PCS

postconcussion syndrome
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Postconcussion syndrome
Author:Randolph W Evans, MD, FAANSection Editor:Michael J Aminoff, MD, DScDeputy Editor:Janet L Wilterdink, MD
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All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Apr 2018. | This topic last updated: Oct 10, 2013.
INTRODUCTION — The postconcussion syndrome (PCS) is a common sequelae of traumatic brain injury (TBI), and it is a symptom complex that includes headache, dizziness, neuropsychiatric symptoms, and cognitive impairment [1]. PCS is most often described in the setting of mild TBI, but it may also occur after moderate and severe TBI, and similar symptoms are described after whiplash injuries as well [2]. Loss of consciousness does not have to occur for PCS to develop.

PCS is controversial, especially in its protracted form [3]. The symptoms are vague, subjective, and common in the general population. The affected patient population is heterogeneous with varying degrees of injury to the head and brain. Individual patient characteristics may alter the expression of the injury. The underlying pathophysiology is undefined. Test results may or may not be abnormal; when present, test abnormalities do not follow a consistently defined pattern.

Mild TBI results after blunt force, nonpenetrating head trauma, and it is most often defined as mild by a Glasgow Coma Scale (GCS) score of 13 to 15, 30 minutes after head injury (table 1). Concussion is a subset of mild TBI, and it is a trauma-induced alteration in mental status that may or may not involve loss of consciousness [4]. This topic will discuss the pathophysiology, clinical features, diagnosis, and management of PCS. The acute presentation and management and other sequelae of concussion and mild TBI are discussed separately. (See "Acute mild traumatic brain injury (concussion) in adults" and "Minor head trauma in infants and children: Evaluation".)

EPIDEMIOLOGY — Thirty to 80 percent of patients with mild to moderate brain injury will experience some symptoms of postconcussion syndrome (PCS). This wide range of reported incidence reflects variabilities in the patient population studied and the criteria by which a diagnosis of PCS is made, either using individual symptoms or defined clinical criteria. Two clinical criteria, the International Classification of Diseases, ICD-10 and the DSM-IV, are commonly used and give widely different results, even within the same patient population [5].

A number of studies have tried to associate the severity of brain injury with PCS among patients with mild traumatic brain injury (TBI) using a variety of measures including the Glasgow Coma Scale (GCS) (table 1), the duration of loss of consciousness or post-traumatic amnesia, and the presence or extent of visualized abnormalities on CT or MRI [2,5-8]. Overall, the severity of injury does not clearly correlate with the risk of PCS. However, at least one study suggests that a history of prior concussion, particularly if recent or multiple, is a risk factor for prolonged symptoms after concussion [9].

Cohort studies of patients with mild and moderate TBI have consistently found that female gender and increasing age are risk factors for PCS [5,6,10,11]. While the nature of the head injury has not been systematically studied as a risk factor, some studies suggest that patients with a sports-related concussion have a better natural history than those with mild TBI resulting from motor vehicle accident, fall, or assault [12]. This may reflect a different severity of the physical and/or psychosocial impact of the injury, and/or a different premorbid predisposition to PCS. This may also contribute to the gender differences, as the relative preponderance of accident and assault versus sports injury as a cause of TBI may be higher in women than men.

PATHOPHYSIOLOGY — There are different theories for the pathogenesis of postconcussion syndrome (PCS). Some hold that the disorder is a structural and biochemical one resulting directly from the brain injury; others postulate a psychogenic origin. It is possible, even likely, that both of these contribute; in particular, these may have a different impact on different symptoms and at different times in the course of the syndrome [13]. (See 'Persistent postconcussion syndrome' below.)

Neurobiologic factors — A number of structural and biochemical changes have been documented in animal models of head injury and in human neuropathological studies. One study compared regional brain volumes on MRI in 19 patients one year after mild TBI to 22 matched control subjects [14]. Patients had measurable global atrophy compared to controls. Certain areas of regional volume loss (eg, cingulate gyrus) correlated with lower neurocognitive measures, clinical scores of anxiety and postconcussive symptoms. The acute and subacute findings associated with mild TBI are described elsewhere. (See "Acute mild traumatic brain injury (concussion) in adults", section on 'Pathophysiology'.)

Physiologic and functional neuroimaging (SPECT, PET and functional MRI) also document more extensive areas of abnormality than is seen on CT, supporting a role for structural or physiologic brain injury in the production of PCS [7,15-23]. However, many of these neuroimaging findings are not specific to head injury and are also noted in patients with migraine and depression. Also, studies do not consistently show a relationship between the extent of abnormalities seen on these studies and the degree of impairment or severity of symptoms experienced by the patient [18,20,24,25]. One exception is a study that correlated acute findings on CT perfusion scans at the time of TBI with disability (although not employment status) at six months [26]. It remains unclear what role these factors have in producing the clinical symptomatology of PCS.

Psychogenic factors — A psychogenic contribution to PCS is suggested by a number of empiric and clinical observations. The symptom complex of PCS (headache, dizziness, and sleep impairment) is similar to the somatization seen in psychiatric disorders including depression, anxiety, and posttraumatic stress disorder. In addition, anxiety and depression can produce subjective and objective cognitive deficits that are similar to those seen in PCS and that improve with antidepressant treatment [27,28].

A number of studies suggest that both psychiatric predispositions (poor coping skills, limited social support and negative perceptions) and psychiatric comorbidity (depression, anxiety and panic, acute and post-traumatic stress disorder) are more prevalent in patients with PCS compared with general population controls and/or with head-injured patients who do not develop persistent PCS [5,8,29-37].

However, studies of the interaction of depression, anxiety, and cognitive performance in mild traumatic brain injury (TBI) are limited. Some investigators did not find a substantial correlation between the level of depressive symptoms and cognitive deficits in patients with mild TBI [38], while others have found a correlation in the response to antidepressant treatment in a subset of patients [29]. (See 'Treatment' below.)

The association of psychiatric disease and PCS is not established. Limitations in methodology, including cross-sectional design and patient and control group selection bias, preclude firm conclusions. Also, such an association could have several explanations. Patients with premorbid psychiatric disease may be more likely to suffer head injury as a result of more prevalent alcoholism, motor or physical impairments resulting from their disease or medications, and other reasons. Alternatively, patients with psychiatric disease may be more prone to develop PCS after head injury. Finally, head injury may cause or precipitate psychiatric disease in susceptible individuals.

Other factors — The very low, even absent, rates of postconcussion symptomatology, in some countries and in children, that are sometimes reported suggests a prominent role for sociocultural factors in the pathogenesis of PCS, perhaps because of misattribution or litigation [39,40].

●Misattribution — Because patients expect PCS symptomatology after TBI, they and their physicians may mistakenly attribute their complaints to the head injury, when they are actually unrelated. In support of this theory, a number of studies have compared patients with mild TBI to non-head-injured controls finding a high prevalence of the same symptoms in both groups, indicating a high base rate of symptoms in the general population [41-43]. At the same time, surveys of individuals with no history of head injury find that most people identify symptoms of PCS as expected after head injury [44].

●Litigation — The idea that pending compensation claims contribute to the presence and duration of PCS symptomatology dates back to original reports in the late nineteenth century. Studies do show a relationship between persistent PCS and potential financial compensation [45,46]. The association does not clearly imply causation, however. Some patients with pending litigation improve with or without treatment, and PCS occurs in the absence of litigation. On the other hand, failure of patients to recover after claims are settled does not necessarily invalidate this theory, as a financial settlement may in fact reinforce illness behavior. (See 'Persistent postconcussion syndrome' below.)

●Chronic pain — Patients with chronic pain have symptoms of PCS at a rate similar to a comparison group of patients after head injury [47,48]. Similar patterns of cognitive deficits may be seen in patients with chronic pain and PCS [28]. It is not clear whether this reflects a shared prevalence of psychiatric disorders among sufferers of PCS and chronic pain syndromes, suggests that PCS is a manifestation of a chronic pain syndrome, or reflects the ubiquitous nature of these symptoms.

CLINICAL FEATURES — The most common complaints in postconcussion syndrome (PCS) are headaches, dizziness, fatigue, irritability, anxiety, insomnia, loss of concentration and memory, and noise sensitivity. The relative preponderance of these symptoms varies from study to study depending on the clinical setting, the time since injury, and other variables. As an example, among 118 patients who volunteered for a mild traumatic brain injury (TBI) treatment study, at one month following the injury headaches were reported in 78 percent, dizziness in 59 percent, fatigue in 91 percent, irritability in 62 percent, anxiety in 63 percent, sleep disturbance in 70 percent, forgetfulness in 73 percent, and noise sensitivity in 46 percent [49]. Among patients referred to a headache clinic, about half had cognitive complaints, and a quarter had psychological complaints; 17 percent had an isolated complaint of headache [50].

Headaches — Headaches are variably estimated as occurring in 25 to 78 percent of persons following mild TBI [49-51]. Paradoxically, headache prevalence, duration, and severity is greater in those with mild head injury compared with those with more severe trauma [52,53]. A significant number of patients have pre-existing headaches, but studies conflict as to whether this is a risk factor for post-traumatic headaches [54,55].

According to the International Headache Society (IHS) criteria, the onset of the headache should be within seven days after the injury [56]. The seven-day onset is arbitrary, particularly since the etiology of post-traumatic migraine is not understood. Three months seems a more reasonable latency for onset than does seven days [2].

Most post-traumatic headaches can be classified by IHS type similarly to nontraumatic headaches. Migraine and tension headaches predominate [2,50,52,57,58]. In most series, tension-type headaches are most frequent (75 to 77 percent) [2,50]; however, among US soldiers with post-traumatic headaches mainly associated with blast trauma, most were of the migraine-type [57] Many patients (27 to 75 percent) have more than one type of headache [50,52].

Tension type — Tension type headaches may occur daily, either as a constant or intermittent pain with variable duration. Their distribution may be generalized, nuchal-occipital, bifrontal, bitemporal, headband or cap-like, and they are characteristically described as a pressure, tightness, or dull aching. Analgesic overuse complicated 42 percent of post-traumatic headaches in one series [50]. (See "Tension-type headache in adults: Pathophysiology, clinical features, and diagnosis".)

Migraine — Migraine headache is typically lateralized, pounding or throbbing in nature, with associated photophobia and nausea. It occurs with and without visual aura. (See "Pathophysiology, clinical manifestations, and diagnosis of migraine in adults".)

Recurring attacks of migraine with and without aura can result from mild head injury [59]. Impact can also cause acute migraine episodes, often in adolescents with a family history of migraine. Originally termed "footballer's migraine" to describe young men playing soccer who had multiple migraine with aura attacks triggered only by impact, similar attacks can be triggered by mild head injury in any sport [60].

Other post-traumatic headache syndromes — Many other headache syndromes may occur in association with mild TBI. These more specific injuries are not necessarily considered typical features of PCS and can occur in isolation.

●Temporomandibular joint injury can be caused either by direct trauma or jarring associated with the head injury. Patients may complain of jaw pain and ipsilateral hemicranial or frontotemporal aching or pressure headaches. (See "Temporomandibular disorders in adults".)

●Occipital neuralgia may result from direct nerve injury or entrapment from contiguous musculoskeletal injury. The aching, pressure, stabbing, or throbbing pain may be in a nuchal-occipital and/or parietal, temporal, frontal, or periorbital or retroorbital distribution. Digital pressure over the greater occipital nerve at the mid superior nuchal line (halfway between the posterior mastoid and the occipital protuberance) may reproduce the headache. (See "Overview of craniofacial pain", section on 'Occipital neuralgia'.)

●Trigeminal nerve injury produces shooting, tingling, aching, or burning pain that may be paroxysmal or constant. Isolated injuries to the supraorbital or infraorbital branches can accompany minor head injury. (See "Overview of craniofacial pain", section on 'Painful post-traumatic trigeminal neuropathy (anesthesia dolorosa)'.)

●Dysesthesias at the site of scalp lacerations occur frequently. In addition, an aching, soreness, tingling, or shooting pain over the site of the original trauma can develop, whether or not a laceration is present. The symptoms may persist for weeks or months but rarely for more than one year.

●Low CSF pressure may result from trauma causing a CSF leak through a dural root sleeve tear or a cribiform plate fracture. This may produce a headache syndrome with prominent positional exacerbation (headache absent when supine and severe when upright) as is seen in post-lumbar puncture headache. (See "Post-lumbar puncture headache".)

●Cortical contusions can cause a headache, especially if there is associated subarachnoid hemorrhage.

●Traumatic dissection of the carotid and vertebral arteries can cause persistent throbbing headache. (See "Overview of craniofacial pain", section on 'Other causes'.)

●Other headache syndromes attributed to trauma in case reports include cluster headaches [61]; hemicrania continua [62]; short-lasting unilateral neuralgiform headache attacks with conjunctival injection, tearing, sweating, and rhinorrhea (SUNCT) [63]; short-lasting unilateral headache with cranial autonomic symptoms [64], and paroxysmal hemicrania [65]. (See "Cluster headache: Epidemiology, clinical features, and diagnosis" and "Short-lasting unilateral neuralgiform headache attacks: Clinical features and diagnosis" and "Paroxysmal hemicrania: Clinical features and diagnosis".)

Dizziness — About one-half of patients report dizziness after mild head injury. While some patients with PCS have nonspecific dizziness (lightheadedness), others report true vertigo that may be due to benign paroxysmal positional vertigo or to a labyrinthine concussion. A number of studies suggest that complaints of dizziness at the time of injury and afterward identify patients at risk of prolonged recovery [66-69].

(See "Acute mild traumatic brain injury (concussion) in adults" and "Approach to the patient with dizziness" and "Benign paroxysmal positional vertigo".)

Psychological and cognitive symptoms — Over 50 percent of patients report personality change, irritability, anxiety, and depression after mild TBI. They may find themselves intolerant of noise, emotional excitement and crowds, and more susceptible to the effects of alcohol. Family members may report that the patient seems more abrupt, argumentative, stubborn, opinionated, or suspicious.

Patients also report impaired memory and concentration; these may be corroborated by objective deficits on neuropsychological testing. In typical cases, these are most prominent immediately after the injury and resolve over the next weeks and months. Fatigue and disruption of sleep patterns, usually insomnia, are also reported.

A significant number of patients (15 to 20 percent) will develop symptoms meeting criteria for psychiatric disease. These include acute stress and post-traumatic stress disorder as well as anxiety, panic disorder, and depression [5,21,32,70].

DIAGNOSTIC TESTING — The judicious use of testing needs to be individualized for each patient [71]. Referrals to an ophthalmologist or otorhinolaryngologist should be made for patients with persistent complaints of visual symptoms or vertigo. Psychiatric evaluation should be considered for patients with prominent psychiatric symptoms.

Neuropsychological testing — Neuropsychological testing is not helpful in most patients with postconcussion symptoms. Nevertheless, when performed by a knowledgeable and experienced psychologist, neuropsychologic evaluation can be helpful for evaluating selected patients with prominent cognitive or psychologic complaints, providing reassurance as to their mild nature and limited extent.

Follow-up studies of unselected patients after mild traumatic brain injury (TBI) demonstrate small measurable deficits on neuropsychological testing. Cognitive domains that appear particularly vulnerable to the effects of head injury include attention, working memory, processing speed, and reaction time [50]. The deficits are generally mild; gross deficits of intelligence and memory are not associated with mild TBI. Abnormalities are most prominent in the first week after TBI and disappear over time. At three months, patients with mild TBI as a group perform similarly to control subjects [72,73].

The observed cognitive deficits are not specific to mild TBI; similar patterns of abnormalities are seen in patients with psychological illness, pain syndromes, and those taking medications [12,27,74].

Neuropsychological testing may demonstrate findings inconsistent with PCS that can be helpful to the physician in pursuing alternative diagnoses. The referring physician should be aware that neuropsychological testing is not well standardized, and findings are easily subject to misinterpretation and overinterpretation for a variety of reasons, especially in medico-legal cases [71,75].

Neuroimaging — Many patients evaluated for mild TBI will have undergone a CT scan or MRI as part of their acute evaluation. About 10 percent of CT scans in mild TBI are abnormal showing mild subarachnoid hemorrhage, subdural hemorrhage, or contusions [76]. MRI is more sensitive than CT scan showing abnormalities in about 30 percent of patients with normal CT scans [77,78]. (See "Acute mild traumatic brain injury (concussion) in adults", section on 'Imaging'.)

Patient with PCS who have not had an MRI and have disabling complaints should have a brain MRI to exclude more serious pathology that would either identify a worse prognosis or an alternative cause for their symptoms.

Other advanced neuroimaging techniques, including functional MRI, magnetic resonance spectroscopy, and diffusion tensor imaging, are under investigation in the evaluation of patients with TBI [79,80]. In one study, patients with evidence of traumatic axonal injury on diffusion tensor imaging were more likely to demonstrate objective evidence of cognitive impairment compared to patients with normal studies [81].

TREATMENT — Treatment of postconcussion syndrome (PCS) is individualized to the patient's particular complaints. Simple reassurance is often the major treatment, since most patients will improve within three months. A trial of six days of bedrest in 107 patients presenting to the emergency department after a mild head injury reduced complaints of dizziness in the first week after injury but did not alter the severity of post-traumatic complaints at three or six months [6].

In the absence of specific treatments for the prevention or treatment of PCS, most clinicians adopt a symptomatic approach [82].

Headaches — Information about treating headache syndromes specifically in the post-traumatic setting is limited to case series:

●Amitriptyline has been widely used for post-traumatic tension type headaches [83] as well as for the nonspecific symptoms such as irritability, dizziness, depression, fatigue, and insomnia.

●An inpatient program of repetitive intravenous dihydroergotamine and metoclopramide may provide relief of refractory chronic post-traumatic headaches [84].

●Greater occipital neuralgia frequently responds to greater occipital nerve block [85] with a local anesthetic, which can also be combined with an injectable corticosteroid.

●A trial of propranolol or amitriptyline alone or in combination produced a 70 percent response rate in 21 of 30 adequately treated patients with post-traumatic migraine [86].

●Analgesia overuse was a common contributor to post-traumatic headache in 19 to 42 percent of patients [2,50]. These patients responded to analgesic withdrawal as favorably as patients whose headaches were not post-traumatic.

●Patients with post-traumatic paroxysmal hemicrania and hemicrania continua have responded to treatment with indomethacin [62,65].

In the absence of controlled studies specific to PCS, these data suggest that post-traumatic headaches will likely respond to those treatments used for migraine and tension headache that are used in other settings [50]. Clinicians caring for these patients note that delayed recovery from post-traumatic headaches may be due to inadequately aggressive treatment, analgesia overuse, or comorbidity [51]. (See "Acute treatment of migraine in adults" and "Preventive treatment of migraine in adults" and "Tension-type headache in adults: Acute treatment" and "Tension-type headache in adults: Preventive treatment".)

Psychologic and cognitive complaints — Current evidence does not provide information for treatment of these complaints that are specific to the post-traumatic setting.

Donepezil has had positive results in preliminary studies in patients with more severe traumatic brain injury (TBI) but has not been studied extensively in PCS [87,88]. Six patients with chronic symptoms after mild head injury reported subjective cognitive improvement in an open-label study of donepezil [89]. A small, randomized trial of CDP-choline in 14 men with mild to moderate TBI was associated with improvement in PCS symptoms and some, but not all, neuropsychological test results after one month [90].

The use of cognitive retraining for cognitive difficulties after mild head injury is controversial. Because cognitive rehabilitation can be quite costly, prospective studies are needed demonstrating efficacy before widespread application can be recommended. Simple techniques, such as training in the use of a notebook and visual imagery may be helpful for patients who have memory impairments.

When the psychologic symptoms are particularly prominent, supportive psychotherapy and the use of antidepressant and anxiolytic medications may be helpful [37]. Again, there are only limited data supporting a treatment approach specific to the PCS setting. Treatment with oxiracetam was described as being helpful for postconcussion symptoms in a single report [91]. In one study, 15 patients with mild TBI who also met criteria for major depression were treated with sertraline for eight weeks, achieving substantial remission in depressive symptoms as well as improvement in cognitive measures [29]. An open-label study in 20 patients with depression after TBI showed symptomatic improvements with treatment with citalopram and carbamazepine [92]. Two small randomized trials have found that cognitive behavioral therapy improved symptoms of anxiety and/or depression in patients who had had a mild TBI [93,94].

Education — One of the most important roles for the physician is education of the patient and family members, other physicians, and, as appropriate, employers, attorneys, and representatives of insurance companies. Many patients are reassured to discover that their symptoms are not unique or crazy but are instead part of a well-described syndrome. Disbelieving family members may become more supportive with education.

Early education and support may also affect the course of PCS [37]. This was illustrated in a follow-up study of 73 patients with mild TBI [95]. Those who reported a belief at the time of injury that long-lasting negative effects were a probable outcome were more likely to have enduring symptoms at three months than those who did not endorse this belief [95].

A number of controlled studies have examined the role of education and reassurance in ameliorating PCS [96-102]. Interventions have included a single follow-up session with reassurance and education; provision of an information booklet; scheduled follow-up phone calls scripted to address education, reassurance, and reactivation; structured behavioral cognitive interventions; and follow-up sessions with multidisciplinary evaluations. Most, but not all, studies suggest that early intervention with information and reassurance may provide a benefit to patients with mild TBI in reducing the severity of PCS [94,103,104].The more intensive multidisciplinary evaluations do not clearly add substantively to the simpler interventions of education and reassurance.

PROGNOSIS — The symptoms and disability attributed to postconcussion syndrome (PCS) are greatest within the first 7 to 10 days for the majority of patients. At one month, symptoms are improved and in many cases resolved [105]. The vast majority of patients have largely recovered by three months [106]. A minority (10 to 15 percent) have symptoms that persist one year or longer. Because of biased reporting, it is possible that this number is inflated, and the overall prevalence is much lower [12].

Persistent postconcussion syndrome — Patients with disabling symptoms that persist after several months or a year may be more disabled than they were immediately after the injury. While the entire symptom complex persists in most cases, emotional symptoms seem particularly prominent. Studies in general have been unable to define risk factors for this subset; premorbid psychosocial factors or psychiatric disease have not consistently been shown to define those patients at risk of a protracted course.

A comprehensive review of studies examining the prognosis for recovery after mild traumatic brain injury (TBI) made the following points [107]:

●Litigation or compensation issues are a strong consistent risk factor for persistent symptoms and disability after mild TBI.

●Repeated concussions may lead to more severe and more protracted cognitive deficits, but the cross-sectional design of the studies preclude a causal inference.

●Female gender is an inconsistent risk factor for persistent symptoms.

●Patients with a Glasgow Coma Scale (GCS) score of 13 have higher rates of disability than those with a GCS of 15, but this may be attributable to other injuries. Patients with complicated TBI (intracranial hematoma or depressed skull fracture) may also be at risk for more persistent symptoms.

●Limited reports suggest that premorbid physical limitations, prior head injury or other neurologic disease, psychiatric disease, life stressors, student status, TBI after motor vehicle accident, and older age may be risk factors for persistent symptoms.

●Some patients with persistent disability may be malingering. However, studies of this phenomenon are limited by poorly validated measures of malingering, the cross-sectional nature of the studies, and a significant delay between the head injury and evaluation.

Potential indicators of malingering include premorbid antisocial and borderline personality traits, poor work record, and prior claims for injury; uncooperative, evasive, or suspicious behavior; inconsistencies in neuropsychological test performance; or engaging in activities inconsistent with reported deficits, having significant financial stressors, and lack of reasonable follow-through on treatments [46,108]. Caution in diagnosing malingering is advised; comprehensive multidisciplinary evaluations to detect malingering are incompletely validated, and symptom exaggeration is known to occur in biologic disease [109]. (See "Factitious disorder imposed on self (Munchausen syndrome)".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, “The Basics” and “Beyond the Basics.” The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on “patient info” and the keyword(s) of interest.)

●Basics topic (see "Patient education: Concussion in adults (The Basics)" and "Patient education: Closed head injury (The Basics)" and "Patient education: Postconcussion syndrome (The Basics)")

SUMMARY AND RECOMMENDATIONS — Postconcussion syndrome (PCS) refers to a common constellation of symptoms reported by patients after mild traumatic brain injury (TBI).

●The most common complaints include headache, dizziness, cognitive impairment, and psychological symptoms. (See 'Clinical features' above.)

●Women and older patients appear to be more susceptible to the development of postconcussion symptoms. The severity of the brain injury does not clearly correlate with the risk of developing PCS or the prognosis for recovery. (See 'Epidemiology' above.)

●Theories of the pathogenesis of the syndrome include both structural and biochemical brain injury as well as psychogenic mechanisms. These may play different etiologic roles at different times in the course of the disorder. (See 'Pathophysiology' above.)

●In patients who did not have MRI as part of their acute injury evaluation, a brain MRI should be performed if there are persistent and disabling complaints to exclude other causes; reassurance should also be provided. Because of the nonspecific nature of the results, neuropsychological testing should be reserved for selected patients. (See 'Diagnostic testing' above.)

●In the absence of a defined specific treatment for this disorder, symptomatic treatment is suggested, which may include migraine medications, analgesics, psychological counseling, and/or psychotropic medications as dictated by patient complaints and disability (Grade 2C). Education and reassurance shortly after the injury are also suggested (Grade 2B). (See 'Treatment' above.)

●Most patients recover quickly, within several weeks. A minority have prolonged disability. Litigation and comorbidity may play a role in these patients. (See 'Prognosis' above.)

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Topic 4830 Version 13.0