Blunt trauma to the head results in acceleration of the brain within the skull. This takes 2 forms: linear or translational acceleration which produces focal lesions, and rotational acceleration which results in ‘sheering stresses’ with stretching of nerves and bridging veins. Deceleration of the brain within the skull occurs when the head strikes a stationary object (e.g. floor, ring post).
Cerebrovascular events are not infrequently encountered. The most common vascular sequalae is the subdural haematoma, which is also the most frequent cause of death in boxers. Epidural bleeds are rare, and are generally due to deceleration of the brain. Subarachnoid bleeds have been rarely reported, but, like intraparenchymal haemorrhages, they do occur. Sudden flexion/extension of the neck is suggested as the mechanism of the occasional brainstem haemorrhage reported in boxing. Thrombosis of the internal carotid artery can occur secondary to direct blows to the neck or stretching of the contralateral carotid artery.
The best known sequalae of boxing is traumatic encephalopathy — the ‘punch drunk’ syndrome. This is most common in second-rate and slugging type fighters. Severity correlates with the length of a boxer’s career and total number of bouts, with an incidence of approximately 18%. Three stages of clinical deterioration are seen, the encephalopathy may be progressive or may remain clinically stable at any level. The first stage consists of affective disturbances with psychiatric symptoms being most marked. During the second stage an accentuation of the psychiatric symptoms occurs and signs/symptoms of Parkinsonism develop. The final stage consists of a decrease in general cognitive function together with pyramidal tract disease. Generally 2 to 3 years elapse between the first and final stages. Neuropathological studies reveal abnormalities of the septum pellucidum, scarring of the cerebellar and cerebral cortices, and loss of pyramidal neurons in the substantia nigra with neurofibrillary tangles in the absence of senile plaques.
A ‘groggy state’ can occur in some fighters with confusion, impaired active attention and alteration of consciousness. During this period the boxer is at greater risk to suffer brain injury as defensive reflexes are frequently lost. Other neurological syndromes have been reported in addition to the ‘groggy state’. These include a midbrain syndrome, headaches and cervical spinal injuries. Additionally, boxing appears to be a significant risk factor for the development of meningiomas.
Radiological studies in boxers with pneumoencephalography (PEG) reveal cerebral/cerebellar atrophy, cavum septum pellucidum and dilation of the cisterna of lamina terminalis in a majority of boxers. These findings have been replicated with computerised tomography (CT) and appear to be more frequent in the boxers with the greater number of bouts. An association between abnormal CT scans and impairment in neuropsychological testing has been reported. Numerous studies using electroencephalography (EEG) have been reported in boxers, most showing abnormal findings on the EEG — generally slowing of the background rhythm into the theta range. A correlation between the number of bouts and their frequency and EEG abnormalities have been reported. While approximately 60% of boxers with encephalopathy show abnormal EEGs, the correlation is low. A smaller number of studies have failed to demonstrate EEG abnormalities. Currently it appears that EEG has a role in determining when a boxer will return to the ring, and is less of a diagnostic tool for evaluating the encephalopathy. Prospective studies are lacking.
Other laboratory methods have been applied to study brain injury in boxers. Regional cerebral blood flow using xenon-133 inhalation has demonstrated a significant decrease in cerebral blood flow in professional boxers when compared to amateurs or controls. Elevation of brain creatine kinase, a cytoplasmic enzyme of the brain, correlates with the degree of cerebral trauma. Rises in the enzyme are seen in boxers, and appear to correlate with the number of blows suffered to the head.
Two major avenues of change have been advanced to improve the safety of boxing. While studies are lacking, experience suggests that the use of protective headgear is not only ineffective, but may increase injuries, as previously glancing blows become more substantial. Conversely, while removing the head as a target would indeed decrease neurological sequalae, the practicality of this has been questioned. Further prospective studies are needed to answer many of the questions that have arisen.