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Indian J Radiol Imaging. 2019 Oct-Dec;29(4):343-349. doi: 10.4103/ijri.IJRI_344_19. Epub 2019 Dec 31.

Hyperglycemia-induced seizures - Understanding the clinico- radiological association.

Author information

Department of Medical Imaging, The Ottawa Hospital, Ottawa, Ontario, Canada.
Department of Radiodiagnosis, Pushpagiri Institute of Medical Sciences and Research Centre, Tiruvalla, Kerala, India.
Department of Radiodiagnosis, Krishna Institute of Medical Sciences, Karad, Maharastra, India.
Neurology, Pushpagiri Institute of Medical Sciences and Research Centre, Tiruvalla, Kerala, India.



To highlight the typical magnetic resonance imaging (MRI) findings in hyperglycemia-induced seizures and compare the results with similar previous studies with a brief mention of pathophysiological mechanisms.

Materials and Methods:

This retrospective study included medical and imaging records of six consecutive patients with hyperglycemia-induced seizures. The data analysis included a clinical presentation and biochemical parameters at admission. The MRI sequences were evaluated for region involved, presence of subcortical T2 hypo-intensity, cortical hyper-intensity, and restricted diffusion. Similar previous studies from the National Library of Medicine (NLM) were analyzed and compared with our study.


Twenty-four patients were included from four studies in previous literature for comparison. In our study, on imaging, posterior cerebral region was predominantly involved, with parietal involvement in 83.3%, followed by occipital, frontal, and temporal involvement in 33.3% patients compared with occipital in 58.3%, parietal in 45.8%, and frontal and temporal in 16.6% of patients in previous literature. The subcortical T2 hypo-intensity was present in 83.3% of the patients, cortical hyper-intensity in all patients, and restricted diffusion in 66.6% of the patients in our study compared with subcortical T2 hypo-intensity in 95.8% of the patients, cortical hyper-intensity in 62.5%, and restricted diffusion in 58.3% of the patients in previous literature.


Although many etiologies present with subcortical T2 hypointensity, cortical hyperintensity, restricted diffusion, and postcontrast enhancement on MRI, the clinical setting of seizures in a patient with uncontrolled hyperglycemia, hyperosmolar state, and absence of ketones should suggest hyperglycemia-induced seizures to avoid misdiagnosis, unnecessary invasive investigations, and initiate timely management.

Advances in Knowledge:

Our study highlights the presence of posterior predominant subcortical T2, fluid-attenuated inversion recovery (FLAIR), and susceptibility-weighted angiography (SWAN) hypointensity; cortical hyperintensity; and restricted diffusion in hyperglycemia-induced seizures. The presence of T2 and SWAN hypointensity could support the hypothesis of possible deposition of free radicals and iron in the subcortical white matter.


Hyperglycemia; magnetic resonance imaging; seizures

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