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Gayet–Wernicke encephalopathy: a complication not to be overlooked in patients with catatonic schizophrenia

BackgroundGayet–Wernicke's encephalopathy (GWE) is a life-threatening neurological emergency caused by vitamin B1 deficiency. This is a rare complication, which may be reversible if managed promptly. However, any diagnostic or therapeutic delay exposes to the risk of serious sequelae. Although...

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Bibliographic Details
Published in:The Egyptian Journal of Neurology, Psychiatry and Neurosurgery Psychiatry and Neurosurgery, 2023-04, Vol.59 (1), p.50-7
Main Authors: Messedi, Neila, Turki, Mariem, Charfi, Rihab, Ellouze, Sahar, Chaari, Imen, Aribi, Lobna, Halouani, Najla, Aloulou, Jihen
Format: Article
Language:English
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Summary:BackgroundGayet–Wernicke's encephalopathy (GWE) is a life-threatening neurological emergency caused by vitamin B1 deficiency. This is a rare complication, which may be reversible if managed promptly. However, any diagnostic or therapeutic delay exposes to the risk of serious sequelae. Although this pathology frequently occurs in chronic alcohol users, it can also occur in any situation of severe undernutrition. In this context, we report a case of GWE occurring after severe undernutrition complicating prolonged catatonia in a patient suffering from schizophrenia.Case presentationHe was a 47-year-old patient, suffering from esophageal stenosis, and followed in psychiatry for schizophrenia, who was hospitalized for a catatonic relapse. He was put on benzodiazepine with parenteral rehydration. Faced with the persistence of food refusal, and the appearance of signs of undernutrition, a parenteral diet was introduced. The evolution was marked by the deterioration of his general and neurological condition, with the appearance of mental confusion. The examination showed a central vestibular syndrome, and brain magnetic resonance imaging showed a hyperintense signaling in the periaqueductal area, in mammillary bodies, and in medial thalamic nuclei on T2-FLAIR sequences. GWE was suspected and parental vitamin B1 therapy was initiated. Laboratory testing confirmed the diagnosis, showing a low thiamine blood level of 32 nmol/l [normal range: 78 to 185 nmol/l]. Regression of neurological symptoms was observed within 2 weeks of treatment.ConclusionThrough this illustration, we draw the attention of the psychiatrist, who must think about preventing this complication, by supplementing any patient at risk of developing GWE with vitamin B1.
ISSN:1110-1083
1687-8329
DOI:10.1186/s41983-023-00651-5