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  • Title: [Miller Fisher syndrome as the presenting symptom of Wernicke's encephalopathy].
    Author: de la Cruz-Cosme C, Padilla-Parrado F, García-Casares N, Heras-Pérez JA, Sempere-Fernández J, Serrano-Castro V, Romero-Acebal M.
    Journal: Rev Neurol; ; 46(8):472-5. PubMed ID: 18428104.
    Abstract:
    INTRODUCTION: Wernicke's encephalopathy is an acute neuropsychiatric syndrome resulting from a thiamine deficit, which is defined by the characteristic triad of confusion, ophthalmoparesis and ataxia, although rare presentations have been reported that delay its diagnosis. Miller Fisher syndrome is characterised by the triad ophthalmoparesis, ataxia and areflexia and is considered to be a variant of Guillain-Barré syndrome; its differential diagnosis includes Wernicke's encephalopathy. CASE REPORT: A 75-year-old female with chronic digestive disorders, who developed an acute picture of bilateral internuclear ophthalmoplegia, ataxia and areflexia, with proteinocytologic dissociation in cerebrospinal fluid; accordingly, an initial diagnosis of Miller Fisher syndrome was proposed. Results of the neurophysiological studies were normal; anti-GQ1b antibodies were negative; and magnetic resonance imaging of the brain suggested Wernicke's encephalopathy. The response to thiamine was spectacular. CONCLUSIONS: The similarities in the distribution of the lesions of the two conditions, in the signs and symptoms and the lab findings, as well as the influence of certain misleading factors (hyponatremia, advanced age), went to make up a typical syndrome that favoured a wrong presumptive aetiological diagnosis. This was corrected at an early stage, however, in light of the results of certain diagnostic tests and after observing the therapeutic response. In addition to being an atypical presentation for Wernicke's encephalopathy, this case highlights the fact that for there to be an agreement between the syndromic and aetiological diagnoses it is necessary to carry out a correct differential diagnosis based on details from the patient's history, on appropriate complementary tests and on the follow-up study of how the patients progress, even when we come across typical syndromes that are usually related to a predominant aetiopathogenesis.
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