MON-677 A Neuro-Radiological Stroke Mimicker: Non-Ketotic Hyperglycemia Induced Occipital Lobe Hyperdensity Presenting with Seizures

Background: Acute hyperglycemia in absence of DKA or HHS is a common cause for hospitalization and is termed as Non-Ketotic Hyperglycemia (NKH). NKH-related occipital lobe seizure activity is a rare entity and it’s neuroradiological findings can be confused for acute stroke. We describe a case of NKH-related seizure activity presenting with distinct MRI findings. Clinical Case: 19-year-old male with DM-1 presented with complaints of burning and numbness involving the left side of face, left upper and lower extremity. These lasted for a few hours and had resolved upon arrival to the ER. At the time of presentation, vitals were stable. Physical examination was significant for flat affect with delayed response to questions without any focal deficits. History obtained from his father revealed that he has had similar episodes of decreased responsiveness during periods of acute hyperglycemia. Laboratory values were significant for glucose of 779mg/dl and sodium of 126mMol/L. Absence of ketones or acidosis ruled out DKA. Normal serum osmolality of 295 ruled out HHS. HbA1c >15% confirmed his non-compliance to insulin use. UDS was negative. Patient was admitted and started on insulin basal/bolus regimen. On the second day of hospitalisation, rapid response was called for seizure-like activity characterised by twitching of left side of face, staring into space and deviation of eyes to left upper corner. This resolved with IV lorazepam without any residual focal deficits. Glucose at the time of seizure was 425mg/dl. He was started on levetiracetam and EEG thereafter revealed no seizure-like activity. CT head and CT angiogram of the head and neck were negative. However MRI showed T2 hyperintensity and restricted diffusion with edema throughout the right occipital lobe. Neurology suspected stroke. However, extensive stroke workup for infectious, autoimmune and hypercoagulable states remained negative. Glucose control was achieved and patient was subsequently discharged on a strict insulin regimen and outpatient follow up with an endocrinologist. Conclusion: NKH is known to manifest as seizure activity and thus, should be considered an endocrine emergency requiring prompt diabetic management. The suggested pathophysiology for seizures is prolonged hyperglycemia leading to oxidative stress and cellular edema. Furthermore, this may contribute to the unique MRI findings and should not be confused for an acute stroke. References: Hung WL1, Hsieh PF, Lee YC, Chang MH. Occipital lobe seizures related to marked elevation of hemoglobin A1C: report of two cases.Seizure. 2010 Jul;19(6):359-62. doi: 10.1016/j.seizure.2010.05.006. Epub 2010 Jun 16.