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.

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.

Neurological complications of bariatric surgery.

OBJECTIVE: To review and analyze the neurological complications from bariatric surgery in Kingdom of Saudi Arabia. METHODS: This cross sectional study was carried out in King Abdulaziz Medical City, Jeddah, Kingdom of Saudi Arabia from January 2009 to December 2015. Important personal and clinical data were collected from the charts of the patients who underwent bariatric surgery. Data on follow up visit and remote complication if present, was also collected. All patients with neurological complications were reviewed in detail. The significant difference was calculated by using T-test and p-value<0.05 was considered significant. RESULTS: A total of 451 patients underwent bariatric surgery, 15 cases had neurological complications (3%). Axonal polyneuropathy was the most frequent neurological complication, but cases of Wernicke syndrome, vitamin B12 deficiency, Guillain-Barre syndrome and copper deficiency were also identified. Fourteen patients (93.3%) had full recovery from the neurological signs and symptoms; one patient died. CONCLUSION: Bariatric surgery is not free of potential neurological complications. Complications may affect both central and peripheral nervous system and death is a possibility. Multidisciplinary care including consultation of different teams is highly recommended.

Infrequent but serious? Beriberi And Thiamine deficiency among adolescents and young adults after bariatric surgery.

BACKGROUND: Thiamine deficiency (TD) among adolescents following metabolic and bariatric surgery (MBS) has not been assessed. OBJECTIVE: We assessed TD among adolescents following MBS. SETTING: University Hospital. METHODS: A retrospective chart review was conducted for all adolescents and young adults (aged 10-25 years) who had MBS and subsequently presented with TD at our institution (n = 30). Diagnosis used clinical, laboratory, brain imaging, and neurophysiology criteria. Of 1575 patients, 7 subsequently had TD. Another 23 adolescents had MBS at private hospitals or overseas and presented at our institution with TD. RESULTS: Based on MBS undertaken at our institution, TD prevalence was .45 cases per 100 MBS. The mean age of patients was 19.5 ± 3.23 years, 53.3% were male, 96.7% had sleeve gastrectomy, and time from MBS to admission averaged 4.97 ± 11.94 months. Mean weight loss from surgery to admission was 33.68 ± 10.90 kg. Associated factors included poor oral intake (90%), nausea and vomiting (80%), and noncompliance with multivitamins (71%). Signs and symptoms included generalized weakness, nystagmus, numbness, and paraparesis (83.3%-80%). Seven patients had Wernicke encephalopathy full triad; 16 displayed a mixed picture of Wernicke encephalopathy and dry beriberi; and there were no cases of wet beriberi. Half the patients achieved complete resolution of symptoms, whereas 47% and 40% had residual weakness or persistent sensory symptoms, respectively. There was no mortality. Most common concurrent nutritional deficiencies were of vitamins K, D, and A. CONCLUSIONS: This is the first in-depth study of TD among adolescents after MBS. Although TD is uncommon among adolescents after MBS, it is serious, requiring diligent suspicion and prompt treatment. Bariatric teams should emphasize compliance with multivitamin regimens and follow it up.

Time to act on the inadequate management of Wernicke's encephalopathy in the UK.

Wernicke's encephalopathy (WE) is a serious medical emergency whose pathogenesis is well understood and reviewed in this paper. Summarizing the evidence for its prophylaxis and management, the authors suggest that, in the UK, there is evidence that many patients identified as being at risk of WE currently do not receive appropriate treatment, despite the availability (not universal) of guidelines and protocols.

Evolution of Wernicke-Korsakoff syndrome in self-neglecting alcoholics: preliminary results of relation with Wernicke-delirium and diabetes mellitus.

We present a descriptive, retrospective study of initial symptoms, comorbidity, and alcohol withdrawal in 73 alcoholic patients with subsequent Korsakoff syndrome. In 25/73 (35%) of the patients the classic triad of Wernicke's encephalopathy with ocular symptoms, ataxia and confusion, was found. In at least 6/35 (17%) of the initial deliria (95% confidence interval: 10-25%) we observed no other underlying causes, thus excluding other somatic causes, medication, (recent) alcohol withdrawal, or intoxication. We suggest that these deliria may have been representing Wernicke's encephalopathy. A high frequency (15%) of diabetics may reflect a contributing factor of diabetes mellitus in the evolution of the Wernicke-Korsakoff syndrome.

Alcoholic Liver Disease Among Patients with Wernicke Encephalopathy: A Multicenter Observational Study.

BACKGROUND: data regarding the association between Wernicke encephalopathy (WE) and alcoholic liver disease (ALD) are scarce in spite of alcohol consumption being the main risk factor for WE. AIMS: to describe the frequency of ALD in a cohort of patients diagnosed with WE and alcohol use disorders (AUDs) and to compare the characteristics of WE patients with and without ALD. METHODS: we conducted an observational study in 21 centers through a nationwide registry of the Spanish Society of Internal Medicine. WE Caine criteria were applied and demographic, clinical, and outcome variables were analyzed. RESULTS: 434 patients were included in the study, of which 372 were men (85.7%), and the mean age was 55 ± 11.8 years. ALD was present in 162 (37.3%) patients and we found a higher percentage of cases with tremor, flapping and hallucinations in the ALD group. A total of 22 patients (5.0%) died during admission (7.4% with ALD vs 3.7% without ALD; P = 0.087). Among the ALD patients, a relationship between mortality and the presence of anemia (Odds ratio [OR]=4.6 Confidence interval [CI]95% 1.1-18.8; P = 0.034), low level of consciousness (OR=4.9 CI95% 1.1-21.2; P = 0.031) and previous diagnosis of cancer (OR=10.3 CI95% 1.8-59.5; P = 0.009) was detected. Complete recovery was achieved by 27 patients with ALD (17.8%) and 71 (27.8%) without ALD (P = 0.030). CONCLUSION: the association of WE and ALD in patients with AUDs is frequent and potentially linked to differences in clinical presentation and to poorer prognosis, as compared to alcoholic patients with WE without ALD.

Alcohol-related cognitive impairment in New South Wales hospital patients aged 50 years and over.

OBJECTIVES: The aim of this study was to describe the principal reasons for admission, medical comorbidities, interventions and outcomes of patients admitted to New South Wales hospitals with alcohol-related cognitive impairment. METHODS: We extracted data from the NSW Admitted Patient Care Database for nearly 410 000 multi-day hospital admissions from 222 public hospitals ending between July 2006 and June 2007 for people aged 50 and over. Data linkage using a unique patient identifier, derived by the Centre for Health Record Linkage identified hospital transfers and readmissions for individual patients. Using ICD10-AM codes, we identified patients with alcohol-related dementia, amnesic syndrome due to alcohol, and Wernicke's encephalopathy, their principal reasons for admission and medical comorbidities, and procedures undertaken. Outcomes were length of stay, mortality, discharge destination, and readmission. RESULTS: A total of 462 patients diagnosed with alcohol-related dementia (n = 300; 82% male, mean age 63.9 years), Wernicke's encephalopathy (n = 77) or amnesic syndrome due to alcohol (n = 126) were identified with overlap between diagnoses. Alcohol-related dementia occurred in 1.4% of dementia patients, and was more likely to occur in younger age groups and men than other types of dementia. Alcohol-related mental disorder was recorded in 70% of alcohol-related dementia multi-day admissions: dependence (52%), 'harmful use' (11%) and withdrawal (12%). Principal reasons for admission for multi-day stays included alcohol-related mental disorder (18%), liver disease (11%) and injuries/poisonings (10%). Medical comorbidity was common. Like other dementia patients, alcohol-related dementia patients had longer length of stay (mean of 15 days) than non-dementia patients and more transfers to residential care (7%). However, mortality was similar to non-dementia patients (5%). Discharge at own risk was high (3.7%). CONCLUSIONS: Alcohol-related dementia is a preventable and potentially reversible condition. Investigation of intervention strategies initiated during hospitalization are warranted.

Cognitive impairment severity in relation to signs of subclinical Wernicke's encephalopathy in HIV and alcoholism comorbidity.

OBJECTIVES: The comorbidity of HIV infection and alcoholism (ALC) is prevalent. Wernicke's encephalopathy, a neurological disorder resulting from thiamine depletion, has been generally associated with alcoholism but has also been reported in HIV infection. This study examined whether subclinical Wernicke's encephalopathy signs could contribute to the heterogeneity of cognitive and motor deficits observed in individuals with both disease conditions (HIV+ALC). DESIGN: Sixty-one HIV+ALC individuals and 59 controls were assessed on attention and working memory, production, immediate and delayed episodic memory, visuospatial abilities, and upper limb motor function. METHODS: Using Caine criteria (dietary deficiency, oculomotor abnormality, cerebellar dysfunction, and altered mental state), HIV+ALC individuals were classified by subclinical Wernicke's encephalopathy risk factors. RESULTS: Signs of subclinical Wernicke's encephalopathy were present in 20% of the HIV+ALC participants. For attention/working memory, delayed memory, and upper limb motor function, HIV+ALC Caine 2+ (i.e. meeting two or three criteria) demonstrated the most severe deficits, scoring lower than HIV+ALC Caine 1 (i.e. meeting one criterion), HIV+ALC Caine 0 (i.e. meeting no criteria), and controls. CONCLUSION: The high prevalence of subclinical signs of Wernicke's encephalopathy and relevance to performance indicate that this condition should be considered in assessment of HIV-infected individuals, especially when alcoholism comorbidity is known or suspected. Above and beyond clinical factors, such as depression, alcoholism and HIV disease-related variables, AIDS, hepatitis C and drug history known to mediate neuropsychological performance, subclinical Wernicke's encephalopathy signs could partly explain the heterogeneity in patterns and severity of cognitive and motor impairments in HIV-infected individuals with alcoholism comorbidity.

[Thiamin and alcohol use disorder: A national survey of practice]. / Thiamine et trouble de l'usage d'alcool : une enquête de pratique nationale.

OBJECTIVE: The survey aimed to estimate, in the presence of alcohol use disorder, the frequency of systematic prescription of thiamine, the factors associated with it, and those related to the administration (oral, intravenous, intramuscular) when Wernicke's encephalopathy is suspected. METHODS: A self-questionnaire available on Internet was sent by e-mail to doctors and nurses taking care patients with alcohol use disorder. RESULTS: In all, 565 professionals responded. The systematic prescription frequency of thiamine was 84.8 %, addiction care centers and medical-psychological centers prescribed it 5 times less than in psychiatric hospitals (OR=0.2 IC [0.1-0.5] P<0.0001), and medicine/surgery/obstetrics (MSO) services 10 times more than psychiatric hospitals (OR=10.7 IC [2.5-45.3] P<0.0001). The prescription decreased with the exercise period, the interns prescribing it 10 times more systematically (OR=10.9 IC [3.6-32.9] P<0.0001). In the presence of symptoms related to Wernicke's encephalopathy, thiamine administration was mainly oral (67.1 %). Intravenous administration was used more by the MSO services (OR=18.3 IC [10.2-32.7] P<0.0001), while the intramuscular injection was used more in psychiatric hospitals (OR=4.6 IC [1.7-11.9] P=0.0353). CONCLUSION: The prescription of thiamine is rather systematic. In contrast, intravenous administration is underused, in the presence of symptoms related to Wernicke's encephalopathy, in favor of oral administration, and the more specific use of the intramuscular injection in psychiatry.

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.

Nursing assessment and management of alcohol-related brain damage in young people.

The long term consequences of chronic alcohol misuse are increasingly affecting young people. This one part unit outlines the main signs and symptoms of Wernicke's encephalopathy and Korsakoff's syndrome. It details nursing assessment and management of these conditions, as well as regimens for safe detoxification.

Wernicke encephalopathy after bariatric surgery: a systematic review.

OBJECTIVE: To review the clinical essentials of Wernicke encephalopathy (WE) after bariatric surgery. SUMMARY BACKGROUND DATA: An estimated 205,000 bariatric surgical procedures were performed in the United States in 2007. Such procedures may potentially lead to severe nutritional complications. METHODS: Literature searches were performed in Medline, Embase, and abstract collections. Inclusion criteria were WE after bariatric surgery, diagnosed by the presence of two or more of the following signs: mental status changes, eye movement abnormalities, cerebellar dysfunction, and dietary deficiency. RESULTS: Of 104 reported cases of WE after bariatric surgery, 84 cases were included. Gastric bypass or a restrictive procedure had been performed in 80 cases (95%). Admission to hospital for WE occurred within 6 months of surgery in 79 cases (94%). Frequent vomiting was a risk factor in 76 cases (90%) and had lasted for a median of 21 days at admission. Intravenous glucose administration without thiamine was a risk factor in 15 cases (18%). Brain magnetic resonance imaging identified lesions characteristic of WE in 14 of 30 cases (47%). Incomplete recovery was observed in 41 cases (49%); memory deficits and gait difficulties were frequent sequela. The recent increase in the use of bariatric surgery in the United States was associated with an increase in reported WE cases. CONCLUSIONS: The number of WE cases after bariatric surgery is substantially higher than previously reported. Surgeons, allied health providers, and patients need to be aware of the predisposing factors and symptoms to prevent and optimize the management of this condition.

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.

Review on hyperemesis gravidarum.

Hyperemesis gravidarum is severe, intractable nausea and vomiting affecting 0.3-2% of pregnancies. It has a complex multifactorial aetiology. This review explores the current literature relating to the clinical manifestations, differential diagnosis, epidemiology, possible aetiology, maternal and fetal complications, and evidence-based management of hyperemesis.

Myths and misconceptions of Wernicke's encephalopathy: what every emergency physician should know.

First described in 1881, Wernicke's encephalopathy continues to be an unrecognized and often misunderstood disease. The cause of Wernicke's encephalopathy is thiamine deficiency as a result of any nutritionally deficient state, though many physicians erroneously consider this disease to be confined only to alcoholics. Unfortunately, the syndrome is most often recognized only on autopsy, especially among nonalcoholics. Despite advances in magnetic resonance imaging, Wernicke's encephalopathy remains primarily a clinical diagnosis. The common clinical findings include mental status changes, ocular dysfunction, and gait ataxia. Additional signs may be present, or 1 or more of the common findings may be absent. Treatment mandates timely intravenous thiamine therapy, for which the optimum dosage remains controversial. This review traces the history of Wernicke's encephalopathy from the first description to our current understanding of the disease and includes many of the misconceptions, myths, and controversies that surround this disease. Emergency physicians need to be well versed in the varied presentation of Wernicke's encephalopathy because most of these patients will present to the emergency department and are oftentimes unrecognized. Further, physician knowledge of this disease is vital because the failure to diagnose results in severe neurologic morbidity and possible mortality, but the treatment is safe and effective.

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.

Are Psychiatric Inpatients at Risk of Developing Wernicke's Encephalopathy Being Identified and Adequately Treated?

OBJECTIVE: Wernicke's encephalopathy is caused by thiamine deficiency and occurs predominantly in alcohol-dependent individuals but also develops in those who are malnourished due to other reasons including medical and psychiatric disorders. This study examined the frequency rate and management of Wernicke's encephalopathy in alcohol-dependent and non-alcohol-dependent patients admitted to a psychiatric hospital. METHODS: Data were retrospectively collected from electronic medical records of psychiatric inpatients admitted to a teaching hospital located in Texas between September 2013 and March 2014. The diagnostic criteria of Caine and colleagues and thiamine dosing strategies were used to identify cases of suboptimal management. RESULTS: A total of 486 charts were reviewed. Nine patients (1.85%) had clinical signs of Wernicke's encephalopathy, and 36 (7%, n = 486) were at a high risk for developing the disorder. None of these patients received adequate doses of parenteral thiamine, and of those who were prescribed thiamine, the majority, including high-risk patients, were prescribed oral thiamine at the traditional dose of 100 mg/d. CONCLUSIONS: The findings suggest that Wernicke's encephalopathy is underdiagnosed and undertreated. Our study also highlights the need for clarifying diagnostic criteria, identifying the risk factors for thiamine deficiency, and improving awareness among physicians about diagnosis, prevention, and adequate treatment of Wernicke's encephalopathy in alcohol-dependent and non-alcohol-dependent patients.

[Clinical appearance and scalable profile Thiamine deficiency in prison in Guinea: study of thirty-eight observations]. / Aspect clinique et profil évolutif de la carence en thiamine en milieu carcéral en Guinée : étude de trente-huit observations.

Cardiovascular and neurological manifestations associated with thiamine deficiency in Guinean prisons are common but not reported.We performed a prospective study of 38 cases related to vitamin B1 deficiency over a period of 4 years. In this population, the literature of traditional data gathered: frequency peak after thirty (92.6%) and clear representation male (sex ratio M/F: 18/1). The clinical symptomatology remains essentially dominated by sensorimotor polyneuropathy and pure sensory (52.2%), overall heart failure (31.5%) and to a lesser degree by Gayet Wernicke's encephalopathy (7.8%) and shoshin beriberi with severe evolution (5.2%). The study of nutritional status by body mass index (BMI) of the World Health Organization, by the criteria of Detsky and biological markers including albumin, shows that these patients are severely malnourished.

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.