Sports-related Concussions: Diagnosis, Complications, and Current Management Strategies

Jonathan G. Hobbs, MD; Jacob S. Young, BS; Julian E. Bailes, MD


Neurosurg Focus. 2016;40(4):e5 

In This Article

Diagnosis of a Concussion

The diagnosis of concussion is a clinical one and relies on an understanding of the definition of "concussion," which is often used synonymously with "mild traumatic brain injury" (mTBI). However, some authorities believe that concussion actually represents a subset of mTBI and should be separated accordingly.[46] Multiple definitions of concussion and mTBI exist; however, they all contain similar core characteristics.

In general, a concussion (or mTBI) is defined as a traumatically induced transient disturbance of neurological function caused by a complex pathophysiological process.[46] However, there is a lack of unity among various medical bodies about what exactly constitutes this mTBI. The American Congress of Rehabilitation Medicine defines mTBI as a traumatically induced physiological disruption of brain function resulting from the head being struck or striking an object or the brain undergoing an acceleration and deceleration movement as manifested by at least one of the following: a period of loss of consciousness (LOC) up to 30 minutes; posttraumatic amnesia that does not exceed 24 hours; any period of confusion or disorientation; transient neurological abnormalities (focal neurological deficits, seizures, nonsurgical intracranial lesions); and a Glasgow Coma Scale (GCS) score of 13–15 within 30 minutes of presentation.[17,68] The WHO stipulated that none of the aforementioned manifestations can be the result of intoxication (alcohol, medication, and recreational drug), systemic illness, or extracranial injuries. It should be noted that neither the American Congress of Rehabilitation Medicine nor the WHO specified a minimum duration for LOC, amnesia, or disorientation that is necessary to meet the requirements of an mTBI. The US Department of Defense adds a caveat to the definition and states that an mTBI cannot have any abnormality on conventional CT or MRI studies.[17]

In 2012, the 4th International Conference on Concussion in Sport (ICCS) put forth a consensus statement regarding SRCs, which provides the basis of our current diagnosis and management. According to this consensus, a concussion is defined as a complex pathophysiological process affecting the brain. A concussion is induced by biomechanical forces and includes several common features of clinical, pathological, and biomechanical injury constructs, which are used to define the nature of the concussive injury.[95] A concussion results from a transmitted force to the head. It typically manifests as a rapid, transient neurological dysfunction with spontaneous resolution (although the symptoms may evolve over minutes to hours after the traumatic event). Although the concussive event may result in neuropathological changes, the symptomatology reflects a functional disturbance rather than a structural injury, which correlates with the often normal findings on conventional neuroimaging studies. The symptoms are graded and may or may not include LOC, and resolution typically follows a sequential course. However, some cases may include prolonged symptoms.[95]

Signs and Symptoms of a Concussion

The signs and symptoms are numerous and often non-specific. Headache is the most common symptom, followed by dizziness. An LOC is actually quite infrequent in SRCs, occurring in only 10% of cases, even though it is classically associated with mTBI.[9,26,81,90,94,95,101] Amnesia and confusion are other classic symptoms of a concussion, and they are often present following a traumatic blow to the head even if there is no preceding LOC (see Table 1 for signs and symptoms of a concussion). The remaining symptoms of a concussion vary widely from patient to patient, and include multiple health care complaints, such as physical (nausea, vomiting, balance disturbance, visual changes, fatigue, photo- or phonophobia, numbness); cognitive ("foggy" mentation, difficulty concentrating, mental slowness, memory difficulty, slow response time, confusion about recent events); emotional (increased irritability, depression, anxiety, nervousness); and sleep disturbances (drowsiness, hyper- or hyposomnolence).[46] These nonspecific symptoms are commonly seen in other medical conditions, and necessitate a global analysis of the patient, and place particular importance on the recent history of trauma for the diagnosis.

No brain injury will be evident on MRI or CT scans with an uncomplicated concussion; however, structural axonal injury may be present—just not evident on imaging—and concussions may be complicated by coexisting intracranial hematomas, petechial hemorrhages in areas with blood vessel shearing, or cortical contusions. If a concussion occurs while an individual is still symptomatic from an earlier concussive event, the theoretical and controversial second-impact syndrome (SIS) may result.[15,16,93,96] This syndrome describes a situation in which the second trauma causes a loss of cerebral autoregulation with resultant and cerebral edema, which can be seen on brain imaging. This topic is discussed in greater detail later in the review.

Associated Injuries

The CNS pathology most commonly associated with mTBI includes axonal injury, brain contusions, and intracranial hemorrhages (ICHs). The primary pathological feature of TBI is axonal shear injury.[153] The damage to the axons and small blood vessels is generally proportional to applied traumatic force, and the extent of axonal injury is suggested by the duration of LOC or the amnesia and GCS score following the injury. If vessels are damaged along with the neuronal axons, the damaged areas may appear as petechial hemorrhages on CT or MRI scans.

Brain contusions are areas of focal cortical injury either from an external force or from rapid acceleration and deceleration that causes the brain to contact the intracranial surfaces. Contusions are associated with localized edema, ischemia, and mass effect, which collectively result in a worse outcome following an mTBI.[148] Although signs of a contusion depend on its cortical location, any focal neurological signs should raise concern for a brain contusion.

Any type of ICH can occur after an mTBI, particularly if the patient is receiving anticoagulant therapy (albeit this is less common in the younger, athletic population). Any patient in whom an mTBI is diagnosed and who begins to show signs of neurological or clinical deterioration should be evaluated for an intracranial hematoma. It is possible that after an SRC a player may temporarily regain consciousness or have an improvement in neurological status before slipping into an unconscious state. This history of a lucid interval following a serious head trauma is a strong indication that a potentially life-threatening complication of the head injury, classically an epidural hematoma, is causing this rapid deterioration after a period of apparent improvement. During the period in which the patient is improving, blood is collecting in the epidural space, and as it accumulates the intracranial pressure rises, which compresses the brain parenchyma and leads to neurological dysfunction and potentially brain herniation. Although not a typical presentation, other complications, such as a cerebral contusion, subdural hematoma, pseudoaneurysm rupture, or ICH can also cause a lucid interval.

Complications of Mild Head Trauma

Skull fractures can complicate even mild traumatic blows to the head. These fractures can either be linear or depressed. Although linear fractures are often benign, they can be associated with underlying pathology such as brain contusions, dural tears, and vascular trauma.[29] A basilar skull fracture can lead to intracranial infections and CSF leakage if a fistula is created, resulting in otorrhea. Likewise, a frontal bone fracture can lead to CSF rhinorrhea and CNS infection if the ethmoid bone shears the olfactory nerves. Any type of fracture that leads to communication between air and the intracranial compartment is classified as an open head injury and should be evaluated with a neurosurgical consultation.

Screening for cervical spine injury should be performed, with history, examination, and imaging studies. Furthermore, vascular injury within the neck can occur. Additionally, trauma can result in cavernous sinus syndrome. Signs of cavernous sinus syndrome include Horner syndrome, ophthalmoplegia, chemosis, proptosis, and trigeminal sensory loss.

Eye injuries may require an ophthalmology consultation if the trauma involves frontal impact. Any cranial nerve injuries that fail to improve as the perineural edema resolves raise suspicion for a nerve entrapment, and neurosurgical consultation is advised.