Transient lesion in the splenium of the corpus callosum: three further cases in epileptic patients and a pathophysiological hypothesis

Abstract

Objective-Focal lesions limited to the splenium of the corpus callosum (SCC) are rare and little is known about their aetiology. Three patients were examined for presurgical evaluation in epilepsy with a transient lesion in the SCC and a pathophysiological hypothesis is presented. Methods-Three patients were identified with a circumscribed lesion in the centre of the corpus callosum. Follow up MRI was performed, the medical records examined retrospectively, and the literature reviewed. Results-The patients showed identical lesions in the SCC with reduced T1 and increased T2 signal intensity and an unaffected marginal hemline of a few mm. Patients were asymptomatic and control MRIs showed complete normalisation within 2 months. Patients had been treated with antiepileptic drugs (AEDs) without signs of toxicity. In all patients AEDs were rapidly reduced for diagnostic purposes, but only one had psychomotor seizures, 5 days before imaging. Conclusions-A transient lesion in the SCC has so far only been described in 13 patients with epilepsy and has been interpreted either as reversible demyelination due to AED toxicity or transient oedema after secondary generalised seizures. The data confirm neither of these hypotheses. A transient lesion in the SCC seems to be a non-specific end point of diVerent disease processes leading to a vasogenic oedema. This suggests, in these patients, a multifactorial pathology triggered by transient eVects of AEDs on arginine vasopressine and its function in fluid balance systems in a condition of vitamin deficiency. The complete and rapid reversibility in all cases without specific intervention is emphasised and any invasive diagnostic or therapeutic approach is discouraged. (J Neurol Neurosurg Psychiatry 2001;70:459-463) Keywords: corpus callosum; anticonvulsant drugs; brain oedema; argipressine Focal imaging abnormalities of the corpus callosum are rare but have been described in various clinical conditions. We have detected a circumscribed lesion confined to the splenium of the corpus callosum in three patients during presurgical evaluation of therapy for refractory epilepsy. An identical lesion has been reported, but the pathophysiological mechanisms have not been identified. [1][2] We have reviewed the literature on splenial lesions and present a new hypothesis about the underlying mechanisms. Case reportsPATIENT 1 A 34 year old woman had an unclassified epilepsy syndrome with partial and generalised During non-invasive monitoring for 10 days she did not show any ictal event and her EEG was normal even though we had stopped phenytoin medication (serum concentration 21.8 mg/l). Brain MRI showed a hypointense signal in the splenium of the corpus callosum on the T1 weighted and inversion recovery scans that was hyperintense in the T2 weighted as well as in FLAIR images (fig 1).These characteristics suggested an abnormally high water content in these areas. The lesion was not associated with further white matter abnormalities and left about 2 mm of the marginal area aroun...

Encephalitis with Prolonged but Reversible Splenial Lesion

“…Some of the proposed mechanisms are blood-brain barrier breakdown, intramyelinic edema due to inflammation and migration of inflammatory cells, extrapontine osmotic myelinolysis due to sodium and glucose imbalance, and direct viral invasion or hypersensitivity to antiepileptic drugs. Studies about posttraumatic lesions in the corpus callosum generally explain the prevalence of callosal injury by its vulnerability to shearing forces (8). In our patient, we presume the presence of an inflammatory mechanism, with intramyelinic edema lasting for more than one month.…”

Encephalopathy Associated with Psychotropic Drug Therapy

“…Indeed, the same lesion has been reported also in the non-epileptic patients treated with antiepileptic drugs (Maeda et al, 2003;Honda et al, 2006). Some patients developed the lesion on treatment with antiepileptic drugs (Kim et al, 1999;Polster et al, 2001;Maeda et al, 2003), while others subsequent to withdrawal of them (Polster et al, 2001;Gürtler et al, 2005;Honda et al, 2006). …”

“…With widespread use of magnetic resonance imaging (MRI), a characteristic discrete focal lesion limited to the central area of the splenium of the corpus callosum has been recognized to occur in epileptic patients receiving antiepileptic drugs (S.S. Kim et al, 1999;Polster et al, 2001). Although the pathophysiological mechanisms of this lesion are still obscure, antiepileptics appear to be implicated as pathogenetic or triggering factors at least in some cases.…”

Lesão transitória no esplênio do corpo caloso em criança epiléptica com glioma cerebral de baixo grau

“…A revisão da literatura sobre lesões do corpo caloso levou ao encontro de três relatos com descrição de alterações idênticas às observadas no presente caso, em 16 pacientes com epilepsia do lobo temporal 1 -4 . Os mecanismos fisiopatológicos ainda não estão adequadamente identificados, tendo sido levantada a hipótese de toxicidade a vigabatrina/fenitoína 2 e de tratar-se de disfunção axonal transitória dependente das crises epilépticas 3 . O objetivo deste relato é chamar a atenção par a que o encontro para alteração do esplênio do c o r p o caloso no estudo de neuroimagem por ressonância magnética (RM) em crianças com crises epilépticas parciais pode ser uma manifestação transitória.…”