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SYNOPSIS The brains of 15 retired boxers have been studied and the lives of the men concerned have been investigated in retrospect. A characteristic pattern of cerebral change has been identified which appears not only to be a result of the boxing but also to underlie many features of the punchdrunk syndrome.157 35

The repeated head trauma experienced by boxers can lead to the development of dementia pugilistica (DP)-punch drunk syndrome. The neuropathology of DP in a classic report by Corsellis et al describes the presence of numerous neurofibrillary tangles in the absence of plaques, in contrast to the profusion of tangles and plaques seen in Alzheimer's disease (AD). The DP cases used in that report were re-investigated with immunocytochemical methods and an antibody raised to the f-protein present in AD plaques. We found that all DP cases with substantial tangle formation showed evidence of extensive #-protein immunoreactive deposits (plaques). These diffuse "plaques" were not visible with Congo-red The final stage consists of a decrease in general cognitive functioning-progressing to dementia together with pyramidal tract disease. Several years elapse between stages.The neuropathology of the condition, described in a classic study,5 consists of abnormalities of the septum pellucidum, focal scarring of the cerebellum and loss of pigmented neurons in the substantia nigra. A striking finding was the presence of numerous neurofibrillary tangles in the cortex (particularly in the temporal lobe) in the absence of appreciable numbers of plaques. A marked contrast to the situation typically seen in Alzheimer's disease (AD). While most of the damage present in DP brains is accountable in terms of trauma suffered during the linear and rotational acceleration caused by blows to the head,5 the extensive neurofibrillary change in the absence of plaque formation is a puzzling phenomenon. The tangles of DP are structurally and immunologically6 indistinguishable from the tangles which are thought to be central to the disease process in AD. On this basis it has been suggested that studies of DP may provide aetiological insight for AD.56 However, this suggestion has been dismissed on the basis that plaques are the central component of AD and as cases of DP show no appreciable plaque formation then the processes involved must be radically different.The

SYNOPSIS The neuropathological results from a prospective, systematically assessed, series of 56 schizophrenic patients and 56 age-and sex-matched normal controls have been presented.When compared with the normal controls, the brains of the schizophrenic subjects showed a significant reduction in brain weight and brain length with a concomitant increase in ventricular size. (All findings relate to measurements made after formalin fixation). In addition, the brains of the schizophrenic patients contained significantly more non-specific focal pathology and fibrillary gliosis than the controls.After exclusion of cases with moderate and severe Alzheimer-type change, cerebro-vascular disease and all forms of focal pathology, the structural brain changes (i.e. decrease in brain weight and brain length) continued to distinguish the schizophrenia group from the controls. Furthermore, an analysis of the clinical data showed that the structural brain changes were correlated in the schizophrenic patients with a measurement of pre-morbid function.The findings and their possible aetiological implications have been discussed.

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