Selected Somatic Disorders Associated With Mild Traumatic Brain Injury: Fatigue, Dizziness and Balance Impairment, and Whiplash Injury

Michael Henrie and Elie P. Elovic

Common somatic aliments seen in association with mild traumatic brain injury (MTBI) include balance deficits, dizziness, fatigue, headache, nausea, visual disturbances, tinnitus (particularly with blast injury or MTBI associated with damage to the internal auditory canal), slurred speech, dysesthesias, generalized nonspecific weakness, and musculoskeletal complaints such as cervical spine injury and whiplash-associated disorders (WADs). In general, the initial symptoms directly attributable to traumatic brain injury (TBI) occur as a result of neurometabolic processes [1]. One must also consider that some symptoms may result from the associated cranial injury that often accompanies MTBI. The most important of these manifestations that are not discussed elsewhere in this text are discussed in the following sections.

FATIGUE

Definition

Fatigue is defined as (a) that state following a period of mental or bodily activity, characterized by a lessened capacity for work and reduced efficiency of accomplishment, usually accompanied by a feeling of weariness, sleepiness, or irritability; (b) a sensation of boredom and lassitude due to absence of stimulation, monotony, or lack of interest in one’s surroundings [2].

Classification

Fatigue can be classified as (a) central fatigue, resulting from supratentorial structures, or (b) peripheral fatigue, which has a physical, metabolic, or muscular origin. It can be further subdivided as either physical or mental/cognitive. There is substantial overlap between central and peripheral processes governing fatigue [3]. In addition, excessive daytime sleepiness is common following TBI [4] and should be viewed as a separate but related construct; it should be differentiated from fatigue, although they often coexist.

Epidemiology

Twenty-one percent of individuals with MTBI complain of fatigue [5]. It is one of the most common postconcussion symptoms, and may persist even after other symptoms have resolved [6].

Pathophysiology

Centrally mediated fatigue results from direct injury to central structures such as the reticular activating system and basal ganglia. A number of other factors that may contribute to fatigue include depression, decreased levels of the amino acids tryptophan and tyrosine, and alterations in cholinergic, serotonergic, and histaminergic pathways [3]. Endocrine disease, including deficiencies in growth hormone, cortisol, testosterone, and thyroid hormones, can also produce fatigue [7]. In addition, there is evidence to suggest that the injured brain is subject to fatigue because it needs to “work harder” in order to compensate for cognitive impairments such as decreased processing speed and attention [8].

Diagnosis

Clinical Presentation

Fatigue can affect an individual’s cognitive function, ability to successfully perform activities of daily living, quality of life, and employment. When obtaining a history, the line of questioning should help differentiate between fatigue and sleepiness and should include identification of possible psychological, neurological, or endocrine abnormalities.

Examination and Laboratory Assessment

Several subjective scales have been used to measure fatigue in brain-injured patients—Fatigue Severity Scale, Visual Analog Scale for Fatigue, Fatigue Impact Scale, Barrow Neurological Institute (BNI) Fatigue Scale, and Cause of Fatigue (COF) Questionnaire. The BNI and COF Questionnaire were designed specifically for brain-injured patients [3,9]. Systematic screening for endocrine dysfunction is recommended in all patients with TBI [7]. More recently, a computer assessment tool stressing endurance, processing speed, and attention was able to demonstrate a difference in performance between a mild TBI group and a control group, hypothesized to be a result of mental fatigue. If correct and reproducible, this tool holds promise as an objective measure of mental fatigue [10].

Treatment

Nonpharmacologic management of fatigue includes the following: Establish a routine home exercise program with the goal of optimizing cardiovascular health and improving physical well-being. Follow good dietary habits with the goal of weight reduction to improve energy efficiency. Educate patients on appropriate sleep hygiene and address any treatable sleep disorders. Address depression if present. Introduce compensatory activities and activity modification to conserve energy [3]. Pharmacologic management should be initiated if conservative measures fail. Management includes discontinuation or appropriate substitution of any medications with the potential to cause fatigue. One common problem (particularly in the setting of moderate to severe TBI) is the inappropriately prolonged use of anticonvulsants. If posttraumatic epilepsy is present, the least sedating medication should be used. Other medications that are commonly prescribed in this population will include muscle relaxants, pain medications and hypnotics. While sometimes necessary the risk/benefit ratio of using these medications must be evaluated.

Endocrine deficiencies requiring immediate treatment include: diabetes insipidus, adrenal insufficiency, and secondary thyroid insufficiency. Replacement of gonadal and growth hormone deficiencies should be postponed until the need for such therapy is confirmed by appropriate retesting, typically at least 1 year after injury [7].

Few well-designed studies have looked at the use of stimulants in the management of posttraumatic fatigue. However, a number of papers have shown efficacy of stimulants for treatment of decreased cognition (processing speed, alertness, etc.) in TBI [11]. In other populations these agents have demonstrated a positive effect on fatigue. The dopaminergic agents methylphenidate and dextroamphetamine have demonstrated benefit in treating HIV-related fatigue [12]. These agents can be dosed to coincide with periods of important activity during the day. Modafinil, thought to work through multiple pathways (including histaminergic, dopaminergic, serotonergic, GABA, and glutaminergic), and thought to work primarily through histaminergic pathways, has been reported to be of benefit in stroke, multiple sclerosis, and depression [13]. Its utility in TBI is unclear; while at least one study reported that the drug is effective in addressing excessive daytime sleepiness after TBI [14], a recent meta-analysis concluded that the evidence is inconsistent and a recommendation for its use in TBI could not be made [15]. Ginkgo biloba, an over-the-counter agent, also has some evidence for its efficacy in the treatment of chronic fatigue syndrome [16].

BALANCE AND DIZZINESS

Definition

The term dizzy is nonspecific and can refer to presyncopal lightheadedness or a sense of an impeding fainting episode, vertigo or the illusion of movement, a sense of imbalance, or multisensory dizziness, which occurs with pathology affecting multiple organ systems [17].

Classification

Dizziness following brain injury can be broadly categorized by etiology as vestibular and nonvestibular.

Epidemiology

Dizziness may affect up to 20% to 50% of individuals with mild to moderate TBI. It is also one of the five most common complaints that distinguish postconcussive patients from healthy controls [18]. In the military population, 80% of service members identified as having sustained a TBI reported balance dysfunction [19].

Pathophysiology

The balance system is complex and consists of multiple sensory inputs including the visual, somatosensory, and proprioceptive systems in addition to the vestibular end organs. Injury to any of the components can lead to complaints of dizziness and imbalance [20]. In addition, injury to the head, which does not necessarily result in TBI, may account for the symptoms. Vestibular causes include benign positional vertigo that may result from displacement of calcium crystals from the otoliths into the semicircular canal, and labyrinthine concussion caused by violent head movements. Labyrinthine concussion can occur in the absence of a temporal bone fracture and is often used to describe the spectrum of inner ear symptoms that occur following brain injury. Less common causes include ischemia, hemorrhage, or direct trauma to one or more components of the vestibular system, as well as perilymphatic fistula and posttraumatic Menier’s syndrome. Decreased processing speed, migraine headache, and concomitant injuries to the visual system or musculoskeletal system should also be considered as potentially affecting the vestibular system’s output [17]. There is little information available in the literature regarding nonvestibular causes of dizziness following TBI. Causes likely include positional orthostasis, cervical spine injury, medications such as antihypertensives and anticonvulsants, hyponatremia, and rarely vestibular epilepsy [17]. In the military population, development of these symptoms probably occurs via the effect of the blast pressure wave on inner ear structures [19].

Diagnosis

Clinical Presentation

Symptoms are often poorly or vaguely described. Common complaints include lightheadedness, feeling drunk, a spinning or rotating sensation, and balance problems [17]. This condition may contribute to balance difficulty, falls, problems with transfers and ADLs, as well as psychological distress [17]. A detailed neurotologic history is the most important factor in determining treatment course, and therefore must be accurately obtained [20].

Examination

Metrics used to assess physical functioning include both objective and self-reported measures, with the Dynamic Gait Index and measures of gait velocity being examples of the former; and the Dizziness Handicap Inventory, Vertigo Handicap Questionnaire, and Vertigo Symptom Scale being examples of the latter [17]. Balance can also be measured with metrics such as the Balance Error Scoring System [21]. If benign positional vertigo is suspected, the Dix-Hallpike test should be performed [20].

Laboratory and Radiologic Assessment

Formal audiometric testing should be strongly considered given the anatomic relationship between the peripheral vestibular and auditory systems. Radiographic evaluation and laboratory vestibular/balance testing can confirm a lesion site, but are less likely to drive treatment decisions [20].

Treatment

Balance rehabilitation therapy (BRT), also known as vestibular rehabilitation, is the most frequently used form of treatment for dizziness and vestibular disorders [17,20]. Vestibular rehabilitation employs balance exercises that enhance central nervous system compensation for vestibular dysfunction. Although a few studies have looked at BRT in TBI, some with encouraging results, it is still unclear if this intervention is effective [17].

The most common use of medications is the short-term use of vestibular suppressants. Vestibular suppressants include anticholinergics (scopolamine), antihistamines (meclizine and promethazine), benzodiazapines, and phenothiazine. Vestibular suppressants have an effect that can significantly slow the body’s natural compensation process, and can exacerbate cognitive complaints; they should only be used on a short-term “as needed” basis. Chronic medication use has little benefit, unless directed at treatment of secondary causes of dizziness/poor balance such as migraine headaches or psychologic disorders. Surgery is generally reserved for cases involving temporal bone fracture or perilymphatic fistula.

WHIPLASH-ASSOCIATED DISORDERS

Definition

The Quebec Task Force on WAD defines whiplash as “… an acceleration–deceleration mechanism of energy transfer to the neck. It may result from rear-end or side-impact motor vehicle collisions, but can also occur during diving or other mishaps. The impact may result in a variety of clinical manifestations” [22].

Classification

The Quebec Task Force developed the following classification taxonomy [23]:

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