Terminology

“Traumatic brain injury” refers to an alteration in brain function or other evidence of brain pathology caused by external force6 and traditionally is classified as mild, moderate, and severe based on the Glasgow Coma Scale (GCS).7 TBI with GCS score of 13 or more is classified as mild, 9 to 12 as moderate, and 8 and lower as severe.8 mTBI is defined as a traumatically induced physiologic disruption of brain function as manifested by at least 1 of the following: (1) any period of loss of consciousness up to 30 minutes, (2) any loss of memory for events before or after the accident not exceeding 24 hours, (3) any alteration in mental state at the time of the accident, and (4) focal neurologic deficits that may or may not be transient.9,10 Concussion is a form of mTBI, and “concussion” is a term commonly used in sports, whereas “mTBI” is used more often in the medical context.11

Pathophysiology

Pathophysiologically, TBI involves 2 phases of tissue injury: primary and secondary. Whereas primary injuries are almost immediate and generally irreversible, secondary injuries are delayed and can continue for an extended period of time and thereby provide an opportunity for therapy.12 The primary injury phase involves direct and indirect mechanical damage from impact and acceleration/deceleration that could result in cortical contusions, subdural or epidural hematomas, axonal shearing, and microvascular injury. Secondary injury is the nonmechanical damage that results from a complex metabolic cascade set off by neuronal cell membrane disruption and axonal stretch.13 Neuronal membrane deformity leads to ionic flux and release of excitatory neurotransmitters. Attempts to restore homeostasis lead to a cellular energy crisis. Depletion of cellular energy stores leads to initiation of apoptosis and neuronal death. Impaired cerebrovascular autoregulation that leads to decreased cerebral blood flow (CBF), inflammatory response with activation of microglia,14 and release of free radicals are additional mechanisms of tissue damage during the secondary injury phase of TBI.

Diffuse axonal injury (DAI) is best described after severe TBI and is characterized by axonal stretching leading to axolemmal disruption, ionic flux, neurofilament compaction, and microtubule disassembly. The effect of these pathophysiologic processes is axonal swelling and eventual disconnection.15,16 Although best described in severe TBI, DAI occurs in mTBI as well and is recognized as an important determinant of long-term cognitive and neuropsychiatric outcome in mTBI.17,18 As discussed in subsequent sections, key advances in neuroimaging of mTBI involve newer techniques that can detect disruption of axonal integrity.

Symptomatology

mTBI can lead to a wide range of symptoms, including loss of consciousness, if any, at the time of injury and memory loss, if any, for events before and after the injury. Postconcussion syndrome refers to symptoms from multiple “symptom categories” that develop within a maximum of 4 weeks following head trauma.19 Broad symptom categories include somatic, cognitive, affective, and sleep-related. Typical symptoms include headache, dizziness, memory impairment, difficulty concentrating, insomnia, mood alteration, and anxiety. Most people with mTBI recover within a few days to weeks with rest and minimal symptomatic treatment. Approximately 15% of patients with mTBI suffer from long-term complications.4,5

Chronic traumatic encephalopathy (CTE) is a rare progressive degenerative condition that is thought to be a consequence of repetitive TBI. First described as dementia pugilistica in boxers,20 CTE is equally concerning for other professional athletes who are at risk for repeated concussions. For instance, retired professional football players with history of 3 or more concussions are 5 times more likely to develop mild cognitive impairment.21 From the autopsy studies of 3 professional athletes with CTE, we know that it is related to deposition of tau protein in neurons and resultant progressive degeneration of the central nervous system.22

General Considerations

The goals of neuroimaging of TBI are to identify treatable injuries, assist in prevention of secondary damage, and provide prognostic information about long-term clinical outcome. Conventional neuroimaging continues to play a crucial role in the initial management of TBI. CT is generally the imaging modality of choice for initial screening to exclude serious intracranial injury in patients who present with head injury. MRI, particularly at 3 T strength, improves structural sensitivity and is indicated in acute TBI when neurologic findings cannot be explained by CT. MRI...