Wernicke's Encephalopathy in Acute and Chronic Kidney Disease: A Systematic Review.

Thiamine (vitamin B1) deficiency is relatively common in patients with kidney disease. Wernicke's encephalopathy (WE) is caused by vitamin B1 deficiency. Our aim was to systematically review the signs and symptoms of WE in patients with kidney disease. We conducted a systematic literature review on WE in kidney disease and recorded clinical and radiographic characteristics, treatment and outcome. In total 323 manuscripts were reviewed, which yielded 46 cases diagnosed with acute and chronic kidney disease and WE published in 37 reports. Prodromal characteristics of WE were loss of appetite, vomiting, weight loss, abdominal pain, and diarrhea. Parenteral thiamine 500 mg 3 times per day often led to full recovery, while Korsakoff's syndrome was found in those receiving low doses. To prevent WE in kidney failure, we suggest administering high doses of parenteral thiamine in patients with kidney disease who present with severe malnutrition and (prodromal) signs of thiamine deficiency.

Behavioural effects of light intervention in people with Korsakoff Syndrome: A pilot study.

Korsakoff Syndrome (KS) is commonly associated with behavioural symptoms such as agitation, apathy, and disinhibition. People with KS often reside in long-term care facilities, which reduces their exposure to natural light. Little is known regarding positive effects of light intervention in KS. Our objective was to evaluate the influence of a dawn simulation therapy on behavioural symptoms in KS. 38 patients residing in a 24-hour care facility were exposed for 6 weeks to a dawn simulation system in their bedrooms, which gradually increased from 0 lux to 290 lux. Behavioural symptoms were measured over 9 weeks. Weeks 1-3 consisted of the baseline phase and weeks 3-9 consisted of the light intervention phase. Our study showed that total severity of neuropsychiatric symptoms was less prominent during light intervention. More specifically, a decrease on the apathy, disinhibition, behaviour at night and appetite and eating behaviour subscales was found during the light intervention phase compared to the baseline phase. Additionally, a significant effect was found on decreasing emotional distress for caregivers. Results suggest that light intervention therapy has a positive effect on reducing behavioural symptoms in KS as well as the levels of stress experienced by the patients' caregivers.

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

BACKGROUND: Wernicke-Korsakoff syndrome (WKS) is a neurological disorder typically found in alcohol use disorder. The fact that it also occurs in nonalcoholic patients is less well known and often ignored. For the first time, this review offers a systematic investigation of the frequency and associated features of nonalcoholic WKS in the published literature. METHOD: We included 11 recent systematic reports, with a total of 586 nonalcoholic WKS cases following hyperemesis gravidarum (n = 177), cancer (n = 129), bariatric surgery (n = 118), hunger strike (n = 41), soft drink diet in children (n = 33), depression (n = 21), Crohn's disease (n = 21), schizophrenia (n = 15), anorexia nervosa (n = 12), ulcerative colitis (n = 10), and incidental thiamine-deficient infant formula (n = 9). FINDINGS: Vomiting and extreme weight loss were strong predictors of nonalcoholic WKS in adults. Blurred vision was a common presenting sign in about one-fourth of the patients. The classic triad of WKS is characterized by confusion, ataxia, and eye-movement disorders. All reviewed studies reported high percentages of patients presenting with an altered mental status, while both motor symptoms were variably present. INTERPRETATION: The foregoing observations led to several important conclusions. First, we can see that nutritional impoverishment leads to profound brain damage in the form of WKS. Second, it seems that physicians are either unaware of or underestimate the risks for nonalcoholic WKS. Physicians must be specifically vigilant in detecting and treating WKS in patients with sudden and severe weight loss and vomiting. Third, lower doses of thiamine frequently lead to chronic Wernicke-Korsakoff syndrome. We noticed that when thiamine treatment for WKS was administered, in many cases doses were too low. In line with proven interventions we therefore recommend a parenteral thiamine treatment of 500 mg 3 times per day in adults.

Wernicke's encephalopathy in Crohn's disease and ulcerative colitis.

Crohn's disease (CD) and ulcerative colitis (UC) are chronic and debilitating inflammatory conditions of the gastrointestinal tract. Thiamine can deplete rapidly in CD and UC, which can lead to Wernicke's encephalopathy (WE), is an acute neurologic disorder. Our objective was to systematically review the presentation of WE in CD and UC. We conducted our search from inception using the MeSH terms "Crohn's disease," "ulcerative colitis," and "Wernicke's encephalopathy." Our search yielded 28 case studies reporting on 31 cases. CD was diagnosed in 21 cases, and UC in 10. The first signs of WE were nausea and vomiting (13 cases), double vision (10), blurred vision (10), and hearing loss (4). In 12 cases, partial or complete bowel resection was one of the etiologies of thiamine depletion. In nine cases, thiamine was not supplemented intramuscularly or intravenously while parenteral nutrition or glucose was given to the patient. In 10 cases, detailed descriptions of thiamine treatment were given. Thiamine treatment at suboptimal levels (7 of 10 cases) turned out to lead to residual cognitive deficits in three cases. In three cases with optimal treatment (1500 mg/d intravenously), complete remission of WE symptoms was achieved. Rapid treatment with high doses (500 mg, 3 times/d) of thiamine saves lives, and treats WE in its core symptomatology.

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.

Unraveling Apathy in Korsakoff Syndrome Patients Receiving Long-Term Care With and Without Cerebrovascular Comorbidity.

BACKGROUND: Korsakoff syndrome (KS) is a severe neuropsychiatric disorder caused by acute deficiency of vitamin B1 and concomitant alcoholism. Patients with KS are particularly vulnerable for cerebrovascular comorbidity. KS is characterized by cognitive and neuropsychiatric symptoms, one of which is apathy. Apathy is a pathological lack of goal-directed behaviors, goal-directed cognitions, and goal-directed emotions. Cerebrovascular accidents are known to carry a risk for developing apathy. Apathy has a dramatic effect on the autonomy and daily lives of patients suffering from this condition. METHODS: We assessed general apathy and related subconstructs in fifteen patients with KS, fifteen patients with KS and cerebrovascular comorbidity who reside in a 24-hour care facility, and fifteen healthy controls. RESULTS: Compared with healthy controls, both KS patient groups showed higher levels of apathy as rated by a close informant. We found no difference between both KS patient groups and the healthy control group on the self-report section of the Pleasant Activities List, suggesting that motivation is still intact in KS patients. It is important to note a discrepancy was found between self-reporting and proxy reporting on this list. KS patients with cerebrovascular comorbidity showed more severe emotional blunting compared to both KS patients without cerebrovascular comorbidity and healthy controls. The competency to consent was lower in patients compared with healthy controls, but no difference was found between KS patients with cerebrovascular comorbidity and those without. CONCLUSIONS: Our results suggest that KS patients show increased levels of general apathy compared with healthy controls. Patients show a diminished competency to consent and increased emotional blunting, while motivation is not compromised. Cerebrovascular comorbidity in KS forms a high risk for emotional blunting. The results of this study suggest that apathy is a severe problem in KS. More attention in both the literature and clinical practice would benefit this complex patient population.

Vitamin D supplementation after malnutrition associated with time-related increase of cancer diagnoses: A cohort study of 389 patients with Wernicke-Korsakoff syndrome.

OBJECTIVES: Vitamin deficiencies may reflect less-than-optimal health in select populations. The aim of this study was to determine whether vitamin D supplementation (VDs) after malnutrition may be adversely related to cancer diagnoses in a selected group of patients with alcoholic Wernicke-Korsakoff syndrome (WKS). METHOD: This was a retrospective cohort study of all patients admitted to Slingedael Korsakoff Center, from 1996 to 2018. The patients were subdivided into three predefined groups depending on differences in VDs: "early" supplementation, which started during or before the previous hospital admission, before the transfer to our center; "late" supplementation, which started later in our center; and "no" VDs received. Data collection involved patients' ages, sex, body mass index, skin type, baseline serum 25-hydroxyvitamin D concentrations if available, doses of cholecalciferol (vitamin D3) supplementation, other vitamins, sun exposure, malnutrition, alcohol use, smoking, cognitive diagnoses, somatic comorbidity, cancer diagnoses, cause of death, and length of stay in Slingedael. New tumors (dependent variable) may have been diagnosed during VDs (exposed cases) or before the start of VDs, if any (unexposed cases). RESULTS: New cancers were diagnosed in 87 of 389 (22.4%) patients after median 3 y of follow-up (interquartile range, 1.1‒5.8 y). In logistic regression analysis, age, smoking, and length of stay in log (y) showed odds ratios of 1.021, 2.74, and 1.68, respectively. The temporal relationship of VDs and cancer diagnosis was significant in VDs that started in the year leading up to the diagnosis (Wilcoxon signed-ranks test of positive ranks corresponding with supplementation and negative ranks corresponding with non-supplementation: Z score 2.54; P = 0.011). CONCLUSION: VDs was time-related to cancer diagnosis in a cohort of patients with alcoholic WKS. The study may suggest the proliferation of cancer as an adverse effect of VDs, particularly in malnourished patients.

Preventing Wernicke's encephalopathy in anorexia nervosa: A systematic review.

Anorexia nervosa (AN) is a common eating disorder that affects 2.9 million people worldwide. Not eating a balanced diet or fasting can cause neurological complications after severe vitamin B1 malnourishment, although the precise signs and symptoms of Wernicke's encephalopathy (WE) are not clear. Our aim was to review the signs and symptoms of WE in patients with AN. We searched MEDLINE, EMBASE, Scopus, and PiCarta on all case descriptions of WE following AN. All case descriptions of WE in AN, irrespective of language, were included. Twelve WE cases were reviewed, suggesting that WE following AN is still a relatively rare neuropsychiatric disorder. WE is characterized by a triad of: mental status change, ocular signs, and ataxia. In alcoholism, this triad is present in 16% of cases, but eight out of 12 AN cases presented themselves with a full triad of symptomatology. Importantly, patients often had a more complex triad than has been previously described, involving vertigo, diplopia, and the consequences of refeeding syndrome. The development of a full triad and additional symptomatology suggests a late recognition of signs and symptoms of WE in AN. A complicating factor is the overlap between symptoms of thiamine deficiency and the symptoms of WE. Specifically, patients who show rapid weight loss are vulnerable for the development of WE. Eating disorders, such as AN, can lead to WE. Prophylactic thiamine checks and treatment in patients with AN are relevant, and in case of suspicion of WE, adequate parenteral thiamine supplementation is necessary.