RESUMO
Transient lesions at the splenium of the corpus callosum (SCC) have been reported after withdrawal of specific antiepileptic drugs (AED), though the pathophysiology of the lesions remains unclear. We examined and treated a schizophrenic patient who developed a transient SCC lesion after withdrawal of the AED, carbamazepine. Interestingly, the SCC lesion was accompanied by the onset of diabetes insipidus, a state of arginine-vasopressin (AVP) insufficiency. Because carbamazepine is shown to potentiate the effect of AVP, our case suggests that an insufficiency of AVP followed by withdrawal of AED could contribute to the pathogenesis of a transient SCC lesion.
Assuntos
Encefalopatias/induzido quimicamente , Encefalopatias/diagnóstico , Carbamazepina/efeitos adversos , Corpo Caloso/efeitos dos fármacos , Corpo Caloso/patologia , Síndrome de Abstinência a Substâncias/diagnóstico , Doença Aguda , Anticonvulsivantes/efeitos adversos , Humanos , Imageamento por Ressonância Magnética/métodos , Masculino , Pessoa de Meia-Idade , Fatores de TempoRESUMO
We report the characteristics of three patients with spinocerebellar degeneration (SCD) with negative-type electroretinograms (ERGs). None of the patients showed retinal degeneration, but all had severe cerebellar ataxia, and brain MRIs showed cerebellar atrophy. Negative-type ERGs have been implicated in the selective functional impairment of the inner retinal layer, but few studies have reported dysfunction of the inner nuclear layer in SCD patients. Our subjects may be the first reported SCD cases with negative-type ERGs. Our results suggest that an etiologic relationship exists between cerebellar ataxia and negative-type ERGs. Further investigation of ERGs in patients with SCD could potentially lead to the identification of an increased number of SCD patients with negative-type ERGs and retinal pathogenesis.