Concussion Clinical Presentation

Updated: Jul 26, 2017
  • Author: David T Bernhardt, MD; Chief Editor: Craig C Young, MD  more...
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Athletes with an MTBI often appear acutely with a confused or blank expression or blunted affect. Delayed response to simple questioning may be demonstrated, along with emotional lability. The emotional lability may become more evident as the athlete attempts to cope with their confusion. Many athletes report an associated headache and dizziness. Visual complaints may include seeing stars, blurry vision, or double vision. [22]

In a study of 48 athletes aged 9-23 years with a diagnosed protracted concussion, Kontos et al found that those who have vestibular symptoms after concussion may have slower reaction times than those who do not and thus may be at greater risk for new injury. [23]

Patients with vestibular dizziness and those with vestibulo-ocular symptoms had significantly slower reaction times than those without these impairments (P = .05 and P = .04, respectively). [23] Athletes with vestibular dizziness and vestibulospinal and vestibulo-ocular impairments also had more total symptoms than those without these impairments. Furthermore, vestibular impairments were associated with greater cognitive impairment and somatic symptoms. Abnormal (>6 cm) convergence distance was associated with a significantly slower reaction time (P = .05). [23]

Both pretraumatic (retrograde) amnesia and posttraumatic (antegrade) amnesia may be present. Usually, the duration of retrograde amnesia is quite brief, with a more variable duration of posttraumatic amnesia (seconds to minutes), depending upon the injury.

A history of persistent vomiting may suggest a significant brain injury with associated elevated intracranial pressure. Other signs of increased intracranial pressure include worsening headache, increasing disorientation, and changing level of consciousness. Possible causes of increasing intracranial pressure include subdural hematomas, epidural hematomas, or some other type of intracranial hemorrhage.

It is important to document a previous history of concussions. Multiple concussions with prolonged neurologic symptoms (eg, headache, hyperacusis, dizziness) suggest postconcussive syndrome and should influence return-to-play decisions. [2, 3, 7, 24, 25, 26, 27]

Assessment tools

The Glasgow Coma Scale (GCS) is routinely used to assess head injuries in an emergency department. This 15-point scale is used to assess eye (spontaneous opening = 4 to no response = 1), motor (obeys commands = 6 to no response = 1), and verbal responses (oriented = 5 to no response = 1) in an attempt to quantify the patient's level of consciousness. This tool is not sensitive enough to evaluate more mild injuries and should not be used on the playing field to judge playability. See the Glasgow Coma Scale calculator.

McCrea et al developed a sideline evaluation to help the practitioner evaluate the more subtly injured brain. [20, 28] A 30-point scale is used to assess an athlete's orientation, concentration, immediate memory, and delayed recall. Preseason testing must be done if a practitioner is hoping to use this tool as a supplement to the neurologic and mental status exam; if the baseline status of an individual is not known, assessment for change after a head injury is useless. McCrea's sideline evaluation uses recitation of the months of the year in reverse order after a study by Young et al showed the lack of reliability of the "serial 7s" test (serial subtraction by 7 from 100) in the baseline evaluation of mental status even in non–head-injured athletes. [29]

Interestingly, the results from one study noted that administering preseason baseline neurocognitive tests in a group versus individual setting resulted in significantly lower verbal memory, visual memory, motor processing speed, and reaction time scores and a greater rate of invalid baselines. [30]

Sport Concussion Assessment Tool, 3rd edition, (SCAT3) is another standardized tool. SCAT3 combines multiple assessments into a single instrument. This combined tool was first produced as a part of the Summary and Agreement Statement of the Second International Symposium on Concussion in Sport, [31] and it has been updated twice since then (SCAT2, 2009; SCAT3, 2013).

A study investigated acute lower extremity musculoskeletal injury rates pre- and post-concussion in concussed (n=44) and matched control athletes (n=58). The study reported that within 1-year post-concussion, the concussed group was 1.97 times more likely to have suffered an acute lower extremity musculoskeletal injury like an ankle sprain, post-concussion than prior to concussion, and 1.64 times more likely to have suffered an acute lower extremity musculoskeletal injury post-concussion than their matched non-concussed cohort over the same time period. [32]


Many different classification schemes have been proposed over the last 2 decades. No one classification system is necessarily better than another classification system. No scientific basis for any of the classification systems exists.

Cantu's guidelines, [7, 33] Ommaya and Gennarelli's guidelines, [34] the Colorado guidelines, [35] and the 1997 American Academy of Neurology (AAN) guidelines [36] were proposed to aid in the evaluation of a concussion. The free CDC Tool Kit on Concussion for High School Coaches is available online in English and Spanish and uses the 1997 AAN guidelines to support a classification scheme. [37] The authors prefer to characterize concussions as follows [37] :

  • A simple concussion injury progressively resolves after 7-10 days without complication. The key to return to play is to hold the athlete from practice or competition until all symptoms have resolved.
  • A complex concussion consists of persistent symptoms that may include those that recur with exertion, specific sequelae such as seizure associated with the injury, prolonged LOC (>1 min), or prolonged impairment of cognitive function.

Some studies have suggested that LOC may not be a great predictor of short-term or long-term neurologic functioning, which makes the guidelines more controversial. [38, 39]

Regardless of the classification scheme that is used, all concur with the ultimate recommendation: Do not allow the concussed athlete to return to play until the patient is completely asymptomatic. The athlete must be free of headache, dizziness, amnesia, blunted affect, and delayed verbal or ocular responses, and all cognitive functioning must have returned to normal.



Perform a thorough, organized assessment to better define the degree of injury when a player is brought to the sidelines or emergency department for evaluation.

The initial evaluation should focus on airway, breathing, and circulation for any unconscious patient. Assume all unconscious or mentally impaired patients have sustained an injury to their cervical spine until proven otherwise.

For conscious patients, the remainder of the examination should be performed in a quiet place, on the sidelines or in the locker room away from teammates and coaches, or in a private room in an emergency department in order to get an accurate assessment of the cognitive status of the injured athlete.

The initial clinical examination should include a careful inspection of the athlete's general appearance.

Palpating the head and neck is important when looking for an associated skull or cervical injury.

Palpate the facial bones and the periorbital, mandibular, and maxillary areas after any head trauma. (See also the Medscape Drugs & Diseases articles Sports-Related Facial Trauma, Maxillary and Le Fort Fractures, and Management of Panfacial Fractures [in the Plastic Surgery section].)

Open and close the mouth to help in the evaluation of possible temporomandibular joint (TMJ) pain, malocclusion, or mandible fracture. (See also the Medscape Drugs & Diseases articles Initial Evaluation and Management of Maxillofacial Injuries [in the Trauma section], Mandibular Fracture Imaging [in the Radiology section], and Mandibular Body Fractures [in the Otolaryngology and Facial Plastic Surgery section].)

Inspect the nose for deformity and tenderness, which may indicate a possible nasal fracture. (See also the Medscape Drugs & Diseases articles Nasal and Septal Fractures [in the Otolaryngology and Facial Plastic Surgery section], Nasal Fracture [in the Sports Medicine section], and Nasal Fracture Surgery [in the Plastic Surgery section].)

Persistent rhinorrhea or otorrhea (clear) indicates a possible associated skull fracture. (See also the Medscape Drugs & Diseases articles Imaging in Skull Fractures [in the Radiology section] and Skull Fracture [in the Neurosurgery section].)

Perform a careful detailed neurologic examination to include examinations of the visual fields, extraocular movements, pupillary reflexes, and level of the eyes.

Assess upper-extremity and lower-extremity strength and sensation.

Assess coordination and balance. Concussed patients often have difficulty with the finger-nose-finger test and will use slow, purposeful movements to complete the task. [40]

Catena et al compared the immediate versus long-term effects of concussion on balance control. [41] Individuals with concussion (n = 30) and matched controls (n = 30) performed a single task of level walking, attention divided walking, and an obstacle-crossing task at 2 heights, with testing occurring 4 times postinjury.

The investigators demonstrated no significant difference between the 2 groups in the single-task level walking task. However, although concussed individuals walked slower within 48 hours of the injury and had less motion of their center of mass in the sagittal plane with divided attention during walking, there were no group differences by day 6 for the same task. [41]

In addition, there were no significant group differences in balance control during obstacle crossing during the first 2 testing sessions, but by day 14, concussed individuals had less mediolateral motion of their center of mass. Catena et al concluded that attention divided gait is better at distinguishing gait adaptations immediately postconcussion, but obstacle crossing can be used further along in the recovery process to detect new gait adaptations. [41]

Significant sway in Romberg testing may indicate persistent injury.

Adding a simple vision test performed on the sidelines to standard tests based on balance symptoms and cognition tasks can improve the detection of concussion in sports players who have experienced a head injury, according to a study of 217 young athletes. The King-Devick test involves reading a series of numbers and takes about 1 minute to complete. A baseline test is given at the start of the season, and tests are repeated after injuries occur. Concussion is diagnosed if the injured athlete takes longer to complete the test. [42]

Among the 30 study subjects with a first concussion, 79% showed worsening of time scores on the King-Devick vision test, while the Standardized Assessment of Concussion (SAC) test detected 52% of concussions and the Balance Error Scoring System (BESS) test detected 70%. Combining the King-Devick vision test with the SAC detected 89% of concussions, and combining all 3 tests identified 100% of concussions. [42]

When examining an athlete on the sideline, perform repeat examinations every 15 minutes until the symptoms have cleared. Repeat the examinations even if the athlete is allowed to return to play.

The patient should not be allowed to return to competition if his/her symptoms or physical examination findings do not return to normal after 15 minutes. For a few hours after the initial injury, close observation and monitoring of the athlete for worsening mental status or neurologic status is warranted on the sideline or in the emergency department.



A previous concussion is a significant risk factor for sustaining a concussion. [2, 3, 7, 24, 25, 26, 27]

One study reported that the risk of sustaining a concussion was 4-5 times higher in patients who had at least 1 concussion in the past. Another study reported that athletes with a history of 3 or more previous concussions were 3-fold more likely to have a concussion than players who had no history of concussion. [26]

Other risk factors for sustaining a concussion that have been suggested but not proven include not wearing mouth guards, poor fitting helmets, and genetic predisposition. [43, 44] Research in all of these areas continues.



Chronic Traumatic Encephalopathy (CTE) 

Persons with a history of repetitive brain trauma, including boxers and football players, are at risk for developing chronic traumatic encephalopathy (CTE), a progressive degenerative disease. Degenerative changes, which can begin months to decades after the patient’s last brain trauma, include atrophy of the cerebral hemispheres, medial temporal lobe, thalamus, mammillary bodies, and brainstem. The condition is also characterized by ventricular dilatation and by fenestration of the cavum septum pellucidum, as well as the accumulation of phosphorylated tau in the brain, with deposits of the protein being found in the sulci and in perivascular areas of the cerebral cortex. Symptoms of CTE include memory loss, confusion, impaired judgment, reduced impulse control, aggression, explosive anger, depression, and progressive dementia. [45, 46, 47, 48]

According to a report from the US Department of Veterans Affairs and Boston University, 87 of 91 deceased former players for the National Football League (NFL) (96%) who donated their brains for study were found to have changes consistent with CTE. These finding need to be tempered by the fact the donors had, prior to death, expressed concern that they might have CTE and so may have had a higher proportion of the disease than does the overall population of former NFL players. In addition these individuals had not necessarily had clinical symptoms of CTE, but felt they might be at risk. [49, 50]

A study by Mez et al diagnosed CTE in 177 (78%) of 202 samples from deceased American football players. The samples included 111 former NFL players of which, 110 (99%) were diagnosed with CTE. The study also found that among the 26 participants diagnosed with mild CTE, 96% had behavioral or mood symptoms or both, 85% had cognitive symptoms, and 33% had signs of dementia. In the 84 participants diagnosed with severe CTE, 89% had behavioral or mood symptoms, 95% had cognitive symptoms, and 85% had signs of dementia. [51]