Postconcussion Syndrome

Handbook of Clinical Neurology, Vol.
158 (3rd series)

Sports Neurology
B. Hainline and R.A. Stern, Editors
https://doi.org/10.1016/B978-0-444-63954-7.00017-3
Copyright © 2018 Elsevier B.V. All rights reserved
Chapter 17
Postconcussion syndrome
BRIGID DWYER AND DOUGLAS I. KATZ*
Department of Neurology, Boston University School of Medicine, Boston, MA, United States
Abstract
Postconcussion syndrome (PCS) is a heterogeneous condition comprised of a set of signs and symptoms in
somatic, cognitive, and emotional domains. PCS is a controversial concept because of differing consensus
criteria, variability in presentation, and lack of specificity to concussion. Whereas symptoms of concussion
resolve in most individuals over days to weeks, a minority of individuals experience symptoms persisting
months to years. The clinical consequences of concussion may be best conceptualized as two multidimen-
sional disorders: (1) a constellation of acute symptoms termed early-phase posttraumatic disorder (com-
monly headache, dizziness, imbalance, fatigue, sleep disruption, impaired cognition, photo- and
phonophobia); and (2) late-phase posttraumatic disorder, consisting of somatic, emotional, and cognitive
symptoms. This phase is highly influenced by various psychosocial factors and is much less specific to the
brain injury itself. Risk factors for development of a late-phase disorder include a high early symptom
burden (e.g., headache, fatigue), a history of multiple concussions, psychiatric conditions (anxiety, depres-
sion), longer duration of unconsciousness or amnesia, and younger age. Successful treatment requires
thoughtful differential diagnosis, including consideration of comorbid and premorbid conditions and other
possible contributing factors. Treatment should include a hierarchic, sequential approach to management
of treatable symptoms that impact functioning, such as depression, anxiety, insomnia, headache, muscu-
loskeletal pain, and vertigo. A guided prescription of aerobic exercise is beneficial for early- and late-phase
disorders after concussion.
INTRODUCTION reports. So fallacious retrospective diagnosis of concus-

sion or mTBI based on the nonspecific symptom profile
Postconcussion syndrome (PCS) has been the subject of
of PCS is a common clinical pitfall.
extensive study but there remain controversy and debate
This chapter addresses aspects of definition and diag-
regarding its definition, etiology, pathophysiology, and
nosis, clinical features, expected clinical course, and
prognosis. Multiple signs or symptoms are required to
variability in prognosis of PCS. The review concludes
meet criteria for most consensus definitions of PCS,
with a brief discussion on treatment and future directions.
but the presenting constellation of symptoms may differ
significantly among individuals. The lack of specificity
DEFINITIONS
of symptoms to brain injury is also problematic. Identical
symptom profiles can occur among different disorders Several definitions of PCS, including those focused on
and, to a large extent, even in the normal population sports concussion, have been used for both clinical man-
(Iverson et al., 2015; Hunt et al., 2016b). Diagnosis of agement and research, but there remains lack of consen-
mild traumatic brain injury (mTBI) or concussion (used sus on a precise definition (Table 17.1). Reliance on one
synonymously here) still lacks established objective bio- or another definition can lead to wide variations in diag-
markers so the diagnosis is based on clinical examination nosis and inclusion criteria for epidemiologic and other
of early signs and symptoms or unreliable retrospective research, as well as clinical decision making.
*Correspondence to: Douglas I. Katz, MD, Department of Neurology, Boston University School of Medicine, 72 E Concord St C3,
Boston MA 02118, United States. Tel: +1-781-348-2500, E-mail: [email protected]
164 B. DWYER AND D.I. KATZ
Table 17.1
Definitions for postconcussion syndrome and related disorders
5th International
Consensus Conference
ICD-10 DSM-IV DSM-V on Concussion in Sport
Terminology Postconcussion Postconcussional Major or mild Sports-related

syndrome disorder neurocognitive disorder: concussion:
traumatic brain injury symptoms and signs
Trauma History of head History of head Impact to head or rapid Impulsive force
trauma injury movement/displacement transmitted to the
of brain head
Loss of “Usually Suggested criterion: Not required Not required
consciousness sufficiently > 5 minutes
(LOC) severe to result
in loss of
consciousness”
Altered Yes Relative attention or Yes, or (+) imaging/ “Impairment of
consciousness / memory neurologic exam neurologic
cognitive impairment on functioning”
impairment neuropsychologic
testing
Maximum 4 weeks N/A Immediate or when Minutes to hours
symptom delay conscious
for attribution to
trauma
Minimum duration N/A 3 months “Past the acute injury phase” Adults: 10–14 days
Children: 4 weeks
Objective evidence Not required Required Not required Not required
DSM-IV, Diagnostic and Statistical Manual of Mental Disorders, fourth edition; DSM-V, Diagnostic and Statistical Manual of Mental Disorders,
fifth edition; ICD-10, International Statistical Classification of Diseases and Related Health Problems, 10th revision.
The International Statistical Classification of in this definition, as it is for the Diagnostic and Statistical
Diseases and Related Health Problems (ICD-10) clinical Manual of Mental Disorders (DSM)-IV definition
criteria for postconcussional syndrome proposed in 1992 (American Psychiatric Association, 2000).
(World Health Organization, 1992) require that a head The DSM-IV criteria for PCS also require a history
trauma is sufficiently severe to cause loss of conscious- of head injury and stipulate: that relative attention or
ness, and is followed within 4 weeks by at least three of memory impairment be present on neuropsychologic
the following features: (1) complaints of unpleasant testing; that symptoms cause clinically significant
sensation and pains such as headache, dizziness, general impairment in social or occupational functioning; and
malaise and excessive fatigue, or noise intolerance; (2) that the duration of these symptoms exceeds 3 months.
emotional changes such as irritability, emotional lability, At least three of the following must be present, either
or some degree of depression and/or anxiety; (3) subjec- as new-onset symptoms or as a substantial clinical wors-
tive complaints of difficulty in concentration and in ening following head injury (although no maximum
performing mental tasks, and of memory problems with- delay in onset is stipulated): becoming fatigued easily;
out clear objective evidence; (4) insomnia; (5) reduced disordered sleep; headache; vertigo or dizziness; irrita-
tolerance to alcohol; and (6) preoccupation with the bility or aggression with little or no provocation; anxiety,
above symptoms and fear of permanent brain damage, depression, or affective lability; changes in personality
to the extent of hypochondria and adoption of a sick role. (e.g., social or sexual inappropriateness); and apathy or
The lack of specificity of these symptoms to TBI is lack of spontaneity (American Psychiatric Association,
problematic, and the vague requirement of loss of con- 2000). The definition of head injury is more detailed than
sciousness challenges inclusion of the large majority of in the ICD-10, and is described as “significant cerebral
mild brain injuries without complete unconsciousness. concussion.” Although it is pointed out that there is
Objective evidence of cognitive deficits is not included insufficient evidence to establish a definitive threshold,
POSTCONCUSSION SYNDROME 165
suggested criteria are loss of consciousness greater than The consensus statement from the 5th International
5 minutes, posttraumatic amnesia greater than 12 hours, Conference on Concussion in Sport (McCrory et al.,
or posttraumatic onset of seizures. As with ICD-10, 2017) describes the symptoms and signs after sports-
this definition excludes the majority of concussed related concussion (SRC) that “evolve over minutes
patients for whom there is no loss of consciousness. to hours” and “may or may not involve loss of con-
ICD-10 criteria have been criticized for their focus sciousness.” Symptoms are described among somatic,
on the presence of symptoms independent of cause, pos- cognitive, and/or emotional categories. Problems in
sibly resulting in misdiagnosis of PCS in patients other clinical domains may include physical signs
without a TBI-related disorder. The DSM-IV criteria (e.g., loss of consciousness, amnesia, neurologic defi-
are similarly criticized, although estimated rates of cit), balance impairment, behavioral changes, cognitive
PCS in TBI populations according to this definition are impairment, and sleep/wake disturbance. The statement
much lower. The 3-month minimum time threshold describes resolution of clinical and cognitive problems
of the DSM-IV criteria excludes many individuals with that “typically follows a sequential course” but “in some
similar symptoms that resolve more quickly. Boake cases symptoms may be prolonged.” The statement
and colleagues (2004) applied diagnostic criteria to147 also emphasizes that the term “persistent symptoms”
patients with mild or moderate TBI; 64% were diagnosed should only be used clinically when an individual does
with PCS according to ICD-10 criteria, versus 11% not recover within the usual recovery time of 10–14
according to DSM-IV criteria. Forty percent of controls days for adults and 4 weeks for children. There is a
with extracranial trauma but no TBI also met ICD-10 cri- caveat that a “single physiologic time window for
teria for PCS. At 6 months postinjury, no significant dif- SRC recovery” is not established. Persistent postcon-
ferences were found between ICD-10 and DSM-IV cussive symptoms are described as a “constellation
definitions (McCauley et al., 2005). A World Health of non-specific post-traumatic symptoms.” It is not
Organization task force review found no empiric support required that these symptoms share a common cause,
for either set of criteria due to their lack of specificity and the consensus statement encourages consideration
(Carroll et al., 2004). A recent study of nonconcussed of confounding factors. These criteria are still in the
college athletes demonstrated that 16.3% had baseline early stages of being applied to clinical and research
symptoms meeting criteria for the ICD-10 definition of settings.
PCS, further demonstrating the lack of specificity of Not surprisingly, a notable lack of consensus
these criteria (Asken et al., 2017). remains among practicing clinicians regarding the
The latest version of the DSM (DSM-V), published in numbers of symptoms and their duration required to
2013, abandons the label “postconcussion syndrome” define PCS. In 2015, Rose et al. surveyed 597 physi-
and instead refers to “major or mild neurocognitive dis- cians regarding the minimum duration of symptoms
order due to traumatic brain injury” within the spectrum needed to diagnose PCS; 26.6% of responders indicated
of other neurocognitive disorders (American Psychiatric that less than 2 weeks was required, 20.4% required
Association, 2013). This definition requires evidence of 2 weeks to 1 month, 33% required 1–3 months, and
TBI, described as an “impact to the head or other mech- 11.1% required more than 3 months. Those seeing more
anisms of rapid movement or displacement of the brain patients with concussion in their practice, or for whom
within the skull.” One or more associated findings are over 50% of their concussion patients were pediatric,
also necessary, including loss of consciousness, posttrau- were more likely to require at least a month of symp-
matic amnesia, “disorientation and confusion,” or neuro- toms ( p < 0.001). Regarding the number of symptoms
logic signs either detected clinically (“new onset of required, 55.9% required only one symptom, 17.6%
seizures; a marked worsening of a preexisting seizure dis- required two, 14.6% required three, and 3.2% required
order; visual field cuts; anosmia; hemiparesis”) or evident at least four symptoms. It should be noted that this
on neuroimaging. The disorder must develop immedi- survey took place prior to the 5th International Confer-
ately after injury or upon recovery of consciousness ence on Concussion in Sport (McCrory et al., 2017),
and should “persist past the acute post-injury period.” and so it is unknown if similar findings would still
These criteria are more in keeping with other widely used occur.
clinical and research concepts of the spectrum of neuro- One of the main ambiguities among these definitions
cognitive problems across the range of severity of TBI and in clinical use is when to apply the term PCS after
from mild to severe. The criteria specify immediate onset mTBI. Does it cover the immediate symptoms after
of neurocognitive disorder immediately after injury or mTBI? Should it be reserved for symptoms that are pre-
recovery of consciousness with postacute time durations sent after the acute period? Should there be a minimal
that more clearly depict the expected recovery after differ- time threshold such as included in the DSM-IV defini-
ent severities of TBI, usually up to 3 months after mTBI. tion? The term persistent PCS is often used for those with
longer-lasting symptoms, although there is no consensus 1996; Lew et al., 2006, Lucas and Blume, 2017). Other
of when to apply the term – 3 months, 6 months, 1 year. headache types may be related to musculoskeletal inju-
Symptom profiles usually vary over time as recovery ries, such as cervical whiplash and craniomandibular
evolves. Although most persons experiencing PCS after injury (Horn et al., 2013); some patients may have a
SRC and other causes of injury recover fully, persistent mix of headache types (Couch and Bearss, 2001). Other
and sometimes severe residual symptoms occur in a posttraumatic headache syndromes include: localized
minority of individuals after mTBI. The causes of symp- pain at the site of scalp trauma or laceration that may
toms may be more or less directly related to the brain persist for months; occipital neuralgia from direct
injury or may be a consequence of other associated occipital nerve injury or entrapment with pain from the
injuries and conditions. Further, the causes of symptoms nuchal-occipital area radiating to parietal, temporal and
may vary over time. Thus, it may be more meaningful to frontal, periorbital areas; and trigeminal nerve injury
consider PCS as having two phases: an early-phase post- with constant or paroxysmal facial pain in one or more
traumatic disorder, occurring in the days to weeks after of the trigeminal nerve distributions. Other headache
injury, which may be more closely linked to the brain types are less common after trauma. These include
injury and associated injuries; and a less common late- trigeminal autonomic cephalalgias, such as cluster head-
phase posttraumatic disorder, which may persist months ache, hemicrania continua, short-lasting unilateral neur-
or more, and likely has a more complex etiology of algiform headache with conjunctival injection and
multiple interacting factors (Katz et al., 2015). It might tearing, short-lasting unilateral headache, and paroxys-
be argued that we should abandon the term PCS entirely, mal hemicrania (Matharu and Goadsby, 2001; Putzki
because of the ambiguities of symptom profile, etiology, et al., 2005; Jacob et al., 2008). Additional uncommon
and time duration in the use of this diagnostic label. posttraumatic causes of headache include traumatic
dissection of carotid or vertebral arteries and low cere-
CLINICAL FEATURES brospinal fluid pressure. These are characterized by
prominent exacerbation with upright position, usually
The most common symptoms of PCS are headache,
caused by cribiform plate fracture or dural root sleeve
dizziness, fatigue, irritability, anxiety, sleep disorder,
tear (Siavoshi et al., 2016).
impaired attention and memory, and sensitivity to noise
Common cervical injuries accompanying mTBI
and light. Symptoms associated with PCS in both early-
include myofascial pain in the cervical musculature
and late-phase disorders are often divided into somatic,
following whiplash injury; associated symptoms can
cognitive, and emotional domains, mostly for conve-
include vertigo, tinnitus, a sense of fullness in the ear,
nience. Symptoms in each domain may overlap and have
and even external ear pain (Horn et al., 2013). It is
multiple interacting etiologies that can change over time.
thought that the proximity of sensory afferents from
After confusion clears, the early phase may include
cranial nerves V, VII, IX, and X may play a role in this
headache, dizziness, nausea, sleep disruption, mental
connection, referred to as the convergence projection
fogginess, anxiety, light sensitivity, noise sensitivity,
theory (Arendt-Nielsen et al., 2000). Cervical afferents
fatigue, emotional lability, and irritability. At least 80%
also contribute to vestibular integrations of head, neck,
of those with mTBI report one or more symptoms in this
and eye movement, further adding to the plausibility of
early phase, but there is no pathognomonic or mandatory
whiplash-induced symptoms (including dizziness), sep-
set of symptoms. Up to 20% of those with mTBI report
arate from those more directly related to TBI. Temporo-
no symptoms after a brief period of altered consciousness
mandibular joint disorder is another possible contributor
(Levin et al., 1987; Dikmen et al., 2010). Symptoms
that should be assessed.
improve in the vast majority of patients within 1–3 weeks
Dizziness occurs in about half of individuals with
after SRC and 1–3 months after other causes of mTBI
mTBI; it may result from a variety of injuries affecting
(Levin et al., 1987; Ponsford et al., 2000; McCrea
vestibular function, or may have a nonvestibular etiol-
et al., 2003; Bleiberg et al., 2004).
ogy. Some complaints of dizziness are nonspecific and
difficult to characterize clinically. Dizziness after sports
Somatic symptoms of mTBI
injury may be a predictor of more prolonged recovery
Somatic symptoms after mTBI include headache, dizzi- (De Kruiijk et al., 2002; Lau et al., 2011).
ness, fatigue, insomnia, photophobia, phonophobia, and Some individuals with mTBI report true vertigo,
tinnitus. Headache and dizziness are the most common – which may be caused by benign paroxysmal positional
headache may occur in up to 90% of those with mTBI vertigo (BPPV), labyrinthine concussion, perilymphatic
(Guskiewicz et al., 2000; Kraus et al., 2005; Faux and fistula, or migraines (Swartz and Longwell, 2005). Lab-
Sheedy, 2008). Headache types include, most com- yrinthine concussion can cause both auditory and vestib-
monly, tension and migraine-type headache (Haas, ular symptoms. BPPV, caused by otolith displacement
into the semicircular canals, is associated with episodic At 5 days postinjury, neuropsychologic testing results
vestibular symptoms maximal in particular positions were similar after concussion in persons with or without
and triggered by movement. Posttraumatic endolym- cognitive complaints (Meares et al., 2006). In a meta-
phatic hydrops (or Menière syndrome) presents with ver- analysis of several studies of cognitive dysfunction after
tigo, a sense of aural fullness, unilateral low-frequency mTBI, the effect size of neuropsychologic test scores
hearing loss, and tinnitus. BPPV is the most common diminished to very small levels, below one standard
of these complications after concussion (Shepard deviation after 24 hours and well below a half standard
et al., 2013). deviation compared to controls after 6 days postinjury
Autonomic nervous system dysfunction has also been (Iverson et al., 2013). Dikmen and colleagues (2017)
suggested as a contributor to PCS pathophysiology in reported on 421 adults followed prospectively, divided
cases where somatic symptoms are exacerbated by exer- into groups based on initial Glasgow Coma Scale score
cise (Ellis et al., 2016). For example, patients with PCS between 13 and 15 or positive computed tomography
have higher resting heart rates (King et al., 1997; Gall (CT) findings, and compared them to non-TBI trauma
et al., 2004; Leddy et al., 2007) and abnormal cerebral controls. They demonstrated differences on a neuropsy-
blood flow regulation (Clausen et al., 2016) during chologic battery only in those with positive CT findings
exercise. In cases of PCS associated with cervicogenic at 1 month postinjury, and no differences at 1 year in
complaints, the sympathetic nervous system also has a any group with mTBI.
proposed role via multiple mechanisms, including mod-
ulation of the contractility of muscle fibers and of both
proprioceptive and nociceptive inputs (Passatore and
Emotional symptoms of mTBI
Roatta, 2006).
Emotional symptoms after mTBI include irritability,
anxiety, depression, or emotional lability. Irritability
Cognitive symptoms of mTBI
and anxiety may be early-phase symptoms, but depres-
Cognitive symptoms include difficulty with concentra- sion tends to occur later. In all cases of mTBI, rates of
tion, decreased attention, impaired memory, and reduced depression are between 11% and 44% within the first
processing speed. In the early phase after concussion, 3 months postinjury (Mooney and Speed, 2001; Levin
typical complaints are feelings of fogginess, losing et al., 2005). In a retrospective review of pediatric
track of thoughts and conversations, slowed thinking, patients referred to a sports concussion program, half
forgetfulness, word-finding problems, and distractibility. the group reported at least one emotional symptom
In SRC, a number of tools and measures are used to char- and 11.5% were diagnosed with a psychiatric disorder,
acterize impairments and track recovery, such as the either new since injury or exacerbation of a premorbid
Immediate Post-concussion Assessment and Cognitive condition (Ellis et al., 2015). Female sex, a higher initial
Test (ImPACT: Lovell and Maroon, 2000). Studies using concussion symptom score, a higher emotional early
this tool show recovery of cognitive signs (including postconcussion symptom subscore, presence of a prein-
verbal and visual memory, visual motor processing speed, jury psychiatric history, and presence of a family history
and reaction times) in most athletes within 4 weeks after of psychiatric illness were significantly associated with
injury (Henry et al., 2016). However, early ImPACT psychiatric outcomes.
scores (24–48 hours after injury) do not necessarily There is substantial overlap between common symp-
predict scores at a week postinjury (Sufrinko et al., 2017). toms of depression, such as fatigue, insomnia, and cog-
A recent systematic review of ImPACT showed that nitive complaints, and symptoms attributed to PCS. Over
reliability for most ImPACT composite scores was poor 85% of patients with depression without a history of head
to moderate, and might therefore be of limited utility in trauma endorse postconcussion-like symptoms (Iverson,
concussion assessment and management. In individuals 2006). Depression also has a significant effect on PCS
without a history of concussion, 22–46% experienced symptom reporting, as demonstrated in a study compar-
what was considered a reliable change on at least one ing patients with or without depression after mTBI and a
ImPACT subscore on serial assessments, and 40–80% group with depression without trauma (Suhr and
of all participants were misclassified on at least two of Gunstad, 2002; Lange et al., 2011). There is also consid-
three serial ImPACT testings for any given ImPACT erable overlap of symptoms of PCS and posttraumatic
composite. ImPACT should not be used as a stand-alone stress disorder (Lagarde et al, 2014). Although posttrau-
tool in assessing postconcussive status (Alsalaheen matic stress disorder occurs in mTBI not caused by
et al., 2016). sports, especially in the military (Gil et al., 2005; Hoge
Neuropsychologic testing may not correlate well et al., 2008), it is probably very uncommon after sports
with self-reported cognitive symptoms after concussion. concussion.
CLINICAL ASSESSMENT the SAC does not differ between concussed and noncon-
cussed athletes at 1 week postinjury. The BESS has been
Clinical evaluation of mTBI and PCS in sports is increas-
a popular clinical tool for measuring recovery after SRC,
ingly occurring earlier at the sidelines (see Chapter 8),
but it has shown poor sensitivity after 3 days postinjury
immediately following injury, but often occurs later in
(Finnoff et al., 2009; King et al., 2014; Murray
emergency rooms (see Chapter 9), primary care offices,
et al., 2014).
or specialty clinics (see Chapters 10 and 11). Early iden-
The PCSS is often used in serial assessments. It is a
tification of concussion and proper protocol-driven
22-item tool reflecting commonly encountered cogni-
management, including clearance to return to sports and
tive, physical, and affective symptoms in PCS, rated
other activities, increases the likelihood of a more rapid,
on a seven-point Likert scale (Pardini et al., 2004). This
uncomplicated recovery (Paniak et al., 2000; Mittenberg
instrument is part of the ImPACT test mentioned above
et al., 2001; Lane and Arciniegas, 2002; Ponsford et al.,
(Lovell and Maroon, 2000). In 2013 Meehan et al. dem-
2002; Willer and Leddy, 2006; Leddy et al., 2012). Those
onstrated that total PCSS score was independently asso-
with delayed diagnosis, inadequate management, and
ciated with symptoms persisting at least 28 days after
associated comorbidities make up a significant proportion
concussion in 182 pediatric sports concussion patients
of the group with more prolonged symptoms who present
of mean age 15.2 3.04 years. A 2014 study by Meehan
for later clinical evaluation. Accurate evaluation and
et al. showed that the majority of pediatric SRC patients
effective management of this late-phase posttraumatic dis-
(86%; 95% confidence interval 80–90%) with an initial
order can be a more complex, multidisciplinary process.
PCSS score of <13 experienced resolution of their
The first challenge in evaluating symptomatic
symptoms within 28 days of injury.
patients is determining the nature and severity of con-
The Rivermead Post-Concussion Symptom Ques-
cussion or brain injury, if one occurred at all. Subconcus-
tionnaire (Crawford et al., 1996) has also been widely
sive head injuries or other soft-tissue injuries, such as
used; if administered in the acute period, it can predict
cranial impact injuries and cervical injuries after whip-
endorsement of at least one PCS symptom in early
lash, can produce similar symptoms without brain injury
follow-up at 3–15 days (Ganti et al., 2016). The Pediatric
(Horn et al., 2013). A history of the injury, obtained not
Quality of Life Inventory and PedsQL Cognitive Func-
only from the patient but also from available bystanders,
tioning scale were recently studied in adolescent athletes
emergency responders, and other acute care providers, is
with concussion. Those who developed PCS had signif-
important. If available, videos of the event can be useful
icantly worse physical and cognitive performance at
in characterizing the injury and early consequences.
initial consultation (median of 6.5 days postinjury)
and a slower rate of recovery in these domains, compared
with those who recovered in less than 30 days (Russell
Screening tools
et al., 2017).
An increasing number of screening and diagnostic tools Saccadic eye movements, vergence, and smooth
are available for sideline and office assessment of post- pursuit are commonly negatively affected after mTBI,
concussive symptoms. These tests are described and but methods of assessment and clinical management
reviewed in greater detail in Chapters 10 and 11. Some have not yet been established (Hunt et al, 2016a). There
of the tools that are utilized in the assessment of uncom- is no widely accepted test that can universally identify all
plicated mTBI without PCS are also used for patients concussion-related vestibulo-ocular or related impair-
with presumed PCS. The acute diagnostic tests identified ments (Heinmiller and Gunton, 2016).
by the American Academy of Neurology (AAN) in its Aerobic treadmill testing, usually administered dur-
guidelines on the evaluation and management of concus- ing physical therapy evaluation, can also be incorporated
sion in sports include the Post-Concussion Symptom into clinical assessment of PCS symptom thresholds and
Scale (PCSS) and Graded Symptom Checklist, Standard- recovery. It may play a role in classifying sports-related
ized Assessment of Concussion (SAC), the Balance PCS into operational subtypes, as proposed by Ellis and
Error Scoring System (BESS), and the Sensory Organi- colleagues (2016).
zation Test (SOT) and formal neuropsychologic testing.
Both the BESS and SOT have low to moderate sensitivity
Clinical assessment and pathophysiologic
for concussion, while the remainder have better sensi-
subtypes of PCS
tivity and specificity (Giza et al., 2013).
These assessments have been studied in the early In the approach described by Ellis et al. (2016), clinical
phase of recovery, but their validity as clinical monitor- history, a systematic neurologic examination and aerobic
ing tools is more questionable. For example, McCrea and treadmill testing suggest pathophysiologic underpin-
colleagues (2003, 2005) concluded that performance on nings of persisting PCS symptoms defined in three or
more postconcussion disorders. Diagnosis of these Although this approach will need further validation
subtypes of PCS can inform clinical management of and support with diagnostic biomarkers and outcome
patients with a late-phase disorder. This conceptualiza- research, it represents a principled clinical protocol that
tion is largely empiric and the authors suggest a research may be useful for differential diagnosis and treatment.
agenda to evaluate this diagnostic schema.
The physiologic postconcussion disorder includes
NATURAL HISTORY AND PROGNOSIS
symptoms characteristic of acute concussion and is
worsened by physical or cognitive activity. It may be Following a brief period of unconsciousness or, at least,
mediated by a mismatch between the brain’s metabolic partially altered awareness, early-phase postinjury
needs and energy delivery capacity. In this group, a sub- disorder symptoms usually arise immediately or within
maximal exercise program could help to improve symp- hours. In a 2016 study by Henry and colleagues of
toms. Those with the physiologic subtype of mTBI 66 adolescents and young adults with SRC (age range
demonstrated worsened symptoms on graded exercise 14–23 years; 64% male), most postconcussion symp-
assessments such as the Buffalo Concussion Treadmill toms improved in the 2 weeks postinjury but in some
Test usually within 5–15 minutes of initial testing cases took up to 28 days to resolve fully as measured
(Leddy et al., 2013, 2015, 2016; Ellis et al., 2016). Those by ImPACT testing, PCSS, a modified Dizziness Hand-
with persisting PCS symptoms who are not symptomatic icap Inventory, and vestibulo-ocular examination and
with treadmill testing are assessed for vestibulo-ocular or were slower to improve after week 2. Males were more-
cervicogenic disorders. likely than females to be symptom-free by 4 weeks
The vestibulo-ocular postconcussion disorder may postinjury. The population studied was notable in that
represent pathologic functioning of both the vestibular all pre-existing neurologic or psychiatric diagnoses
and oculomotor systems for maintenance of balance, except migraine served as exclusion criteria.
postural control, and gaze stability. There may be objec- In a study by Iverson and colleagues (2015), adoles-
tive evidence of dysfunction in convergence, accommo- cent athletes reported symptoms of PCS at substantial
dation, smooth pursuits, saccades or vestubulo-ocular rates, even without a history of recent concussion.
reflexes, and BPPV. Patients may complain of dizziness, Gender and pre-existing conditions predicted PCS
gait instability, headaches triggered or worsened by symptoms in these uninjured high school athletes.
visually challenging activities, difficulty focusing, and Symptoms associated with PCS were reported in 19%
intermittent blurred vision or diplopia. Vestibular or of boys and 28% of girls in the absence of concussion,
vision-based physical therapy may be of benefit depend- with much higher rates in those with pre-existing
ing on the underlying etiology (Ellis et al., 2016). conditions – 60–82% of boys and 73–97% of girls –
The cervicogenic postconcussion disorder may derive including depression, preinjury migraines, substance
from dysfunction of the complex sensory and autonomic use, and attention deficit-hyperactivity disorder (Iverson
interconnections between the spinal cord, brainstem, et al., 2015).
and cerebellum as they mediate dynamic head, neck, The usual trajectory of recovery of symptoms after
and eye positions. Cervical muscle spasm may also play mTBI evolves over days to weeks and the vast majority
a role in symptoms such as cervicogenic headaches and recover from the early-phase postinjury disorder by
occipital neuralgia. Associated symptoms include neck 3 months (Kashluba et al., 2004). A small subset have
pain, neck stiffness, dizziness with activity, occipital persisting symptoms and a late-phase postinjury disorder
headaches (even occipital neuralgia), and fatigue or (Ruff, 2011). One often-cited prospective study by
fogginess. Evaluation of paraspinal and suboccipital Rutherford et al. (1979) reported that 15% of patients
muscles, cervical range of motion, cervical dizziness, hospitalized with mTBI had persisting PCS symptoms
and palpation of the greater and lesser occipital nerves at 1 year or more. Although 15% had one symptom
should be incorporated into the examiner’s assessment. or more at 1 year, the percentage dropped to less than
Cervical spine rehabilitation is recommended for this 5% in those with multiple (four or more) symptoms.
group (Ellis et al., 2016). A recent study by Dikmen and colleagues (2017)
New-onset or worsened migraine headaches after reported three or more symptoms at 1 year in 53–55%
concussion characterize a fourth group, which may of 336 patients with mTBI of all etiologies, compared
benefit from a submaximal exercise regimen and tradi- to 27% in non-TBI trauma controls. However, inclusion
tional pharmacologic treatments for migraine. Among criteria requiring a period of loss of consciousness, post-
members of this subgroup, both graded aerobic treadmill traumatic amnesia over 1 hour, or CT abnormalities
testing and formal neuropsychologic testing were recom- describe more severe injuries than is typical among those
mended by Ellis et al. (2016) in determining medical with SRC. In a series of 64 adults with sports concussion
clearance. followed prospectively, the mean duration of symptoms
was 32 days ( 48 days) and early PCSS score predicted more important than the brain injury in explaining the
more prolonged symptoms (Meehan et al., 2016). Over- clinical symptoms as they extend from days and weeks
all, the proportion with persistent PCS symptoms and a to months and years postinjury. The lack of specificity
late-phase posttraumatic disorder after sports concussion of concussion to persisting symptoms of PCS has been
is probably very low, but further prospective studies are reported in a number of studies, including some demon-
necessary to clarify the risk. strating that late symptoms attributed to PCS are simi-
In general, SRC confers a better outcome than mTBI larly prevalent after mTBI and trauma without brain
associated with motor vehicle accidents or other injury (such as mild orthopedic injuries), especially
mechanisms (Ponsford et al., 2000). This may relate to when eliminating other confounds such as litigation
a number of factors. including younger age, better condi- (Mickeviciene et al., 2004).
tioning, better health status and, perhaps, more incentive
to achieve baseline functional status. SRC is less likely
Differential diagnosis and factors
associated with multiple concomitant orthopedic, skin,
contributing to late-phase posttraumatic
and soft-tissue injuries predisposing to chronic pain
disorder
and loss of physical functioning. SRCs also tend to lack
the life-threatening aspects of injury causes such as com- For any set of ongoing late-phase symptoms and loss
bat, assault, or motor vehicle accidents that predispose to of function, the clinician should assess for multiple
posttraumatic stress disorder and other psychologic potential etiologies, including contributions from coex-
traumas (Carroll et al., 2004; Stulemeijer et al., 2006, isting mood disorders, chronic pain syndromes, vestibu-
2008; Jacobs et al., 2010). lar dysfunction, musculoskeletal injuries, psychosocial
stressors, and personality factors such as resilience.
A comprehensive medical, surgical, family, and social
Transition from early- to late-phase
history, including a detailed description of preinjury
posttraumatic disorder
social, occupational, and academic functioning, is criti-
The transition from early- to late-phase posttraumatic cal to account for multiple potential contributing factors.
disorder is not clearly defined in timing or symptom Mood and anxiety disorders are among the most
profiles (Katz et al., 2015). Although there is consider- common contributors to late-phase symptoms. Any his-
able overlap, early- and late-phase symptom profiles tory of depressed mood, anxiety, irritability, attention or
after mTBI probably have different characteristics concentration difficulties, fatigue, and sleep disturbance
(Rees, 2003). Physical symptoms, most commonly head- should be explored. These could all indicate a diagnosis
ache and dizziness, are predominant in the early phase of depression, anxiety disorder, adjustment disorder,
(1–2 weeks) and emotional disturbances are more likely posttraumatic stress disorder, or other psychiatric disor-
in the later phase (4–8 weeks) (Yang et al., 2007). ders. A history of mood disturbance may precede the
Dischinger et al. (2009) evaluated mTBI admissions to injury, or emerge as a consequence. Athletes can have
a trauma service at 3–10 days and at 90 days after injury; particular psychosocial stressors during concussion
prevalence of physical symptoms declined more rapidly recovery, such as alienation from desired social experi-
than emotional and cognitive symptoms. ences, interruption of roles as player and teammate,
Symptoms associated with a late-phase posttraumatic and deterioration in academic performance. Prolonged
disorder should evolve from an early-phase postinjury disability after concussion can lead to adjustment
disorder to be considered related at all to the injury. It difficulties and mood disorder associated with a di-
is a common diagnostic pitfall to misattribute symptoms minished sense of self and identity (Charmaz, 2002;
after injury to PCS even if symptom onset occurs after a Fenech, 2013). Depression can influence multiple
considerable gap in time postinjury. As the Berlin and symptoms attributed to PCS (Trahan et al., 2001; Suhr
Zurich consensus conferences emphasize, PCS after and Gunstad, 2002; Garden and Sullivan, 2010), in-
sports injury is a graded set of clinical symptoms follow- cluding deficits on neuropsychologic testing (Zakzanis
ing a “sequential course,” prolonged in a small percent- et al., 1998; Austin et al., 1999; McDermott and
age (McCrory et al., 2017), not a course associated with Ebmeier, 2009). Symptoms and neuropsychologic
late onset of symptoms. impairments can be clinically indistinguishable between
Although the early-phase symptoms after concussion depression and mTBI.
have a closer link to the injury, the later-phase symptoms Factitious disorder and malingering should be consid-
are less clearly directly associated with the concussion ered with any neurologic complaints that may lack objec-
and concomitant injuries. The concussion itself may no tive signs or atypical symptoms, and in persons who
longer be a factor causing the prolongation of PCS symp- display exaggeration of symptoms, inconsistent neuro-
toms. Other comorbid and premorbid factors tend to be logic examination findings, and a discrepancy between
reported distress and objective findings. Factitious not be directly related to the injury. The timing of
disorders involve the deliberate reporting of false symp- early-phase symptoms should be considered in attribut-
toms, exaggeration of minor symptoms, or even the sur- ing etiology. Chronic pain from musculoskeletal injuries
reptitious induction of self-harm (“making oneself or other disorders is a common factor that may prolong
sick”). There is little or no reward other than the attention other PCS symptoms such as insomnia, irritability,
and sympathy of others and administration of symptom- fatigue, and cognitive disturbance. Vestibular symptoms,
relevant treatment. Malingering involves similar behav- potentially from disorders of the inner ear, cervical
iors, but the reward is not intrinsic to having an ill injuries, or migraines, may also worsen and prolong late
or injured status and instead relates to rewards such as symptoms. Endocrine disorders such as hypothyroidism
monetary gain and freedom from work, school, or finan- can mimic many of the somatic, mood, and cognitive
cial responsibilities. The DSM-IV (American Psychiatric symptoms of both TBI and depression (Davis and
Association, 2000) describes the distinction as follows: Tremont, 2007). Concurrent use of illicit substances or
“Malingering differs from factitious disorder [by proxy] alcohol abuse can mimic and exacerbate the cognitive,
in that motivation for the symptom production in mood, and behavioral disturbances attributed to PCS.
Malingering is an external incentive, whereas in Facti- Undiagnosed structural lesions, or a more severe brain
tious Disorder external incentives are absent.” The risk injury than initially diagnosed, are possible consider-
of encountering a malingering patient is increased in a ations in those with prolonged symptoms. Structural
medicolegal context, poor compliance with evaluation lesions on routine neuroimaging are uncommon after
and treatment, or a history of antisocial personality concussion. Focal findings on examination and persis-
disorder (Guilmette, 2013). tent symptoms such as headache are a frequent justifica-
Efforts are currently underway to efficiently identify tion for brain imaging such as magnetic resonance
patients who are manipulating symptom reporting, imaging (MRI) in the postacute setting, but reveal a very
especially in military populations (Dretsch et al., 2017; low incidence of abnormalities and an even lower
Lippa et al., 2017). As baseline neurocognitive testing incidence of abnormalities for which an intervention
becomes more routine within athletic programs, clini- would be indicated (Morgan et al., 2015). Brain MRI
cians and researchers have also examined the notion should be considered in PCS patients who present with
that athletes could paradoxically attempt to underper- a history of abnormal CT findings, focal neurologic
form on baseline testing for the purposes of being cleared deficits, or seizures. Other brain imaging techniques such
to return to play sooner, despite the presence of ongoing as diffusion tensor imaging, functional MRI, quantitative
postconcussive signs and symptoms. Systems can be cerebral blood flow sequences, and cerebrovascular
developed to detect such purposeful underperformance. reactivity mapping are important research tools, but
A study by Siedlik et al. in 2016 examined the perfor- currently are not a part of routine clinical management
mance of 20 male collegiate rugby players who were of PCS (Ellis et al., 2016).
instructed to intentionally underperform on ImPACT
without making their attempts to score poorly obvious.
Risk factors for developing a late-phase
ImPACT detected 70% of malingering attempts using
disorder
internal validation measures, and clinician reviewers
identified 80% of malingering attempts. Underreporting A number of risk factors may prolong PCS symptoms,
of concussive events or symptoms after concussion including: older age of injury (King, 2014), high school
is another problem that defies detection in athletes. age of play or younger, female sex, attention deficit-
McCrea et al. (2004) studied a group of Wisconsin hyperactivity disorder, learning disabilities, and spe-
varsity high school football players who reported con- cific symptoms such as cognitive deficits, headaches,
cussions only 47.3% of the time. A significant dizziness and disequilibrium, mood disorders, and
proportion (41%) with identified concussion failed to disturbances of oculomotor functioning (Table 17.2).
report symptoms in an effort to avoid being withheld GRIN2A promotor polymorphisms (McDevitt et al.,
from competition. 2015), and SLC17A7 promotor variations (Madura
Differential diagnosis of the clinical features associ- et al., 2016) have been shown in prospective cohort
ated with PCS should include a number of consider- studies to be associated with longer recovery times after
ations. Headache is a common symptom and a primary SRC. ApoE4 genotype (Merritt et al., 2016) has been
headache disorder is a possibility, both as a premorbid associated with more severe symptom reporting after
condition, exacerbated by injury, and as a headache SRC. Early headache and dizziness increased the
condition of new onset. New onset of migraine and other chance of symptoms at 1 month postinjury in a general
primary headache disorders is particularly common mTBI sample (Savola and Hillbom, 2003). Significant
among adolescents and young adults, and may or may symptoms at 6 months postinjury correlated with
Table 17.2
Factors mediating risk of posttraumatic disorder (early and late phase)
Pre-existing factors Injury characteristics Postinjury factors
Prior traumatic brain injury Early symptom burden Adjustment (psychosocial, personality factors)
Psychiatric disease Nonsports-related context Malingering
Personality disorder Factitious disorder
Headache disorder Treatment compliance
Attention deficit-hyperactivity disorder Litigation
Genetics Employment status
Younger age
Female gender
complaints of headache, dizziness, and nausea in the Although a history of prior mTBI was a risk factor for
emergency room following an mTBI of all causes longer PCS in some studies, the extent of the influence of
(De Kruijk et al., 2002). A multivariate analysis identi- prior injury is unclear among athletes and in the general
fied postinjury anxiety, noise sensitivity, and female population. Apart from the risk of so-called second-
gender as a cluster of predictors with the highest proba- impact syndrome, the occurrence of a repeat concussion
bility of later symptoms (Dischinger et al., 2009). shortly after a previous concussion may be particularly
The 5th International Conference of Concussion in problematic in worsening and extending symptoms
Sport concluded that the severity of symptoms in the (Guskiewicz et al., 2000, 2003; Giza et al., 2013). The
first or initial few days after SRC is the “strongest and recent 5th International Conference acknowledged that
most consistent predictor” of slowed recovery, while multiple past mTBIs are associated with increased
minimal symptoms on the first day conferred a favor- “physical, cognitive and emotional symptoms” before
able prognosis (McCrory et al., 2017). In line with this participation in a sporting season, although the specific
statement, several studies of athletes presenting to sports symptoms most suggestive of poor outcome or pro-
concussion clinics found that early symptom burden longed recovery are still a subject of debate (McCrory
predicted more prolonged symptoms after SRC (Lau et al., 2017).
et al., 2009; Meehan et al., 2014). Lau et al. (2009), using Pre-existing and postinjury psychiatric conditions are
computerized cognitive testing in male high school associated with a higher risk of prolonged PCS symp-
football players, also found that those with symptoms toms (Greiffenstein and Baker, 2001; Mooney and
lasting over 10 days were more likely to show relative Speed, 2001; Evered et al., 2003; Meares et al., 2006).
deficits with visual memory and processing speed. In a Anxiety in particular may increase the likelihood of
later study, longer recovery occurred in those with reporting of PCS symptoms (Ponsford et al., 2000;
primarily migrainous complaints associated with slowed Mooney and Speed, 2001; Snell et al., 2010; Cooper
reaction times and increased visual and/or verbal et al., 2011; King and Kirwilliam, 2011), which may in
memory impairment (Lau et al., 2011). Risk factors for turn increase an individual’s degree of anxiety (Kay
more prolonged symptoms included unconsciousness, et al., 1992; Bay and de-Leon, 2011). A history of psy-
posttraumatic amnesia, and more severe acute symptoms chiatric conditions or headaches is an important risk
in a prospectively studied group of 570 high school factor for >1 month of symptoms among youth with
and college athletes, who experienced concussion and SRC (McCrory et al., 2017). Personality features such
took longer to recover (10% of the group) (McCrea as histrionic, narcissistic, and compulsive personality
et al., 2013). disorders appear to increase the risk (Evered et al.,
The AAN guidelines on the evaluation and manage- 2003). Psychosocial stress factors also play an important
ment of concussion in sports concluded that a prior role in symptom prolongation (Kay et al., 1992; Ruff
history of concussion is likely associated with more et al., 1996; Evered et al., 2003; Wood, 2004).
severe and longer-lasting symptoms (Giza et al., 2013). Those with symptoms lasting beyond 3 months are
The AAN guidelines identified probable risk factors more likely to plateau in their trajectory of improvement
for prolonged recovery, including younger age of play, (Kashluba et al., 2008; McLean et al., 2009; Snell et al.,
early posttraumatic headache, fatigue, early amnesia, 2010). Although patients may demonstrate recovery in
alteration in mental status, and disorientation. Possible the 3–12-month postinjury period, if symptoms persist
risk factors included dizziness, playing the position of beyond 1 year, total remission is much less likely among
quarterback in American football, and wearing a half- patients who continue to present for care, even when
face shield in ice hockey. confounding factors such as litigation are no longer
involved (Fee and Rutherford, 1988; Packard, 1992). can facilitate recovery. For patients with persistent symp-
Tiersky et al. (2005) reported that clinical improvement toms, the consensus statement recommends a “detailed,
with cognitive behavioral therapy was less significant multimodal clinical assessment” aimed at the identifica-
between 3 and 6 months than between 1 and 3 months tion of both primary and secondary pathologies that may
on a prospectively followed group of 20 adults with be underlying the persisting symptoms. There is early
mTBI; however, only one member of this group had evidence to support the use of several therapies, includ-
an SRC. ing aerobic exercise in patients with persistent PCS who
In 2010 Barlow et al. prospectively followed 670 are thought to have clinically significant deconditioning
children (mean ages 7.62 and 9.44 years) in a consecutive or autonomic instability. If there is cervical spine pathol-
controlled cohort study of patients presenting to an ogy or vestibular dysfunction, physical therapy targeting
emergency department with concussion or extracranial these specific pathologies may be of benefit. Finally, if
injury. Approximately 25% of the mTBI group was mood or behavioral issues are prominent, psychotherapy,
injured while playing sports. Nine percent of children particularly cognitive behavioral therapy, may be benefi-
with mTBI met ICD criteria for PCS at 3 months; approx- cial (Al-Sayegh et al., 2010; McCrory et al., 2017). How-
imately 21% remained symptomatic at 1 year. ever, the statement underscores that there is limited
evidence to support use of pharmacotherapy and warns
that pharmacotherapy should be considered carefully
TREATMENT
in athletes who are returning to play.
Successful treatment of PCS involves early postconcus-
sion management and includes assessment, recognition
CONCLUSIONS
of early complications, education about symptoms
and expectations for recovery, recommendations for PCS remains controversial because of its lack of specific-
activity modifications, and follow-up assessment. These ity to concussion, particularly at times more remote from
interventions are key to successful recovery and mini- the injury. There is no consensus for its definition, and
mizing the risk of early-phase symptoms evolving to limited understanding of its epidemiology, pathophysiol-
a late-phase disorder with more prolonged symptoms. ogy, time course, and prognosis. It may be more useful to
Treatment of persisting symptoms in a late-phase divide postconcussion symptoms into early- and late-
disorder involves thoughtful differential diagnosis, con- phase posttraumatic disorders. The early-phase disorder
sideration of comorbid and premorbid conditions, and is more clearly causally linked to TBI, whereas late-
other factors that may impact symptoms. A hierarchic, phase symptoms lack specificity and are often driven
sequential approach to symptom management should by comorbid or noninjury conditions. Early-phase symp-
be undertaken, emphasizing problems with a signifi- toms are more commonly somatic or cognitive and
cant impact on the late-phase symptom profile and those include dizziness, headache, imbalance, fatigue, sleep
with available, effective treatments (e.g., depression, disruption, impaired cognition, photophobia, and phono-
anxiety, insomnia, headache, and vertigo). A program phobia. Autonomic dysfunction likely contributes to
of exercise, avoiding levels above the symptom thresh- early-phase symptoms and exacerbations with activity
old, is of benefit for those with both early- and late-phase and exertion. Late-phase symptoms feature a greater
disorders after concussion (Willer and Leddy, 2006; impact of emotional factors on the symptom profile,
Leddy et al., 2010, 2013; Baker et al., 2012). but chronic headaches, other pain problems, vestibular
Recent literature reviews examining interventions for problems, and disequilibrium are also common factors.
PCS meant to speed recovery or ameliorate prolonged Cognitive problems more likely emerge as a result
PCS symptoms concluded that there is no evidence to of these other factors in the late-phase disorder. The tran-
support the use of any particular treatment (Burke sition between early- and late-phase disorders is not well
et al., 2015). However, the recent consensus statement defined temporally or symptomatically. Risk factors for
on concussion in sport (McCrory et al., 2017) describes developing a late-phase disorder include elevated early
a clinical approach capturing emerging, evidence-based symptom burden, a history of multiple concussions,
support for multimodal, symptom-guided plans of care. comorbid or premorbid psychiatric conditions, longer
Recognizing that SRC can cause a number of symptoms duration of unconsciousness or amnesia, and younger
and problems, including injury to the cervical spine age of play.
and vestibular system, they argue that existing data Treating providers should construct a thoughtful
provide support for specific interventions, including differential diagnosis, mindful of potentially coexisting
cervical and vestibular rehabilitation, as well as psycho- mood, sleep, and primary headache disorders; musculo-
logic treatment. In contrast to previous statements, the skeletal injuries, vestibular pathology; undiagnosed
authors now report that data indicate that controlled, structural lesions; and other complications, especially
subsymptom-threshold, submaximal exercise programs when evaluating individuals with a late-phase disorder.
Successful early-phase treatment should include educa- American Psychiatric Association (2000). Diagnostic and sta-
tion about symptoms and recovery, recommendations tistical manual of mental disorders, 4th ed.American
for activity modifications, graded return to activities Psychiatric Association, Washington DC.
(including a program of subsymptom threshold exer- American Psychiatric Association (2013). The diagnostic and
statistical manual of mental disorders, 5th ed.American
cise), and follow-up assessment. In those with late-phase
Psychiatric Association, Arlington, VA.
disorder, clinicians should institute a hierarchic, sequen-
Arendt-Nielsen L, Laursen RJ, Drewes AM (2000). Referred
tial approach to symptom management, emphasizing pain as an indicator for neural plasticity. Prog Brain Res
problems with a significant functional impact and 129: 343–356.
available, effective treatments. Asken BM, Snyder AR, Clugston JR et al. (2017). Concussion-
Further research focusing on biomarkers, epidemiol- like symptom reporting in non-concussed collegiate ath-
ogy, symptom profiles, natural history, prognosis, and letes. Arch Clin Neuropsychol: 1–9.
treatment will need to clarify the disorders now referred Austin MP, Mitchell P, Wilhelm K et al. (1999). Cognitive
to as PCS, and to elucidate the distinctions and transition function in depression: a distinct pattern of frontal impair-
between the early- and late-phase posttraumatic disor- ment in melancholia? Psychol Med 29: 73–85.
ders. Protein biomarkers such as MAP-2 (as a marker Baker JG, Freitas MS, Leddy JJ et al. (2012). Return to full
functioning after graded exercise assessment and progres-
of axonal damage) and CNPase (as a marker of oligoden-
sive exercise treatment of postconcussion syndrome.
drocyte activity) show promise as correlates of chronic
Rehabil Res Pract 2012: 705309.
postconcussive symptomatology (Broglio et al., 2017). Barlow KM, Crawford S, Stevenson A et al. (2010).
Another protein biomarker study that merits further Epidemiology of postconcussion syndrome in pediatric
study is neurofilament light protein that has been demon- mild traumatic brain injury. Pediatrics 126 (2):
strated to correlate with a late-phase posttraumatic e374–e381.
disorder in athletes with symptoms more than 1 year after Bay E, de-Leon MB (2011). Chronic stress and fatigue-related
injury, as well as with a greater number of lifetime con- quality of life after mild to moderate traumatic brain injury.
cussions (Shahim et al., 2016). Significantly lower cere- J Head Trauma Rehabil 26: 355–363.
brospinal fluid beta-amyloid levels were also seen in this Bleiberg J, Cernich AN, Cameron K et al. (2004). Duration of
population. Multimodal neuroimaging, using structural cognitive impairment after sports concussion. Neurosurgery
54: 1073–1078; discussion 1078–1080.
and functional imaging tools, is also potentially impor-
Boake C, McCauley SR, Levin HS et al. (2004). Limited agree-
tant as a biomarker to improve detection and understand-
ment between criteria-based diagnoses of postconcussional
ing of early and late symptoms after concussion (Broglio syndrome. J Neuropsychiatry Clin Neurosci 16: 493–499.
et al., 2017). Further study is necessary to develop more Broglio SP, McCrea M, McAllister T et al. (2017). A national
sensitive, reliable concussion assessment tools to track study on the effects of concussion in collegiate athletes and
natural history, trajectory of recovery and response to US military service academy members: the NCAA-DoD
treatment, such as the efforts underway by the National Concussion Assessment, Research and Education (CARE)
Collegiate Athletic Association–Department of Defense consortium structure and methods. Sports Med 47:
Concussion Assessment, Research and Educatio consor- 1437–1451.
tium (McCrea et al., 2005; Broglio et al., 2017) Assess- Burke MJ, Fralick M, Nejatbakhsh N et al. (2015). In search of
ments should involve more than symptom reporting and evidence-based treatment for concussion: characteristics of
current clinical trials. Brain Inj 29: 300–305.
objectively reflect clinical features such as cognitive
Carroll LJ, Cassidy JD, Peloso PM et al. (2004). Prognosis for
impairment, postural stability, and oculovestibular
mild traumatic brain injury: results of the WHO
functioning. Further research is also needed to clarify Collaborating Centre Task Force on Mild Traumatic
the individual and interacting contributions of risk fac- Brain Injury. J Rehabil Med (43 Suppl): 84–105.
tors for the development of late-phase posttraumatic dis- Charmaz K (2002). The self as habit: the reconstruction of self
orders after concussion and interventions that may in chronic illness. OTJR 22 (1 suppl): 31S–41S.
modify these risks and improve outcomes. Clausen M, Pendergast DR, Willer B et al. (2016). Cerebral
blood flow during treadmill exercise is a marker of physi-
ological postconcussion syndrome in female athletes.
REFERENCES
J Head Trauma Rehabil 31: 215–224.
Alsalaheen B, Stockdale K, Pechumer D et al. (2016). Cooper DB, Kennedy JE, Cullen MA et al. (2011). Association
Measurement error in the Immediate Postconcussion between combat stress and post-concussive symptom
Assessment and Cognitive Testing (ImPACT): systematic reporting in OEF/OIF service members with mild traumatic
review. J Head Trauma Rehabil 31: 242–251. brain injuries. Brain Inj25: 1–7. https://doi.org/
Al-Sayegh A, Sandford D, Carson AJ (2010). Psychological 10.3109/02699052.2010.531692.
approaches to treatment of postconcussion syndrome: a Couch JR, Bearss C (2001). Chronic daily headache in the
systematic review. J Neurol Neurosurg Psychiatry 81: posttrauma syndrome: relation to extent of head injury.
1128–1134. Headache 41: 559–564.
Crawford S, Wenden FJ, Wade DT (1996). The Rivermead Giza CC, Kutcher JS, Ashwal S et al. (2013). Summary of
head injury follow up questionnaire: a study of a new rating evidence-based guideline update: evaluation and manage-
scale and other measures to evaluate outcome after head ment of concussion in sports: report of the Guideline
injury. J Neurol Neurosurg Psychiatry 60: 510–514. Development Subcommittee of the American Academy
Davis JD, Tremont G (2007). Neuropsychiatric aspects of of Neurology. Neurology 80: 2250–2257.
hypothyroidism and treatment reversibility. Minerva Greiffenstein FM, Baker JW (2001). Comparison of premorbid
Endocrinol 32: 49–65. and postinjury MMPI-2 profiles in late postconcussion
De Kruijk JR, Leffers P, Menheere PP et al. (2002). Prediction claimants. Clin Neuropsychol 15: 162–170.
of post-traumatic complaints after mild traumatic brain Guilmette T (2013). The role of clinical judgment in symptom
injury: early symptoms and biochemical markers. validity assessment. Mild traumatic brain injury: symptom
J Neurol Neurosurg Psychiatry 73: 727–732. validity assessment and malingering, Springer, New York,
Dikmen S, Machamer J, Fann JR et al. (2010). Rates of symp- NY.
tom reporting following traumatic brain injury. J Int Guskiewicz KM, Weaver NL, Padua DA et al. (2000).
Neuropsychol Soc 16: 401–411. Epidemiology of concussion in collegiate and high school
Dikmen S, Machamer J, Temkin N (2017). Mild traumatic football players. Am J Sports Med 28: 643–650.
brain injury: longitudinal study of cognition, functional sta- Guskiewicz KM, McCrea M, Marshall SW et al. (2003).
tus, and post-traumatic symptoms. J Neurotrauma 34: Cumulative effects associated with recurrent concussion
1524–1530. in collegiate football players: the NCAA concussion study.
Dischinger PC, Ryb GE, Kufera JA et al. (2009). Early predic- JAMA 290: 2549–2555.
tors of postconcussive syndrome in a population of trauma Haas DC (1996). Chronic post-traumatic headaches classified and
patients with mild traumatic brain injury. J Trauma 66: compared with natural headaches. Cephalalgia 16: 486–493.
289–296; discussion 296–287. Heinmiller L, Gunton KB (2016). A review of the current prac-
Dretsch MN, Williams K, Staver T et al. (2017). Evaluating the tice in diagnosis and management of visual complaints
clinical utility of the Validity-10 for detecting amplified associated with concussion and postconcussion syndrome.
symptom reporting for patients with mild traumatic brain Curr Opin Ophthalmol 27: 407–412.
injury and comorbid psychological health conditions. Henry LC, Elbin RJ, Collins MW et al. (2016). Examining
Appl Neuropsychol Adult 24: 376–380. recovery trajectories after sport-related concussion with a
Ellis MJ, Ritchie LJ, Koltek M et al. (2015). Psychiatric out- multimodal clinical assessment approach. Neurosurgery
comes after pediatric sports-related concussion. 78: 232–241.
J Neurosurg Pediatr 16: 709–718. Hoge CW, McGurk D, Thomas JL et al. (2008). Mild traumatic
Ellis MJ, Leddy J, Willer B (2016). Multi-disciplinary manage- brain injury in U.S. soldiers returning from Iraq. N Engl
ment of athletes with post-concussion syndrome: an evolv- J Med 358: 453–463.
ing pathophysiological approach. Front Neurol 7: 136. Horn LJ, Siebert B, Patel N et al. (2013). Headache. In:
Evered L, Ruff R, Baldo J et al. (2003). Emotional risk factors ND Zasler, DI Katz, RD Zafonte (Eds.), Brain injury med-
and postconcussional disorder. Assessment 10: 420–427. icine, 3rd edn Demos Medical Publishing, New York, NY,
Faux S, Sheedy J (2008). A prospective controlled study in the pp. 932–953.
prevalence of posttraumatic headache following mild trau- Hunt AW, Mah K, Reed N et al. (2016a). Oculomotor-based
matic brain injury. Pain Med 9: 1001–1011. vision assessment in mild traumatic brain injury: a system-
Fee CR, Rutherford WH (1988). A study of the effect of legal atic review. J Head Trauma Rehabil 31: 252–261.
settlement on post-concussion symptoms. Arch Emerg Hunt AW, Paniccia M, Reed N et al. (2016b). Concussion-like
Med 5: 12–17. symptoms in child and youth athletes at baseline: what is
Fenech AM, Shaw Fisher K (2013). Lifelong and therapeutic "typical"? J Athl Train 51: 749–757.
recreation and leisure, Demos Medical Publishing, New Iverson GL (2006). Misdiagnosis of the persistent postconcus-
York, NY. sion syndrome in patients with depression. Arch Clin
Finnoff JT, Peterson VJ, Hollman JH et al. (2009). Intrarater Neuropsychol 21: 303–310.
and interrater reliability of the Balance Error Scoring Iverson GL, Rael TL, Gaetz MB et al. (2013). Mild traumatic
System (BESS). PMR 1: 50–54. brain injury. In: ND Zasler, DI Katz, R Zafonte (Eds.),
Gall B, Parkhouse WS, Goodman D (2004). Exercise following Brain injury medicine: principles and practice, 2nd edn.
a sport induced concussion. Br J Sports Med 38: 773–777. Demos Medical Publishing, New York, NY.
Ganti L, Daneshvar Y, Ayala S et al. (2016). The value of neu- Iverson GL, Silverberg ND, Mannix R et al. (2015). Factors
rocognitive testing for acute outcomes after mild traumatic associated with concussion-like symptom reporting in high
brain injury. Mil Med Res 3: 23. school athletes. JAMA Pediatr 169: 1132–1140.
Garden N, Sullivan KA (2010). An examination of the base Jacob S, Saha A, Rajabally Y (2008). Post-traumatic short-
rates of post-concussion symptoms: the influence of demo- lasting unilateral headache with cranial autonomic symp-
graphics and depression. Appl Neuropsychol 17: 1–7. toms (SUNA). Cephalalgia 28: 991–993.
Gil S, Caspi Y, Ben-Ari IZ, Koren D et al. (2005). Does mem- Jacobs B, Beems T, Stulemeijer M et al. (2010). Outcome pre-
ory of a traumatic event increase the risk for posttraumatic diction in mild traumatic brain injury: age and clinical vari-
stress disorder in patients with traumatic brain injury? ables are stronger predictors than CT abnormalities.
A prospective study. Am J Psychiatry 162: 963–969. J Neurotrauma 27: 655–668.
Kashluba S, Paniak C, Blake T et al. (2004). A longitudinal, Leddy JJ, Cox JL, Baker JG et al. (2013). Exercise treatment
controlled study of patient complaints following treated for postconcussion syndrome: a pilot study of changes in
mild traumatic brain injury. Arch Clin Neuropsychol 19: functional magnetic resonance imaging activation, physi-
805–816. ology, and symptoms. J Head Trauma Rehabil 28:
Kashluba S, Paniak C, Casey JE (2008). Persistent symptoms 241–249.
associated with factors identified by the WHO Task Force Leddy JJ, Baker JG, Merchant A et al. (2015). Brain or strain?
on Mild Traumatic Brain Injury. Clin Neuropsychol 22: Symptoms alone do not distinguish physiologic concussion
195–208. from cervical/vestibular injury. Clin J Sport Med 25:
Katz DI, Cohen SI, Alexander MP (2015). Mild traumatic 237–242.
brain injury. Handb Clin Neurol 127: 131–156. Leddy JJ, Baker JG, Willer B (2016). Active rehabilitation of
Kay TNB, Cavallo M, Ezrachi O et al. (1992). Toward a neu- concussion and post-concussion syndrome. Phys Med
ropsychological model of functional disability after mild Rehabil Clin N Am 27: 437–454.
traumatic brain injury. Neuropsychology 6: 371–384. Levin HS, Mattis S, Ruff RM et al. (1987). Neurobehavioral
King NS (2014). A systematic review of age and gender factors outcome following minor head injury: a three-center study.
in prolonged post-concussion symptoms after mild head J Neurosurg 66: 234–243.
injury. Brain Inj 28: 1639–1645. Levin HS, McCauley SR, Josic CP et al. (2005). Predicting
King NS, Kirwilliam S (2011). Permanent post-concussion depression following mild traumatic brain injury. Arch
symptoms after mild head injury. Brain Inj 25: 462–470. Gen Psychiatry 62: 523–528.
King ML, Lichtman SW, Seliger G et al. (1997). Heart-rate Lew HL, Lin PH, Fuh JL et al. (2006). Characteristics and
variability in chronic traumatic brain injury. Brain Inj 11: treatment of headache after traumatic brain injury: a
445–453. focused review. Am J Phys Med Rehabil 85: 619–627.
King LA, Horak FB, Mancini M et al. (2014). Instrumenting Lippa SM, Lange RT, French LM et al. (2017). Performance
the balance error scoring system for use with patients validity, neurocognitive disorder, and post-concussion
reporting persistent balance problems after mild traumatic symptom reporting in service members with a history of
brain injury. Arch Phys Med Rehabil 95: 353–359. mild traumatic brain injury. Arch Clin Neuropsychol:
Kraus J, Shafer K, Ayers K (2005). Physical complaints med- 1–13.
ical service use and social and employment changes fol- Lovell M, Maroon J (2000). ImPACT: Immediate Post-
lowing mild traumatic brain injury: a 6-month Concussion Assessment and Cognitive Testing,
longitudinal study. J Head Trauma Rehabil 20: 239–256. NeuroHealth Systems, Pittsburgh, PA.
Lagarde E, Salmi LR, Holm LW et al. (2014). Association of Lucas S, Blume HK (2017). Sport-related headache. Neurol
symptoms following mild traumatic brain injury with post- Clin 35: 501–521.
traumatic stress disorder vs. postconcussion syndrome. Madura SA, McDevitt JK, Tierney RT et al. (2016). Genetic
JAMA Psychiatry 71 (9): 1032–1040. variation in SLC17A7 promoter associated with response
Lane JC, Arciniegas DB (2002). Post-traumatic headache. to sport-related concussions. Brain Inj 30: 908–913.
Curr Treat Options Neurol 4: 89–104. Matharu MJ, Goadsby PJ (2001). Post-traumatic chronic par-
Lange RT, Iverson GL, Rose A (2011). Depression strongly oxysmal hemicrania (CPH) with aura. Neurology 56 (2):
influences postconcussion symptom reporting following 273–275.
mild traumatic brain injury. J Head Trauma Rehabil 26: McCauley SR, Boake C, Pedroza C et al. (2005).
127–137. Postconcussional disorder: are the DSM-IV criteria an
Lau B, Lovell MR, Collins MW et al. (2009). Neurocognitive improvement over the ICD-10? J Nerv Ment Dis 193:
and symptom predictors of recovery in high school athletes. 540–550.
Clin J Sport Med 19: 216–221. McCrea M, Guskiewicz KM, Marshall SW et al. (2003). Acute
Lau BC, Collins MW, Lovell MR (2011). Sensitivity and spec- effects and recovery time following concussion in colle-
ificity of subacute computerized neurocognitive testing and giate football players: the NCAA concussion study.
symptom evaluation in predicting outcomes after sports- JAMA 290: 2556–2563.
related concussion. Am J Sports Med 39: 1209–1216. McCrea M, Hammeke T, Olsen G et al. (2004). Unreported
Leddy JJ, Kozlowski K, Fung M et al. (2007). Regulatory and concussion in high school football players: implications
autoregulatory physiological dysfunction as a primary for prevention. Clin J Sport Med 14: 13–17.
characteristic of post concussion syndrome: implications McCrea M, Barr WB, Guskiewicz K et al. (2005). Standard
for treatment. NeuroRehabilitation 22: 199–205. regression-based methods for measuring recovery after
Leddy JJ, Kozlowski K, Donnelly JP et al. (2010). sport-related concussion. J Int Neuropsychol Soc 11: 58–69.
A preliminary study of subsymptom threshold exercise McCrea M, Guskiewicz K, Randolph C et al. (2013). Incidence,
training for refractory post-concussion syndrome. Clin clinical course, and predictors of prolonged recovery time
J Sport Med 20: 21–27. following sport-related concussion in high school and col-
Leddy JJ, Sandhu H, Sodhi V et al. (2012). Rehabilitation of lege athletes. J Int Neuropsychol Soc 19: 22–33.
concussion and post-concussion syndrome. Sports Health McCrory P, Meeuwisse W, Dvorák J et al. (2017). Consensus
4: 147–154. statement on concussion in sport – the 5th international
conference on concussion in sport held in Berlin, October disorders (WAD) as a model. Eur J Appl Physiol 98:
2016. Br J Sports Med 51: 838–847. 423–449.
McDermott LM, Ebmeier KP (2009). A meta-analysis of Ponsford J, Willmott C, Rothwell A et al. (2000). Factors
depression severity and cognitive function. J Affect influencing outcome following mild traumatic brain injury
Disord 119: 1–8. in adults. J Int Neuropsychol Soc 6: 568–579.
McDevitt J, Tierney RT, Phillips J et al. (2015). Association Ponsford J, Willmott C, Rothwell A et al. (2002). Impact of
between GRIN2A promoter polymorphism and recovery early intervention on outcome following mild head injury
from concussion. Brain Inj 29: 1674–1681. in adults. J Neurol Neurosurg Psychiatry 73: 330–332.
McLean SA, Kirsch NL, Tan-Schriner CU et al. (2009). Health Putzki N, Nirkko A, Diener HC (2005). Trigeminal autonomic
status, not head injury, predicts concussion symptoms after cephalalgias: a case of post-traumatic SUNCT syndrome?
minor injury. Am J Emerg Med 27: 182–190. Cephalalgia 25: 395–397.
Meares S, Shores EA, Batchelor J et al. (2006). The relation- Rees PM (2003). Contemporary issues in mild traumatic brain
ship of psychological and cognitive factors and opioids in injury. Arch Phys Med Rehabil 84: 1885–1894.
the development of the postconcussion syndrome in gen- Rose SC, Fischer AN, Heyer GL (2015). How long is too long?
eral trauma patients with mild traumatic brain injury. The lack of consensus regarding the post-concussion syn-
J Int Neuropsychol Soc 12: 792–801. drome diagnosis. Brain Inj 29: 798–803.
Meehan 3rd WP, Mannix RC, Stracciolini A et al. (2013). Ruff RM (2011). Mild traumatic brain injury and neural recov-
Symptom severity predicts prolonged recovery after ery: rethinking the debate. NeuroRehabilitation 28:
sport-related concussion, but age and amnesia do not. 167–180.
J Pediatr 163: 721–725. Ruff RM, Camenzuli L, Mueller J (1996). Miserable minority:
Meehan WP, Mannix R, Monuteaux MC et al. (2014). Early emotional risk factors that influence the outcome of a mild
symptom burden predicts recovery after sport-related con- traumatic brain injury. Brain Inj 10: 551–565.
cussion. Neurology 83 (24): 2204–2210. Russell K, Selci E, Chu S et al. (2017). Longitudinal assess-
Meehan 3rd WP, O’Brien MJ, Geminiani E et al. (2016). Initial ment of health-related quality of life following adolescent
symptom burden predicts duration of symptoms after con- sports-related concussion. J Neurotrauma 34: 2147–2153.
cussion. J Sci Med Sport 19: 722–725. Rutherford WH, Merrett JD, McDonald JR (1979). Symptoms
Merritt VC, Ukueberuwa DM, Arnett PA (2016). Relationship at one year following concussion from minor head injuries.
between the apolipoprotein E gene and headache following Injury 10: 225–230.
sports-related concussion. J Clin Exp Neuropsychol 38: Savola O, Hillbom M (2003). Early predictors of post-
941–949. concussion symptoms in patients with mild head injury.
Mickeviciene D, Schrader H, Obelieniene D et al. (2004). Eur J Neurol 10: 175–181.
A controlled prospective inception cohort study on the Shahim P, Tegner Y, Gustafsson B et al. (2016).
post-concussion syndrome outside the medicolegal con- Neurochemical aftermath of repetitive mild traumatic brain
text. Eur J Neurol 11: 411–419. injury. JAMA Neurol 73: 1308–1315.
Mittenberg W, Canyock EM, Condit D et al. (2001). Treatment Shepard NT, Clendaniel RA, Ruckenstein M (2013). Balance
of post-concussion syndrome following mild head injury. and dizziness. In: N Zasler, D Katz, R Zafonte (Eds.),
J Clin Exp Neuropsychol 23: 829–836. Brain injury medicine. Demos Medical Publishing,
Mooney G, Speed J (2001). The association between mild trau- New York, NY.
matic brain injury and psychiatric conditions. Brain Inj 15: Siavoshi S, Dougherty C, Ailani J et al. (2016). An unusual
865–877. case of post-traumatic headache complicated by intracra-
Morgan CD, Zuckerman SL, King LE et al. (2015). Post- nial hypotension. Brain Sci 7 (1).
concussion syndrome (PCS) in a youth population: defin- Siedlik JA, Siscos S, Evans K et al. (2016). Computerized neu-
ing the diagnostic value and cost-utility of brain imaging. rocognitive assessments and detection of the malingering
Childs Nerv Syst 31: 2305–2309. athlete. J Sports Med Phys Fitness 56: 1086–1091.
Murray N, Salvatore A, Powell D et al. (2014). Reliability and Snell DL, Siegert RJ, Hay-Smith EJ et al. (2010). An exami-
validity evidence of multiple balance assessments in ath- nation of the factor structure of the Revised Illness
letes with a concussion. J Athl Train 49: 540–549. Perception Questionnaire modified for adults with mild
Packard RC (1992). Posttraumatic headache: permanency and traumatic brain injury. Brain Inj 24: 1595–1605.
relationship to legal settlement. Headache 32: 496–500. Stulemeijer M, van der Werf SP, Jacobs B et al. (2006). Impact
Paniak C, Toller-Lobe G, Reynolds S et al. (2000). of additional extracranial injuries on outcome after mild
A randomized trial of two treatments for mild traumatic traumatic brain injury. J Neurotrauma 23: 1561–1569.
brain injury: 1 year follow-up. Brain Inj 14: 219–226. Stulemeijer M, van der Werf S, Borm GF et al. (2008). Early
Pardini D, Stump J, Lovell M et al. (2004). The Post- prediction of favourable recovery 6 months after mild trau-
concussion Symptom Scale (PCSS): a factor analysis. Br matic brain injury. J Neurol Neurosurg Psychiatry 79:
J Sports Med 38: 661–662. 936–942.
Passatore M, Roatta S (2006). Influence of sympathetic ner- Sufrinko A, McAllister-Deitrick J, Womble M et al. (2017).
vous system on sensorimotor function: whiplash associated Do sideline concussion assessments predict subsequent
neurocognitive impairment after sport-related concussion? Wood RL (2004). Understanding the ‘miserable minority’: a
J Athl Train 52: 676–681. diasthesis-stress paradigm for post-concussional syn-
Suhr JA, Gunstad J (2002). Postconcussive symptom report: drome. Brain Inj 18: 1135–1153.
the relative influence of head injury and depression. World Health Organization (1992). International statistical
J Clin Exp Neuropsychol 24: 981–993. classification of diseases and related health problems,
Swartz R, Longwell P (2005). Treatment of vertigo. Am Fam 10th ed.World Health Organization, Geneva, Switzerland.
Physician 71: 1115–1122. Yang CC, Tu YK, Hua MS et al. (2007). The association
Tiersky LA, Anselmi V, Johnston MV et al. (2005). A trial of between the postconcussion symptoms and clinical out-
neuropsychologic rehabilitation in mild-spectrum traumatic comes for patients with mild traumatic brain injury.
brain injury. Arch Phys Med Rehabil 86: 1565–1574. J Trauma 62: 657–663.
Trahan DE, Ross CE, Trahan SL (2001). Relationships Zakzanis KK, Leach L, Kaplan E (1998). On the nature and
among postconcussional-type symptoms, depression, and pattern of neurocognitive function in major depressive dis-
anxiety in neurologically normal young adults and victims order. Neuropsychiatry Neuropsychol Behav Neurol 11:
of mild brain injury. Arch Clin Neuropsychol 16: 435–445. 111–119.
Willer B, Leddy JJ (2006). Management of concussion and
post-concussion syndrome. Curr Treat Options Neurol 8:
415–426.

Postconcussion Syndrome

Uploaded by

Copyright:

Available Formats

Postconcussion Syndrome

Uploaded by

Document Information

Original Title

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

Postconcussion Syndrome

Uploaded by

Copyright:

Available Formats

Handbook of Clinical Neurology, Vol.

158 (3rd series)

INTRODUCTION reports. So fallacious retrospective diagnosis of concus-

Terminology Postconcussion Postconcussional Major or mild Sports-related

Pre-existing factors Injury characteristics Postinjury factors

You might also like