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issue for many years usually with the conclusion that the condition does not exist and that any apparent relationship is super cial and coincidental Most such patients probably had early symptoms of Parkinson disease, brought to light by the head injury There are, however, rare cases, such as the one reported by Doder and colleagues, in which traumatic necrosis of the lenticular and caudate nuclei was followed, after a period of 6 weeks, by the onset of predominantly contralateral parkinsonian signs, including tremor, which progressed slowly and were unresponsive to L-dopa, and there are undoubted instances of parkinsonism following severe closed head injury and the vegetative state (Matsuda et al) An exception to these statements may be a parkinsonian syndrome in ex-boxers, as a manifestation of the punch-drunk syndrome (see below) Cerebellar ataxia is a rare consequence of cranial trauma unless the latter was complicated by cerebral anoxia (causing ataxia with myoclonus) or a by a hemorrhage strategically placed in the deep midbrain or cerebellum When cerebellar ataxia is due to the trauma itself, it is frequently unilateral and the result of injury to the superior cerebellar peduncle An ataxia or apraxia of gait may also re ect the presence of a communicating hydrocephalus (see below and Chap 30) Punch-Drunk Encephalopathy (Dementia Pugilistica) The cumulative effects of repeated cerebral injuries, observed in boxers who had engaged in many bouts over a long period of time, constitute a type of head injury that is dif cult to classify What is referred to is the development, after many years in the ring (sometimes toward the end of the boxer s career, more often within a few years of retirement), of dysarthric speech and a state of forgetfulness, slowness in thinking, and other signs of dementia Movements are slow, stiff, and uncertain, especially those involving the legs, and there is a shuf ing, wide-based gait In other words, a parkinsonian and dementing syndrome emerges and sometimes a moderately disabling ataxia, but there is no mistaking these for idiopathic Parkinson disease The plantar re exes may be extensor on one or both sides The EEG contains slow waves of theta and sometimes delta frequency The clinical syndrome was reanalyzed by Roberts and colleagues, who found it present to some degree in 37 of the 224 professional boxers they examined More recent studies have shown that in about one-half of all professional boxers, both active and retired, the CT scan discloses ventricular dilatation and/or sulcal widening and a cavum septi pellucidi (why the latter, which is a developmental anomaly, would be overrepresented in boxers is unclear) These abnormalities had been demonstrated many years before, by pneumoencephalography, and were found to be related to the number of bouts (Ross et al; Casson et al) A thorough pathologic study of this disorder has been made by Corsellis and associates They examined the brains of 15 retired boxers who had shown the punch-drunk syndrome and identi ed a group of cerebral changes that appear to explain the clinical ndings Mild to moderate enlargement of the lateral ventricles and thinning of the corpus callosum were present in all cases Also, practically all of them showed a greatly widened cavum septi pellucidi and fenestration of the septal leaves Readily identi ed 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 Of the 15 cases, 11 showed varying degrees of loss of pigmented cells of the substantia nigra and locus ceruleus, and many of the.

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remaining cells showed the Alzheimer neuro brillary change; Lewy bodies were not observed, however The neuro brillary 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 senile plaques in this material; however, all cases showed extensive immunoreactive deposits of -amyloid ( diffuse plaques ) In three boxers who developed a parkinsonian syndrome, Davie and colleagues found a reduction of N-acetylaspartate in the putamen and pallidum by protein magnetic resonance spectroscopy This probably re ected a loss of neurons in these regions and was said by these authors to differentiate it from idiopathic Parkinson disease The pathogenesis of the punch-drunk state remains unclear Posttraumatic Hydrocephalus This is an uncommon complication of severe head injury 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 (normalpressure hydrocephalus) Postmortem examinations have demonstrated an adhesive basilar arachnoiditis Since a similar syndrome is observed occasionally after the rupture of a saccular aneurysm with subarachnoid hemorrhage, the same mechanisms, ie, blocking of the aqueduct and fourth ventricle by blood clot and basilar meningeal brosis, may also be operative in traumatic hydrocephalus Response to ventriculoperitoneal shunt may be dramatic Zander and Foroglou have had extensive experience with this condition and have written informatively about it

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Posttraumatic Nervous Instability (Postconcussion Syndrome)