Ataxia is a common finding in patients who have recovered from severe head injury. This report delineates the clinical and pathological findings in a patient who recovered from a head injury but was left with ataxia of gait. A lesion of the superior cerebellar peduncle, demonstrated post mortem 2% years after injury, was the only explanation for the ataxia. This lesion is part of the spectrum of changes seen in diffuse axonal injury thought to be due to shearing forces which tear white matter at the time of the initial injury.
Chester CS, Reznick BR: Ataxia after severe head injury: the pathological substrate. Ann Neurol22: [77][78][79] 1987 Clinicopathological studies of head in juries have generally been limited to patients who died soon after injury or to those dying after prolonged coma. Unexplained focal deficits are common in patients who survive a serious injury, but the pathological correlates of the focal lesions are not well defined. This report describes a patient who recovered from a head injury, but was left with ataxia and died 2'/2 years later. Demyelination of the superior cerebellar peduncle, demonstrated post mortem, was the only explanation for the ataxia. The occurrence of lesions in the cerebellar peduncle and corpus callosum after trauma is well known, but this is usually associated with a prolonged vegetative state.
Case Report
A 32-year-old salesman was found unconscious with Cheyne-Stokes respirations after his car hit a telephone pole. Subsequent examiners described fixed, dilated pupils and withdrawal to painful stimuli. Six hours later, decerebrate posturing of the right limbs developed. A skull film demonstrated a right parietal fracture. Computed tomography showed the lateral ventricles were displaced to the right by a large hematoma within the left temporal lobe as well as contusions in the right parietal lobe. At surgery, the left tempo-From the * D e p m e n t of