Parkinsomism immediately following a single episode of acute head injury is rare (180) but has been reported with direct penetrating lesions of the midbrain (181) and with subdural hematoma (182). Epidemiologic studies have shown a history of remote head trauma to be a risk factor for PD, however the mechanism is unclear (183-184). Repeated head injury may result in a syndrome that includes psychiatric symptoms, memory loss, and/or parkinsonism (dementia pugilistica, punch-drunk syndrome). This most often occurs in professional and amateur boxers, with the onset of symptoms occurring several years after the end of their athletic career. Pathological studies have shown loss of pigmented neurons in the substantia nigra and the presence of widespread AD-like pathology, with numerous tau-immunoreactive NFTs and amyloid p (Ap) containing SPs (185,186). A direct link between these pathological changes and preceding trauma is supported by studies showing Ap deposits in the brains of individuals dying a few weeks following severe head injury (187) and evidence that both Ap and phosphorylated tau accumulate following brain injury in experimental animals (188,189). Anatomical-pathologic correlation for movement disorder in some of these patients is supported by in vivo neuroimaging, showing damage or dysfunction of the nigrostriatal system (190-192).
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