Neuropathology of cyanate toxicity in rhesus monkeys. Preliminary report.
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Biomedical subjects
Publications and source records attributed to C M Shaw.
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The neuropathological findings at necropsy are described in three cases of basilar artery injuries and their consequences after head trauma and the mechanism of injuries is discussed. The first case was that of massive pontine infarct due to an occlusion of the basilar artery trapped in the fracture of the clivus, 13 days before death. The second case, also with a pontine infarct, survived for two and two-thirds months; the trauma was probably similar, but the presence of the basal skull fracture and the occlusion of the basilar artery can be surmised only in retrospect. The third case was one of delayed rupture of the basilar artery occurring three to four weeks after the injury, which caused aneurysmal formation in the left posterior cerebral artery.
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Small daily doses of methylmercury hydroxide were administered to rhesus monkeys for periods of up to 17 months. Behavioral tests of peripheral vision and of the accuracy and rapidity of hand movements did not disclose any early subtle deficits preceding the onset of obvious signs of neurotoxicity. These signs appeared suddenly and involved reduced food intake (anorexia), clumsiness of jumping, loss of fine control of the digits, and uncoordinated mastication. With a constant daily dose of 0.1 mg/kg or less, blood concentration of mercury reached a peak after about 2 months, and then decreased to about half the peak value. Subsequently, increasing the daily dose level above 0.1 mg/kg (range of 0.12-0.21 mg/kg) produced an increase of blood concentration which tended to stabilize in the range of 2.0-2.5 ppm. After several months at these elevated concentrations all animals exhibited signs of neurotoxicity.