Postconcussion symptoms fall into three categories: (1) physical (e.g., headaches, vertigo, fatigue); (2) cognitive (e.g., forgetfulness, difficulty learning and remembering, difficulty concentrating, slowed thinking); and (3) emotional/behavioral (e.g., insomnia, irritability, depression, anxiety). They are caused by an interaction among biologic, psychological, and social factors. The most consistent predictor of persistent postconcussion symptoms is preinjury psychiatric history. Cognitive deficits found on neuropsychological testing usually resolve within three months of mild traumatic brain injury except for those with intracranial lesions on initial computed tomography (CT) scan. However, there is evidence to suggest that there can be subtle long-term cognitive sequelae related to brain injury in some patients. Cognitive impairment can also be caused by headache, insomnia, depression, and anxiety.
Education and reassurance are the most important early interventions. There is no convincing evidence that complete rest contributes to recovery. However, some reduction in activity is warranted, especially in athletes. Athletes should not go back to competitive sports until they are free of symptoms and have gone through a program of graded exertion without symptoms. The rehabilitation of postconcussion symptoms is best approached by first addressing those that are most amenable to treatment and/or most likely to contribute to other symptoms.
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. 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 to 15; and
post-traumatic amnesia not longer than 24 hours.
“Complicated” mTBI is characterized by the addition of intracranial abnormalities on computed tomography (CT) scan on the day of injury.
In 2010, the Centers for Disease Control and Prevention reported the incidence of mTBI among civilians in the United States to be about 1.875 million annually. However, the true numbers are probably considerably higher given that a large percentage of people do not seek treatment. In the military, studies of recently deployed soldiers or veterans of the Iraq and Afghanistan wars have reported a prevalence of mTBI in the range of 6.8% to 20%.
Over time, most people with mTBI make a complete clinical recovery. The incidence of persistent multiple postconcussion symptoms or persistent postconcussion syndrome varies extensively in the literature due to variations in the population studied. Although some authors have estimated that less than 5% still have symptoms 1 year after injury, others have reported a much higher frequency of multiple symptoms. These high numbers may not take into account the numerous concussions without long-term sequelae that are never seen by clinicians or the frequency of such symptoms in a control group. Dikmen et al. found that 70% of study participants with mTBI and normal head CT scans had at least three symptoms one year after injury, but this was also true of 53% of the control group with orthopedic injuries but no mTBI. The prevalence of the symptoms associated with concussion is relatively high in healthy populations, people with whiplash and other painful conditions, depression, post-traumatic stress disorder (PTSD), acute stress, and people litigating non-head injuries.
The most common postconcussion symptoms are headache, dizziness (often vertiginous), poor balance, nausea, vomiting, forgetfulness, difficulty learning or remembering, difficulty concentrating, slowed thinking, hypersomnolence, fatigue, insomnia, irritability, sensitivity to noise and light, blurred vision, diplopia, depressed feelings, and anxiety. A 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. Criteria for “postconcussional syndrome” (sometimes referred to as “postconcussion syndrome” or similar terms) have been established by the International Statistical Classification of Diseases and Related Health Problems, Tenth Revision. The criteria require symptoms from at least three of six categories. Unlike the Rivermead, it includes a category with mental health symptoms (e.g., depression, anxiety) and another category that includes only preoccupation with symptoms. However, after concussion, symptoms may be present in a wide variety of both limited and extensive constellations and as such do not always constitute a true syndrome. 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.
The etiology of postconcussion symptoms is often multifactorial. 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 can lead to considerable anxiety and depression and a “shaken sense of self.” In those who have persistent problems, a complex of symptoms often feed one on the other, exacerbating the cognitive impairment, which may then take on a life of its own even as the underlying brain injury continues to recover. 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. Early on, the aspect of the symptoms attributable to brain injury gradually improves, but 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 cycle ensues ( Fig. 148.1 ). Difficulty in concentrating can also result in headaches, which exacerbates the complex.
PTSD should be suspected in individuals who have re-experiences 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.
The most consistent predictor of PPCS is preinjury psychiatric symptoms history. Some studies have found that when there is a control group with orthopedic injuries, mTBI does not even predict acute PCS or PPCS. Other factors variably associated with persistence of symptoms include age; preinjury physical health; anxiety or acute post-traumatic stress shortly after the injury; a high number of early symptoms; acute headache, nausea, dizziness, or balance problems; early impaired memory; intoxication at the time of injury; Glasgow Coma Scale score less than 15; post-traumatic amnesia; intracranial lesions on the day of injury CT scan; serum S100B levels; recent adverse events; preexisting social and vocational difficulties; lack of social support; less education; lower socioeconomic status; 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 brain (including prior mTBI) and other neurologic problems. 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.
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. 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. Most studies have been done with relatively young people, often athletes. Some studies have found subtle differences from controls or differences on more demanding tests, such as dual-task performance, months or years after injury. 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. Athletes who have had multiple concussions have been found to do worse on neuropsychological testing than controls. There is a greater prevalence of mild cognitive impairment in later life among professional football players who have had concussions than among those who have not had a concussion. Although these findings could be related to preinjury characteristics of those who have concussions, they suggest the possibility that a single concussion may result in some chronic loss of brain function, possibly subclinical, in many people. In addition, individuals who have had one or more concussions months or years ago have in some studies been found to have evidence for loss of white matter integrity on diffusion tensor imaging compared to controls, and differences from control subjects on functional magnetic resonance imaging (fMRI) and event-related potentials. However, until those who have persistent impairment are studied with these modalities both before and after injury, cause and effect will remain unclear.
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, as an impaired patient’s retrospective assessment of their status may be unreliable. On the other hand, mental status testing noted in records may not have picked up more subtle deficits if only orientation is evaluated, and becomes less reflective of the immediate postinjury state as time passes since the injury.
Tension, migraine, whiplash-associated (cervicogenic), 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. Post-traumatic headache that starts within seven days of the injury or upon regaining consciousness is considered secondary type according to the International Classification of Headache Disorders.
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 with heavy snoring suggests obstructive sleep apnea. Difficulty in falling asleep and maintaining sleep can be determined by history.
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 [BPPV]), brainstem injury, migraine-associated vertigo, labyrinthine concussion, perilymph fistula, or may be cervicogenic. Those with BPPV often report vertigo when rolling in bed. Perilymph fistula and labyrinthine concussion are usually associated with hearing loss and tinnitus as well. Nonvertiginous dizziness is less common following concussion. Medication-induced dizziness (e.g., by tricyclic antidepressants, gabapentin) and other causes should be considered, including psychogenic dizziness (see also Chapter 8 ).
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, particularly within a few weeks of injury. Memory problems are most often related to attention deficits or difficulty with retrieval. The contribution of attention, encoding/consolidation, 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. However, findings on mental status testing may be normal; more extensive evaluation by neuropsychological testing, including reaction time and/or continuous performance tasks, may be necessary to reveal the deficits. Findings inconsistent with present functioning or more severe than would be expected for someone with mTBI indicate that there may be poor effort or other contributing factors. See the section on differential diagnosis for potential contributing factors.
Assessment of affect, demeanor, and behavior may reveal evidence of depression, anxiety, irritability, 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 (fifth edition) for major depression. It has been found to be valid and reliable in people with traumatic brain injury. The Primary Care PTSD Screen is another useful instrument. Those who screen in for PTSD should then receive a more thorough assessment.
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 pain elicited by compression of the occipital nerves in those with occipital neuralgia (see Chapter 103 , Chapter 106 ).
Physical examination can help to localize a vestibular disorder. If a saccadic correction is seen after a head thrust of 20 to 30 degrees while fixating on a target (head thrust maneuver), a peripheral mechanism is likely. Saccadic pursuit during extra-ocular muscle testing suggests a central etiology. When BPPV is the cause, the Dix-Hallpike 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. The test is positive if vertigo is experienced and nystagmus seen after a lag of up to 30 seconds. 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.
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, or vascular, vestibular, attentional, or psychological problems. Frequently nothing will be found on routine examination. Oculomotor exercises can retrain the muscles when accommodative dysfunction is present, and may help with diplopia as well.
The sense of smell and taste may be affected by damage to branches of the olfactory nerve as they pass through the cribriform plate or by focal cortical contusion. Smell test kits can be useful for confirming loss of smell.
Other cranial nerve testing, muscle strength, cerebellar testing, deep tendon reflexes, plantar stimulation, and sensation are usually normal.
The extent to which postconcussion symptoms interfere with function varies with the extent of the associated pathologic process but depends also on the psychological reaction to the postconcussion impairments. The most common consequences of postconcussion symptoms are limitations in home and community living skills or social, academic, or vocational disability. Patients may be forgetful and inattentive, may have difficulty following conversations, and may find crowded, noisy environments difficult to tolerate. Headaches are often exacerbated by attentional demands and other stresses and may themselves contribute to inattentiveness. Vertigo or other illusory motion causes difficulty in tolerating motion, including, for some, moving vehicles, and may be associated with balance problems. Depression, anxiety, and irritability can contribute heavily to functional limitations.
The brain CT scan is the standard for the acute assessment of intracranial lesions after mTBI. Headache, vomiting, loss of consciousness or amnesia, alcohol intoxication, age older than 60 years, post-traumatic seizure, physical evidence of trauma above the clavicles, and current anticoagulant use are definitive indications for obtaining emergent CT but it is also recommended for patients with continued or worsening headaches, mental status changes, and focal neurological changes who have not had previous imaging. Standard MRI has improved detection of intracranial lesions such as microhemorrhages associated with diffuse axonal injury over CT, but abnormal findings do not correlate with worse neuropsychological outcomes at one month and one year. , Diffusion tensor imaging, which evaluates the integrity of nerve fiber tracts, white matter, and myelin, can show both acute and chronic changes after mTBI. However, abnormalities can also be seen in people with depression, mild cognitive impairment, and white matter hyperintensities, as well as in older adults, and these factors can influence the results of studies if not taken into account. When Ilvesmaki et al. controlled for gender and age, there was no association between DTI findings and acute mTBI. Biomarkers such as S100B, serum glial fibrillary acidic protein (GAFP), and ubiquitin C-terminal hydrolase-L1 (UCH-L1) are emerging as potential tools to diagnose brain injury or predict intracranial lesions on CT scan shortly after injury. However, when sensitivity is set at 100%, only UCH-L1 has a specificity high enough to be of value in decision-making about whether or not a CT scan is needed. Concomitant cervical spine injury such as fracture or dislocation must be ruled out with cervical spine radiographs when the patient has associated neck pain.
If cognitive deficits persist more than 3 to 6 months, then neuropsychological testing is warranted for further evaluation and treatment. The goal is to gain a more enhanced understanding of cognitive strengths and weaknesses as well as the role of emotional, behavioral, and somatic sequelae. A sleep study (polysomnography) is indicated to rule out sleep apnea and other disorders when excessive daytime sleepiness does not improve despite the absence of sedating medications and insomnia. Referral to vestibular therapy and further testing such as electronystagmography is indicated when complaints of dizziness, balance, and disequilibrium remain prominent months after the injury. Referral to audiology should be made when there is concern for hearing loss, continued tinnitus, and associated complaints. Ophthalmology or optometry evaluation should be considered when visual symptoms persist. Neuroendocrine testing is warranted in individuals with mTBI who have persistent fatigue, cognitive difficulties, behavioral changes, or depression, as these can be symptoms of post-traumatic hypopituitarism. Other manifestations include decreased libido, amenorrhea, myopathy, and life-threatening complications such as sodium dysregulation and adrenal crisis. Recommended screening includes serum free thyroxine, thyroid-stimulating hormone, morning cortisol, prolactin, and insulin-like growth factor 1 levels; testosterone concentration in men; and follicle-stimulating hormone concentration in postmenopausal women or premenopausal women with amenorrhea.