Diabetic striatopathy and concurrent peri-ictal cortical diffusion restriction in nonketotic hyperglycemia: A rare stroke mimic
Source: PubMed Central Open Access, NCBI / U.S. National Library of Medicine
Diabetic striatopathy is a rare neurological complication of nonketotic hyperglycemia, classically associated with hemichorea-hemiballismus and characteristic striatal imaging abnormalities, although atypical presentations may mimic acute cerebrovascular disease. We report a 77-year-old woman with insulin-treated type 2 diabetes mellitus who presented with afebrile status epilepticus and a 1-week history of progressive left hemiplegia. Laboratory testing revealed marked hyperglycemia (480 mg/dL) without ketosis or metabolic acidosis. Electroencephalography demonstrated focal ictal onset in the right parietotemporal region. Noncontrast head CT showed spontaneous hyperdensity of the right caudate nucleus and putamen without mass effect. Brain MRI demonstrated corresponding right striatal T1 hyperintensity and T2/FLAIR hypointensity without diffusion restriction, consistent with diabetic striatopathy. In addition, a right frontal lesion showed FLAIR hyperintensity with diffusion restriction, favored to represent a peri-ictal abnormality related to status epilepticus; however, acute cortical infarction could not be fully excluded in the absence of follow-up imaging. MR angiography showed left M1 and A1 atheromatous stenoses, while the right anterior circulation was patent, and arterial spin labeling demonstrated no focal hyperperfusion. Following antiseizure treatment and intensive glycemic correction, seizures resolved and neurological improvement was observed. This case highlig
Abstract
Diabetic striatopathy is a rare neurological complication of nonketotic hyperglycemia, classically associated with hemichorea-hemiballismus and characteristic striatal imaging abnormalities, although atypical presentations may mimic acute cerebrovascular disease. We report a 77-year-old woman with insulin-treated type 2 diabetes mellitus who presented with afebrile status epilepticus and a 1-week history of progressive left hemiplegia. Laboratory testing revealed marked hyperglycemia (480 mg/dL) without ketosis or metabolic acidosis. Electroencephalography demonstrated focal ictal onset in the right parietotemporal region. Noncontrast head CT showed spontaneous hyperdensity of the right caudate nucleus and putamen without mass effect. Brain MRI demonstrated corresponding right striatal T1 hyperintensity and T2/FLAIR hypointensity without diffusion restriction, consistent with diabetic striatopathy. In addition, a right frontal lesion showed FLAIR hyperintensity with diffusion restriction, favored to represent a peri-ictal abnormality related to status epilepticus; however, acute cortical infarction could not be fully excluded in the absence of follow-up imaging. MR angiography showed left M1 and A1 atheromatous stenoses, while the right anterior circulation was patent, and arterial spin labeling demonstrated no focal hyperperfusion. Following antiseizure treatment and intensive glycemic correction, seizures resolved and neurological improvement was observed. This case highlights the coexistence of diabetic striatopathy and a probable peri-ictal cortical lesion in nonketotic hyperglycemia, resulting in a misleading stroke-like presentation. abs0001