Cortical damage in Wernicke's encephalopathy with good prognosis: a report of two cases and literature review.

Wernicke's encephalopathy (WE) is a thiamine deficiency-related condition, in which lesions are usually present in the periventricular and subcortical areas of the brain. However, lesions have also been found in atypical areas, such as the cerebral cortex. The present study summarizes the clinical outcomes and radiological features of WE with cortical impairment. We report two cases of cortical involvement in patients with WE, and review 22 similar cases from other reports. Among all 24 cases, 4 patients had a confirmed history of chronic daily alcohol abuse, and 19 of them had an identified causes of thiamine deficiency. 17 cases reported specific clinical information, among which 11 patients had symptoms of cortical impairment. 23 cases reported prognostic information at the end of treatment or at follow-up. The mortality rate was 26.1 % in our review. All patients had abnormal magnetic resonance imaging (MRI) signals or pathological findings in the bilateral cortex. Among patients with available MRI, 89.0 % had banding-like signs along the para-central sulcus. 13 cases underwent follow-up MRI examinations and 76.9 % displayed normal images. We suggest that WE with bilateral cortical involvement may have an acceptable prognosis, but that the mortality rate is higher than that among typical cases, especially if patients are not treated promptly and correctly. We identified the frontal and parietal lobes, especially around the central sulcus, to be the most susceptible areas, and suggest that the banding signs may be characteristic of WE. Persistent hyper-intensity on T2-weighted-fluid-attenuated inversion recovery, or gadolinium enhancement, may predict poor outcome.

Epileptic seizures in nonalcoholic Wernicke's encephalopathy: a case report and literature review.

Wernicke encephalopathy (WE) is characterized by eye signs, cerebellar dysfunction, and confusion. Epileptic seizures are rare in nonalcoholic WE. We reviewed the clinical, laboratory, radiological, and prognostic characteristics of nonalcoholic WE accompanied by epileptic seizures. We reported 1 case and searched similar cases using PubMed, WoK, Ovid, and Embase. WE was diagnosed according to dietary deficiencies, clinical symptoms and brain magnetic resonance imaging (MRI). We reviewed 13 patients (median age, 27 years; 5 men) with clear histories of thiamine deficiency and symptoms of typical WE. The type of epileptic seizures reported in the 13 cases reviewed was generically reported as seizures or convulsions in 4 patients; 7 patients had generalized tonic-clonic seizures, 1 partial seizure, and 1 generalized convulsive status epileptics. Two patients had epileptic seizures as the first symptom of WE. Laboratory tests mainly indicated metabolic acidosis and electrolyte disturbances. Electroencephalography may present as normal patterns, increased slow waves or epileptic discharge. Six patients had cortical lesions on brain MRI. These lesions were usually diffuse and band-like, and sometimes involved all lobes either symmetrically or asymmetrically, with the frontal lobe as the most susceptible area. All cortical lesions were accompanied by non-cortical lesions typical of WE. Brain MRI abnormalities, after thiamine treatment, mostly disappeared on follow-up MRIs. The patients had good prognoses. Only 1 patient had repeated seizures, and there were no comas or deaths. Patients with nonalcoholic WE accompanied by seizures are young and generally have good prognoses. Most patients experienced generalized convulsive seizures, which may have been related to abnormal cerebral cortical metabolism due to subacute thiamine deficiency.

A Case Report of Nonalcoholic Gayet-Wernicke Encephalopathy: Don't Miss Thiamine.

Gayet-Wernicke encephalopathy (WE) is an acute neurological disorder resulting from deficiency of thiamine, commonly related to chronic abuse of alcohol, but frequently missed or overlooked as a diagnosis when a nonalcoholic patient presents with atypical signs and symptoms of the disease. The diagnosis of the disease is clinical, and confirmation is done by magnetic resonance imaging. We aim to highlight a case of WE in a nonalcoholic postoperative surgical patient receiving total parental nutrition where high-dose intravenous administration of thiamine in time mitigated the symptoms of disease and prevented permanent neurological sequelae. We spotlight the significance of adequate thiamine for postoperative malnourished surgical patients.

Starvation-induced diplopia and weakness: a case of beriberi and Wernicke's encephalopathy.

A 56-year-old teetotaller man with hypertension and gout presented with a week duration of painless worsening diplopia on a background of loss of weight and appetite, generalised lethargy and weakness for 1 year. On examination, he was noted to be hypothermic and tachycardic with generalised muscle wasting. Proximal myopathy, lower limb fasciculations and areflexia, restricted bilateral eye abduction and nystagmus were observed. Blood investigations demonstrated compensated lactic acidosis, acute kidney injury and leucocytosis. A nerve conduction study showed severe length-dependent axonal sensorimotor polyneuropathy. This was a diagnostic dilemma until an MRI brain revealed symmetrical signal abnormality and enhancement in the periaqueductal area indicative of Wernicke's encephalopathy, caused by thiamine deficiency from poor nutrition. Beriberi, also caused by thiamine deficiency, accounted for his tachycardia, polyneuropathy, areflexia, hypothermia and biochemical abnormalities. Both beriberi and Wernicke's encephalopathy are medical emergencies, which were treated with intravenous thiamine to good effect.