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Acute Clinical Symptoms of Concussion

Assessing Prognostic Significance

Paul R. McCrory, MBBS, PhD
Karen M. Johnston, MD, PhD

THE PHYSICIAN AND SPORTSMEDICINE - VOL 30 - NO. 8 - AUGUST 2021


In Brief: The acute symptoms of concussion provide the basis for assessment, classification, and ultimately, management of this common problem in sport. The only concussive symptoms that have been scientifically validated are loss of consciousness, headache, dizziness, nausea, blurred vision, attentional deficit, and memory loss. Although many symptoms have been anecdotally attributed to concussive injury, their clinical significance is unknown. An evidence-based analysis of concussive symptoms and their prognostic significance can aid physicians who must make management and return-to-play decisions.

The clinical manifestations of concussion as a transient neurologic syndrome without structural brain injury have been known since the 10th century AD. The term "concussion" was first used by one of the greatest Muslim physicians and philosophers, Rhazes (850-923 AD).1,2 The fundamental distinction that he made—describing concussion as an abnormal physiologic state without gross traumatic lesions of the brain—is the critical turning point in history of the medical understanding of this condition. Despite more than 1,000 years of medical research, the nature and pathophysiologic basis of the clinical symptoms of concussion remain unclear.

Definition of Concussion

No universal agreement on the standard definition or nature of concussion exists.3,4 The Congress of Neurological Surgeons proposed a consensus definition of concussion5 that was subsequently endorsed by various medical associations. However, this definition does not address many of the predominant clinical features of concussion, such as headache and nausea. Several common features that incorporate clinical, pathologic, and biomechanical injury constructs define the nature of a concussive head injury, including:

  • Concussion may be caused either by a direct blow to the head or elsewhere on the body from an "impulsive" force transmitted to the head;
  • Concussion may cause an immediate and short-lived impairment of neurologic function;
  • Concussion may cause neuropathologic changes; however, the acute clinical symptoms largely reflect a functional disturbance rather than structural injury;
  • Concussion may cause a graded set of clinical syndromes that may or may not involve loss of consciousness. Resolution of the clinical and cognitive symptoms typically follows a sequential course; and
  • Concussion is manifest by conventional neuroimaging studies.

There is agreement on the above descriptions, but no single definition adequately reflects the importance of the various postconcussive symptoms. (See "Summary and Agreement Statement of the First International Conference on Concussion in Sport, Vienna 2021") Thus, proposed definitions remain flawed.

Clinical Symptoms of Concussion

The acute symptoms of concussion have been examined in prospective studies. The only validated symptoms are amnesia, loss of consciousness, headache, dizziness, blurred vision, attentional deficit, and nausea.6-8 Headache, of course, is not confined to concussion—up to 50% of athletes report exercise-related headaches.9,10

In addition, a wide variety of anecdotal symptoms (eg, vacant stare, irritability, emotional lability, impaired coordination, sleep disturbance, noise or light intolerance, lethargy, behavioral disturbance, and altered sense of taste or smell)11 may be encountered in concussed athletes. The prognostic significance of these symptoms is unknown, although they are widely cited by clinicians. Symptom aggravation with altitude, atmospheric pressure, and high ambient temperature are also anecdotally described. One area of concern that has not been studied in detail is after apparent recovery when deficits may still be evident if subjects are assessed during physiologic stress.12

Despite these symptoms being attributable to concussion, surprisingly few athletes recognize the injury. In one study,13 four of five professional football players did not recognize their own concussions, even though many had symptoms lasting more than a day. Of all symptoms evaluated, confusion (getting "dinged") was most common.13 Numerous reports describe recurrent concussional symptoms with exertion. The physiologic basis for this finding is not known, but current return-to-play guidelines reflect caution in this regard, with asymptomatic exertional provocative testing being an important qualifier for return to play.

Predicting Injury Severity

Do clinical symptoms predict injury severity? The importance of this question rests on the fact that numerous grading systems have been developed to measure concussion severity and predict prognosis and outcome. These grading systems include assessment of many concussion parameters, including loss of consciousness (LOC), orientation, and posttraumatic amnesia (PTA).

Loss of consciousness. Most grading systems currently used, including the most recent American Academy of Neurology guidelines, heavily weigh LOC as predictive of injury severity.14 However, brief (<1 minute) LOC as an isolated marker of injury severity has not been found to reflect either severity or neuropsychological performance,8,15,16 and it has not been shown to be associated with neuroimaging or electrophysiologic abnormalities in concussion.17,18

Orientation. Recent studies of sports-related concussion have noted that standard orientation questions (eg, time, place, and person) were less sensitive in discriminating concussed from nonconcussed football players when compared with questions of recently acquired memory. Tests pertaining to sport-specific concepts have demonstrated the highest yield.6,19 These factors have a number of clinical implications, given that the assessment of posttraumatic amnesia is usually contingent on orientation.20

Posttraumatic amnesia. The duration of PTA has been found to correlate with the severity and outcome of severe traumatic brain injury.21-28 The few studies6,29-31 that investigated the qualitative features of PTA in mild concussion did not find PTA to be a prognostic marker.

Retrograde amnesia. The period of lost recall for events prior to brain injury has been extensively documented in traumatic brain injury.31-35 Retrograde amnesia is a time-variable entity with a lengthening of the amnesic period in the first few minutes after injury31 and then subsequent shortening,32 leaving a small period of permanent retrograde amnesia. Although retrograde amnesia is considered to be a consistent feature of traumatic brain injury, neither its presence nor its duration is considered a reliable indicator of injury severity or outcome.36

Other symptoms. Headache, dizziness, blurred vision, and nausea have been noted in prospective studies of concussion,6,7 but their prognostic significance remains unclear. Postconcussive headache has not been clearly studied; however, anecdotal observations suggest a vascular source that responds to standard antimigraine therapy. Clinical differentiation from the many other nonconcussive conditions that manifest as headache on the athletic field may be difficult.

Postconcussion Syndrome

The issue of a constellation of physical and cognitive symptoms labeled as the postconcussive syndrome (PCS) remains as controversial today as when it was first proposed in the 19th century.37 Symptoms include headache, vertigo, dizziness, nausea, memory complaints, blurred vision, noise and light sensitivity, difficulty concentrating, fatigue, depression, sleep disturbance, loss of appetite, anxiety, incoordination, and hallucinations.38-41

Two distinct schools of thought have arisen regarding the pathophysiology of PCS. The first proposes that the symptoms associated with PCS are a direct consequence of brain injury.42,43 The second proposes that the symptoms are functional and represent psychological or emotional sequelae of the brain injury. The relative contribution of these two mechanisms remains unclear.44,45

The role of preinjury, injury-related, environmental, and personality factors have been evaluated in adults46 and children.47 The issue of malingering and compensable litigation is also often proposed as a mechanism for symptom prolongation.44,48-50

In general, PCS is uncommon in most collision and contact sports, although relatively few studies have followed athletic populations for significant periods. Comparison with impact forces in motor vehicle crash studies remains speculative.7,16,39,43,47,51-58

Neuropsychological Deficits

Only in the past few decades have the neuropsychological consequences of concussion been studied, particularly in sport. While there is now acceptance of an organic basis to the problems associated with concussion, controversy remains regarding the nature of the cognitive deficits as well as the speed and extent of recovery from them.27,28,31,41,50,59-67 A range of neuropsychological deficits has been reported after mild concussive injury. The major areas of deficit include:

  • Disturbances of new learning and memory,12,16,36,39,53,56,60,61,65,68 planning and the ability to switch mental "set,"16,53,68,69 and
  • Reduced attention and speed of information processing, including test strategies such as the Paced Auditory Serial Addition Test, choice reaction time, sustained concentration and vigilance task, letter cancellation task, digit symbol subtest of the Wechsler Abbreviated Scale of Intelligence, and Smith Symbol Digit Modalities Test.7,53,57,61,62,70-77

Isolated reports suggest that impairments may be evident on tasks involving visuospatial constructional ability, language, and sensorimotor function.16,53

Tracking Symptoms

Baseline testing of neuropsychological function is important. Preinjury testing addresses the potential methodologic problems inherent in some published studies4,11,54 that used nonsporting controls for comparison of results. Several groups have developed strategies using baseline neuropsychological testing, suggesting that such techniques are feasible in a clinical setting. Studies7,72,78,79 in both American and Australian football dating from the mid-120210s testify to the usefulness of this approach. Recent attempts to consolidate and shorten extensive test batteries have led to success and results comparable to longer formats.80-82

The association of poor performance on testing with postconcussive symptoms has not been firmly established. Recent findings of abnormalities in executive function and working memory, as seen by functional magnetic resonance imaging (MRI) scanning and neuropsychological testing, indicate that postconcussive symptoms may be a marker for injury.13 Parallel studies19,83 measuring event-related potentials while performing attention tasks may also indicate transient injury and recovery on resolution of symptoms. Another study83 of long-latency-evoked potentials have suggested a possible role in the assessment of traumatic brain injury, although their clinical significance remains unclear.

Optimal Neuroimaging

Evidence obtained over the past 15 years40,84-91 reveals that MRI is more sensitive and specific than computed tomography, particularly in the evaluation of mild head injury and in some sports-related head injuries. Recent preliminary data18 indicate that the addition of diffusion-weighted imaging to standard MRI sequences increased the finding of signal abnormalities in concussed athletes from 20% to 33%. Noteworthy is that all subjects who tested positive in this study had ongoing PCS, although the study lacks baseline control imaging.

Specific Postconcussion Risks

Research highlights the importance of two postconcussion complications.

Second impact syndrome. Diffuse cerebral edema is a rare but well-recognized complication of mild traumatic brain injury in sports. It occurs predominantly in children and teenagers. A head injury, however trivial, can trigger the rapid development of cerebral swelling that usually results in brain stem herniation and death. Its cause is unknown but is thought to involve disordered cerebral vascular autoregulation.92

Although repeated concussions have been proposed as the basis for this syndrome, the evidence is not compelling.93 It is more likely that a single impact of any severity may result in this rare complication.

Convulsions. Concussive or impact convulsions in collision sport are an uncommon but dramatic complication of minor head injury. A recent study94 has delineated the nature of these convulsions; they occur within 2 seconds of impact and are not associated with structural brain injury.

Among players who suffer concussive convulsions, the universally good outcome and absence of structural injury or long-term neuropsychological damage reflect the benign nature of these episodes. From a clinical standpoint, late seizures do not occur, antiepileptic therapy is not indicated, and prohibition from collision sport is unwarranted. The treating clinician can reassure the patient that concussive convulsions are benign, and overall management should center on the appropriate treatment of the concussion alone.

Making Headway

By its very nature, a concussion is diagnosed by its presenting symptoms. Grading scales have been established based on symptom parameters such as LOC and PTA. Definitions of concussion are based on neurologic symptoms. In spite of this, the prognostic contribution of symptoms to the clinical picture is not well established. Therefore, adoption of certain concussion management guidelines by key medical and sporting bodies is premature based on the available scientific data. The need for case-controlled studies is paramount.

Because few prospective studies have validated the significance of particular symptoms, good clinical judgment is vital. The vade mecum should be clear: An athlete with postconcussive symptoms should not return to play or training.

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Dr McCrory is a neurologist and sports physician in the Brain Research Institute and the Centre for Sports Medicine Research and Education at the University of Melbourne in Australia. Dr Johnston is a neurosurgeon in the department of neurosurgery at McGill University in Montreal. Address correspondence to Paul R. McCrory, MBBS, PhD, PO Box 93, Shoreham, VIC 3916, Australia; e-mail to [email protected].

Disclosure information: Drs McCrory and Johnston disclose no significant relationship with any manufacturer of any commercial product mentioned in this article. No drug is mentioned in this article for an unlabeled use.


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