (Elovic et al., 2005).
Both subjective and objective measures can be used to screen for and/or diagnose sleep disorders. Commonly used self-reported questionnaires include: the Pittsburgh Sleep Quality Index and Insomnia Severity Index to assess sleep quality (Bastien et al., 2001; Buysse et al., 1989); the Epworth Sleepiness Scale and Stanford Sleepiness Scale to assess daytime sleepiness (Johns, 1991; Shahid et al., 2012); and, the STOP-Bang questionnaire to assess for obstructive sleep apnea (Chung et al., 2016). None of these measures have been validated in persons with ABI, although they may be used in this population for research and clinical purposes. Commonly used objective measures of sleep dysfunction include: sleep diaries (Aaronson et al., 1999), polysomnography (Ouellet et al., 2015; Zasler et al., 2012), actigraphy, multiple sleep latency tests (Zasler et al., 2012) and maintenance of wakefulness tests (Zasler et al., 2012). As with the subjective measures, most of these have not been validated in persons with ABI, aside from actigraphy (Kamper et al., 2016), although these tests are commonly used. These objective and subjective measures may be useful to clinicians as they work to screen, assess, and treat sleep disorders and/or fatigue in persons with ABI.
Factors associated with higher rates of sleep dysfunction vary across studies. Higher Glasgow Coma Scores (GCS >7) at time of injury, better immediate memory, pre-ABI presence of fatigue, a history of substance abuse, older age and female gender have been associated with higher frequency of sleep complaints by some researchers (Thaxton & Patel, 2007). In contrast, others report that increased injury severity is associated with more disturbances in sleep and wake cycles (Duclos et al., 2014), as well as fatigue and sleepiness (El-Khatib et al., 2019).
The presence of sleep disturbance has multiple negative implications for persons with ABI. Sleep disturbances may negatively impact satisfaction with life, and scores on the Functional Independence Measure and Disability Rating Scale (Fogelberg et al., 2012). Affected Individuals tend to have longer lengths of stay in hospital (Duclos et al., 2014; Nakase-Richardson et al., 2013; Sandsmark et al., 2016). Moreover, Nakase-Richardson et al. (2013) discovered that the moderate to severe sleep disorders were correlated with longer durations of post-traumatic amnesia, which has negative prognostic implications. The negative sequelae of sleep dysfunction are further underscored by Sandsmark et al. (2016) who reported that in the acute post ABI setting, sleep was associated with good outcomes, such as increased likelihood to be discharged home, shorter intensive care unit and hospital length of stays, and decreased mortality. Gardani et al. (2015) report that in severe brain injuries, insomnia and poor sleep quality are associated with anxiety during subacute and chronic rehabilitation. Moreover, Cantor et al. (2012) found that at one-year post ABI, insomnia was associated with the presence of anxiety, major depression, and poor sleep quality. At two years post ABI, the presence of anxiety, higher discharge cognitive Functional Independence Measure scores, and poorer sleep quality were predictors of insomnia (Cantor et al., 2012). Fichtenberg et al. (2000) found an association between insomnia and pain and depression. Although determination of causality is not possible for these studies, they highlight that sleep dysfunction can accompany multimorbidity that may interfere with recovery post ABI.
Management of Sleep Disorders
The management of sleep disorders varies based on the specific disorder and can be achieved through non-pharmacological and/or pharmacological approaches. To date, few studies have investigated effectiveness of treatment options for sleep disorders in the ABI population. In this following section, we present an overview of the literature examining pharmacological as well as nonpharmacological interventions for managing sleep disorders post ABI.
7.5 Non-Pharmacological Interventions for Sleep Disorders
7.5.1 Relaxation Strategies
7.5.2 Lifestyle Management Strategies
7.5.3 Cognitive Behavioural Therapy
Similarly, Nguyen et al. (2017) reported individuals who received CBT showed significant improvements in sleep quality, insomnia, anxiety, and depression, but not in sleepiness. A secondary analysis of the previous study, and another involving stroke patients, found that participants who were younger, had better verbal memory, and with comorbid symptoms of depression were more likely to respond to CBT treatment (Nguyen et al., 2018).
7.5.5 Sleep Hygiene
7.6 Pharmacological Interventions for Sleep Disorders
7.6.3 Lorazepam and Zopiclone
Melatonin may not improve sleep onset latency or daytime sleepiness.
There is level 1b evidence (from one randomized controlled trial; Grima et al., 2018) that melatonin treatment may not affect sleep onset latency or daytime sleepiness in patients post TBI.
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7.1 Fatigue Post ABI