Thalamic Hyperintensity on Diffusion-Weighted MRI in a Patient with Nonconvulsive Status Epilepticus
A 70-year-old woman with altered mentality and unresponsiveness arrived at our emergency room. She had a medical history of Alzheimer’s disease, hypertension and chronic obstructive pulmonary disease, but no seizure or stroke. Her vital signs were stable. On the initial neurologic examination, she was drowsy and mute. She had left homonymous hemianopsia and right gaze preponderance. She showed symmetric withdrawal response to noxious stimuli. Electrocardiogram revealed atrial fibrillation and the cardiac enzymes were normal. Since eight hours before arrival, she had a cluster of generalized tonic clonic seizures at an interval of about ten minutes without full recovery of consciousness for just prior two hours. The convulsive seizure subsided with intravenous lorazepam injection. However, her drowsiness and unresponsiveness did not return to the baseline normal status. We took the DWI and the EEG to identify the cause of sustained abnormal mentality. The DWI revealed an ill-defined high signal intensity in the right thalamus and subtly in the right temporal area, in which the values of apparent diffusion coefficient (ADC) were reduced (). In the MR angiography, there was no significant steno-occlusive lesion. These DWI findings suggested a possibility of a clustered seizure-related change or an acute ischemic stroke. EEG recording showed a right temporal ictal onset zone with persisting ictal discharges with rhythmic alpha to theta activity ().\nAfter the confirmation of ictal EEG, we applied intravenous phenytoin to control the NCSE. Oral topiramate and intravenous levetiracetam were added to suppress remnant ictal discharges. Finally, ictal discharges disappeared (). Though she was gaining alertness, her mutism sustained. Follow-up DWI at the 5th day clarified a brighter lesion localized to the pulvinar (). Transthoracic and transesophageal echocardiographies revealed a small echogenic nodular mass (7.5 × 3.5 mm sized) attached to the posterior mitral valve leaflet and a severely dilated left atrium. Other studies including CSF examination and serologic markers for autoimmune and paraneoplastic diseases were normal. The cause of status epilepticus remained unknown despite extensive work-ups. We suspected a ringt posterior cerebral artery (PCA) infarction when we took her atrial fibrillation and the infarction territory into account. As CHA2DS2-VASc score was 3, it was reasonable to start anticoagulation irrespective of the feasible mechanism of the seizure. Altered mentality with global aphasia persisted despite the adequate treatment.