Diagnostic Neuroradiology

Neuroradiology

, Volume 49, Issue 4, pp 299-305

Focal neuronal loss, reversible subcortical focal T2 hypointensity in seizures with a nonketotic hyperglycemic hyperosmolar state

  • S. RaghavendraAffiliated withDepartment of Neurology, Sree Chitra Tirunal Institute for Medical Sciences and Technology
  • , R. AshalathaAffiliated withDepartment of Neurology, Sree Chitra Tirunal Institute for Medical Sciences and Technology
  • , Sanjeev V. ThomasAffiliated withDepartment of Neurology, Sree Chitra Tirunal Institute for Medical Sciences and Technology Email author 
  • , C. KesavadasAffiliated withDepartment of Imaging Sciences and Interventional Radiology, Sree Chitra Tirunal Institute for Medical Sciences and Technology Email author 

Rent the article at a discount

Rent now

* Final gross prices may vary according to local VAT.

Get Access

Abstract

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.

Keywords

Nonketotic hyperglycemia Reversible T2 hypointensity Magnetic resonance imaging Bilateral striatal hyperintensity Diffusion-weighted imaging Seizures