The term mild traumatic brain injury has generally been used synonymously with the word “concussion”; however, at the Third International Conference on Concussion in Sport, held in Zurich in 2008, “[the panel of experts] acknowledged that the terms refer to different injury constructs and should not be used interchangeably.”¹ Concussion is defined as a complex pathophysiological process affecting the brain, induced by traumatic biochemical forces.¹ It may be caused by a direct blow to the head or any other part of the body that leads to impulsive forces transmitted to the head, causing the rapid onset of short-lived neurologic impairment, which may or may not involve the loss of consciousness.¹ Acute symptoms result from a functional disturbance rather than a structural brain injury, which is further supported by the absence of abnormalities on standard neuroimaging.

Concussions are metabolic injuries with cellular dysfunction as the culprit for the acute and subacute symptoms. Immediately after a concussion, there are multiple cascades of ionic, metabolic, and physiologic events. The earliest changes involve the release of excitatory amino acids and a large efflux of potassium causing hyperglycolysis. This is followed by persistent calcium influx thought to cause neurovascular contriction which protects the brain from massive swelling. These events result in an increase in energy demand but a decrease in energy supply, which leads to a cellular energy crisis.^2,3 It is this crisis that is thought to be the mechanism for postconcussive vulnerability because the brain is thought to be less equipped to respond to a second head injury leading to longlasting effects. After hyperglycolysis, the brain experiences depressed metabolism, complicated by the persistent and elevated calcium levels, which may impair oxidative metabolism and activate pathways leading to cell death.³ Animal models have shown that the metabolic dysfunction lasts up to 2 weeks; it is postulated that the period of derangement is longer in humans.⁴

Symptoms of concussion can be somatic, cognitive, and/or emotional. Headache is the most common symptom of concussion⁵ and may develop immediately or minutes to hours after injury.² Loss of consciousness can occur but is relatively uncommon and, contrary to prior practice, is not a necessary sign for the diagnosis of concussion. In fact, confusion and retrograde and/or anterograde amnesia are the more common forms of altered mental status after a concussion,² with one study suggesting that amnesia is most predictive of postinjury difficulties and those with persistent memory deficits were more likely to have more symptoms, longer duration of symptoms, and poorer performance on neurocognitive tests.⁶ One or more of the following additional symptoms and signs can be experienced or observed with a concussion: loss of consciousness, immediate motor phenomena, dizziness, blurry vision, poor balance,
tinnitus, confusion, sleep disturbances, fatigue, slow mental processing, and mood disturbances.⁷

Resolution of symptoms, clinical and cognitive, occurs in a sequential order, with most adult concussions resolving in 7 to 10 days, and it is considered within normal limitations for symptoms to last up to 3 months postinjury.⁸ Multiple studies have revealed that younger athletes are more likely to have a longer recovery time when compared with college and professional athletes.^9,10 There is also evidence suggesting that athletes with a history of multiple concussions may take longer to recover from a concussion.¹¹

Postconcussion syndrome is a controversial term, lacking a generalized consensus among medical professionals on a universally accepted definition; it is a collection of symptoms occurring within the initial week of an injury and lasting up to 3 months or more. Signs and symptoms are the same as those associated with a concussion and cause social and vocational difficulties requiring a multidisciplinary team approach for testing and treatment. The team may consist of a neuropsychologist, physiatrist, neurologist, psychiatrist, and/or primary care physician providing the following resources: cognitive rehabilitation, psychotherapy, stress management, vocational counseling, and medications.¹²

Second impact syndrome (SIS), a term coined in 1984 by Saunders and Harbaugh,¹³ is a rare occurrence where an athlete, still suffering from postconcussive symptoms from an initial head injury, sustains a second head injury that results in a loss of autoregulation of cerebral vasculature, leading to vascular engorgement, cerebral swelling, and brain herniation that is usually fatal. Other than boxers, reports of SIS have never been described in anyone older than 19 years of age. There is controversy over the actual incidence of SIS and little epidemiologic data about supporting the existence of SIS.¹⁴ The United States has a higher incidence of cases among football players as compared with Australia. In Australia, the injury rate is higher but reported less.¹⁴