Wernicke Encephalopathy in schizophrenia: a systematic review

Abstract

Introduction: In schizophrenia, patients can experience delusions or hallucinations regarding their food or health status, leading to diminished intake. Fasting or not eating a balanced diet can cause neurological complications after severe vitamin B1 malnourishment. The precise signs and symptoms of Wernicke's Encephalopathy (WE) in schizophrenia are not clear. Our aim, therefore, was to conduct a systematic review of the characteristics of WE in patients with schizophrenia. Methods: We conducted our search from inception using Mesh terms schizophrenia, Wernicke Encephalopathy, Korsakoff's syndrome. We searched Pubmed, ISI Web of Science, and Scopus. We defined WE as mental, oculomotor, and motoric alterations and thiamine deficiency; schizophrenia was defined as psychosis, hallucinations and/or delusions; adequate WE treatment as >500 mg/day intramuscular or intravenous. Our search yielded 15 WE cases. Results: WE is characterised by a triad of mental status change, ocular signs and ataxia. In alcohol use disorder, this triad is present in 16% of the cases, but 12 out of the 15 published schizophrenia cases presented themselves with a full triad. Importantly, as an additional characteristic, patients often lost weight within a short period of time. Conclusions: The development of a full triad and additional symptomatology suggests a late recognition of signs and symptoms of WE in schizophrenia. Prophylactic thiamine checks and treatment in patients with schizophrenia are relevant, and if WE is suspected adequate parenteral thiamine supplementation is necessary. KEY POINTS Only few cases of schizophrenia-related WE have been published in the literature, though challenges in diagnosing and recognising WE suggest that the vast majority of cases go undetected. Acute thiamine deficiency leads to Wernicke's Encephalopathy. Patients diagnosed with schizophrenia are at risk to develop Wernicke's Encephalopathy. Timely treatment with high doses of thiamine can adequately treat Wericke's Encephalopathy.

Wernicke-Korsakoff syndrome despite no alcohol abuse: A summary of systematic reports

“…The clinical presentation of WKS is a triad of altered mental status, ocular signs, and ataxia which was present in all cases of hunger strike. In other populations, the full triad was present in at least half the patients for hyperemesis gravidarum (62.1%) [10], bariatric surgery (52.4%) [12], schizophrenia (12/15) [17], and anorexia nervosa 8/12 [18]. For the three largest samples, the classical triad was more frequently present in WKS following hyperemesis gravidarum compared to cancer (χ 2 = 31.92, p < .00001).…”

“…This characteristic was not statistically the most pronounced in any of the three largest samples (ps > 0.11). In pediatric patients, an altered mental status was sometimes reflected by altered consciousness, irritability, and lethargy, as described in the study on soft drink diet in children [13] and in the accidental thiamine deficient infant formula report [17].…”

“…In babies and children on a soft drink diet [14], vomiting was evident in 22/33 cases. In 6/21 patients with depression [15], 8/21 patients with Crohn's disease [16], 2/15 schizophrenia patients [17], 5/10 ulcerative colitis patients [16], and 8/9 accidental thiamine deficient infant formula cases [18], vomiting was evident.…”

“…In modern medicine, patients who have a severely diminished intake or practice fasting for a prolonged time, can resemble the patients described by DeWardener and Lennox in their development of WKS. Famine, which often leads to the consumption of a diet with only polished rice, hunger strikes, food refusal in anorexia nervosa, depression and schizophrenia, are some of the examples that can lead to WKS [4,5,[13][14][15][16][17]. Less familiar is the risk of giving total parenteral nutrition without thiamine to already weakened individuals, or accidentally giving babies and children a diet without thiamine [14,16,19].…”

“…Because WKS is under-recognized and undertreated among patients without AUD, and because of the fast-rising number of both case reports and reviews on nonalcoholic WKS [3,[10][11][12][13][14][15][16][17][18][19], we have brought together for the first time a complete overview of the systematic reports on nonalcoholic WKS. Our primary goal was to increase the clinician's awareness and recognition for nonalcoholic WKS by describing symptomatology, method of diagnosis, and outcome of treatment.…”