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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

1
Department of Medical Imaging, The Ottawa Hospital, Ottawa, Ontario, Canada.
2
Department of Radiodiagnosis, Pushpagiri Institute of Medical Sciences and Research Centre, Tiruvalla, Kerala, India.
3
Department of Radiodiagnosis, Krishna Institute of Medical Sciences, Karad, Maharastra, India.
4
Neurology, Pushpagiri Institute of Medical Sciences and Research Centre, Tiruvalla, Kerala, India.

Abstract

Objectives:

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.

Results:

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.

Conclusion:

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.

KEYWORDS:

Hyperglycemia; magnetic resonance imaging; seizures

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