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Postconcussion syndrome
Author: Randolph W Evans, MD, FAAN
Section Editor: Michael J Aminoff, MD, DSc
Deputy Editor: Janet L Wilterdink, MD

All topics are updated as new evidence becomes available and our peer review process is complete.

Literature review current through: Aug 2022. | This topic last updated: Apr 09, 2021.

INTRODUCTION

The 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], but it is more accurate to use
the term "post-TBI syndrome," as it 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.

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.

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 [4].

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) [5-9]. 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 [10].

Cohort studies of patients with mild and moderate TBI have consistently found that
female sex and increasing age are risk factors for PCS [6,7,11,12]. 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 [13].
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 [14]. (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 [15,16]. One study compared regional brain volumes on magnetic
resonance imaging (MRI) in 19 patients one year after mild traumatic brain injury
(TBI) with 22 matched control subjects [17]. 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 computed
tomography (CT), supporting a role for structural or physiologic brain injury in the
production of PCS [8,18-26]. 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 [21,23,27,28]. 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 [29]. 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 [30,31].

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 [6,9,32-40].

The association of TBI and subsequent PTSD has been well established in combat
veterans [41,42]. (See "Posttraumatic stress disorder in adults: Epidemiology,
pathophysiology, clinical manifestations, course, assessment, and diagnosis",
section on 'Combat' and "Medical care of the returning veteran" and "Medical care
of the returning veteran", section on 'Psychological complications of traumatic brain
injury'.)

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 [43], while others have found a
correlation in the response to antidepressant treatment in a subset of patients [32].
(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 [44,45].
 ● 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 [46-48]. 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 [49].

● 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 [50,51]. 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 [52,53]. Similar
patterns of cognitive deficits may be seen in patients with chronic pain and
PCS [31]. 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 [54]. 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 [55].

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 [56-59]. (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 [6,24,35,60].

DIAGNOSTIC TESTING

The judicious use of testing needs to be individualized for each patient [61].
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 [55]. 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 [62,63].

The observed cognitive deficits are not specific to mild TBI; similar patterns of
abnormalities are seen in patients with psychological illness, those with pain
syndromes, and those taking medications [13,30,64].
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 [61,65].

Neuroimaging — Many patients evaluated for mild TBI will have undergone a

computed tomography (CT) scan or magnetic resonance imaging (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 [66]. MRI is more sensitive than CT scan, showing abnormalities in
approximately 30 percent of patients with normal CT scans [67,68]. (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 [69,70]. In one study, patients with evidence of
traumatic axonal injury on DTI were more likely to demonstrate objective evidence
of cognitive impairment compared with patients with normal studies [71]. A meta-
analysis concluded that although DTI is sensitive to a wide range of group
differences in diffusion metrics, DTI currently lacks the specificity necessary for
meaningful clinical application in individuals [72].

Electroencephalography — Electroencephalography (EEG) is not indicated in most

patients with PCS. There are no certain EEG or quantitative EEG features unique to
mild TBI or useful for identifying mild TBI as the cause of PCS [73]. 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 [74].

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 [75].

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 [7,76]. 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 "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'.)

Psychologic 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 [77,78]. Six patients with
chronic symptoms after mild head injury reported subjective cognitive improvement
in an open-label study of donepezil [79]. 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
[80].

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 [81,82].
Cognitive-behavioral therapy and psychotherapy may be more effective than
cognitive rehabilitation in reducing chronic PCS [83]. 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 [40]. 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 [32]. An open-label study in 20 patients with depression after TBI showed
symptomatic improvements with treatment with citalopram and carbamazepine
[84]. Small randomized trials have found that cognitive-behavioral therapy improved
symptoms of anxiety and/or depression in patients who had had a mild TBI [85-87].

Posttraumatic stress disorder (PTSD) is associated with mild TBI, particularly in

veterans of combat. The treatment of PTSD is discussed separately. (See
"Management of posttraumatic stress disorder in adults" and "Psychotherapy and
psychosocial interventions for posttraumatic stress disorder in adults".)

Randomized, sham-controlled studies of hyperbaric oxygen in the treatment of

persistent PCS have not consistently shown a benefit on symptoms or cognitive
testing [88,89].

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 [40]. This was
illustrated in a follow-up study of 73 patients with mild TBI [90]. 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 [90].

A number of controlled studies have examined the role of education and

reassurance in ameliorating PCS [91-97]. 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 [86,98,99]. 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 [100]. 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 [101]. The vast majority of patients have largely
recovered by three months [102,103].

A minority of patients with PCS have cognitive deficits that persist one year or
longer [103]. 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 [104].

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
TBI made the following points [105]:

● 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
[51,106]. 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 [107]. (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: 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.)

● 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.)

● In patients who did not have magnetic resonance imaging (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, 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'.)

● 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 20.0
GRAPHICS

Glasgow Coma Scale (GCS)

  Score

Eye opening

Spontaneous 4

Response to verbal command 3

Response to pain 2

No eye opening 1

Best verbal response

Oriented 5

Confused 4

Inappropriate words 3

Incomprehensible sounds 2

No verbal response 1

Best motor response

Obeys commands 6

Localizing response to pain 5

Withdrawal response to pain 4

Flexion to pain 3

Extension to pain 2

No motor response 1

Total  

The GCS is scored between 3 and 15, 3 being the worst and 15 the best. It is composed
of three parameters: best eye response (E), best verbal response (V), and best motor
response (M). The components of the GCS should be recorded individually; for example,
E2V3M4 results in a GCS score of 9. A score of 13 or higher correlates with mild brain
injury, a score of 9 to 12 correlates with moderate injury, and a score of 8 or less
represents severe brain injury.

Graphic 81854 Version 9.0

Overview of sleep-wake disorders in patients with traumatic brain
injury

Sleep-wake disturbances are among the most prevalent and persistent sequelae of TBI.
Patients suffering from TBI of any severity, in both the acute and chronic phases,
commonly report EDS, increased sleep need, insomnia, and sleep fragmentation.
Identification and treatment of sleep disorders in patients with TBI is important and can
complement other efforts to promote maximum functional recovery. Refer to UpToDate
topic review on sleep-wake disorders in patients with TBI for more information.

PSG: polysomnography; OSA: obstructive sleep apnea; RLS: restless legs syndrome; TBI:
traumatic brain injury; EDS: excessive daytime sleepiness; PTSD: posttraumatic stress
disorder; REM: rapid eye movement.

Graphic 131183 Version 1.0

Contributor Disclosures
Randolph W Evans, MD, FAAN Consultant/Advisory Boards: Lundbeck [Migraine]. Speaker's
Bureau: Abbvie [Migraine]; Amgen [Migraine]; Biohaven [Migraine]; Eli Lilly [Migraine]; Impel
[Migraine]; Teva [Migraine]. Other Financial Interest: Elsevier [Royalties]; Oxford University
Press [Royalties]; Medscape Neurology [Royalties]. All of the relevant financial relationships
listed have been mitigated. Michael J Aminoff, MD, DSc Consultant/Advisory Boards: Brain
Neurotherapy Bio [Parkinson disease].
All of the relevant financial relationships listed have
been mitigated. Janet L Wilterdink, MD No relevant financial relationship(s) with ineligible
companies to disclose.

Contributor disclosures are reviewed for conflicts of interest by the editorial group. When
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