Wernicke Encephalopathy in schizophrenia: a systematic review.

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 pointsOnly 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.

Preventing Wernicke Encephalopathy After Bariatric Surgery.

Half a million bariatric procedures are performed annually worldwide. Our aim was to review the signs and symptoms of Wernicke's encephalopathy (WE) after bariatric surgery. We included 118 WE cases. Descriptions involved gastric bypass (52%), but also newer procedures like the gastric sleeve. Bariatric WE patients were younger (median = 33 years) than those in a recent meta-analysis of medical procedures (mean = 39.5 years), and often presented with vomiting (87.3%), ataxia (84.7%), altered mental status (76.3%), and eye movement disorder (73.7%). Younger age seemed to protect against mental alterations and higher BMI against eye movement disorders. The WE treatment was often insufficient, specifically ignoring low parenteral thiamine levels (77.2%). In case of suspicion, thiamine levels should be tested and treated adequately with parenteral thiamine supplementation.

Wernicke's encephalopathy in exclusive breastfed infants.

BACKGROUND: Kashmir has a population that largely consumes polished rice which is deficient in thiamine. Furthermore, lactating women in this region are prone to severe thiamine deficiency because of their traditional food avoidance practices. Infantile beriberi is common in exclusively breastfed infants of thiamine deficient mothers in Kashmir. METHODS: This was a one year prospective hospital-based study. We included 50 exclusively breastfed infants in our study. All patients were evaluated as per unit protocol including complete septic workup and metabolic workup. Most of our patients belonged to low and middle income group families, and mothers were on customary dietary restriction. Demographic and anthropometric data were collected from all the study participants. In addition, data regarding the treatments received by the study population and overall mortality were collected. RESULTS: The mean age, male:female ratio, and mean weight of the study population were 3.15±0.97 months, 1.5:1, and 5.1±1.1 kg, respectively. Traditional food avoidance practices were followed by 80% of the mothers. Irritability was observed in 40 (80%) patients. Blepharoptosis was observed in 30 (60%). Septic workup including cerebro spinal fluid analysis was normal in all patients. Predominant magnetic resonance imaging finding was bilateral basal ganglia hyperintensity. Whole blood thiamine diphosphate levels showed a drastic decrease (10-49 nmol/L). Ten percent of the study infants died. CONCLUSION: In exclusively breastfed infants, we observed acute infantile encephalopathy with epidemiological, clinical, biochemical, and radiological features suggestive of infantile Wernicke's encephalopathy and a favourable therapeutic response to thiamine supplementation during the acute stage.

Rare Neurological Complications After Sleeve Gastrectomy.

BACKGROUND: Bariatric surgery is considered to be the most effective treatment of morbid obesity and improvement of obesity-related comorbidities, such as type II diabetes. However, both peripheral and central neurological complications can occur after bariatric surgery. Such complications tend to occur more frequently after bypass surgery than after sleeve gastrectomy (SG). The objective of this study was to identify the patients that presented post-operative neurological complications after undergoing SG and describe the incidence, presentation, and management of these complications. METHODS: This was a retrospective study of 592 cases of SG performed between 2009 and 2014 with a special focus on patients who presented neurological complications. RESULTS: Of the 592 SG cases, only seven (1.18 %) patients presented neurological complications. All patients had uneventful post-operative course, but all reported feeding difficulties, accompanied by severe dysphagia, and rapid weight loss, with a mean weight loss of 35 kg (30-40 kg) 3 months after SG. All patients were readmitted owing to neurological symptoms that included paresthesia, abolition of deep tendon reflexes of the lower limbs, muscle pain, and motor and sensitive deficits in some cases. There were two cases of Wernicke's encephalopathy. All patients were treated for neuropathy secondary to vitamin B1 deficiency and had a significant improvement and/or resolution of their symptoms. CONCLUSIONS: Neurological complications after SG are rare and are often preceded by gastrointestinal symptoms, rapid weight loss, and lack of post-operative vitamin supplementation. Re-hospitalization and multidisciplinary team management are crucial to establish the diagnosis and initiate treatment.

Risk of thiamine deficiency and Wernicke's encephalopathy after gastrointestinal surgery for cancer.

BACKGROUND: Cancer patients submitted to gastrointestinal surgery are at risk of thiamine deficiency (TD) and Wernicke's encephalopathy (WE). Although permanent neurological damage and death could be prevented by a timely replacement therapy, they often remain undiagnosed and untreated. We hypothesized that WE remains unrecognized because most cases may manifest several months after hospital discharge. METHODS: WE frequency was investigated in a sample of cancer patients who underwent gastrointestinal surgery, by using the diagnostic criteria proposed to improve diagnosis among alcoholics. Patients were evaluated at discharge through the examination of medical records and 6 months after by telephonic interview. RESULTS: Forty-five patients were selected. Signs of WE resulted in 4.4% at discharge. At 6 months, 21 patients were interviewed. Among them, 90.4% had signs of WE. The number of affected patients was significantly higher 6 months after discharge than at discharge (90.4 vs 9.5%, p < 0.0001). CONCLUSIONS: Further studies with larger samples are needed to establish the prevalence of TD and related WE in cancer patients after gastrointestinal surgery. This study suggests that the problem is understated. Even in absence of symptoms of TD, the use of prophylactic thiamine supplementation should be taken in consideration, as consequences of misdiagnosis can be severe.

Wernicke's syndrome during parenteral feeding: not an unusual complication.

OBJECTIVE: Wernicke's encephalopathy (WE) is an acute disorder due to thiamine deficiency, characterized by ophthalmoplegia, ataxia, and mental confusion, similar to that classically observed in alcoholism. Some cases of WE were reported to coincide with other conditions such as hyperemesis gravidarum, bariatric surgery, and total parenteral nutrition. In this study the objective was to retrospectively evaluate the prevalence of WE among intravenously fed patients in our hospital during the previous 2 y. METHODS: Among all cases of WE diagnosed by cranial magnetic resonance scan during a 2-y period in the Azienda Ospedaliera of Padua, we identified patients who exhibited WE during parenteral feeding. Albumin plasma levels, measured at the onset of WE symptoms, were used to estimate nutritional status. RESULTS: We found seven cases of WE that coincided with intravenous feeding. WE occurred, on average, 13 d after the start of glucose infusion. The five subjects with albumin plasma levels lower than 35 g/L at the onset of WE received glucose infusion for fewer days. In six cases the clinical signs disappeared the day after thiamine infusion. In one case mental function did not normalize and the patient developed Korsakoff's syndrome despite prolonged thiamine treatment. CONCLUSION: During a 2-y period we observed a high prevalence of WE in intravenously fed patients due to lack of thiamine supplementation. A prophylactic treatment must be performed in at-risk patients and multivitamin infusion containing thiamine must be administered daily during the course of intravenous feeding.

Wernicke encephalopathy after obesity surgery: a systematic review.

OBJECTIVE: To characterize the clinical features, risk factors, radiographic findings, and prognosis of Wernicke encephalopathy after bariatric surgery. METHODS: We performed a systematic review of MEDLINE, Embase, Ovid, ISI (Science Citation Index), and Google Scholar for case reports, case series, or cohort studies of Wernicke encephalopathy after bariatric surgery. RESULTS: We found 32 cases (27 of whom were women) reported, from 2 weeks to 18 months after the procedure. Most patients had vomiting as a risk factor (n = 25) and presented with the triad of Wernicke encephalopathy (confusion, ataxia, and nystagmus; n = 21). Optic neuropathy, papilledema, deafness, seizures, asterixis, weakness, and sensory and motor neuropathy were also reported. Characteristic radiographic findings were hyperintense signals in the periaqueductal gray area and dorsal medial nucleus of the thalamus; radiographs were normal in 15 patients. One series from Brazil reported 4 patients (among 50 patients) with Wernicke encephalopathy; all presented with vomiting and concomitant peripheral neuropathy at a median of 2.5 months (1.5 to 3 months) after bariatric surgery. Another series identified 2 of 23 patients (both women) with Wernicke encephalopathy after bariatric surgery. CONCLUSION: Wernicke encephalopathy after bariatric surgery usually occurs between 4 and 12 weeks postoperatively, especially in young women with vomiting. Atypical neurologic features are common. The diagnosis is mainly clinical, because radiographic findings are normal in some patients. Prospective studies to determine the prevalence of this problem and protocols for preventive thiamine supplementation need evaluation.

The treatment of patients at risk of developing Wernicke's encephalopathy in the community.

AIM: To review the process of identifying alcohol-dependent patients at risk of developing Wernicke's encephalopathy (WE) in the community, and prophylactic treatment options. METHODS: Non-systematic literature review of the diagnosis of thiamine deficiency and of its treatment in the community. The role of supplementation of beer and bread with thiamine was evaluated. RESULTS: The diagnosis of thiamine deficiency is not always made, and treatment apparently may sometimes be inadequate. CONCLUSIONS: Alcohol-dependent patients in the community who are at risk of developing WE should be given thiamine 250 mg, intramuscularly, daily for 3-5 days as part of a community detoxification programme. Further work is essential to determine the optimum dose of thiamine required to prevent permanent brain damage (Korsakoff's Psychosis). Neurotoxicity, due to the metabolism of excessive alcohol in patients with chronic and severe alcohol dependence, must be considered as an important factor in determining the long-term outcome of treatment.

[Prevalence, prophylaxis and treatment of Wernicke encephalopathy. Thiamine, how much and how do we give it?]. / Prévalence, prophylaxie et traitement de l'encéphalopathie de Gayet-Wernicke. Quelle dose et quel mode d'administration de la thiamine?

Wernicke's encephalopathy (WE) is an acute neuropsychiatric condition due to thiamine deficiency (vitamin B1) most commonly associated with chronic alcohol abuse. WE is difficult to diagnose because the classical triad of signs (confusion, ataxia and ophthalmoplegia) occurs in only 10% of cases. The presentation is often one of a non-specific confusional state which may easily be attributed to intoxication, alcohol withdrawal or to a concurrent morbidity such as head injury. To improve the outcome, it is important to make a presumptive diagnosis of WE and treat the patients as soon as possible with high-dose parenteral thiamine. Patients with an alcohol problem associated with malnutrition should all be offered a preventive treatment with parenteral thiamine in view of the impaired oral thiamine absorption.

A survey of the current clinical practice of psychiatrists and accident and emergency specialists in the United Kingdom concerning vitamin supplementation for chronic alcohol misusers.

Although it is well known that B-vitamin deficiencies directly affecting the brain are common in alcohol misuse, no concise guidelines on the use of vitamin supplements in alcohol misusers currently exist in the UK. The purpose of this study was to assess current practice and opinion among UK physicians. Questionnaires were completed by a total of 427 physicians comprising Accident and Emergency (A&E) specialists and psychiatrists, with a response rate of 25%. The main findings were that vitamin deficiency was perceived as being uncommon amongst alcohol misusers (<25%) and there was no consensus as to which B vitamins are beneficial in treatment or the best method of administration of B-vitamin supplementation. The majority of psychiatrists favoured oral administration for prophylaxis against the Wernicke-Korsakoff syndrome in chronic alcohol misusers and parenteral therapy in patients with signs of Wernicke-Korsakoff syndrome. Whilst only just over half the A&E specialists expressed a preference, most favoured parenteral therapy in both cases. Most respondents did not currently have a unit policy/protocol on the management of vitamin supplementation in chronic alcohol misusers. Overall, the findings suggest that there is wide variation in current practice and highlight the need for guidelines in this area.

Prevalence of Wernicke-Korsakoff syndrome in Australia: has thiamine fortification made a difference?

OBJECTIVE: To determine the prevalence of the Wernicke-Korsakoff syndrome (WKS) in Australia and compare this with previous studies. DESIGN AND SETTING: Prospective autopsy study at the New South Wales Institute of Forensic Medicine, 1996-1997. METHODS: Brains of deceased people (aged over 15 years) derived from 2212 sequential autopsies performed between 1 January 1996 and 31 December 1997 were studied macroscopically and microscopically to identify cases of WKS. MAIN OUTCOME MEASURES: Standard histological criteria for WKS and any available clinical data. RESULTS: Twenty-five cases of WKS were identified (prevalence, 1.1%), mostly among the 5.9% of the 2212 people who had a history suggestive of alcohol abuse. Only four cases (16%) had been diagnosed during life. CONCLUSIONS: There has been a significant reduction in the prevalence of WKS in Australia since the introduction of thiamine enrichment of bread flour. While the prevalence is still higher than in most other Western countries, further research is needed before adding thiamine to alcoholic beverages can be recommended.

Wernicke-Korsakoff syndrome in Sydney hospitals after 6 years of thiamin enrichment of bread.

OBJECTIVES: To estimate the incidence of Wernicke's encephalopathy (WE) and Korsakoff's psychosis (KP) before and after the introduction of thiamin enrichment of bread in Australia. DESIGN AND SUBJECTS: Inpatient records were examined in 17 major public general hospitals in greater Sydney for the 4 years 1993-96 (inclusive) with the International Classification of Diseases (ICD) 9 diagnoses 265.1 (WE), 291.1 and 294.0 (KP). Relevant clinical data were recorded on a specially designed form so that cases could be classified as confirmed or probable WE, confirmed or probable KP, confirmed or probable Wernicke-Korsakoff syndrome (WE + KP) or not WE or KP. The average number of cases of WE + KP was 38 acute (new) cases and 69 total (acute + chronic) cases per annum for all the hospitals combined. RESULTS: This study used the same methods as our earlier retrospective examination of Wernicke-Korsakoff cases in essentially the same hospitals for 1978-93. Records for 1993 were thus pulled twice and, while individual cases (using hospital index number) did not always coincide, the total numbers for 1993 were 69 and 70. For the 5 years after 1991 the number of acute cases of WE and KP in Sydney hospitals was 61% of the number for the 5 years before 1991 (P<0.01). There is, however, no continuing downward trend. CONCLUSIONS: These results are consistent with a 40% reduction of the incidence of acute WE and KP since bread has been enriched with thiamin. The disease complex has, however, not been eliminated. To achieve this, further public health action would be needed, such as addition of thiamin to beer.

[Wernicke's encephalopathy]. / Wernickes encefalopati.

Wernicke's encephalopathy (WE) is a neuropsychiatric disorder caused by thiamine (vitamin B1)-deficiency. WE is most commonly seen among patients with alcohol abuse, and thiamine deficiency is here caused by several factors, among others inadequate diet, insufficient gastrointestinal absorption and enzymatic abnormalities. The syndrome, however, is also seen among non-alcoholic, undernourished patients, e.g. certain patients with cancer or AIDS. The diagnosis WE has traditionally been given when the triad of confusion, ataxia and ophthalmoplegia was present. However, it should be recognised, that these three symptoms are not always present at the same time, partly because the mental symptoms often dominate and cloud, possible ocular abnormalities and ataxia. The syndrome is, according to the author's opinion, still underdiagnosed. The treatment of WE, consisting of large doses of intravenous thiamine, is effective and safe, and therefore it is important to be aware of WE among risk-patients, especially among patients with alcohol abuse, and to institute treatment with intravenous thiamine at the slightest suspicion.

Wernicke-Korsakoff syndrome in Sydney hospitals: before and after thiamine enrichment of flour.

OBJECTIVE: To estimate the incidence of Wernicke-Korsakoff syndrome (WKS) before and after the introduction of thiamine enrichment of bread flour in 1991. DESIGN: Retrospective survey of hospital records. Patient records with the diagnostic codes for Wernicke's encephalopathy (WE) or Korsakoff's psychosis (KP) were reviewed and details of acceptable cases were entered onto a data form. SETTING: All 17 major public general hospitals in the Sydney area (New South Wales), between 1978 and 1993. OUTCOME MEASURES: Numbers of confirmed or probable diagnoses of WE, KP or WKS and associated deaths, patient demographic and social characteristics and alcohol intake. RESULTS: 1,267 patients with WKS were found, with 1,012 acute cases. Although numbers of acute cases may have started to fall before 1991, numbers for the last two years were the lowest of all the 16 years (P = 0.004). Cases of KP outnumbered those of WE by about 3:1 and men outnumbered women 4:1. The peak age was 60-64 years (17%) and beer was the most commonly cited alcoholic drink (71%). The red-cell transketolase test was seldom used for diagnosis (3% of acute cases). CONCLUSIONS: The lower number of "acute" cases in 1992 and 1993 is consistent with a preventive effect of mandatory enrichment of bread with thiamine, but is not conclusive evidence. Longer follow-up of Sydney hospitals, results of postmortem examinations and follow-up in other areas of Australia are required.

An international perspective on the prevalence of the Wernicke-Korsakoff syndrome.

In the Western world previous studies have shown that the majority of cases of the Wernicke-Korsakoff syndrome (WKS), which is caused by thiamine deficiency, occur in alcoholics. However, in France, a country with one of the highest per capita consumptions of alcohol, the prevalence of the WKS was found to be only 0.4% in a small retrospective autopsy study. This figure is compared with data sent to the authors by a number of neuropathologists from the U.S.A., Europe, Scandinavia and Australia. There was no obvious correlation between the prevalence rates of the WKS, which were highest in Australia (2.8%-previously published), and per capita consumption of alcohol. Other issues such as diet, National programs for supplementation of foods with thiamine, and drinking habits are considered. The pathological diagnosis of the WKS can often be made on macroscopic examination of the brain after fixation in formalin. The mammillary bodies are smaller than normal in most cases of chronic WKS. However in this study it was found that the most common causes of small mammillary bodies were Alzheimer's disease and atrophy due to transneuronal degeneration secondary to lesions in the hippocampus.

Thiamin in beer: a health promotion perspective.

Wernicke's encephalopathy (WE) is a serious disease resulting from excessive alcohol intake. As well as the disastrous consequences for the individual, patients with WE place a heavy burden for continuing care on the community. Australia appears to have a higher rate of WE than other western countries, probably due to differences in the consumption patterns of alcoholic beverages. Unlike most other western countries, Australia does not fortify flour with thiamin. On the other hand the USA does fortify flour and has higher thiamin intakes and lower rates of WE. In Australia it has been proposed that thiamin be added to alcoholic beverages. Given that technical problems related to stability, taste and absorption can be solved, the fortification of a substance which is potentially harmful, raises serious problems for health educators. The labeling of alcoholic beverages as 'vitamin enriched' could result in changes in the community's beliefs about alcohol and in increased alcohol consumption. The nutrition and education implications of this proposal are discussed. The conclusion is drawn that Australia should follow the example of other western countries and fortify flour with thiamin.

The Wernicke-Korsakoff syndrome: a reappraisal in Queensland with special reference to prevention.

The Wernicke-Korsakoff syndrome occurs most frequently in alcoholic patients when they become thiamin deficient. First admissions to psychiatric units with the chronic component of this syndrome, Korsakoff's psychosis, peaked in Queensland in 1975-1976. The fall in hospital admission rates since this time could relate to a decline in per-capita alcohol consumption in Australia, or to more awareness of the thiamin needs of drinkers. Alternatively, the improvement may be illusory: although many cases of Wernicke's encephalopathy are being diagnosed, many of these patients are not receiving psychiatric assessment and treatment, perhaps because admission to psychiatric hospital beds is more difficult than it was formerly. Patients who are diagnosed as having Korsakoff's psychosis fare badly in the community, and have a greatly increased mortality rate than do such patients in hospital. Optimal care for such patients is necessarily costly of medical resources. Of available preventive measures, evidence is presented to support the fortification of beer with thiamin and the provision of community educational programmes. The fortification of flour with thiamin may have little impact on the thiamin-deficiency syndromes that arise in problem drinkers in Queensland.