CT and MRI of Wernicke's encephalopathy.

05:45 EDT 26th May 2015 | BioPortfolio

Summary of "CT and MRI of Wernicke's encephalopathy."

The purpose of this pictorial essay is to present the computed tomography (CT) and magnetic resonance imaging (MRI) findings of Wernicke's encephalopathy, a rare, severe, acute neurological syndrome due to thiamine (vitamin B1) deficiency, associated with high morbidity and mortality. The classical clinical triad, which includes ocular signs, altered consciousness and ataxia, can be found in only one-third of patients. Although chronic alcoholic patients are the most commonly affected, Wernicke's encephalopathy may complicate malnutrition conditions in nonalcoholic patients, in whom it is greatly underestimated. CT and above all MRI of the brain play a fundamental role in diagnosing the condition and ruling out other diseases. MRI is the most sensitive technique and is required in all patients with a clinical suspicion of Wernicke's encephalopathy. Medial thalami, mamillary bodies, tegmentum, periaqueductal region, and tectal plate are typical sites of abnormal MRI signal. The dorsal medulla, red nuclei, cranial nerve nuclei, cerebellum, corpus callosum, frontal and parietal cerebral cortex are less common sites of involvement although they are more frequently affected in nonalcoholic patients. Paramagnetic contrast material may help to identify lesions not otherwise visible.

Affiliation

UOC NINT Neuroimmagini e Neurointerventistica, Dipartimento di Neuroscienze, Azienda Ospedaliera Universitaria Senese, Policlinico "Santa Maria alle Scotte", Viale Mario Bracci, 16, 53100, Siena, Italy, alfonsocerase@aliceposta.it.

Journal Details

This article was published in the following journal.

Name: La Radiologia medica
ISSN: 1826-6983
Pages:

Links

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Medical and Biotech [MESH] Definitions

A type of fluent aphasia characterized by an impaired ability to repeat one and two word phrases, despite retained comprehension. This condition is associated with dominant hemisphere lesions involving the arcuate fasciculus (a white matter projection between Broca's and Wernicke's areas) and adjacent structures. Like patients with Wernicke aphasia (APHASIA, WERNICKE), patients with conduction aphasia are fluent but commit paraphasic errors during attempts at written and oral forms of communication. (From Adams et al., Principles of Neurology, 6th ed, p482; Brain & Bannister, Clinical Neurology, 7th ed, p142; Kandel et al., Principles of Neural Science, 3d ed, p848)

Impairment in the comprehension of speech and meaning of words, both spoken and written, and of the meanings conveyed by their grammatical relationships in sentences. It is caused by lesions that primarily affect Wernicke's area, which lies in the posterior perisylvian region of the temporal lobe of the dominant hemisphere. (From Brain & Bannister, Clinical Neurology, 7th ed, p141; Kandel et al., Principles of Neural Science, 3d ed, p846)

An acute neurological disorder characterized by the triad of ophthalmoplegia, ataxia, and disturbances of mental activity or consciousness. Eye movement abnormalities include nystagmus, external rectus palsies, and reduced conjugate gaze. THIAMINE DEFICIENCY and chronic ALCOHOLISM are associated conditions. Pathologic features include periventricular petechial hemorrhages and neuropil breakdown in the diencephalon and brainstem. Chronic thiamine deficiency may lead to KORSAKOFF SYNDROME. (Adams et al., Principles of Neurology, 6th ed, pp1139-42; Davis & Robertson, Textbook of Neuropathology, 2nd ed, pp452-3)

A transmissible spongiform encephalopathy of cattle associated with abnormal prion proteins in the brain. Affected animals develop excitability and salivation followed by ATAXIA. This disorder has been associated with consumption of SCRAPIE infected ruminant derived protein. This condition may be transmitted to humans, where it is referred to as variant or new variant CREUTZFELDT-JAKOB SYNDROME. (Vet Rec 1998 Jul 25;143(41):101-5)

A rare transmissible encephalopathy most prevalent between the ages of 50 and 70 years. Affected individuals may present with sleep disturbances, personality changes, ATAXIA; APHASIA, visual loss, weakness, muscle atrophy, MYOCLONUS, progressive dementia, and death within one year of disease onset. A familial form exhibiting autosomal dominant inheritance and a new variant CJD (potentially associated with ENCEPHALOPATHY, BOVINE SPONGIFORM) have been described. Pathological features include prominent cerebellar and cerebral cortical spongiform degeneration and the presence of PRIONS. (From N Engl J Med, 1998 Dec 31;339(27))

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