Diabetic Ketoacidosis Related Focal Status Epilepticus Associated with T1 Hyperintensity on the Caudate Nucleus, a Finding Specific to Hyerglycemic Movement Disorders
Maryam Bahadori1, Wumy Oderinde1, Dan Michael Pineda2, james thomas2
1Tufts Medical Center, 2Lahey Clinic and Medical Center
Background:
Seizures can complicate hyperglycemic emergencies, being more common in Nonketotic hyperglycemic hyperosmolar (NKHH) than diabetic ketoacidosis (DKA) because ketones may decrease neuron excitability and increase seizure threshold. A characteristic radiologic feature of NKHH is subcortical T2 hypointensity, known as the “dark white matter” sign. Our case presents an unusual instance of DKA manifesting as focal status epilepticus with MRI findings typical of hyperglycemic movement rather than a seizure disorder.
Results:
67 year old man with poorly controlled diabetes presented with a week of subacute confusional state. No facial or limb weakness or dyskinesias were observed. High urinary ketones, uremia, and a serum glucose of 422 mg/dL led to his admission for diabetic ketoacidosis. Bicarbonate levels were elevated, while sodium, calcium, and liver function tests were normal. An EEG showed focal status epilepticus from the left temporal lobe, which was eventually controlled with levetiracetam and lacosamide. MRI revealed multifocal cortical and subcortical diffusion restrictions, FLAIR hyperintensities in the left parietal, occipital, and posterior temporal regions, and T1 hyperintensity on the left caudate extending to the lentiform nucleus. Empiric IV acyclovir was initiated. CSF analysis was negative for pleocytosis, HSV PCR, and autoimmune and infectious panels. He improved over 48 hours with glucose correction, becoming alert, oriented, and conversational. Follow-up imaging showed resolution of the diffusion restrictions. His rapid recovery and imaging suggested seizure caused by DKA rather than encephalitis, leading to the discontinuation of antivirals. He was discharged to rehab and recovered after two weeks of physical therapy.
Conclusions:
DKA can present with focal seizures, similar to NKHH. While T1 hyperintensity of the basal ganglia has been linked to hyperglycemic movement disorders, this case shows that it can also be associated with seizures. This radiologic feature may help differentiate hyperglycemic-induced seizures from other causes such as encephalitis.
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