wernicke encephalopathy/edema

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Diffusion-weighted imaging abnormalities in wernicke encephalopathy: reversible cytotoxic edema?

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BACKGROUND Wernicke encephalopathy (WE) is a metabolic disorder of the central nervous system resulting from vitamin B(1) deficiency. The exact mechanisms underlying the pathogenesis of the lesions in WE are not completely understood. Vitamin B1 deficiency is associated with intracellular and

Fundus Findings in Wernicke Encephalopathy.

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Wernicke encephalopathy (WE) is an acute neuropsychiatric syndrome resulting from thiamine (vitamin B1) deficiency, classically characterized by the triad of ophthalmoplegia, confusion, and ataxia. While commonly associated with chronic alcoholism, WE may also occur in the setting of poor nutrition

Irreversible optic neuropathy in wernicke encephalopathy and leber hereditary optic neuropathy.

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A 52-year-old woman with alcohol abuse presented with recent worsening of vision, imbalance, and confusion. Examination revealed counting fingers acuity in both eyes with central scotomas, color vision loss, horizontal nystagmus, and gait ataxia. Thiamine was initiated as treatment for a presumptive

Visual Loss, Retinal Hemorrhages, and Optic Disc Edema Resulting From Thiamine Deficiency Following Bariatric Surgery Complicated by Prolonged Vomiting.

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BACKGROUND Vision loss resulting from thiamine deficiency is a recognized complication of bariatric surgery. Most patients with such vision loss have Wernicke encephalopathy with characteristic changes seen on neuroimaging. Other patients may have retinal hemorrhages, optic disc edema, and

[Wernicke encephalopathy in a chronic peritoneal dialysis patient--correlation between diffusion MR and pathological findings].

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Wernicke encephalopathy (WE) is a neurologic disorder caused by a nutritional deficiency of thiamine. Since the lesion in WE consists of brain edema, diffusion weighted imaging (DWI) is quite useful for detecting the pathologic changes in WE, and can differentiate between reversible extracellular

Visual loss due to Wernicke syndrome following gastric bypass.

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OBJECTIVE To report a case of Wernicke encephalopathy after gastric bypass surgery resulting in vision loss, ophthalmoplegia, and ataxia, all of which reversed with a single dose of IV thiamine. METHODS Observational case report. RESULTS A 34-year-old woman presented with decreased vision and

Edematous necrosis in thiamine-deficient encephalopathy of the mouse.

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Acute encephalopathy was produced in the adult male Swiss mouse by pyrithiamine injection in conjunction with a thiamine-deficient diet. The condition of some mice was reversed within 24 hours by a treatment of a high dose of thiamine. The lesions occurred selectively in the thalamus, pontine

Toxic-induced cerebellar syndrome: from the fetal period to the elderly.

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The cerebellum is a brain region which is particularly susceptible to intoxication. Clinical presentation is heterogeneous. It is often considered that elderly patients and patients presenting pre-existing structural lesions of the posterior fossa are particularly at risk of developing a

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