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Callosotomy for intractable epilepsy from bihemispheric cortical dysplasias

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Summary

Four patients suffering for severe drug-resistant epilepsy from bihemispheric cortical dysplasias underwent anterior callosotomy. One of these patients also presented mental retardation of mild degree associated with the epileptic syndrome. There were no operative complications in this series. Clinical signs of interhemispheric disconnection were not detectable postoperatively.

Twenty-eight to 53 months after surgery, the generalized seizures were completely suppressed in 2 cases, and were reduced by 89–97% in frequency in the other 2 cases. Partial seizures were less affected by callosotomy being reduced by 14–87%.

In an additional fifth case of intractable epilepsy from bihemispheric cortical dysplasias with associated severe mental retardation operated upon elsewhere for callosotomy and followed at our institution, the outcome for seizures was completely unsatisfactory.

Neurophysiological studies revealed that the interhemispheric transfer (IHT) of visuo-motor responses was functionally impaired after callosotomy only in one patient who harboured bilateral cortical dysplasias in the occipital lobes. This malformation might affect the pattern of axonal projection to the posterior portion of the corpus callosum which is considered of crucial importance for the integration of crossed visuo-motor responses.

From this paper the following conclusions can be drawn:

  1. a)

    epileptic patients with severe drug-resistant epilepsy due to bihemispheric cortical dysplasias are good candidates for callosotomy,

  2. b)

    one-stage extensive anterior callosotomy sparing the splenium is the procedure of choice,

  3. c)

    associated severe mental retardation seems to contra-indicate callosotomy,

  4. d)

    the neurophysiological study of the IHT can yield information on the functional status of the corpus callosum.

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Pallini, R., Aglioti, S., Tassinari, G. et al. Callosotomy for intractable epilepsy from bihemispheric cortical dysplasias. Acta neurochir 132, 79–86 (1995). https://doi.org/10.1007/BF01404852

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