Hyperglycemia with Occipital Seizures: Images and Visual Evoked Potentials

Abstract

Summary:Purpose: Hyperglycemia may rarely be seen with visual seizures. Observation of both visual evoked potentials (VEPs) and magnetic resonance imaging (MRI) in visual status epilepticus (SE) has not been reported. We describe acute and follow-up VEP and MRI findings of a patient with hyperglycemia-related visual SE of occipital origin.Methods: In a 59-year-old diabetic woman, complex visual hallucinations and illusions developed with ≤10 seizures per hour as an initial manifestation of nonketotic hyperglycemia.Results: Neurologic examination revealed ictal nystagmus to the right and continuous right hemianopsia. Ictal electroencephalography (EEG) and Tc-99m hexamethylpropylene amine oxime (HMPAO) single-photon emission computed tomography (SPECT) revealed an epileptogenic focus in the left occipital lobe. MRI with fluid-attenuated inversion recovery showed focal subcortical hypointensity and gyral hyperintensity. Followup MRI showed only minimal gyral hyperintensity at 6 months. The P100 amplitude of VEP was significantly higher at the right occipital area during SE, but slightly higher on the left after the patient had been seizure free for 6 months.Conclusions: Occipital seizures and hemianopsia can be caused by hyperglycemia and may be accompanied by special MRI and VEP findings. Key Words: Nonketotic hyperglycemia-Hemianopsia-Visual evoked potentialsMagnetic resonance imaging.Nonketotic hyperglycemia (NKH) is a clinical syndrome consisting of severe hyperglycemia, hyperosmolality, and intracellular dehydration without ketoacidosis. Only a few cases of NKH-related occipital visual seizures have been reported (1-4).Partial status epilepticus (SE) can be defined as (a) >30 min of abnormal neurologic function at the time of EEG, and (b) at least two discrete EEG seizures or continuous rapid (≥1.5 Hz) epileptiform discharges (5).Observation of both visual evoked potential (VEP) and magnetic resonance imaging (MRI) abnormalities in hyperglycemia-related visual SE has never been reported. We describe immediate and follow-up VEP and MRI findings of a patient with visual SE due to NKH.

Homonymous hemianopia in nonketotic hyperglycemia is an ictal phenomenon

“…There is other evidence of occipital seizures in the setting of hyperglycemia in NKH. 2,3 Two separate reports in patients with right HH described left occipital hyperperfusion on SPECT in conjunction with left occipital rhythmic beta activity on EEG, 4 and fMRI blood oxygenation level-dependent activation in Brodmann area 18 in conjunction with left occipital ictal activity. 5 To our knowledge, there are no reports of brain FDG-PET with EEG to confirm the ictal nature of NKH-associated HH.…”

Neuroimaging in Patients with Abnormal Blood Glucose Levels

“…33 Sporadic reports of 1 H-MR spectroscopy have described reduced NAA in the involved regions. 38 There are few case reports of ictal hyperperfusion in the involved regions on technetium Tc99m hexamethylpropyleneamine oxime SPECT imaging, in contrast to HC-HB in a similar subgroup of patients, which shows hypoperfusion. 19,34,38 Besides NKHG, subcortical T2 shortening may also be seen in viral encephalitis, meningitis, hypoxic insult, and Moyamoya disease.…”

“…38 There are few case reports of ictal hyperperfusion in the involved regions on technetium Tc99m hexamethylpropyleneamine oxime SPECT imaging, in contrast to HC-HB in a similar subgroup of patients, which shows hypoperfusion. 19,34,38 Besides NKHG, subcortical T2 shortening may also be seen in viral encephalitis, meningitis, hypoxic insult, and Moyamoya disease. 33 Overlying leptomeningeal enhancement, if present, would add metastasis, sarcoidosis, and lymphoma to the list of differential considerations.…”

“…33 NCCT is often negative, though rare cases with both HC-HB and seizures may show basal ganglia hyperattenuation. 38,39 On MR imaging, the involved regions are usually isointense on T1WI but may show focal T2 prolongation in the cortex and T2 shortening in the underlying WM. [33][34][35] Similar hypointense subcortical signal is also noted on gradient-echo images.…”

“…Postulated mechanisms include mineral deposition and ischemia. 33,34,38 A hypointense signal on the gradient-echo image would support free radical accumulation. 33 NCCT is often negative, though rare cases with both HC-HB and seizures may show basal ganglia hyperattenuation.…”