Search

Introduction: Neuroimaging in seizures associated with nonketotic hyperglycemia (NKH) is considered normal. We report magnetic resonance imaging (MRI) abnormalities in four patients with NKH and seizures., Methods: We prospectively evaluated clinical and radiological abnormalities in four patients with NKH during the period March 2004 to December 2005., Results: All patients presented with seizures, either simple or complex partial seizures or epilepsia partialis continua. Two of them had transient hemianopia. MRI showed subcortical T2 hypointensity in the occipital white matter and in or around the central sulcus (two patients each), T2 hyperintensity of the overlying cortex (two patients), focal overlying cortical enhancement (three patients) and bilateral striatal hyperintensity (one patient). Diffusion-weighted imaging (DWI) performed in three patients showed restricted diffusion. The ictal semiology and electroencephalographic (EEG) findings correlated with the MRI abnormalities. On clinical recovery, the subcortical T2 hypointensity and striatal hyperintensity reversed in all patients. The initial cortical change evolved to FLAIR hyperintensity suggestive of focal cortical gliosis. The radiological differential diagnosis considered initially included encephalitis, malignancy and hemorrhagic infarct rendering a diagnostic dilemma., Conclusion: We identified subcortical T2 hypointensity rather than hyperintensity as a characteristic feature of seizures associated with NKH. Only very few similar reports exist in literature. Reversible bilateral striatal T2 hyperintensity in NKH has not been reported to the best of our knowledge.

Although a wide spectrum of reversible periictal magnetic resonance imaging (MRI) abnormalities (RPMA) are being increasingly identified, the clinicians are often in a dilemma about their localization significance. This prompted us to analyze the clinical, MRI, electroencephalographic (EEG) and follow-up data of 12 patients with RPMA seen in a tertiary referral epilepsy center. RPMA occurred after a single or a cluster of focal seizures with or without secondary generalization. The interictal and ictal EEG abnormalities were localized to the site of RPMA in nine patients. RPMA involved areas remote from the site of EEG abnormalities in four patients. We have developed a comprehensive classification to account for the wide spectrum of RPMA involving gray matter, white matter and leptomeninges with or without contrast enhancement or mass effect. Follow-up MRIs showed complete resolution of RPMA in all, except in four patients, who developed residual focal atrophy. During median follow-up period of 3 years, recurrence of RPMA was observed in two patients. Diffusion weighted MRI in two patients and histopathological finding in one patient favored causal role of hypoxia in the pathogenesis of RPMA. Our observations help to understand the electroclinical profile, radiological spectrum, localization significance and natural history of RPMA better.