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Year : 2022  |  Volume : 70  |  Issue : 2  |  Page : 828--829

MRI in Non-Ketotic Hyperglycemia in an Infant

Mahesh Kamate1, Narendranadha Reddy2, Virupaxi Hattiholi3,  
1 Department of Pediatric Neurology, KAHER's J N Medical College, Belagavi, Karnataka, India
2 Department of Paediatrics, KAHER's J N Medical College, Belagavi, Karnataka, India
3 Department of Radiology, KAHER's J N Medical College, Belagavi, Karnataka, India

Correspondence Address:
Dr. Mahesh Kamate
Professor of Paediatric Neurology, KAHER's J N Medical College, Belgaum - 590 010, Karnataka

How to cite this article:
Kamate M, Reddy N, Hattiholi V. MRI in Non-Ketotic Hyperglycemia in an Infant.Neurol India 2022;70:828-829

How to cite this URL:
Kamate M, Reddy N, Hattiholi V. MRI in Non-Ketotic Hyperglycemia in an Infant. Neurol India [serial online] 2022 [cited 2022 Jun 25 ];70:828-829
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Full Text

Non-ketotic hyperglycemia (NKH) seen mainly in adults with noninsulin-dependent diabetes mellitus is rare in children and can be seen in the setting of monogenic diabetes secondary to mutations in potassium channels. NKH presents as focal motor seizures/epilepsia partialis continua and occipital lobe seizures. The seizures are more related to chronic hyperglycemia due to diabetes mellitus and are associated with increased hemoglobin A1c (Hb1Ac) levels. Chronicity of hyperglycemia is more important than the degree of hyperglycemia.[1] It responds to treatment of underlying hyperglycemia than to use of anti-epileptic drugs. It is associated with characteristic hypointensities on T2 and FLAIR (fluid-attenuated inversion recovery) sequences which could be due to the effect of seizure that occurs in the setting of chronic hyperglycemia without ketosis. We here present the neuroimaging findings of 45-day-old boy, who presented with left focal motor clonic seizures. There was history of frequent feeding and passing frequent urine 2 weeks prior to the seizure. His blood sugar on admission was 536 mg/dL and Hb1Ac was 14.3 mg/dL. There was no acidosis and urine ketones were negative. The seizures did not respond to full doses of phenytoin and levetiracetam but responded to control of sugar with insulin. Electroencephalogram (EEG) showed right occipital and central epileptiform discharges. Cerebrospinal fluid examination was normal and magnetic resonance imaging (MRI) showed hypointensities in right occipital lobe on T2W and FLAIR images [Figure 1]. Genetic tests revealed defect in KCNJ11 gene. To the best of our knowledge, this is the first report of MRI changes in NKH in a young infant.{Figure 1}

Accumulation of iron associated with disruption of axonal transportation, due to early cortical ischemia or excitotoxic damage from seizures, are potential mechanisms of T2 hypointensities.[2] Differentials for this MRI findings include rare presentation of ischemia, multiple sclerosis, leptomeningeal metastasis, and meningitis or meningoencephalitis. This MRI finding should prompt one to think of NKH in a given setting.

ATP-sensitive potassium (KATP) channels have been recently shown to play a role in hyperglycemia-induced seizures. KATP channels that have a role in insulin secretion by pancreatic cells are present even in neurons (e.g., hippocampal and neocortical). These channels are responsible for increasing neuronal excitability in a hyperglycemic environment and these are the ones that are mutated in monogenic diabetes mellitus.[3]

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2Sasaki F, Kawajiri S, Nakajima S, Yamaguchi A, Tomizawa Y, Noda K, et al. Occipital lobe seizures and subcortical T2 and T2* hypointensity associated with nonketotic hyperglycemia: A case report. J Med Case Rep 2016;10:228.
3Moien-Afshari F, Tellez-Zenteno JF. Occipital seizures induced by hyperglycemia: A case report and review of literature. Seizure 2009;18:382-5.