Neuroimaging in uncontrolled hyperglycemia: a case series and literature review

Abstract

Abstract Background There are wide-ranging differential diagnoses for the myriad of neurological symptoms associated with non-ketotic hyperglycemia. Similarly, various secondary complications of diabetic ketoacidosis present with nonspecific clinical symptoms. These are inadvertently misdiagnosed as epilepsies and strokes with associated hyperglycemia. Direct association between these nonspecific symptoms and hyperglycemia has been proved by demonstrating their resolution with correction of the latter. This case series portrays the spectrum of few rare neuroimaging findings of uncontrolled hyperglycemia, which helps in proper and prompt diagnoses. Case presentation Five diabetic patients with uncontrolled hyperglycemia were observed. Striatal hyperdensity on computed tomography or striatal T1 hyperintensity on magnetic resonance imaging was observed in three patients who presented with movement disorders. The abnormality was bilateral in one case. These observations were consistent with hyperglycemia-induced hemichorea–hemiballismus syndrome. In another patient who had presented with focal seizures, magnetic resonance imaging revealed subcortical T2/FLAIR hypointensity in bilateral occipital regions, which has been described to be characteristic for non-ketotic hyperglycemia-related seizures. Yet another patient who had been treated for diabetic ketoacidosis had developed bilateral lower-limb weakness. In correlation with a background of rapid correction of hyponatremia, magnetic resonance imaging revealed symmetric areas of altered signal intensity in the bilateral perirolandic region showing an open ring pattern of diffusion restriction, suggesting extrapontine myelinolysis. Conclusions In all the cases, the clinical differentials were wide. Neuroimaging was mandatory in establishing hyperglycemia as the underlying cause for the movement disorders and seizures. Also, neuroimaging aided in timely identification of extra-pontine myelinolysis, which might have prevented further central pontine involvement in the patient with diabetic ketoacidosis.