Wernicke encephalopathy presenting as a stroke mimic: A case report

Table 1 Key diagnostic distinctions between ischemic stroke and Wernicke encephalopathy

	Ischemic stroke	WE
Origin	Vascular	Metabolic
Mechanism	Thrombotic or embolic occlusion of a cerebral artery which interrupts blood flow depleting the brain from of oxygen and glucose, which leads to disrupted adenosine triphosphate synthesis and energy deficiency, as well as impaired ion homeostasis and acid-base imbalance. Cytotoxic edema is developed rapidly after ischemic stroke, followed by vasogenic and mixed edema	Krebs cycle (tricarboxylic acid cycle) and the pentose phosphate pathway due to thiamine deficiency leading to both vasogenic and cytotoxic edema
Associated risk factors	High blood pressure, atrial fibrillation, cardiac failure, diabetes mellitus, vasculopathies, hypercoagulability, carotid stenosis, dyslipidemia etc.	Chronic alcoholism, hyperemesis gravidarum, gastric surgery procedures, anorexia nervosa etc.
Clinical presentation	Depends on the vascular territory: Dysarthria, aphasia, hemiparesis, hemianopia, hemi paresthesia, ataxia etc.	Typical triad: Confusion, ophthalmoplegia, ataxia
Laboratory findings	No specific changes. Changes of international normalized ratio, prothrombin time, activated partial thromboplastin time if specific anticoagulation therapy is taken, elevated d-dimer or fibrinogen activity may be found	Low thiamine concentration in blood, low red blood cell transketolase activity. Elevated transaminases, bilirubin and glutamyl transpeptidase, and low serum concentration of hepatic proteins in chronic alcoholism
Radiological features	Vascular territory. CT perfusion: Hypoperfusion of the affected area. CT: Hypodensity. MRI findings: Hypointense in T1, Hyperintense in T2/FLAIR. High diffusion weighted imaging signal, with corresponding low ADC. Radiological findings corresponding to encephalomalacia of the affected area	Non-vascular territory. CT perfusion: Normal. CT is normal in the majority of WE cases in the acute phase of the disease. MRI findings: Symmetrical bilateral. Hyperintensities of medial thalami, mammillary bodies, and periaqueductal region in T2/FLAIR. Atrophy of the mammillary bodies may be absent initially but is a typical finding. ADC varies from normal to reduced but less than that in most cases of ischemic stroke. Reversal of radiological findings with the adequate treatment
Treatment	Anticoagulants, antiplatelet drugs, symptomatic measures such as antihypertensive and/or antidiabetic agents etc.	Thiamine replacement

ADC: Apparent diffusion coefficient; CT: Computed tomography; FLAIR: Fluid attenuation inversion recovery; MRI: magnetic resonance imaging; WE: Wernicke encephalopathy.