Evaluation of posttraumatic fatigue
Introduction
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Fatigue is one of the most commonly reported symptoms after brain injury (BI); reported rate of fatigue varies.
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One study reported fatigue in 53% of those studied.
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Other studies have suggested 21% to 70% of individuals with traumatic brain injury (TBI) experience fatigue, greater than estimates for the general population of 3% to 22%.
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Definition
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No standardized uniform definition exists. It has been described as an awareness of a negative balance between available energy and the mental and physical requirements of activities.
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Distinction between central fatigue and peripheral fatigue :
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Central fatigue: Dysfunction of supratentorial structures involved in mentation
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Peripheral fatigue: Of physical, metabolic, or muscular origin
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Often both are involved after TBI.
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Fatigue versus excessive daytime sleepiness (EDS): Although they are similar, there is a difference in that sleepiness typically responds to appropriate amount of rest. Sleepiness is more defined by difficulty maintaining wakefulness, whereas fatigue is multidimensional.
Etiology
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The exact etiology is unknown and is likely multifactorial.
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There are associations with conditions that are frequently reported after TBI, such as depression, pain, and disturbed sleep.
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Chronic pain can lead to symptoms of fatigue.
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It has been reported with neuroendocrine abnormalities.
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Coping hypothesis is a theory that fatigue after BI is caused by an increase in mental effort needed to overcome impaired attention and processing speed, thus the brain compensates to overcome these cognitive deficits.
Scales/metrics used
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There is no one universally applied scale, although a number of scales have been used to measure fatigue after BI ( Table 37.1 ).
TABLE 37.1
Measures of Assessing Fatigue
Measure
Key Features
Global Fatigue Index (GFI)
One of the most widely used measures of fatigue, used with a variety of populations with chronic conditions, including human immunodeficiency virus, multiple sclerosis, and cancer
Epworth Sleepiness Scale
Measures daytime sleepiness rather than fatigue but has been used in studies in those with traumatic brain injury (TBI). There are eight items, each of which rates a routine daytime situation on a 4-point scale from 0 (would never doze) to 3 (high chance of dozing). Subjects who score 10 or more are considered to have excessive daytime sleepiness.
Fatigue Severity Scale (FSS)
A one-dimensional fatigue scale composed of nine items each ranging from 1 (no impairment) to 7 (severe impairment), with higher scores indicating more severe fatigue. Has been used in trials of individuals with TBI and used in trials of modafinil for fatigue after TBI.
Modified Fatigue Impact Scale
A multidimensional fatigue measure found to be reliable and has been used in studies in individuals with TBI. A 21-item self-report instrument in which subjects rate the extent to which fatigue has caused problems for them from 0 (no problem) to 4 (extreme problem), with higher scores indicating a greater impact of fatigue. Subscales for cognitive, physical, and psychosocial functioning can also be calculated.
Barrow Neurological Institute Fatigue Scale
Designed for use in early stages of measuring fatigue, such as on acute rehabilitation.
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“Measurement overlap” is important to keep in mind, in that measures of depression, pain, and other health problems often pertain to fatigue and thus are likely to correlate with fatigue measures.
General medical workup
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Initial testing can include erythrocyte sedimentation rate (ESR), complete blood count, chemistry panel, liver panel, and fasting blood glucose.
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Cardiopulmonary
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Obstructive sleep apnea, chronic obstructive pulmonary disease (COPD), heart failure
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Metabolic
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Anemia/iron deficiency
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Endocrine
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Anterior pituitary dysfunction
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Thyroid/growth hormone/testosterone/cortisol
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Psychiatric
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Alcohol or drug dependence
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Infectious
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Neoplastic
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Medication induced
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Assessing necessity of medications that increase fatigue:
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Antiepileptics
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Antihistamines
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Antipsychotics
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Antihypertensives (propranolol, verapamil)
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Antiemetics (Phenergan, Zofran)
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Sleep disorders (see later)
Management
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Home exercise program
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Rehabilitation approach
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Compensatory strategies with energy conservation
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Instructions to pace oneself/brain breaks
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Dietary counseling and weight reduction
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Psychiatric counseling or referral to mental health specialists as indicated
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Cognitive behavioral therapy (CBT) has been shown to help with fatigue in other conditions but is not proven to help with fatigue specifically after TBI
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Pharmacological treatments of fatigue
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Modafinil is US Food and Drug Administration (FDA) approved for treatment of EDS associated with narcolepsy, obstructive sleep apnea, and shift work sleep disorder.
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Modafinil has been shown to help with Excessive Daytime Sleepiness (EDS) but not with measures of fatigue.
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Methylphenidate has been shown to benefit in one class III crossover study of 24 patients.
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Hormone replacement can be considered for endocrine abnormalities, but more research is needed.
Evaluation of sleep dysfunction
Introduction
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Sleep disorders are common after a TBI, with one study finding incidence to be three times higher compared with the general population.
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Prevalence is higher in those with severe TBI compared with mild TBI.
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Sleep dysfunction is a component of fatigue but not necessarily the primary cause of fatigue.
Overview of normal sleep
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Sleep stages divided into nonrapid eye movement (NREM) and rapid eye movement (REM)
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Five stages overall: wake (W), N1, N2, N3, and R
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N1–N3 are considered NREM
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Characteristics of each stage
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W: As individuals become drowsy and the eyes close, the alpha rhythm is the predominant pattern. An epoch is considered stage W if it contains greater than 50% alpha waves
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N1: Very short duration, considered light sleep
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N2: Presence of sleep spindles and K complexes
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N3: Considered the deepest stage of sleep and characterized by delta waves
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REM sleep: electroencephalogram (EEG) is the same as in awake state but characterized by muscle atonia and episodic bursts REMs; stage when dreams occur
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Slow-wave/deep NREM sleep is more prominent in the first third of the night, and REM sleep is more prominent in the last part of the night or morning hours.
Pathophysiology/changes to sleep after traumatic brain injury
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A metaanalysis of polysomnography data after TBI showed that TBI patients had poorer sleep efficiency, shorter total sleep duration, and greater wake after sleep onset time. Although sleep architecture was similar between the groups, a trend suggested that TBI patients may spend less time in REM sleep. TBI patients reported greater subjective sleepiness and poorer perceived sleep quality.
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Biochemical substrates have been found to be altered after TBI.
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Lower levels of cerebrospinal fluid of a neuropeptide called hypocretin-1 (orexin) are associated with excessive daytime sleepiness in TBI in acute phase but return to baseline in chronic phase. Low cerebrospinal fluid (CSF) orexin is initially found to be low in narcolepsy.
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Lowered melatonin is found to be associated with altered REM sleep post TBI.
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Damage to the hypothalamus, brainstem, and reticular activating system can disrupt arousal and the sleep–wake cycle.
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Coup-contrecoup injury most frequently damages inferior frontal and anterior temporal regions, including the basal forebrain, which is an area involved in sleep initiation.
Etiology
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Types of sleep disorders most commonly reported after TBI ( Table 37.2 )
TABLE 37.2Related posts:
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