Abstract
Falconer and Taylor1 have recently inferred from retrospective studies of case records that the primary cause of ammonshorn sclerosis—as classically found in the brains of many epileptics—may be anoxia during febrile convulsions in childhood. It would seem more than coincidental that to create selective ammonshorn sclerosis in guinea-pigs I have used repetitive seizures under hypoxia2, or hypoglycaemia, accompanied by hyperthermia (rectal temperature of 43°–45° C attained by running the experiments within a glass-doored oven) in order to accelerate the appearance of the lesions. If this experimental combination of “exhaustion” stresses approximates to the combination of circumstances during febrile convulsions in human childhood, then the primary lesions at that age might be prevented by the administration of hypothermia and hyperbaric oxygen, and perhaps intravenous glucose, rather than of anti-epileptics. Again, because I have observed that premedication with amphetamine tends to prevent the occurrence of pathology in the ammonshorn of guinea-pigs3, there might be prophylactic value in the administration of amphetamine as well.
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References
Falconer, M. A., and Taylor, D. C., Arch. Neurol., 19, 353 (1968).
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Turner, E. A., J. Neurol. Neurosurg. Psychiat., 26, 285 (1963).
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MCLARDY, T. Ammonshorn Pathology and Epileptic Dyscontrol. Nature 221, 877–878 (1969). https://doi.org/10.1038/221877a0
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DOI: https://doi.org/10.1038/221877a0
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