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
