Definition

Postconcussion symptoms are a set of symptoms commonly seen after concussion. The term concussion is generally used as a synonym for mild traumatic brain injury (mTBI). A number of definitions with varying lower and upper limits of severity for diagnosis have been proposed [1]. One commonly used definition of mTBI is a traumatically induced physiologic disruption of brain function, manifested by at least one of the following:

• any period of loss of consciousness;

• any loss of memory for events immediately before or after the accident;

• any alteration in mental state at the time of the accident (e.g., feeling dazed, disoriented, or confused); and

• focal neurologic deficits, which may or may not be transient;

but in which the severity of injury does not exceed the following:

• loss of consciousness of approximately 30 minutes or less;

• after 30 minutes, an initial Glasgow Coma Scale score of 13-15; and

• post-traumatic amnesia not longer than 24 hours [1].

“Complicated” mTBI is characterized by the addition of intracranial abnormalities on computed tomography (CT) scan on the day of injury [2].

There are also several classification systems [3]. Table 147.1 presents a classification established by the American Academy of Neurology [4].

Bazarian and colleagues [5] reported the incidence of emergency department visits for mTBI to be 503 per 100,000, which is about 1.4 million emergency department visits for mTBI in the United States per year. This is similar to the Centers for Disease Control and Prevention estimate of 1.375 million [6]. However, the true numbers are probably considerably higher, given that a large percentage of people do not seek hospital treatment.

Symptoms

The most common postconcussion symptoms are headache, dizziness (often vertiginous) or poor balance, forgetfulness, difficulty in learning or remembering, difficulty in concentrating, slowed thinking, hypersomnolence, fatigue, insomnia, depression, anxiety, irritability, sensitivity to noise and light, and visual problems [7,8]. The most commonly used instrument for assessing the number and severity of postconcussion symptoms is the Rivermead Post-Concussion Symptoms Questionnaire, which has been found to have adequate divergent validity and reliability [9–11]. Criteria for “postconcussion syndrome” have been established by the International Classification of Diseases, Ninth Revision [12], the International Statistical Classification of Diseases and Related Health Problems, Tenth Revision [13], and the fourth edition of the Diagnostic and Statistical Manual of Mental Disorders [14]. However, symptoms may be present in a wide variety of both limited and extensive constellations and as such do not constitute a true syndrome [7,8]. There may be a lag of days or weeks between the concussion and the patient’s first complaints, and some related phenomena, such as depression, may not become manifest until months after the initial injury. Although these symptoms can be seen with any severity of injury, they are often most pronounced in the context of mTBI. Over time, most people make a complete clinical recovery [11]. Although some authors have estimated that less than 5% still have symptoms 1 year after injury [15], studies vary considerably in this regard [16–18]. The prevalence of postconcussion symptoms is relatively high in healthy populations [15]; in people with whiplash and other painful conditions, depression, post-traumatic stress disorder (PTSD), and acute stress; and in people litigating non-head injuries [19]. Nevertheless, one study found a difference of 31% between those who had mTBI and a non–head-injured control group with orthopedic injuries with respect to the number who had three or more symptoms 1 year after injury. However, these differences were significant only among those who were married and those who had higher levels of education [17].

The etiology of postconcussion symptoms is often multifactorial, and much of it is still not well understood. The usual inciting factors are mTBI with residual impairment of cognition, whiplash or other soft tissue injury to the head and neck, and at times disruption of the vestibular apparatus or central vestibular insult. Problems with attention, forgetfulness, and fatigue coupled with the frequent development of headaches, insomnia, and vertigo often lead to considerable anxiety and depression and a “shaken sense of self” [20]. In those who have persistent problems, a complex of symptoms often feed one on the other [7], exacerbating the cognitive impairment, which may then take on a life of its own even as the underlying brain injury continues to recover [20,21]. A common scenario is one in which pain, anxiety (including, at times, PTSD), and depression contribute to insomnia, which in turn exacerbates headaches, and all of these symptoms contribute to cognitive impairment [11]. Early on, as the symptoms attributable to brain injury gradually improve, the patient may not experience any cognitive improvement because other factors are driving these symptoms. The lack of improvement often increases the patient’s anxiety and can bring about depressive feelings. A vicious circle ensues (Fig. 147.1). Difficulty in concentrating can also result in headaches, which exacerbates the complex. PTSD should be suspected in individuals who have reexperiences of the original injury (“flashbacks”), avoidance of situations similar to that which caused the injury (e.g., riding in a car), a feeling of emotional “numbness,” and hyperarousal. There are high prevalence rates of PTSD, mTBI, and their co-occurrence in recently deployed soldiers [5].

There is evidence to suggest that persistence of symptoms is associated with a high number of early symptoms: acute headache, multiple painful areas, nausea, dizziness, or balance problems; early impaired memory; intoxication at the time of injury; intracranial lesions on the day of injury CT scan; loss of white matter integrity on diffusion tensor imaging; preexisting social, psychological, and vocational difficulties; lack of social support; less education; lower socioeconomic status; age older than 40 years; being married; female gender; current student status; litigation or compensation; being out of work secondary to injury; motor vehicle crash as cause of injury; lack of fault for a collision; preexisting physical impairment; APOε4 genotype; and preexisting brain (including prior mTBI) and other neurologic problems. Studies vary with respect to some of these findings [8,11,15,22–26]. However, the total body of evidence regarding the causes of poor outcome after mTBI suggests a complex interaction among biologic, psychological, and social factors, with different factors varying in significance by the individual [27]. It is notable that people with mTBI have been found to underestimate the frequency of symptoms that they had before the injury, demonstrating a bias toward attributing current symptoms to the mTBI (“good old days bias”) [17].

Most authors have not defined a particular time frame for the designation of “persistent” postconcussion symptoms; those who have done so have used 3 months as a cutoff [16,28]. The question of persistence of cognitive impairment after mTBI has been a subject of considerable controversy. Most controlled studies and meta-analyses indicate that cognitive deficits found on neuropsychological testing resolve within 3 months of mTBI, with the notable exception of complicated mTBI [2,29]. Most studies have been done with relatively young people, often athletes. Some studies have found subtle differences from controls [30,31] or differences on more demanding tests, such as dual-task performance, months or years after injury [32]. Subtle differences in balance have also been found among college football players who have had one or more concussions compared with those who have not [32]. Athletes who have had multiple concussions have been found to do worse on neuropsychological testing than controls [22,33]. There is a greater prevalence of mild cognitive impairment in later life [34] among professional football players who have had concussions than among those who have not had a concussion. These findings suggest that a single concussion may result in some loss of brain function, possibly subclinical in most people. In addition, individuals who have had one or more concussions months or years ago have been found to have evidence for loss of white matter integrity on diffusion tensor imaging [26] and differences from control subjects on functional magnetic resonance imaging (fMRI) [35] and event-related potentials [32].

Cognition

The patient should be questioned about the inciting event with regard to whether there was a loss of consciousness, loss of anterograde or retrograde memory, other alteration in mental status, or focal neurologic findings. A patient’s subjective feeling of being dazed or confused may or may not reflect actual brain injury. It is common for people to feel dazed because of the emotional shock experienced after an accident. There is often limited or no documentation of the details of the patient’s mental status immediately after the accident, and a clinician must do his or her best to reconstruct the situation largely on the basis of the history given by the patient. The observations of others may help clarify whether the patient was responding slowly or otherwise appeared confused. Emergency medical records should be obtained whenever possible but may or may not reflect the patient’s mental status at the scene of the accident and may not pick up more subtle deficits if only orientation is evaluated.

Headaches

Tension, migraine, cervicogenic (musculoskeletal), and mixed headaches are the most frequent types seen after concussion. Pain from soft tissue injury at the site of impact, occipital neuralgic pain, and dysautonomic cephalgia can be seen as well. The patient should be questioned with respect to severity, quality, location and radiation, date of onset, duration, frequency, exacerbating or ameliorating factors, and frequency of medication use in addition to associated symptoms, such as nausea, vomiting, visual phenomenon, diaphoresis, rhinorrhea, and sensitivity to light and noise [36,37].

Vestibular/Balance Disorder

Vertigo and other illusory motion related to head movement or position as well as impaired balance can be caused by cupulolithiasis or canalithiasis (benign paroxysmal positional vertigo), brainstem injury, migraine-associated vertigo, labyrinthine concussion, or perilymph fistula or may be cervicogenic. Perilymph fistula and labyrinthine concussion are usually associated with hearing loss and tinnitus as well. Nonvertiginous dizziness is not usually directly related to concussion; medication-induced dizziness (e.g., by nonsteroidal anti-inflammatory drugs and antidepressants) and other causes should be considered, including psychogenic dizziness [38]. See also Chapter 8.

Sleep

A history of fatigue or daytime sleepiness should suggest the possibility of a sleep disorder. Delayed sleep phase syndrome and disrupted sleep-wake cycles can usually be diagnosed by history. Being overweight or obese or heavy snoring suggests obstructive sleep apnea. Difficulty in falling asleep and maintaining sleep can be determined by history [11].

Other

The physician’s history of the events surrounding the initial accident should also include exploration of other associated injuries, seizure, vomiting, and drug or alcohol intoxication. A preinjury medical, social, psychological, vocational, and educational history should be obtained, including any history of attention deficit disorder or learning disability.

The examination of the individual with postconcussion symptoms will often elicit problems with attention, memory, and executive function on mental status evaluation. Memory problems are most often related to attention deficits or difficulty with retrieval [39]. The contribution of attention, encoding, and retrieval problems to verbal memory can be evaluated with the presentation of a word list followed by immediate recall, recall after 5 minutes, and then a multiple choice recognition task, which provides the structure needed to assist retrieval when information has been encoded. The Montreal Cognitive Assessment, which contains subtests that challenge executive function as well as memory and attention, is a useful tool to assess for cognitive impairment, although it has not been studied in traumatic brain injury [40]. However, findings on mental status testing may be normal; more extensive evaluation by neuropsychological testing, including reaction time [31] and continuous performance tasks, may be necessary to reveal the deficits. Findings inconsistent with daily functioning or more severe than would be expected for someone with mTBI indicate that there may be poor effort or other contributing factors [19,41]. See the section on differential diagnosis for potential contributing factors [20].

Psychological

Assessment of affect, demeanor, and behavior may reveal evidence of depression, anxiety, and other psychological characteristics. The Patient Health Questionnaire-9 is one approach to assessing depression. It is a brief questionnaire that mirrors the diagnostic criteria of the Diagnostic and Statistical Manual of Mental Disorders (fourth edition) for major depression. It has been found to be valid and reliable in people with traumatic brain injury [42]. The Primary Care PTSD Screen is another useful instrument. Those who screen in for PTSD should then receive a more thorough assessment [43].

Headaches

Examination of the head and neck often elicits restriction of motion, tender points, or trigger points radiating to the head. There may be tenderness at the site of the original head injury and occasionally pain elicited by compression of the occipital nerves [36,37]. See Chapters 102 and 105.

Vestibular/Balance Disorder

During acute vertigo, nystagmus will often be present, generally stronger with peripheral than with central vertigo. As adaptation begins to occur, nystagmus may be seen only with certain maneuvers (e.g., after 20 horizontal head shakes) or may not be seen at all. When benign paroxysmal positional vertigo is the cause, the Hallpike-Dix maneuver is usually positive. This maneuver is performed from the sitting position on a flat surface with the head rotated 45 degrees to either side. The patient is quickly lowered from the sitting to the lying position, until the head, still rotated, is extended over the edge of the examining table. Vertigo is experienced and nystagmus seen after a lag of up to 30 seconds [38]. Neck range of motion and tender points or trigger points should be assessed for contributions from cervicogenic dizziness (see also Chapter 8). Patients with vertigo and other illusory movement may also have balance problems, but impaired balance with difficulty on tandem walk, standing on one leg, hopping, and other maneuvers may be seen without vertigo. The Balance Error Scoring System can provide a quantifiable assessment of balance [11].

Visual

Some patients complain of a feeling of visual disorientation or intermittent blurred vision. The symptoms can be related to a need for changes in refraction, accommodative dysfunction [44], or vascular, vestibular, attentional, or psychological problems. Frequently nothing will be found on routine examination.

Olfactory

The sense of smell may be affected by damage to branches of the olfactory nerve as they pass through the cribriform plate or by focal cortical contusion.

Other cranial nerve testing, muscle strength, cerebellar testing, deep tendon reflexes, plantar stimulation, and sensation are usually normal.

Functional Limitations