Wernicke's Encephalopathy Mimicking Acute Onset Stroke Diagnosed by CT Perfusion

Background. Metabolic syndromes such as Wernicke’s encephalopathy may present with a sudden neurological deficit, thus mimicking acute onset stroke. Due to current emphasis on rapid admission and treatment of acute stroke patients, there is a significant risk that these stroke mimics may end up being treated with thrombolysis. Rigorous clinical and radiological skills are necessary to correctly identify such metabolic stroke mimics, in order to avoid doing any harm to these patients due to the unnecessary use of thrombolysis. Patient. A 51-year-old Caucasian male was admitted to our hospital with suspicion of an acute stroke due to sudden onset dysarthria and unilateral facial nerve paresis. Clinical examination revealed confusion and dysconjugate gaze. Computed tomography (CT) including a CT perfusion (CTP) scan revealed bilateral thalamic hyperperfusion. The use of both clinical and radiological findings led to correctly diagnosing Wernicke’s encephalopathy. Conclusion. The application of CTP as a standard diagnostic tool in acute stroke patients can improve the detection of stroke mimics caused by metabolic syndromes as shown in our case report. 1. Case Report A fifty-one-year old Caucasian male was admitted to our hospital with sudden onset confusion, dysarthria, and a unilateral facial palsy. The patient was in his usual health prior to admission. His medical history consisted of hypothyroidism, peptic ulcer disease, and previous alcoholism complicated by alcoholic polyneuropathy. Home nursing services noticed an acute onset dysarthria and a unilateral facial nerve paresis so they contacted the emergency medical services. Due to the acute deterioration of his speech, he was admitted as a possible candidate for thrombolytic treatment-flown into the hospital by air ambulance. Upon admission the patient was fully conscious but was perceived to be somewhat perplexed. He was oriented for neither date nor time. On examination, pupils were equal and reactive with corneal reflexes present bilaterally. Both visual fields were intact. Yet, his gaze in the midline was dysconjugate with abduction weakness present bilaterally (Figure 1). This was manifested clinically with double vision on lateral gaze. No nystagmus was observed. There was no facial asymmetry and on clinical testing no facial nerve paresis was noted. The tongue was not deviated from the midline with no appreciable atrophy or fasciculations. Examination of strength was consistent with a generalized weakness but there were no formal pareses. No involuntary movements were seen. Deep tendon