The American Society for Metabolic and Bariatric Surgery (ASMBS) Wernicke's Task Force issues the following guidelines to enhance the quality of care in patients undergoing bariatric surgery and for other populations at risk of thiamine deficiency and Wernicke's encephalopathy (WE). This paper examines the current literature regarding the prevention, diagnosis, and treatment of WE. These guidelines intend to provide an objective summary of current peer-reviewed literature and provide clinical practice recommendations based on this literature and expert opinions. The goal is to enhance awareness and reduce the incidence of WE and the Wernicke-Korsakoff syndrome (WKS). This statement is not intended to establish a local, regional, or national standard of care and may be revised in the future as additional evidence becomes available.

Wernicke encephalopathy is a well-described neurological complication of thiamine deficiency that is classically characterized by a triad of mental confusion, ophthalmoplegia, and gait ataxia. Although most commonly linked to alcoholism and thiamine deficiency in adults, it can present in pediatric patients. Wernicke encephalopathy presenting as dysnatremias is not well described. This report describes a developmentally delayed 21-month-old male with restrictive dietary habits who eventually developed focal neurological deficits. He was found to be hyponatremic consistent with syndrome of inappropriate antidiuretic hormone (SIADH). Additionally, he had brain magnetic resonance imaging findings consistent with Wernicke encephalopathy. He improved with thiamine administration and correction of his hyponatremia. His case highlights the importance of broadening the differential for altered mental status in the setting of SIADH. Similarly, his case provides an example for why primary care pediatricians should remain vigilant in caring for patients with developmental delay and restricted diets, as even rare complications are possible.

Objective: Wernicke encephalopathy (WE) related to hyperemesis gravidarum (HG) is a devastating neuropsychiatric syndrome that remains frequently undiagnosed in pregnant women. Although many cases have been published, more studies are required to establish guidelines for the early detection and treatment of this condition. Material and Methods: We conducted a retrospective study to analyze the available data concerning 12 cases of WE complicating HG in the Mother and Child Hospital's Obstetric Intensive Care Unit, belonging to Mohamed VI University Hospital of Marrakesh. Results: Twelve out of 76 HG admitted cases developed WE. Pregnant WE patients became depleted after 11 weeks of vomiting at median gestational weeks of 16.2. They had a severe weight loss of more than 5% of their body and had all presented prodromal signs of WE before the actual onset of the clinical triad. WE diagnosis was clinically made based on Caine's operational criteria as they allow early identification of the disease. A good tool that could also aid diagnosis is an encephalic MRI; however, it should not delay treatment with prompt administration of high doses of thiamin of > 500 mg/day. Chronic sequelae in this study occurred in 45.5% and death in one case. Conclusion: In HG, thiamin rapidly depletes which can lead to WE with adverse outcomes for the mother and fetus. Therefore, physicians must be vigilant in detecting early signs of WE to promptly provide a high dose of thiamin with targeted multimodal therapies as this could be lifesaving.

Wernicke Encephalopathy (WE), a neurological disorder often linked to alcohol use, can also occur under non-alcoholic conditions, including in pediatric populations.

This systematic review examines 88 pediatric WE cases reported over the past 30 years, encompassing diverse etiologies such as cancer (25 cases), gastrointestinal diseases (19), malnutrition (17), psychiatric disorders (13), obesity surgery (5), renal disease (4), COVID-19 (2), PICU complications (1), hyperemesis gravidarum (1), and a genetic mutation (1).

Prodromal symptoms included nausea (60%) and vomiting (55%). In total, 37% of the patients received parenteral nutrition without thiamine before WE diagnosis, often progressing to Wernicke-Korsakoff syndrome (WKS). Key findings revealed the classic triad of WKS, eye movement disorders (80%), mental status changes (75%), and ataxia (63%), with MRI demonstrating high diagnostic sensitivity (85%). Treatment varied widely; higher parenteral thiamine doses correlated with faster recovery and better outcomes, while insufficient dosages led to adverse effects. Full remission was achieved in 61% of cases, with improved outcomes in more recent reports due to refined dosing protocols.

These findings underscore the importance of early recognition of nausea and vomiting as predictors of pediatric WE and the critical need to incorporate thiamine in parenteral nutrition for children. Optimal dosing remains vital for recovery, particularly in severe cases.

Wernicke-Korsakoff encephalopathy is a metabolic disease caused by vitamin B1 deficiency that predominantly affects alcoholic patients. Its clinical picture is characterized mainly by altered mental status with memory deficits, ophthalmoparesis, and ataxia, although other clinical manifestations may also be present. The current case presents certain clinical difficulties regarding the diagnosis when confronting an atypical presentation of a classical disease in an acute setting when a decision to administer an intravenous thrombolytic agent needs to be made.

This case involves a young male patient, with a history of chronic alcohol abuse, malnourished, and in poor general health, who presented with right-sided hemiparesis and language disturbance of acute onset, suggesting a left hemispheric stroke. The psychological examination was difficult due to a mix of confusion and aphasia, the latter being challenging to assess as the patient had a dismissive and highly deflective attitude toward the examiner. The initial cerebral computed tomography scan was unremarkable, in line with early imaging in ischemic stroke patients. On subsequent magnetic resonance imaging, lesions were observed in the medullo-pontine tegmentum, around the aqueduct of Sylvius, in the mamillary bodies, in the medial thalami, but also extensive bilateral cortical involvement in the frontal lobes. After receiving intravenous vitamin B1 treatment, the patient made a slow, but full, recovery, after eight weeks of hospitalization, and was subsequently transferred to a psychiatry clinic for treatment of his addiction.

Atypical Wernicke-Korsakoff encephalopathy can closely mimic stroke, usually akin to a vertebro-basilar lesion. Our case is the first report we are aware of Wernicke-Korsakoff encephalopathy feigning a left hemispheric stroke with aphasia and right hemiparesis. This has implications for the emergency medicine doctor, neurologist and the stroke specialist when considering an emergency differential diagnosis for a patient with an initial normal computed tomography scan, especially in regard to deciding acute therapy.

Acute encephalopathy is a common presenting symptom in the emergency room and complicates many hospital and intensive care unit admissions. The evaluation of patients with encephalopathy poses several challenges: limited history and examination due to the patient's mental status, broad differential diagnosis of systemic and neurologic etiologies, low yield of neurodiagnostic testing due to the high base rate of systemic causes, and the importance of identifying less common neurologic causes of encephalopathy that can be life-threatening if not identified and treated. This article discusses the differential diagnosis of acute encephalopathy, presents an approach to the history and examination in a patient with encephalopathy, reviews the literature on the yield of neurodiagnostic testing in this population, and provides a diagnostic framework for the evaluation of patients with altered mental status.

There is an increasing awareness of the link between chronic alcohol consumption and the development of cognitive, behavioural and functional deficits. Currently, preventative strategies are limited and require engagement in dedicated long-term rehabilitation and sobriety services, the availability of which is low. The acute alcohol withdrawal syndrome is an episode of neurochemical imbalance leading to autonomic dysregulation, increased seizure risk and cognitive disorientation. In addition to harm from symptoms of alcohol withdrawal (e.g. seizures), the underpinning neurochemical changes may also lead to cytotoxicity through various cellular mechanisms, which long-term, may translate to some of the cognitive impairments observed in Alcohol-Related Brain Damage (ARBD). Here we review some of the pharmacological and neurochemical mechanisms underpinning alcohol withdrawal. We discuss the cellular and pharmacological basis of various potential neuroprotective strategies that warrant further exploration in clinical populations with a view to preventing the development of ARBD. Such strategies, when integrated into the clinical management of acute alcohol withdrawal, may impact large populations of individuals, who currently face limited dedicated service delivery and healthcare resource.

Alcohol use, while commonly associated with liver damage, also has significant neurologic implications, which often mimic hepatic encephalopathy and complicate diagnosis and management. Alcohol mediates its acute central nervous system effects by altering neurotransmitter balance, notably between gamma-aminobutyric acid and glutamate. Its chronic neurotoxicity, compounded by thiamine deficiency, results in chronic neurologic complications. Clinically, alcohol-related neurologic disorders present a spectrum from acute intoxication and withdrawal to chronic conditions like Korsakoff syndrome, dementia, cerebellar degeneration, and peripheral neuropathy. This review underscores differentiating these conditions from hepatic encephalopathy and highlights the importance of history-taking and physical examination in clinical practice.

This case report presents the clinical findings of a female patient diagnosed with Wernicke's encephalopathy, characterized by pinpoint pupils. While pupillary changes can occur in Wernicke's encephalopathy, the presence of pinpoint pupils is exceedingly rare. In this report, we aim to document and discuss this unusual presentation, as well as speculate on the potential mechanisms underlying this atypical manifestation of the disease.

The thalamus, with its reciprocal connections to and from cortical, subcortical, and cerebellar regions, is a central active participant in multiple functional brain networks. Structural MRI studies measuring the entire thalamus without respect to its regional or nuclear divisions report volume shrinkage in diseases including HIV infection, alcohol use disorder (AUD), and their comorbidity (HIV+AUD). Here, we examined relations between thalamic subregions (anterior, ventral, medial, and posterior) and neuropsychological functions (attention/working memory, executive functioning, episodic memory, and motor skills). Volumes of thalamic subregions were derived from automatic segmentations of standard T1 weighted MRIs of 65 individuals with HIV, 189 with AUD, 80 with HIV+AUD comorbidity, and 141 healthy controls (CTRL). Total thalamic volume was smaller and cognitive and motor composite scores were lower in the three diagnostic groups relative to the CTRL group. The AUD and HIV+AUD groups had significantly smaller thalamic subregional volumes than the CTRL group. The HIV+AUD group had smaller anterior thalamic volume than the HIV-only group and smaller ventral thalamic volume than the AUD-only group. In the HIV+AUD group, memory scores correlated with anterior thalamic volumes, attention/working memory scores correlated with posterior and medial thalamic volumes, and motor skill scores correlated with posterior thalamic volumes. Exploratory analyses focused on the HIV+AUD group indicated that within the posterior thalamic region, the pulvinar and medial geniculate nuclei were related to attention/working memory scores, and the pulvinar was related to motor skills scores. This study is novel in locating volume deficits in specific thalamic subregions, in addition to the thalamus as a whole, in HIV, AUD, and their comorbidity and in identifying functional ramifications of these deficits. Taken together, this study highlights the relevance of thalamic subregional volume deficits to dissociable cognitive and motor processes.

Wernicke encephalopathy (WE) is a rare but severe neurological syndrome characterized, in its classic form, by the acute onset of ocular disturbances, ataxia, and cognitive impairment. It is caused by a deficiency of thiamine (vitamin B1) and mainly affects chronic alcoholics, although it can also affect patients with pathologies that lead to malnutrition. We present a case of a 58-year-old woman, who presented with significant weight loss over the past 6 months and who came to the emergency department for episodes of repetitive vomiting and a sleepy state. The patient underwent blood chemistry tests and a brain CT scan, which revealed symmetrical and bilateral hypodensity of the medial portion of the thalamus, tectal plate, and periaqueductal gray matte, suggestive of WE. She was subsequently referred to the Department of Neurology and underwent a brain MRI, which confirmed the clinical suspicion. She also had an abdominal CT scan and ileo-colonoscopy and was diagnosed with Crohn's disease. Immediately after the clinical diagnosis of WE, a replacement therapy based on intravenous thiamine at high doses was promptly set up, and the patient improved from a clinical point of view. Wernicke encephalopathy can be difficult to diagnose when it occurs in non-alcoholic patients; WE associated with IBD is a rare condition, and it can present with atypical and more subtle symptoms. Radiologists and physicians must be aware of this condition and imaging findings for rapid diagnosis and treatment.

Vitamin B1 (thiamine) deficiency (TD) after metabolic and bariatric surgery (MBS) is often insidious and, if unrecognized, can lead to irreversible damage or death. As TD symptoms are vague and overlap with other disorders, we aim to identify predictors of recurrent TD and failure to collect B1 labs.

We analyzed a large sample of data from patients with MBS (n = 878) to identify potential predictors of TD risk. We modeled recurrent TD and failure to collect B1 labs using classical statistical and machine learning (ML) techniques.

We identified clusters of labs associated with increased risk of recurrent TD: micronutrient deficiencies, abnormal blood indices, malnutrition, and fluctuating electrolyte levels (aIRR range: 1.62-4.68). Additionally, demographic variables associated with lower socioeconomic status were predictive of recurrent TD. ML models predicting characteristics associated with failure to collect B1 labs achieved 75-81% accuracy, indicating that clinicians may fail to match symptoms with the underlying condition.

Our analysis suggests that both clinical and social factors can increase the risk of life-threatening TD episodes in some MBS patients. Identifying these indicators can help with diagnosis and treatment.

Wernicke's encephalopathy (WE) is a dangerous and potentially fatal neurological condition associated with thiamin deficiency. The standard treatment for WE is intravenous (IV) thiamin, but limited research describes optimal dosing. We present a case of a 40-year-old male with severe alcohol use disorder (AUD) and chronic malnourishment who developed WE. Upon administration of 100 mg IV thiamin, symptoms of WE persisted, but when the dose was increased to 500 mg, altered mental status and ophthalmoplegia resolved rapidly. IV thiamin is a reliable and low-risk treatment for WE, even when administered at high doses. High-dose IV thiamin (i.e., >/100 mg) can treat neurological symptoms and cognitive dysfunction in WE and should be considered for first-line treatment. Further study of WE diagnostic and treatment guidelines is warranted to maximize recovery potential.

Clinical features of Wernicke's encephalopathy (WE) confirmed strictly through the low blood vitamin B1 (VB1) levels are limited. This study aimed to analyse magnetic resonance imaging (MRI) findings, and clinical characteristics, in patients with WE who have confirmed low blood VB1 levels.

Clinical and laboratory records of 12 consecutive patients with WE admitted to our hospital during the past 11 years were reviewed. The WE diagnosis was confirmed based on low blood VB1 levels and the presence of at least one of the classical triad.

Ophthalmoplegia and nystagmus were recorded in 75% and 50% of the patients, respectively. Eleven of 12 patients presented with consciousness disturbance/memory loss. All patients experienced gait disturbances. Eight of the 12 patients exhibited MRI abnormalities at typical sites (the dorsal midbrain [n = 7], medial thalamus [n = 6], mammillary bodies [n = 5], and dorsal pons [n = 5]). Of the 12 patients, six showed abnormalities at atypical sites (the splenium of the corpus callosum [n = 4], fornix [n = 3], cerebral cortex [n = 2], cerebellar vermis [n = 2], and dorsal medulla [n = 1]). Patients with positive MRI abnormalities had significantly lower blood VB1 levels than those without abnormalities (9.5 vs. 16.0 ng/mL).

In cases of confirmed WE with low blood VB1 levels, the corpus callosum, fornix, and cerebral cortex were more frequently involved than in previous studies. MRI abnormalities at both typical and atypical sites were correlated with low blood VB1 levels in WE, suggesting that lower blood VB1 levels are associated with more severe brain damage in patients with WE.

In this case series, the simultaneous occurrence of Wernicke's encephalopathy (WE) and dry beriberi was reported in three patients who underwent vertical sleeve gastrectomy (VSG) between May 2021 and May 2023. All patients were obese women who underwent vertical sleeve gastrectomy (VSG) without immediate postoperative complications, but two weeks later, hyperemesis and subsequent encephalopathy with ocular movement abnormalities and weakness were observed over the following thirty days. Patients were referred to neurology, where due to the high suspicion of WE, thiamine replacement therapy was initiated; meanwhile, diagnostic neuroimaging and blood tests were conducted. Neurological and psychiatric evaluations and neuroconduction studies were performed to assess the clinical evolution and present sequelae. One year after diagnosis, all patients exhibited affective and behavioral sequelae, anterograde memory impairment, and executive functioning deficits. Two patients met the criteria for Korsakoff syndrome. Additionally, peripheral nervous system sequelae were observed, with all patients presenting with sensorimotor polyneuropathy. In conclusion, Wernicke's encephalopathy requires a high diagnostic suspicion for timely intervention and prevention of irreversible sequelae, which can be devastating. Therefore, raising awareness among medical professionals regarding the significance of this disease is essential.

[Objective] To investigate association between Wernicke encephalopathy (WE) and brain MRI. [Subjects] 26 patients (7 females, mean age 63.9 ± 12.7 years) with WE admitted to our department between May 2008 and September 2022. [Methods] Wernicke's encephalopathy in patients with MRI lesions was defined as "MRI-positive group" (MPG), and those without MRI lesions as "MRI-negative group" (MNG). The following parameters were assessed between the two groups: age, sex, alcoholism, neurological symptoms, vitamin B1, lymphocyte, total cholesterol, albumin, and outcome at discharge. [Results] There were 17 patients in MPG. Compared to MNG, MPG had lower rates of alcohol abuse (10.0% vs 77.8%, P = 0.025), lower vitamin B1 (median 10.0 ‍ng/ml vs 29.0 ‍ng/ml, P < 0.001), and more vitamin B1 treatment dose (median 1900 ‍mg vs 600 ‍mg, P = 0.016). [Conclusion] Alcoholic WE may be overlooked if the focus is solely on brain MRI findings.

Wernicke encephalopathy (WE) is an acute and potentially fatal neuropsychiatric disorder resulting from thiamine deficiency: its etiology and clinical presentation can be heterogeneous and arduously recognized, especially in children and adolescents.

An 8-year-old girl arrived to the emergency room with ataxic gait, nystagmus, and mental confusion after a 10-day history of repeated severe vomiting; her recent clinical history was characterized by restricted nutrition due to a choking phobia, which caused substantial weight loss. Brain magnetic resonance imaging revealed a bilaterally increased T2 signal in the medial areas of the thalami and cerebral periaqueductal region. Diagnosis of WE based on clinical and neuroradiological findings was established and confirmed after labwork showing low serum thiamine. Following psychiatric evaluation, the patient was also diagnosed with avoidance-restrictive food intake disorder (ARFID), which required starting cognitive behavioral therapy and introducing aripiprazole. The patient displayed improvement of the radiological findings after one month and complete resolution of her neurological symptoms and signs.

Eating disorders like ARFID might forerun acute signs of WE; this possibility should be considered even in pediatric patients, especially when atypical neurological pictures or feeding issues come out.

While Wernicke's encephalopathy (WE) is mostly caused by thiamine deficiency secondary to chronic alcohol use, other conditions that may affect one's nutritional status, such as bariatric surgery, hyperemesis gravidarum, chronic gastrointestinal disease, HIV/AIDS, and certain malignancies, may also lead to this outcome. We are discussing one such case, WE, in a young man with acute myeloid leukemia (AML) who underwent chemotherapy. The patient presented with blurred vision, paresthesia, weakness, and vomiting. Although he denied alcohol abuse, his symptoms, physical exam findings, and MRI results were consistent with WE. Treatment with thiamine resulted in a significant improvement in his visual disturbances and mental status. The authors highlight the importance of recognizing WE in non-alcoholic patients, particularly those undergoing prolonged hospitalization and chemotherapy, as nutritional deficiencies can develop. They recommend thiamine supplementation for patients receiving chemotherapy and those with poor oral intake. The case underscores the need for high clinical suspicion and early intervention in atypical cases of WE.

Wernicke's encephalopathy (WE) is a serious neurological disorder that is underdiagnosed. Despite limited clinical guidelines, the standard use of intravenous (IV) thiamine is underutilized and remains an area of research deserving much attention.

We conducted a systematic review using Medline, Embase, and CENTRAL databases to identify and summarize the literature on IV thiamine treatment in WE. Human studies with WE patients who received ≥100 mg of thiamine IV met inclusion criteria. Randomized controlled trials, cross-sectional studies, and case reports were included.

A total of 27 studies were included: 20 case reports, five retrospective studies, one prospective study and one randomized control trial. Of the case reports, 11 (55%) cases were female, and the average age of all cases was 45 years (SD = 15). The other seven studies included 688 patients; the average age was 52 years (SD = 9), and 266 (38.7%) were female. Among the case reports, neurological and clinical findings were used to diagnose WE in 16 (80%) cases. MRI was utilized to diagnose 15 (75%) cases. 500 mg IV thiamine TID was reported in 12 case reports (60%). 18 (90%) of case reports had partial or complete resolution of symptoms following IV thiamine.

IV thiamine can alleviate neurological symptoms, cognitive dysfunction, and brain imaging lesions associated with WE. We found key limitations in the evidence for IV thiamine and diagnostic standards for WE. Future targeted research should establish clear diagnostic and treatment guidelines for WE to prevent this serious condition from being underdiagnosed or undertreated.

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.

Wernicke Encephalopathy (WE) is a neurological acute syndrome related to vitamin B1 deficiency and is relatively common in patients with chronic alcoholism. In the case of Hyperemesis Gravidarum, thiamine body stores become unable to meet the increased demand, resulting in acute deficiency. WE is associated with typical clinical and radiological findings. Treatment pathways rely on thiamine replacement. The case herein reported is centered around a 33-year-old diabetic patient at 12 weeks of gestation, with WE due to hyperemesis gravidarum. The disease manifested itself with weakness, mental confusion, headache, and impaired vision. The diagnosis was established after the detection of typical findings by MRI. Thirty days after therapy was started, most of the patient's neurological disorders were resolved. The patient was discharged 40 days later with instructions to continue daily thiamine supplementation. The pregnancy outcome was good. Unfortunately, mild ataxia persisted in 2-year follow-up as a long-term consequence. When diagnosed and treated, WE has a favorable prognosis. However, roughly 80% of patients experience memory loss, which may continue for a long time, while gait disorders reportedly affect about 35% of patients. Mild ataxia and dysmetria may persist, too. We reviewed the scientific literature on WE in women with HG until February 2023. Hardly any authors report data on long-term sequelae. Our report emphasizes how important it is to take into consideration this complication in clinical practice, referring to published guidelines and recommendations. Neurological maternal sequelae can demonstrably persist despite early diagnosis and appropriate management. For this reason, a long-term follow-up is recommended. Wernicke syndrome management cannot yet rely on well-established conclusive guidelines; hence, a cautionary approach ought to be prioritized in order to ensure medicolegal soundness.

Vitamin and mineral deficiencies are prevalent nutritional disorders following bariatric surgery. Although they are more prevalent after malabsorptive procedures such as bypass, they also occur in restrictive procedures such as gastric sleeve. The mechanisms that lead to the occurrence of these deficits are related to the presence of poor nutritional intake or poor adherence to multivitamins and multimineral supplementation. Wernicke-Korsakoff syndrome (WKS) is an acute neurological disorder resulting from thiamine deficiency. This syndrome is composed of two distinct phases: first, Wernicke Encephalopathy (WE), the acute phase of this syndrome, which is characterized by a triad of mental confusion, ocular signs, and ataxia, followed by the chronic phase of WKS, called Korsakoff's syndrome (KS), which is known for the presence of anterograde amnesia and confabulation. We aimed to report a case of a patient with WKS after bariatric surgery. The patient's retrospective chart review was performed in order to retrieve the relevant clinical data. The patient was a 24-year-old female student with a BMI of 48 kg/m2 who underwent sleeve gastrectomy surgery for morbid obesity. Over the following 2 months, recovery from surgery was complicated by non-specific symptoms such as nausea, recurrent vomiting, and a significant reduction in food intake, which led the patient to visit the emergency department six times with hospitalization on the last occasion for a definitive diagnosis. During the 15 days of hospitalization, the patient developed ocular diplopia, nystagmus, complaints of rotatory vertigo, and gait abnormalities. A magnetic resonance imaging of the head was performed but revealed no significant changes. After a formal neurological assessment, treatment with parenteral thiamine (100 mg, three times a day) was started without prior dosing. The observed clinical improvement confirmed the diagnosis of WKS. Bariatric surgery may contribute to thiamine deficiency and, consequently, to WKS. Education about the adverse consequences of malnourishment is mandatory before and after the surgery. Investigation of nutritional deficiencies both pre- and post-operatively is crucial in order to prevent complications such as WKS.

Pregnancy, a nutritionally demanding situation in terms of macro- and micronutrient supply owing to heightened maternal, placental, and fetal needs, significantly affects thiamine reserves. Thiamine deficiency during pregnancy and the postpartum period, presenting with varied manifestations and outcomes, is a relatively common condition in our population. The study aimed to understand the various manifestations and outcomes of acute thiamine deficiency in pregnant and postpartum women, emphasizing the significance of early recognition and thiamine therapy to prevent serious complications during pregnancy and after childbirth.

This prospective study conducted in a tertiary care center in North India enrolled consecutive pregnant and postpartum women presenting with clinical features consistent with thiamine deficiency disorders, such as thiamine deficiency-related neuropathy, high-output heart failure, heart failure with reduced ejection fraction, Wernicke's encephalopathy, gastric beriberi, and thiamine-responsive acute pulmonary hypertension. In addition to capturing medical history including drug intake, dietary consumption, and comorbidities, women underwent brief relevant clinical examinations and laboratory assessments, including whole-blood thiamine levels. Response to intravenous thiamine supplementation was also monitored.

Data of 31 women (12 pregnant, 19 postpartum) with a diagnosis of acute thiamine deficiency and a mean age of 28.88 ± 2.69 years were analyzed. The mean thiamine level was 1.28 ± 0.44 μg/dL with mean blood lactate of 3.46 ± 3.33. The most common presentation was gastric beriberi (n = 10), followed by paraparesis (n = 6), high-output heart failure (n = 6), acute pulmonary hypertension, heart failure with reduced ejection fraction (n = 3 each), and an acute confusional state (n = 2). All patients responded to thiamine challenge.

In the context of borderline thiamine status, particularly in our population with endemic thiamine deficiency and heightened demand for thiamine during pregnancy and the peripartum period, the deficiency can have varied and serious manifestations of dry and wet beriberi. Early recognition of the clinical features and thiamine therapy can be life-saving. There is a need for validated clinical criteria owing to the non-availability of thiamine testing in resource-limited settings.

Wernicke encephalopathy (WE) is an acute neuropsychiatric emergency that is caused by a deficiency in vitamin B1 (thiamine). This condition is most commonly seen in patients with alcohol use disorder; however, patients with other disorders of severe malnourishment are also at increased risk. In severe cases, this disease may be followed by Korsakoff's psychosis and even death.  We present a case of a 64-year-old African American female with a history of alcohol use disorder who presented to the emergency department on account of an acute confusional state. Neurological examination revealed right beating nystagmus on the left gaze and a wide-based gait. Initial laboratory work-up was unrevealing; however, magnetic resonance imaging (MRI) of the brain demonstrated an abnormal T2 fluid-attenuated inversion recovery (FLAIR) signal involving the bilateral mammillary bodies and surrounding lateral ventricles that extended into the periaqueductal parenchyma. The patient was admitted to the neurology unit, and high-dose intravenous thiamine was commenced. During hospitalization, the patient's confusion improved and they were subsequently discharged with oral thiamine. The spectrum of severity of WE is wide, ranging from fatal disease and can lead to permanent brain damage or even Korsakoff syndrome, characterized by severe memory loss and confabulation. The diagnosis is mainly clinical and based on the presence of symptoms in the classic triad of mental status change, oculomotor abnormality, and ataxia. This triad is only present in about 10% of cases, making the diagnosis very challenging. Laboratory testing can assist in making the diagnosis, but it is not always reliable or available. In situations of clinical uncertainty, imaging may also be used to support diagnosis or rule out other differentials. The mainstay of treatment is with high-dose parenteral thiamine.

Wernicke encephalopathy is an emergent neurological disorder caused by vitamin B1 (thiamine) deficiency. Here, we present a case of Wernicke encephalopathy in a male patient in his 70s with normal serum thiamine levels and MRI findings on admission. He had a history of heavy alcohol consumption and a gradual decrease in food intake. On arrival at the hospital, his consciousness was impaired which persisted even after glucose replacement. Moreover, horizontal nystagmus and cerebellar ataxia were observed. Head CT scan and MRI revealed no abnormal findings. Further, his serum thiamine level was within the normal range. The patient was clinically diagnosed with Wernicke encephalopathy, and high-dose thiamine therapy was started. Then, his symptoms improved immediately. Thus, in case of clinical suspicion, treatment for Wernicke encephalopathy must be initiated promptly even in patients with normal serum thiamine levels.

Alcohol-related liver disease (ALD) is a major cause of liver-related morbidity and mortality. Epidemiological trends indicate recent and predicted increases in the burden of disease. Disease progression is driven by continued alcohol exposure on a background of genetic predisposition together with environmental cofactors. Most individuals present with advanced disease despite a long history of excessive alcohol consumption and multiple missed opportunities to intervene. Increasing evidence supports the use of non-invasive tests to screen for and identify disease at earlier stages. There is a definite role for public health measures to reduce the overall burden of disease. At an individual level, however, the ability to influence subsequent disease course by modifying alcohol consumption or the underlying pathogenic mechanisms remains limited due to a comparative lack of effective, disease-modifying medical interventions. Abstinence from alcohol is the key determinant of outcome in established ALD and the cornerstone of clinical management. In those with decompensated ALD, liver transplant has a clear role. There is consensus that abstinence from alcohol for an arbitrary period should not be the sole determinant in a decision to transplant. An increasing understanding of the mechanisms by which alcohol causes liver disease in susceptible individuals offers the prospect of new therapeutic targets for disease-modifying drugs. Successful translation will require significant public and private investment in a disease area which has traditionally been underfunded when compared to its overall prevalence.

Psychological distress is common following a burn injury, and many burn survivors have pre-morbid psychiatric illnesses including mood and trauma-related disorders, and substance and alcohol use. This article is intended to be used by all interdisciplinary health care team members to improve the identification and treatment of common psychological concerns experienced by survivors and is organized to follow the general recovery timeline.

Despite guidelines and recommendations, Wernicke's encephalopathy (WE) treatment lacks evidence, leading to clinical practice variability.

Given the overall lack of information on thiamine use for WE treatment, we analyzed data from a large, well-characterized multicenter sample of patients with WE, examining thiamine dosages; factors associated with the use of different doses, frequencies, and routes; and the influence of differences in thiamine treatment on the outcome.

This retrospective study was conducted with data from 443 patients from 21 centers obtained from a nationwide registry of the Spanish Society of Internal Medicine (from 2000 to 2012). Discharge codes and Caine criteria were applied for WE diagnosis, and treatment-related (thiamine dosage, frequency, and route of administration) demographic, clinical, and outcome variables were analyzed.

We found marked variability in WE treatment and a low rate of high-dose intravenous thiamine administration. Seventy-eight patients out of 373 (20.9%) received > 300mg/day of thiamine as initial dose. Patients fulfilling the Caine criteria or presenting with the classic WE triad more frequently received parenteral treatment. Delayed diagnosis (after 24h hospitalization), the fulfillment of more than two Caine criteria at diagnosis, mental status alterations, and folic acid deficiency were associated significantly with the lack of complete recovery. Malnutrition, reduced consciousness, folic acid deficiency, and the lack of timely thiamine treatment were risk factors for mortality.

Our results clearly show extreme variability in thiamine dosages and routes used in the management of WE. Measures should be implemented to ensure adherence to current guidelines and to correct potential nutritional deficits in patients with alcohol use disorders or other risk factors for WE.

Individuals with alcohol-related brain damage (ARBD) represent a population whose healthcare needs often go unmet. This is the result of a lack of not only an awareness surrounding the condition by healthcare professionals, but also healthcare service inclusion and delivery, more broadly. The Coronavirus 2019 (COVID-19) pandemic and the associated lockdowns dramatically affected the accessibility and availability of addiction services globally, while also driving changes in alcohol consumption among the most vulnerable. In the absence of change, this culmination of increased high-risk drinking behaviour, lack of awareness by healthcare professionals and severely limited service delivery for individuals living with ARBD post COVID-19, represents a perfect storm that is rapidly approaching our health and care services world-wide. Collectively, this will reduce positive health outcomes in an already at-risk group.

Patients with alcohol use disorders are commonly identified and managed in the emergency department. Although the alcohol-intoxicated patient has a high risk for significant injury and diseases, the majority will be allowed to sober in the emergency department and can be discharged without incident. However, there are metabolic derangements in these patients, such as alcoholic ketoacidosis, Wernicke-Korsakoff, and potomania that very commonly present similar to intoxication and can be misdiagnosed by emergency clinicians.

The aim of this study was to objectively evaluate the hypothesis that the neuropsychological presentation of Korsakoff's syndrome, the chronic phase of Wernicke-Korsakoff syndrome (WKS), is invariably a severe, selective amnesia against a background of relatively preserved general intellectual functions in a consecutive clinical sample. An analysis of the neuropsychological profiles of nine cases with a recorded history of WKS was undertaken. All cases were adult males (ages 32 to 70) with a long history of alcohol use disorder. Eight cases were chosen retrospectively on a consecutive basis from patient referrals. One additional case was recruited prospectively. Conventional understanding and some current opinion of Korsakoff's syndrome predicts anterograde memory to be consistently more impaired than other cognitive abilities, but this was not found in this case series. The Mean Wechsler Delayed Memory Index was not significantly different from the Wechsler Full-Scale IQ (FSIQ), p = 0.130. Regression of Delayed Memory on FSIQ produced a non-significant intercept, p = 0.213. The 'hallmark' criterion of anterograde memory score at least 20 points less than intelligence score was observed in four of eight cases with available data, equating to a 'sensitivity' of 50%. Three of eight cases with available data had an FSIQ less than the memory score. Contrary to a common view, general intellectual function was not consistently preserved in Korsakoff's syndrome relative to memory function. This study illustrates one of the specific merits of case series, namely, to critique an established view. Clinicians and researchers should expand their diagnostic criteria for Korsakoff's syndrome to include more variable cognitive phenotypes, including a potentially reversible dementia-like impairment of variable severity, and focus on potential treatment opportunities.

Objective: Acute encephalopathy is a common symptom encountered in critically ill patients and may be associated with Wernicke's encephalopathy (WE) or serotonin syndrome (SS). We describe a patient who presented with clinical manifestations of both WE and SS and who responded to treatment for both pathologies. Case: A 56-year-old male presented after being found unresponsive and in a questionable tonic-clonic state. Past medical history was significant for depression managed with fluoxetine 20 mg by mouth daily and alcohol use disorder. A physical exam revealed severe clonus in the bilateral lower extremities; diffuse hyperreflexia along with akinesia on the left upper extremity; ophthalmoplegia; and persistent tachycardia despite pharmacologic interventions. It was learned that the patient had been taking his fluoxetine 3 times per day rather than daily as prescribed. Oral cyproheptadine was administered at a 12 mg initial dose followed by 4 mg every 6 hours. A thiamine regimen of 500 mg intravenous (IV) every 8 hours in addition to folic acid 1 mg IV every 24 hours was initiated to treat WE. Physical symptoms of both WE and SS resolved within 48 hours, and the patient was ultimately discharged to home in stable condition. Discussion/Conclusions: The clinical diagnosis of both WE and SS in this case is supported by the Caine and Hunter criteria, respectively, as well as the resolution of symptoms with accepted treatment modalities for each. It is important for clinicians to be cognizant of potential overlapping pathologies when patients present with nonspecific symptoms, especially acute encephalopathy, in the intensive care unit.

This paper begins with a short case report of florid, spontaneous confabulation in a 61-year-old man with an alcohol-induced Wernicke-Korsakoff syndrome. His confabulation extended across episodic and personal semantic memory, as well as orientation in time and place, as measured on Dalla Barba's Confabulation Battery. Five other brief case summaries will then be presented, followed by a summary of the clinical, neurological, and background neuropsychological findings in three earlier series of Korsakoff patients. These observations will be considered in light of Wijnia's recent and my own, earlier reviews of the Korsakoff syndrome. Taken together, they indicate the need for a multi-faceted approach (clinical, neurological, neuropsychological, and neuroimaging) to the assessment and diagnosis of the disorder.

Alcohol-related cognitive disorders have long been an area of study, yet they continue to pose challenges in the diagnosis, treatment, and understanding of underlying neuropsychiatric mechanisms. The present article offers a comprehensive review of Wernicke's Encephalopathy and Korsakoff's Syndrome, two conditions often seen on a continuum of alcohol-related brain damage. Drawing on current medical literature, neuroimaging studies, and clinical case reports, we explore the neuropsychiatric and neuropsychological profiles, symptomatology, and differential diagnoses of these disorders. We delve into the biochemical pathways implicated in the development of WE and KS, notably thiamine deficiency and its impact on neurotransmitter systems and neural networks. The article also addresses the challenges in early diagnosis, often complicated by non-specific symptoms and co-occurring psychiatric conditions. Furthermore, we review the current state of treatment protocols, including pharmacological and non-pharmacological interventions. Finally, the article highlights gaps in current knowledge and suggests directions for future research to improve diagnosis, treatment, and patient outcomes. Understanding the nuanced interplay between the neuropsychiatric and neuropsychological aspects of WE and KS is crucial for both clinicians and researchers alike, in order to provide effective treatment and to advance our understanding of these complex conditions.

BACKGROUND Wernicke encephalopathy is traditionally associated with chronic alcoholism, nutritional imbalance, prolonged intravenous feeding, hyperemesis, anorexia nervosa, and malabsorption syndromes. We report a case of Wernicke's encephalopathy in a 12-year-old girl with avoidant restrictive food intake disorder. CASE REPORT The patient had lost 45.4 kg of body weight due to self-imposed changes to her diet, before presenting with decreased oral intake for 2-3 weeks, intermittent nausea, crampy epigastric pain, and post-prandial emesis. Her weight on admission was 78.2 kg. She received intravenous fluids of dextrose 5% with normal saline while she initially attempted to eat, but the post-prandial emesis persisted. She developed a fear of vomiting, which led to even more severe food intake restriction. After a week, she began to report double vision and blurred peripheral vision, with physical findings of nystagmus and an ataxic gait. She was empirically started on thiamine after negative neurology workup, with improvement of her gait, blurry vision, and nystagmus. Thiamine deficiency was later confirmed. CONCLUSIONS In patients with large amounts of weight loss presenting with neurological symptoms, Wernicke's encephalopathy must be considered in the differential diagnosis. Avoidant restrictive food intake disorder is rarely reported to cause Wernicke's encephalopathy. To the best of our knowledge, this is the first pediatric case demonstrating that Wernicke encephalopathy can occur in this type of eating disorder and not just in anorexia nervosa.

Alcohol consumption is common in many societies and has increased considerably, resulting in many socioeconomic and public health problems. In this sense, studies have been carried out in order to understand the mechanisms involved in alcohol consumption and related harmful effects. This study aimed to identify and map the knowledge and to perform bibliometric analysis of the neurotoxicology of alcohol based on the 100 most cited articles. A search was carried out in the Web of Science Core Collection database and information was extracted regarding the journal, authors, keywords, year of publication, number of citations, country and continent of the corresponding author. For each selected manuscript, the study design, alcohol exposure model, dose, period of exposure, and effect on the central nervous system and research hotspots were mapped. The journal with the highest number of publications was Alcoholism: Clinical and Experimental Research (n = 11 papers), the author who contributed the most was Crews FT (n = 8 papers), the studies had a total of 288 keywords and 75% of the publications were from the United States of America. The experimental studies evaluated the effects of prenatal and postnatal exposure and were conducted in rats and mice using doses ranging from 2.5 to 14 g/kg/day, with administration by subcutaneous, intraperitoneal, intragastric, or inhalation route or with free access through drinking bottles. Among the studies mapped, the oldest one (1989) aimed to understand the systemic damage and mechanisms of action involved, while the most recent focused on understanding the receptors and mechanisms involved in addiction, as well as genetic factors. Our results show the panorama of the most widespread scientific production in the scientific community on the neurotoxicology of ethanol, a high prevalence was observed in studies that addressed fetal alcohol syndrome and/or the effects of ethanol on neurodevelopment.

Wernicke's encephalopathy (WE) and Korsakoff Syndrome (KS) are distinct neurological disorders that may have overlapping clinical features. Due to the overlap, they are collectively known as Wernicke-Korsakoff syndrome. WE is related to diencephalic and mesencephalic dysfunction due to thiamine. WE typically manifests as confusion, ophthalmoplegia, nystagmus, and gait ataxia (Wernicke's triad), although they may not consistently occur together. Although WE mostly occurs in alcoholics, other etiologies, such as post-bariatric surgery, must be considered. Early diagnosis and therapy by intravenous thiamine are essential to prevent WE complications and to reduce morbidity and mortality. Therefore, physicians' and patients' awareness of WE is essential for early diagnosis and therapy. Accordingly, this narrative review aimed to provide an update on WE by reviewing articles published between April 2015 to April 2022 about the etiology, pathophysiology, diagnosis, and WE management updates. EMBASE, PubMed, Google Scholar, Google, and Scopus search engines were used to conduct the literature search.

Ethanol use is common to most cultures but with varying doses and to varying extents. While research has focused on the effects on the liver, alcohol exerts a range of actions on the function and structure of the nervous system. In the central nervous system (CNS) it can provoke or exacerbate neurological and psychiatric disease; its effects on the peripheral nervous system are not included in this review. Sustained alcohol intake can predispose to acute neurochemical changes which, with continued ingestion and incomplete treatment, can lead to chronic structural changes in the CNS: these include generalised cortical and cerebellar atrophy, amnesic syndromes such as Korsakoff's syndrome, and specific white matter disorders such as central pontine myelinolysis and Marchiafava-Bignami syndrome. Alcohol in pregnancy commonly and significantly affects fetal health, though this receives less medical and political attention than other causes of fetal harm. This review looks at the range of disorders that can follow acute or chronic alcohol use, and how these should be managed, and we provide a practical overview on how neurologists might diagnose and manage alcohol addiction.

Anorexia Nervosa (AN) has always been prevalent in adolescents. During the COVID-19 pandemic, the eating disorder community across the world has noted a sharp increase in adolescent patients with AN and the severity of medical compromise. Rarely seen sequelae have become increasingly more common. This case report describes two previously healthy female adolescents with severe malnutrition due to AN admitted for nutritional stabilization who exhibited paranoid delusions responsive to thiamine and olanzapine. Though neither exhibit the full triad or all the Caine criteria for Wernicke's Encephalopathy (WE), the triad will not present completely in most patients with WE, especially in the pediatric population. Having one symptom of the triad is indicative of WE. Due to the decreased number of clinical criteria for Wernicke's encephalopathy coupled with the lack of typical brain MRI findings found in these patients, we recommend a high index of suspicion for WE and investigation with thiamine. Thiamine supplementation should be standard care in AN with oral supplementation in stable conditions. In the case of refeeding syndromes, preventative parenteral thiamine 100 mg IV qd, and in the case of thiamine deficiency, thiamine 500 mg IV TID.

Wernicke encephalopathy (WE), a neurological emergency commonly associated with alcohol use disorder, results from a severe deficiency of vitamin B1. If left untreated, patients either succumb to the illness or develop chronic Korsakoff's syndrome (KS). Recently, an increasing number of nonalcoholic WE case studies have been published, highlighting a lack of understanding of malnutrition-related disorders among high-functioning patients. We present the case of a 26 year old female who developed life-threatening WE after COVID-19-complicated obesity surgery. She experienced the full triad of WE symptoms, including eye-movement disorders, delirium, and ataxia, and suffered for over 70 days before receiving her initial WE diagnosis. Late treatment resulted in progression of WE symptoms. Despite the severity, the patient achieved remission of some of the symptoms in the post-acute phase due to prolonged parenteral thiamine injections and intensive specialized rehabilitation designed for young traumatic brain injury (TBI) patients. The rehabilitation resulted in gradual remission of amnesia symptomatology, mainly increasing her autonomy. The late recognition of this case highlights the importance of early diagnosis and prompt, targeted intervention in the management of nonalcoholic WE, as well as underscores the potential for positive outcomes after delayed treatment through intensive cognitive rehabilitation in specialized treatment centers.

Alcoholic cerebellar degeneration is a restricted form of cerebellar degeneration, clinically leading to an ataxia of stance and gait and occurring in the context of alcohol misuse in combination with malnutrition and thiamine depletion. However, a similar degeneration may also develop after non-alcoholic malnutrition, but evidence for a lasting ataxia of stance and gait and lasting abnormalities in the cerebellum is lacking in the few patients described with purely nutritional cerebellar degeneration (NCD).

We present a case of a 46-year-old woman who developed NCD and Wernicke's encephalopathy (WE) due to COVID-19 and protracted vomiting, resulting in thiamine depletion. We present her clinical course over the first 6 months after the diagnosis of NCD and WE, with thorough neuropsychological and neurological examinations, standardized clinical observations, laboratory investigations, and repeated MRIs.

We found a persistent ataxia of stance and gait and evidence for an irreversible restricted cerebellar degeneration. However, the initial cognitive impairments resolved.

Our study shows that NCD without involvement of alcohol neurotoxicity and with a characteristic ataxia of stance and gait exists and may be irreversible. We did not find any evidence for lasting cognitive abnormalities or a cerebellar cognitive-affective syndrome (CCAS) in this patient.

Wernicke-Korsakoff syndrome is a neuropsychiatric disorder caused by thiamine deficiency composed of two related disorders accounting for an acute presentation and chronic progression. Hyperemesis gravidarum presents a significant risk factor for Wernicke-Korsakoff syndrome as symptoms may rapidly progress in the setting of pregnancy. We present the first-reported case of hyperemesis-gravidarum-associated Wernicke encephalopathy in a patient in the first half of pregnancy in which a missed diagnosis led to septic shock, fetal demise, and eventual profound Korsakoff syndrome.

We present the case of a 33-year-old primigravid African American woman at 15 weeks gestational age who initially presented at a community emergency department with nausea and vomiting that ultimately progressed to severe hyperemesis-gravidarum-associated Wernicke-Korsakoff syndrome, fetal demise, and septic shock. The patient received a total of 6 weeks of high-dose parenteral thiamine. Magnetic resonance imaging of the head and formal neuropsychological assessment following treatment plateau confirmed the diagnosis of Wernicke-Korsakoff syndrome.

The multisystem complications seen in severe thiamine deficiency can delay timely administration of high-dose thiamine, particularly in pregnancy, in which the classic triad of Wernicke-Korsakoff syndrome may not raise clinical suspicion due to rapid progression of neurological sequelae in this population. We advise a low threshold for parenteral thiamine repletion in pregnant women with persistent vomiting as hyperemesis gravidarum-induced severe thiamine deficiency can result in Wernicke-Korsakoff syndrome, sepsis, and fetal demise.

Wernicke encephalopathy (WE) is a neuropsychiatric syndrome caused by thiamine deficiency. Despite its low sensitivity, brain magnetic resonance imaging (MRI) is the most useful diagnostic technique. Our aim was to investigate whether the timing of the imaging study, and thiamine replacement can influence brain MRI findings in these patients.

Retrospective observational study of hospitalized patients between January/2008 and December/2020 with a clinical diagnosis of WE. Data from clinical presentation, diagnostic features, therapeutic approach, and outcomes were collected.

We identified 41 patients (55 ± 13.3 years) with WE. Brain MRI was performed in 36 patients, and one third had T2/FLAIR hyperintensities suggestive of WE. We found an association between a history of poor diet and periventricular hyperintensities (p = 0.023), especially on the ventral surface of the thalamus and the periaqueductal region. It was found that the odds of having a typical imaging of WE decreased by 5.3% for each additional unit (100 mg) of thiamine administered (p = 0.046) (95% CI [0.89, 0.99]). On the other hand, the number of days from clinical presentation was not found to be a viable predictor (p = 0.254) (95% CI [0.88, 1.03]) Recovery was positively correlated with the total dose of thiamine received until discharge (p = 0.020).

MRI hyperintensities seem to be dependent on the timing of thiamine correction and, particularly, on the thiamine dosage prescribed at admission. Nevertheless, thiamine replacement should not be delayed, as its timely prescription is associated with a better prognosis at discharge.