Hiremath SB, Gautam AA, George PJ, Thomas A, Thomas R, Benjamin G, et al.
The Indian journal of radiology & imaging. Date of publication 2019 Oct 1;volume 29(4):343-349.
1. 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.
Hiremath SB(1)(2), Gautam AA(2)(3), George PJ(2), Thomas A(2), Thomas R(4),
Benjamin G(2).
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.
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.
Copyright: © 2019 Indian Journal of Radiology and Imaging.
DOI: 10.4103/ijri.IJRI_344_19
PMCID: PMC6958898
PMID: 31949334
Conflict of interest statement: There are no conflicts of interest.
