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
The patient with dysconjugate eye position.
Due to the acute onset of dysarthria and oculomotor pathologies an urgent cerebral CT was performed revealing hypodense changes in the thalamus bilaterally (Figure
CT on admission. The white arrows show the hypodensities seen medial in the thalamus bilaterally.
CT perfusion on admission. Time-to-peak map (TTP, (a)) showing reduced time-to- peak and cerebral blood flow map (CBF, (b)) and cerebral blood volume map (CBV, (c)) showing increased relative cerebral blood flow and relative cerebral blood volume in thalamus bilaterally.
A complete blood count was noteworthy for a slightly elevated glucose 7.9 mmol/L (reference range 4.0–6.0 mmol/L) and C-reactive protein 14 mg/L (reference range 0–7 mg/L). The remainder of the blood work-up, which included electrolytes, and kidney- and liver-function tests, was normal. Testing for intoxicants in the blood, which included opiates, benzodiazepines, and ethanol, was negative. A lumbar puncture was performed and analysis of the cerebrospinal fluid (CSF) was normal, showing a CSF protein of 0.45 g/L (reference range 0.0–0.5 g/L), 2 white blood cells per microliter (reference range 0–5 cells per microliter), and CSF glucose of 5 mmol/L. A chest X-ray was performed, revealing no pathologies. A transthoracic echocardiogram was also performed with normal findings.
MRI imaging of the brain showed bilateral hyperdense lesions in the thalamus on the fluid attenuated inversion recovery (FLAIR) series. These lesions exhibited slight gadolinium (Gd) contrast enhancement as did both mammillary bodies (Figure
MR at day 3 showing hyperintense changes in both thalami adjacent to the third ventricle on FLAIR series (a) and Gd-enhancement in the thalami (b) and in the mammillary bodies (c).
Both the clinical presentation and the radiological examinations were consistent with Wernicke’s encephalopathy. In addition, caregivers of the patient were contacted and confirmed that he had not been eating normally with increasing bouts of nausea and vomiting over a two- week period. Furthermore they informed us that he had been treated for Wernicke’s encephalopathy several years ago, at another hospital. The patient was promptly treated with intravenous thiamine for three days. After starting treatment he showed significant clinical improvement on a daily basis. Vitamin B1 treatment was continued orally and the patient was discharged on the fourth day after admission, clinically completely restituted.
Wernicke’s encephalopathy is a relatively common, acute onset neuropsychiatric syndrome, arising from vitamin B1 (thiamine) deficiency; it is characterized by ophthalmoplegia, cerebellar dysfunction, and mental changes. Yet, this classical triad of symptoms is seen in only 16% of patients [
The thiamine deficiency seen in Wernicke’s encephalopathy leads to brain lesions usually restricted to more certain vulnerable areas. These lesions usually establish themselves within 2-3 weeks, corresponding well with the time needed for the depletion of the bodies thiamine reserves [
An acute onset stroke was suspected in our patient according to the FAST criteria (Face, Arm, Speech, and Time); the presence of a facial paresis and slurred speech, noted prehospitally, led to rapid admission [
To our knowledge this is the first case report, where a patient admitted to hospital with the suspicion of an acute onset stroke was correctly diagnosed with Wernicke’s encephalopathy, due to demonstrable hyperperfusion on CTP series. Interestingly, the unenhanced CT showed bilateral hypodensities in the thalamus, making basilar artery thrombosis a possible differential diagnosis. In the vast majority of Wernicke’s encephalopathy cases, unenhanced CT is generally interpreted to be normal in the acute stages of the disease [
Due to the increased public awareness of possible stroke symptoms and the emphasis on rapid treatment administration in acute stroke patients, there is an increasing risk of treating stroke mimics with thrombolysis. Studies have shown that up to 30% of patients presenting with acute neurological deficits, considered to be acute onset stroke, have in fact stroke mimics [
The authors declare that there is no conflict of interests regarding the publication of this paper.