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Sports-related injuries account for 10 % of head and spinal cord injuries,1 and yearly 1.5 million Americans suffer traumatic brain injury (TBI) without loss of consciousness or need for hospitalization. Further evidence that a growing public health dilemma is growing comes from the Centers for Disease Control and Prevention (CDC), who attributed 207,830 emergency room visits per year between 2001 and 2005 to non-fatal sports-related head injuries.2 A study of high school athletes found that all sports were at risk for concussions, with boys’ football the highest at 63 % of the total, followed by wrestling (10 %), soccer (6 %), and the rest in basketball, softball, baseball, field hockey, and volleyball.
Concussion is generally defined as a mild injury to the brain caused by traumatic biomechanical forces without radiographic evidence of damage. It may be caused by a direct blow to the head or an impulsive force that leads to acceleration of the head without direct trauma. Loss of consciousness is frequently absent, in fact 90 % of sports-related concussions present this way.3 The most common signs and symptoms are headaches, dizziness, confusion, disorientation, and blurred vision. Although once thought to be benign, there is increasing evidence that concussions or mild traumatic brain injury (MTBI) have more serious complications, particularly when they occur repeatedly. Sports-related chronic traumatic encephalopathy (CTE) manifests as a progressive worsening of cerebral neurologic symptoms, initiated and maintained from repetitive concussions. Recent epidemiologic data has shown that 17 % of the individuals with repetitive MTBI develop CTE, however, the severity and the frequency of repetitive injury needed to cause CTE is still unknown.4–8
Early Concepts of Chronic Traumatic Encephalopathy
In 1928, Martland introduced the term ‘punch drunk’ to describe neurologic symptoms such as confusion, tremors, slowed speech and gait seen in boxers suffering from repeated blows to the head.9 This came to be known as ‘dementia pugilistica’ by Millspaugh,10 and then the term ‘psychopathic deterioration of pugilists’ was introduced by Courville.11 The cause of these symptoms became clear once the neuropathology of CTE was described by Brandenburg and Hallevorden and later Corsellis who found several characteristic areas of damage—septum pellucidum, adjacent periventricular gray, frontal and temporal lobes, substantial nigra, cerebellar scarring, and diffuse neuronal loss.12,13,14 Table 1 lists the four components of punch drunk syndrome with their suspected anatomical substrate. Although the terms ‘punch drunk’ and ‘dementia pugilistica’ came from the original descriptions found in boxers, later reports showed that CTE was also found in athletes practicing other sports besides boxing where there is a risk of repetitive brain injury (football, wrestling, hockey, and soccer).12,13
The gross pathology of CTE includes a reduction in brain weight, enlargement of the ventricular system, especially lateral and third ventricle, thinning of the corpus callosum, atrophy of cerebral hemispheres, mesial temporal lobes, thalamus, mammillary bodies, olfactory bulbs and brainstem, pallor in the substantia nigra and locus coeruleus, a cavum septum pellucidum, and scarring of the cerebellar tonsils.