A pathologic study of this disorder specific to boxers was made by Corsellis and associates. They examined the brains of 15 retired boxers who had shown the “punch-drunk” syndrome and identified a group of cerebral changes that appeared to explain the clinical findings. Mild to moderate enlargement of the lateral ventricles and thinning of the corpus callosum were present in all cases. Also, as mentioned, practically all of them showed a greatly widened cavum septi pellucidi and fenestration of the septal leaves. Readily identified areas of glial scarring were situated on the inferior surface of the cerebellar cortex. In these areas, and well beyond them, Purkinje cells were lost and the granule cell layer was somewhat thinned. Surprisingly, cerebral cortical contusions were found in only a few cases. Notably absent also was evidence of previous hemorrhage but earlier studies by Martland emphasized punctate hemorrhages as the main finding (he may have introduced the term from the ring to medical parlance and his paper has colorful language). Of the 15 cases in Corsellis’s cohort, 11 showed varying degrees of loss of pigmented cells of the substantia nigra and locus ceruleus, and many of the remaining cells showed Alzheimer neurofibrillary change but not Lewy bodies. Neurofibrillary changes were scattered diffusely through the cerebral cortex and brainstem but were most prominent in the mediotemporal gray matter. Noteworthy was the absence of discrete amyloid plaques in this material by the usual staining methods; however, all cases showed extensive immunoreactive deposits of beta-amyloid (“diffuse plaques”).
However, these studies were performed before the advent of modern immunohistochemistry techniques. McKee and her coworkers have drawn attention to the deposition of tau protein in autopsy material that has come to define chronic traumatic encephalopathy. They have found a fairly consistent neuropathologic pattern consisting mainly of perivascular hyperphosphorylated tau protein embedded in astrocytic or neurofibrillary tangles with a predilection for the depths of sulci of the frontal and temporal lobes but also in other areas of cortex, thalamus, and brainstem, and eventually appearing extensively in the medial temporal lobes. For example, among 85 subjects with repetitive mild traumatic brain injury they found these changes to varying degrees in 68. The majority had headaches, depression, impulsivity, and aggression only roughly proportional to the severity of pathologic changes. As evident in others was poor cognitive performance in the spheres of executive function and memory. Only those with the most widespread and densest deposition of tau were overtly demented and many of those had gait difficulty. A few of these also had parkinsonian manifestations. A putative relationship of recurrent trauma to motor neuron disease has also been raised. This form of chronic encephalopathy and tau deposition has evinced great interest in relation to concussion sustained during athletics at all levels.
This is an uncommon complication, but one that is frequently imputed to severe head injury. It usually conforms to the category of normal pressure hydrocephalus, as discussed in Chap. 29 but an ex-vacuo type of ventricular enlargement is seen, particularly in chronic alcoholics. Intermittent headaches, vomiting, confusion, and drowsiness are the initial manifestations. Later on, mental dullness, apathy, and psychomotor retardation are seen; by this time the CSF pressure may have fallen to a normal level (normal-pressure hydrocephalus). Postmortem examinations in some cases have demonstrated an adhesive basilar arachnoiditis. Early subarachnoid hemorrhage may be involved in the mechanisms. The response to ventriculoperitoneal shunt may be dramatic. Zander and Foroglou have written informatively about this condition.