INTRODUCTION — Postconcussion syndrome (PCS) is a common sequelae of traumatic brain injury (TBI) and describes a symptom complex that includes headache, dizziness, neuropsychiatric symptoms, and cognitive impairment [1]. The term "postconcussion syndrome" was coined in 1934 [2]; some authors prefer to refer to the syndrome as "persisting symptoms after concussion" [3]. However, it may be more accurate to use the term "post-TBI syndrome," as PCS may also occur after moderate and severe TBI. Mild TBI can occur after the head being struck, the head striking an object, or the brain undergoing an acceleration/deceleration movement without direct external trauma to the head. Loss of consciousness does not have to occur for PCS to develop. We will use the term "PCS," as it is most commonly used in the published literature.
PCS is controversial, especially in its protracted form [4]. 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.
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".)
●(See "Minor blunt head trauma in infants and young children (<2 years): Clinical features and evaluation".)
●(See "Minor blunt head trauma in children (≥2 years): Clinical features and evaluation".)
●(See "Post-traumatic headache".)
●(See "Sequelae of mild traumatic brain injury".)
●(See "Traumatic brain injury: Epidemiology, classification, and pathophysiology".)
EPIDEMIOLOGY — Thirty to 80 percent of patients with mild traumatic brain injury (TBI) will experience some symptoms of 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 [5].
A number of studies have tried to associate the severity of brain injury with PCS among patients with mild TBI using a variety of measures including the Glasgow Coma Scale (GCS) (table 1), the duration of loss of consciousness or posttraumatic amnesia, and the presence or extent of visualized abnormalities on computed tomography (CT) or magnetic resonance imaging (MRI) [6-10]. 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 [11].
Cohort studies of patients with mild and moderate TBI have consistently found that female sex and increasing age are risk factors for PCS [7,8,12,13]. 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 [14]. 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 sex differences, as the relative preponderance of accident and assault versus sports injury as a cause of TBI may be higher in females than males.
PATHOPHYSIOLOGY — There are different theories for the pathogenesis of 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 [15]. (See 'Persistent postconcussion syndrome' below.)
Neurobiologic factors — A number of structural and biochemical changes have been documented in animal models of brain injury and in human neuropathologic studies [16,17]. One study compared regional brain volumes on MRI in 19 patients one year after mild traumatic brain injury (TBI) with 22 matched control subjects [18]. Patients had measurable global atrophy compared with 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 (single-photon emission computed tomography [SPECT], positron emission tomography [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 [9,19-27]. 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 [22,24,28,29]. 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 [30]. 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 (PTSD) (see "Somatic symptom disorder: Epidemiology and clinical presentation" and "Somatic symptom disorder: Assessment and diagnosis"). 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 [31,32].
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 stress and PTSD) are more prevalent in patients with PCS compared with general population controls and/or with head-injured patients who do not develop persistent PCS [7,10,33-41].
The association of TBI and subsequent PTSD has been well established in combat veterans [42,43]. (See "Posttraumatic stress disorder in adults: Epidemiology, pathophysiology, clinical features, assessment, and diagnosis", section on 'Combat' and "Medical care of the military veteran" and "Medical care of the military veteran", section on 'Chronic postconcussive symptoms'.)
However, studies of the interaction of depression, anxiety, and cognitive performance in other populations with mild 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 [44], while others have found a correlation in the response to antidepressant treatment in a subset of patients [33]. (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 [45,46].
●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 with 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 [47-49]. 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 [50].
●Litigation – The idea that pending compensation claims contribute to the presence and duration of PCS symptomatology dates back to original reports in the late 19th century. Studies do show a relationship between persistent PCS and potential financial compensation [51,52]. 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 [53,54]. Similar patterns of cognitive deficits may be seen in patients with chronic pain and PCS [32]. 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 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 [55]. Among patients referred to a headache clinic, approximately half had cognitive complaints, and a quarter had psychological complaints; 17 percent had an isolated complaint of headache [56].
Headaches — Headaches are variably estimated as occurring in 25 to 78 percent of persons following mild TBI.
Most posttraumatic headaches can be classified by International Classification of Headache Disorders (ICHD) type similarly to nontraumatic headaches with the suffix "like" added to indicate that it is not a primary headache. Migraine-like and tension-type-like headaches predominate.
The clinical features and diagnosis of posttraumatic headache syndromes are described in detail separately. (See "Post-traumatic headache", section on 'Clinical features and diagnosis'.)
Dizziness — Approximately 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 [57-60]. (See "Approach to the patient with dizziness" and "Benign paroxysmal positional vertigo" and "Sequelae of mild traumatic brain injury", section on 'Posttraumatic vertigo and dizziness'.)
Sleep disturbance — Sleep disturbances, usually insomnia, are also reported by approximately one-third of patients in the acute phase after mild injury and approximately half of patients in the chronic phase.
The most common manifestations of sleep-wake disorders after TBI are excessive daytime sleepiness, increased sleep need, and insomnia (figure 1). Less commonly, patients experience circadian rhythm disturbances; abnormal movements or behaviors during sleep, such as sleep talking, bruxism, and dream enactment; and sleep-disordered breathing. (See "Sleep-wake disorders in patients with traumatic brain injury".)
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.
A significant number of patients (15 to 20 percent) will develop symptoms meeting criteria for psychiatric disease. These include acute stress and posttraumatic stress disorder (PTSD) as well as anxiety, panic disorder, and depression [7,25,36,61].
DIAGNOSTIC TESTING — The judicious use of testing needs to be individualized for each patient [62]. 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 evaluation can be helpful for evaluating selected patients with persistent and prominent cognitive or psychological 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 [56]. 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 [63,64].
The observed cognitive deficits are not specific to mild TBI; similar patterns of abnormalities are seen in patients with psychological illness, pain syndromes, insomnia [65], and obstructive sleep apnea [66], and in those taking medications [14,31,67].
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 [62,68].
Neuroimaging — Many patients evaluated for mild TBI will have undergone a CT scan or MRI as part of their acute evaluation. Approximately 10 percent of CT scans in mild TBI are abnormal, showing mild subarachnoid hemorrhage, subdural hemorrhage, or contusions [69]. MRI is more sensitive than CT scan, showing abnormalities in approximately 30 percent of patients with normal CT scans [70,71]. (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 identify either a worse prognosis or an alternative cause for their symptoms.
Other advanced neuroimaging techniques, including functional MRI, magnetic resonance spectroscopy, and diffusion tensor imaging (DTI), are under investigation in the evaluation of patients with TBI [72,73]. According to the American College of Radiology Appropriateness Criteria for head trauma, for "subacute or chronic head trauma with unexplained cognitive or neurologic deficit(s)…there is insufficient evidence to support the routine clinical use of DTI at the individual patient level" [74].
Electroencephalography — Electroencephalography (EEG) is not indicated in most patients with PCS. There are no certain EEG or quantitative EEG (qEEG) features unique to mild TBI or useful for identifying mild TBI as the cause of PCS [75]. After mild TBI, EEG may show slowing of the posterior dominant rhythm and increased diffuse theta slowing, which may return to normal within hours or may clear more slowly over many weeks [76]. According to the guideline committee of the American Clinical Neurophysiology Society, "it was found that for patients with or without symptoms of abnormal cognition or behavior, current evidence does not support the clinical use of qEEG either at the time of the injury or remote from the injury to diagnose [mild] TBI" [77].
TREATMENT — Treatment of PCS is individualized to the patient's particular complaints. Simple reassurance is often the major treatment, since most patients will improve within three months.
In the absence of specific treatments for the prevention or treatment of PCS, most clinicians adopt a symptomatic approach [78].
Cognitive or physical rest — Cognitive and physical rest after a concussion have not shown convincing evidence of benefit in terms of more rapid recovery or in long-term clinical outcomes [8,79]. Patients should avoid activities that might lead to a second concussion while they are symptomatic from the initial event.
We do not formally recommend a rest period otherwise. Patients should limit activities that exacerbate their symptoms in the first days after injury and then gradually return to their former level of activity as tolerated.
The role of cognitive and physical rest has been more extensively studied in children and adolescents. (See "Concussion in children and adolescents: Management", section on 'Physical rest and activity' and "Concussion in children and adolescents: Management", section on 'Cognitive rest'.)
Headache management — The approach to management of posttraumatic headaches is discussed separately. (See "Post-traumatic headache", section on 'Treatment'.)
Management of sleep-wake disorders — Behavioral and pharmacologic treatments are available for the majority of sleep-wake disorders in patients with traumatic brain injury (TBI) (figure 1). Treatment varies according to the dominant symptom or specific sleep disorder as well as relevant comorbidities. Beyond symptomatic improvement, the potential benefits of successful treatment of sleep-wake disorders in the TBI population include improvement in functional outcomes and quality of life. (See "Sleep-wake disorders in patients with traumatic brain injury", section on 'Treatment'.)
Psychological and cognitive complaints — Current evidence does not provide information for treatment of these complaints that are specific to the posttraumatic setting.
Donepezil has had positive results in preliminary studies in patients with more severe TBI but has not been studied extensively in PCS [80,81]. Six patients with chronic symptoms after mild head injury reported subjective cognitive improvement in an open-label study of donepezil [82]. A small, randomized trial of CDP-choline in 14 males with mild to moderate TBI was associated with improvement in PCS symptoms and some, but not all, neuropsychological test results after one month [83].
The use of cognitive rehabilitation for cognitive difficulties after mild TBI is controversial. Although a systemic review found good support for its use in military/veteran populations, studies in other populations are lacking [84-86]. Cognitive-behavioral therapy and psychotherapy may be more effective than cognitive rehabilitation in reducing chronic PCS [87]. 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 psychological symptoms are particularly prominent, supportive psychotherapy and the use of antidepressant and anxiolytic medications may be helpful [41]. Again, there are only limited data supporting a treatment approach specific to the PCS setting. 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 [33]. An open-label study in 20 patients with depression after TBI showed symptomatic improvements with treatment with citalopram and carbamazepine [88]. Small randomized trials have found that cognitive-behavioral therapy improved symptoms of anxiety and/or depression in patients who had had a mild TBI [89-91].
Posttraumatic stress disorder (PTSD) is associated with mild TBI, particularly in veterans of combat. The treatment of PTSD is discussed separately. (See "Posttraumatic stress disorder in adults: Treatment overview" and "Posttraumatic stress disorder in adults: Psychotherapy and psychosocial interventions".)
Randomized, sham-controlled studies of hyperbaric oxygen in the treatment of persistent PCS have not consistently shown a benefit on symptoms or cognitive testing [92,93].
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 [41]. This was illustrated in a follow-up study of 73 patients with mild TBI [94]. 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 [94].
A number of controlled studies have examined the role of education and reassurance in ameliorating PCS [95-101]. 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 [90,102,103]. The more intensive multidisciplinary evaluations do not clearly add substantively to the simpler interventions of education and reassurance.
PROGNOSIS
Natural history — The symptoms and disability attributed to 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 [104]. A greater burden of symptoms at initial presentation appears to be associated with a higher risk that symptoms will persist for more than one month [105]. The vast majority of patients have largely recovered by three months [106,107].
Approximately 15 percent of patients with PCS have cognitive deficits that persist one year or longer [107]. It is not certain whether symptom reporting represents the effects of brain injury and/or is due to secondary gain, preexisting emotional problems, demographics, and stress reactions to the injury or injury event. In one prospective study, 46 percent of patients with mild traumatic brain injury (TBI) reported three or more symptoms at one year; 24 percent, a smaller but still substantial proportion, of trauma patients without head injury also reported such symptoms [108].
Persistent postconcussion syndrome — Patients with disabling symptoms that persist for more than three months after the injury 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 TBI made the following points [109]:
●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 sex 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 [52,110]. 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 [111]. (See "Factitious disorder imposed on self (Munchausen syndrome)".)
SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Increased intracranial pressure and moderate-to-severe traumatic brain injury" and "Society guideline links: Minor head trauma and concussion" and "Society guideline links: Sports-related concussion".)
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 topics (see "Patient education: Concussion in adults (The Basics)" and "Patient education: Head injury in adults (The Basics)" and "Patient education: Postconcussion syndrome (The Basics)")
SUMMARY AND RECOMMENDATIONS
●Clinical features – 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.)
●Pathogenesis and risk factors – Females 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.)
●Evaluation – 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.)
●Management – In the absence of a defined specific treatment for this disorder, management is generally symptomatic and may include medication for headache, psychological counseling, and/or psychotropic medications as dictated by patient complaints and disability. Education and reassurance shortly after the injury are also helpful. (See 'Treatment' above and "Post-traumatic headache", section on 'Treatment'.)
●Prognosis – 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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