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Disorders manifested by both neurological and mental disorders belong to the neuropsychiatric diseases. This category includes Alzheimer's disease, Parkinson's disease, Wernicke–Korsakoff syndrome, delirium tremens, catatonia and anti-NMDA receptor encephalitis. The etiology of psychotic disorders in neuropsychiatric diseases probably differs from that in schizophrenia and other psychoses, which causes both inefficiency and adverse events when using antipsychotics in neuropsychiatry. In the absence of a therapeutic alternative, antipsychotics can be prescribed with caution for neurodegenerative disorders, whereas catatonia is a relative, and anti-NMDA receptor encephalitis is an absolute contraindication to their use.

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. [ABSTRACT FROM AUTHOR]

Hemorrhage inside the mammillary bodies (MMBs) is known to be one of the findings of Wernicke encephalopathy. Brain MRI of two patients with Wernicke-Korsakoff syndrome (WKS) demonstrated high susceptibility values representing hemosiderin deposition in MMBs by using quantitative susceptibility mapping (QSM). QSM provided additional information of susceptibility values to susceptibility-weighted imaging in diagnosis of WKS. [ABSTRACT FROM AUTHOR]

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.

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. [ABSTRACT FROM AUTHOR]

Background: Research on the use of psychotropic drugs in people with alcohol-related neurocognitive disorders is virtually nonexistent. We examined the prevalence of antipsychotic drug use and its effect on mortality among patients with Wernicke–Korsakoff syndrome (WKS) or alcohol-related dementia (ARD). Methods: In this nationwide register study, we collected data on the medication use and mortality of all persons aged ≥40 diagnosed with WKS (n = 1149) or ARD (n = 2432) between 1998 and 2015 in Finland. We calculated the prevalence of antipsychotic use within one year of diagnosis and the adjusted cumulative mortality of antipsychotic users versus non-users in relation to the age-, sex-, and calendar year-matched general population. Results: Of the WKS and ARD patients, 35.9% and 38.5%, respectively, purchased one or more antipsychotic drugs in the year following diagnosis. The adjusted cumulative mortality of the antipsychotic users was significantly lower than that of non-users in both the WKS and ARD groups, where the adjusted hazard ratios (95% CI) were 0.85 (0.72–0.99) and 0.73 (0.65–0.81), respectively. WKS and ARD patients using antipsychotics were less likely to die of alcohol-related causes than antipsychotic non-users, but the difference was significant only in the ARD group. Conclusions: This population-based study shows that antipsychotic use is common in patients with WKS or ARD. In contrast to other dementia studies, our results indicate that the mortality of antipsychotic users is significantly lower than that of non-users. The lower mortality could be explained by decreased alcohol use and better healthcare coverage in antipsychotic users. [ABSTRACT FROM AUTHOR]

Abstract Background 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. Case presentation 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. Conclusions 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.

Background: 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. Case presentation: 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. Conclusions: 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. [ABSTRACT FROM AUTHOR]

The purpose of this research was to investigate the effects of protocatechuic acid (PCA) at doses of 50 and 100 mg/kg on the development of unfavourable changes in cognitive processes in a pyrithiamine-induced thiamine deficiency (PTD) model of the Wernicke–Korsakoff syndrome (WKS) in rats. The effects of PCA were assessed at the behavioural and biochemical levels. Behavioural analysis was conducted using the Foot Fault test (FF), Bar test, Open Field test, Novel Object Recognition test (NOR), Hole–Board test and Morris Water Maze test (MWM). Biochemical analysis consisting of determination of concentration and turnover of neurotransmitters in selected structures of the rat CNS was carried out using high-performance liquid chromatography. PTD caused catalepsy (Bar test) and significantly impaired motor functions, leading to increased ladder crossing time and multiplied errors due to foot misplacement (FF). Rats with experimentally induced WKS showed impaired consolidation and recall of spatial reference memory in the MWM test, while episodic memory related to object recognition in the NOR was unimpaired. Compared to the control group, rats with WKS showed reduced serotonin levels in the prefrontal cortex and changes in dopamine and/or norepinephrine metabolites in the prefrontal cortex, medulla oblongata and spinal cord. PTD was also found to affect alanine, serine, glutamate, and threonine levels in certain areas of the rat brain. PCA alleviated PTD-induced cataleptic symptoms in rats, also improving their performance in the Foot Fault test. In the MWM, PCA at 50 and 100 mg/kg b.w. improved memory consolidation and the ability to retrieve acquired information in rats, thereby preventing unfavourable changes caused by PTD. PCA at both tested doses was also shown to have a beneficial effect on normalising PTD-disrupted alanine and glutamate concentrations in the medulla oblongata. These findings demonstrate that certain cognitive deficits in spatial memory and abnormalities in neurotransmitter levels persist in rats that have experienced an acute episode of PTD, despite restoration of thiamine supply and long-term recovery. PCA supplementation largely had a preventive effect on the development of these deficits, to some extent also normalising neurotransmitter concentrations in the brain. [ABSTRACT FROM AUTHOR]

Nausea and vomiting affect up to 80% of all pregnancies, sometimes so severely that the condition of hyperemesis gravidarum (HG) is established. HG may in addition be a predisposing factor for Wernicke encephalopathy (WE), a severe and life-threatening condition due to vitamin B1 (thiamin) deficiency. If untreated, WE may progress to Korsakoff's syndrome, an irreversible cognitive disorder. We reported a case that recently occurred at our clinic and performed a systematic review of the literature to investigate the clinical presentation, maternal and perinatal outcomes and treatment of WE in women with HG. We performed a systematic review of case series and case reports searching the Medline database on Pubmed from inception until December 2021. We used as search terms (Wernicke encephalopathy) OR (Wernicke-Korsakoff syndrome) AND (hyperemesis gravidarum) AND (pregnancy) AND (thiamin deficiency). Articles were considered eligible for inclusion in our review if they described at least one case of WE due to thiamin deficiency in relation to HG. An overall of 82 cases of WE due to HG in pregnancy from 66 manuscripts, including our own, were selected. The maternal mean age was 26.38 ± 5.23 years, while mean gestational week at hospitalization was 14.57 ± 4.12 after a mean of 6.6 ± 3.14 weeks of vomiting duration. WE manifestation occurred at a mean gestational age of 16.54 ± 3.06 weeks. Regarding clinical presentation, ocular signs and symptoms were reported by 77/82 (93.9%) women, 61/82 (74.4%) presented with ataxia and 63/82 (76.8%) with confusion. Dysarthria affected 15/82 women (18,3%), while muscular weakness was present in 36/82 (43.9%) and impaired reflexes in 42/82 (51.2%). Memory impairment involved 25/82 (30.5%) of the study population. Almost all cases reported a thiamin administration treatment, however data regarding the clinical course of the neurological condition and the perinatal outcomes were often missing and showed a great heterogeneity when reported. WE is a challenging diagnosis, as its clinical presentation is nonspecific. A high clinical suspicion and the awareness of its possible predisposing conditions such as HG may help clinicians to get a prompt diagnosis and starting treatment, which are vital to prevent possible life-impairing neurological sequelae. [ABSTRACT FROM AUTHOR]

Wernicke’s encephalopathy (WE) is a neurologic disease caused by vitamin B1 or thiamine deficiency (TD), being the alcohol use disorder its main risk factor. WE patients present limiting motor, cognitive, and emotional alterations related to a selective cerebral vulnerability. Neuroinflammation has been proposed to be one of the phenomena that contribute to brain damage. Our previous studies provide evidence for the involvement of the innate immune receptor Toll-like (TLR)4 in the inflammatory response induced in the frontal cortex and cerebellum in TD animal models (animals fed with TD diet [TDD] and receiving pyrithiamine). Nevertheless, the effects of the combination of chronic alcohol consumption and TD on TLR4 and their specific contribution to the pathogenesis of WE are currently unknown. In addition, no studies on TLR4 have been conducted on WE patients since brains from these patients are difficult to achieve. Here, we used rat models of chronic alcohol (CA; 9 months of forced consumption of 20% (w/v) alcohol), TD hit (TDD + daily 0.25 mg/kg i.p. pyrithiamine during 12 days), or combined treatment (CA + TDD) to check the activation of the proinflammatory TLR4/MyD88 pathway and related markers in the frontal cortex and the cerebellum. In addition, we characterized for the first time the TLR4 and its coreceptor MyD88 signature, along with other markers of this proinflammatory signaling such as phospo-NFκB p65 and IκBα, in the postmortem human frontal cortex and cerebellum (gray and white matter) of an alcohol-induced WE patient, comparing it with negative (no disease) and positive (aged brain with Alzheimer’s disease) control subjects for neuroinflammation. We found an increase in the cortical TLR4 and its adaptor molecule MyD88, together with an upregulation of the proinflammatory signaling molecules p-NF-ĸB and IĸBα in the CA + TDD animal model. In the patient diagnosed with alcohol-induced WE, we observed cortical and cerebellar upregulation of the TLR4/MyD88 pathway. Hence, our findings provide evidence, both in the animal model and the human postmortem brain, of the upregulation of the TLR4/MyD88 proinflammatory pathway in alcohol consumption–related WE.

Background: Epidemiological data on alcohol-related cognitive disorders are scarce. Up-to-date population-based incidence and mortality rates for Wernicke-Korsakoff syndrome (WKS) and alcohol-related dementia (ARD) are necessary to understand the burden of these diseases.Methods: We collected diagnostic data from the Finnish Hospital Discharge Register and mortality data from Statistics Finland for all persons aged ≥40 years who had received a diagnosis of WKS (n = 1149) or ARD (n = 2432) between 1998 and 2015 in Finland. We calculated the incidences and mortality in relation to the age-, sex- and calendar year-matched general population. Causes of death were ascertained from death certificates.Results: For WKS, the incidence per 100,000 person-years (95% confidence interval (CI)) was 3.7 (3.4-3.9) in men and 1.2 (1.1-1.3) in women. For ARD, the incidence was 8.2 (7.9-8.6) in men and 2.1 (1.9-2.3) in women. The incidence of WKS peaked in people aged 50-59 years and the incidence of ARD in people aged 70-79 years. The standardized mortality ratio (95% CI) was 5.67 (5.25-6.13) in WKS patients and 5.41 (5.14-5.70) in ARD patients. Most of the excess mortality resulted from alcohol-related causes.Conclusions: To our knowledge, this is the first study describing population-based incidence and mortality rates, sex-segregated data and causes of death in patients with WKS or ARD. Our results establish a point of reference for the incidence of WKS and ARD and show the high mortality and poor prognosis of these disorders. [ABSTRACT FROM AUTHOR]

Background: The primary cause of Wernicke–Korsakoff syndrome (WKS) is thiamine deficiency, and more than 90% of cases are reported in alcohol‐dependent patients. While observational studies show parenteral thiamine administration drastically reduced WKS‐related mortality, relevant treatment trials have never been conducted to determine the optimum thiamine dose. Methods: Two double‐blind, parallel groups, randomized controlled trials (RCTs) were conducted to determine the optimal thiamine dose required for (1) the prevention of Wernicke's encephalopathy (WE), the acute phase of WKS, in asymptomatic but "at‐risk" alcohol misuse patients (Study 1) and (2) the treatment of WE in symptomatic alcohol misuse patients (Study 2). Each study had a dosage regimen comprising three parenteral thiamine doses that were allocated at a ratio of 1:1:1. Study 1: Asymptomatic At‐Risk patients (N = 393) received either 100 mg daily, 100 mg thrice daily, or 300 mg thrice daily, for 3 days. Study 2: Symptomatic patients (N = 127) received either 100 mg thrice daily, 300 mg thrice daily, or 500 mg thrice daily, for 5 days. Cognitive function was the primary outcome, assessed using the Rowland Universal Dementia Assessment Scale, two Cogstate subtests, and an adapted Story Memory Recall test. Secondary analyses examined differences in neurological function (ataxia, oculomotor abnormalities, and confusion) at follow‐up. Results: No significant differences were observed between any of the dosage conditions for either Study 1 or Study 2 on cognition or neurological functioning. This real‐world study found that having a clinically unwell target population with high comorbidity and multiple presentations, coupled with challenges in cross‐cultural assessment is likely to complicate RCT findings. Conclusions: The results of this study showed no clear benefit of high dose thiamine over intermediate or lower doses of thiamine, over the time intervals examined, for the treatment and prevention of cognitive and neurological abnormalities related to WKS. Several study limitations temper the interpretation of these findings. Nevertheless, the absence of conclusive evidence for the superiority of high‐dose thiamine supports a recommendation for patient‐specific treatment, while ensuring that the potential impact of other biochemical factors (e.g., magnesium and other B vitamin deficiencies) are considered and corrected if necessary. [ABSTRACT FROM AUTHOR]

The article presents a case study of a 40-year-old man with severe traumatic brain injury (TBI) and polytraumatic injuries in a single vehicle crash. Topics include demonstrating mild diffuse traumatic subarachnoid hemorrhage and a small subdural hematoma over the left cerebral convexity and along the left aspect of the central falx; and maximum assistance with activities of daily living in the setting of the cognitive and executive impairments.

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Danielle R Isen, 1 Lanning B Kline 2 1Department of Neurology, University of South Alabama School of Medicine, Mobile, AL, USA; 2Department of Ophthalmology, University of Alabama School of Medicine, Birmingham, AL, USACorrespondence: Lanning B KlineDepartment of Ophthalmology, University of Alabama School of Medicine, 700 South 18th Street, Suite 601, Birmingham, AL 35233, USATel +1 205 488 0756Email lkline@uabmc.eduAbstract: Wernicke encephalopathy (WE) is a life-threatening but reversible syndrome resulting from acute thiamine deficiency that is frequently overlooked and underdiagnosed. It is classically characterized by a triad of ocular dysfunction, ataxia, and altered mental status. However, less than 1/3 patients have the complete triad, so it is crucial to have a high index of suspicion. Awareness of the early signs of WE is essential to prevent clinical progression, as patients with the full triad already have a profoundly thiamine-deficient state. This review highlights the neuro-ophthalmic manifestations of WE to guide the clinician in identifying the condition. In addition, we provide an update regarding the clinical characteristics, pathophysiology, neuroimaging and laboratory findings, treatment options, and prognosis of WE.Keywords: Wernicke-Korsakoff Syndrome, thiamine deficiency, ocular findings, review

The purpose of this research was to investigate the effects of protocatechuic acid (PCA) at doses of 50 and 100 mg/kg on the development of unfavourable changes in cognitive processes in a pyrithiamine-induced thiamine deficiency (PTD) model of the Wernicke–Korsakoff syndrome (WKS) in rats. The effects of PCA were assessed at the behavioural and biochemical levels. Behavioural analysis was conducted using the Foot Fault test (FF), Bar test, Open Field test, Novel Object Recognition test (NOR), Hole–Board test and Morris Water Maze test (MWM). Biochemical analysis consisting of determination of concentration and turnover of neurotransmitters in selected structures of the rat CNS was carried out using high-performance liquid chromatography. PTD caused catalepsy (Bar test) and significantly impaired motor functions, leading to increased ladder crossing time and multiplied errors due to foot misplacement (FF). Rats with experimentally induced WKS showed impaired consolidation and recall of spatial reference memory in the MWM test, while episodic memory related to object recognition in the NOR was unimpaired. Compared to the control group, rats with WKS showed reduced serotonin levels in the prefrontal cortex and changes in dopamine and/or norepinephrine metabolites in the prefrontal cortex, medulla oblongata and spinal cord. PTD was also found to affect alanine, serine, glutamate, and threonine levels in certain areas of the rat brain. PCA alleviated PTD-induced cataleptic symptoms in rats, also improving their performance in the Foot Fault test. In the MWM, PCA at 50 and 100 mg/kg b.w. improved memory consolidation and the ability to retrieve acquired information in rats, thereby preventing unfavourable changes caused by PTD. PCA at both tested doses was also shown to have a beneficial effect on normalising PTD-disrupted alanine and glutamate concentrations in the medulla oblongata. These findings demonstrate that certain cognitive deficits in spatial memory and abnormalities in neurotransmitter levels persist in rats that have experienced an acute episode of PTD, despite restoration of thiamine supply and long-term recovery. PCA supplementation largely had a preventive effect on the development of these deficits, to some extent also normalising neurotransmitter concentrations in the brain.

Neuro-ophthalmic manifestations of Wernicke encephalopathy (WE) are uncommon and vary from nystagmus, oculomotor palsies, anisocoria, and optic disc edema to vision loss. We describe a case of a 53-year-old woman presenting with subacute bilateral painless vision decline, lower-extremities weakness with impaired ambulation, headache, and abdominal pain. Neurological examination was pertinent for confabulation, bilateral decreased visual acuity with an absent blink to threat, absent afferent pupillary defect and fundus abnormalities, and significant allodynia in bilateral lower extremities. Besides elevated inflammatory marker with an erythrocyte sedimentation rate (ESR) of 130 mm/hr, her infectious, autoimmune, paraneoplastic, and neuromyelitis optica work-up was overall unremarkable. Brain MRI showed abnormal fluid-attenuated inversion recovery (FLAIR) signaling in bilateral mammillary bodies and around periaqueductal gray matter concerning WE. Due to concerns of Wernicke-Korsakoff syndrome (WKS), parenteral high-dose thiamine was initiated with significant clinical improvement. The patient was also later found to have a positive anti-myelin oligodendrocyte glycoprotein (MOG) antibody, which was deemed false positive given the atypical phenotype and symptomatic improvement with thiamine supplementation. This case encourages the consideration of vision loss as a manifestation of WKS, especially in patients who have risk factors. Testing serum levels of thiamine is strongly encouraged; however, initiating empiric treatment is advocated for high clinical suspicion due to its reversible nature and minimal risk for side effects., Competing Interests: Human subjects: Consent was obtained or waived by all participants in this study. Conflicts of interest: In compliance with the ICMJE uniform disclosure form, all authors declare the following: Payment/services info: All authors have declared that no financial support was received from any organization for the submitted work. Financial relationships: All authors have declared that they have no financial relationships at present or within the previous three years with any organizations that might have an interest in the submitted work. Other relationships: All authors have declared that there are no other relationships or activities that could appear to have influenced the submitted work., (Copyright © 2024, Guagliardo et al.)

Wernicke's encephalopathy (WE) is a prominent neurologic manifestation of thiamine (vitamin B1) deficiency. While often linked to alcoholism, it can also arise from various causes, including malabsorption, inadequate dietary intake, increased metabolic requirement, and among dialysis patients. Here, we present a case of altered mental status from acute metabolic encephalopathy attributed to sepsis, acute kidney injury (AKI), and hypoglycemia. WE was overlooked in the early hospitalization course due to the daily administration of thiamine. However, the patient's cognitive decline persisted despite the improvement of sepsis and AKI. Subsequent brain MRI revealed thalamic T2 signal intensity changes, suggesting either a past infarction or WE. Implementing an empirical regimen of high-dose thiamine resulted in the patient's rapid cognitive recovery. This therapeutic strategy was integrated into the management of her sepsis and AKI, leading to her full recovery and subsequent hospital discharge without complications., Competing Interests: Human subjects: Consent was obtained or waived by all participants in this study. Conflicts of interest: In compliance with the ICMJE uniform disclosure form, all authors declare the following: Payment/services info: All authors have declared that no financial support was received from any organization for the submitted work. Financial relationships: All authors have declared that they have no financial relationships at present or within the previous three years with any organizations that might have an interest in the submitted work. Other relationships: All authors have declared that there are no other relationships or activities that could appear to have influenced the submitted work., (Copyright © 2024, Zhang et al.)

Introduction: Alcohol is the most consumed substance in Western culture and its use is a causal factor in more than 200 diseases and disorders. Our objective was to determine the relationship between alcohol consumption and cognitive impairment in people aged ≥60, and identify which cognitive functions are most affected by prolonged alcohol consumption., Methods: Search in MEDLINE, PsycInfo, Psicodoc, Cochrane and Web of Science databases. The search was limited to articles published from 2010 to 2020. A total of 8716 articles were obtained. Those repeated and unrelated to the topic were eliminated, leaving a total of seven articles: five longitudinal studies, covering the relationship between alcohol and cognitive impairment; and two cross-sectional studies, which helped identify which cognitive functions are more affected. This systematic review was carried out in accordance with the criteria of the PRISMA statement., Results: Most of the studies found conclude that no or excessive alcohol consumption is associated with a higher risk of cognitive impairment, compared to moderate consumption. In addition, excessive and prolonged alcohol consumption can evolve into secondary alcoholic dementia such as Marchiafava-Bignami disease, Wernicke-Korsakoff syndrome or pellagra. In people with alcohol use disorder, the cognitive functions that are most affected are executive functions, visuospatial skills, attention and memory., (Copyright © 2024. Published by Elsevier España, S.L.U.)

About 85% of survivors of acute Wernicke's Encephalopathy (WE), a frequent and serious consequence of thiamine deficiency and alcohol misuse, sustain chronic neurocognitive deficits also known as chronic Wernicke-Korsakoff syndrome (WKS). If alcoholism is combined with smoking, tobacco alcohol optic neuropathy (TAON) may occur which leads to visual impairment. In contrast to WKS, TAON may be treated successfully by early vitamin substitution and detoxification. Little research has been conducted on WKS longterm outcomes. Existing literature suggests poor prognosis. Symptoms remaining beyond the acute treatment with thiamine are thought to be irreversible. Whether neurorehabilitation may be an effective route to help recovery of those persistent symptoms is an open question. At our neurorehabilitation center, which specializes in the treatment of severe chronic deficits after brain injury, the opportunity arose to treat a 35 year old male with WKS, and to conduct follow-up assessments 3- and 7-years post discharge, respectively. Initially MK was admitted to emergency care with suspected postconcussive syndrome, alcohol-related thiamine deficiency, and TAON. Thiamin, cobalamin, and folate substituion improved TAON but major cognitive deficits remained. When admitted to our center 4 months later, he was fully reliant on care staff for all activities of daily living (ADL). Through intensive neurocognive training and psychological treatment he improved gradually and, after 26 months, was well enough to be discharged into the community and pursue work in a sheltered setting. Neuropsychological tests, as well as patient reports obtained at the follow-ups showed that the benefits apparent at discharge had been sustained, and for some scores, improved further. This was particularly evident in the Rey-Osterrieth Complex Figure Test which improved from percentage ranges

Abstract: Objectives consist of updating published reports on the recognition, assessment, and care of patients with Wernicke-Korsakoff syndrome (WKS). Methods included defining relevant terms, describing core clinical phenomena, conducting meaningful reviews for latter-day WKS publications, and selecting instructive case examples. Findings covered epidemiology, precipitants, neuroimaging studies, alternate learning strategies in WKS, adjunctive treatments, and promising research. In conclusion, patients, their family members, clinicians, and public health experts should benefit from this updated knowledge. Countries with substantial alcohol consumption should consider emulating Holland in designating WKS research centers, founding regional clinical facilities, and funding multidisciplinary expert teams. [ABSTRACT FROM AUTHOR]

About 85% of survivors of acute Wernicke's Encephalopathy (WE), a frequent and serious consequence of thiamine deficiency and alcohol misuse, sustain chronic neurocognitive deficits also known as chronic Wernicke-Korsakoff syndrome (WKS). If alcoholism is combined with smoking, tobacco alcohol optic neuropathy (TAON) may occur which leads to visual impairment. In contrast to WKS, TAON may be treated successfully by early vitamin substitution and detoxification. Little research has been conducted on WKS longterm outcomes. Existing literature suggests poor prognosis. Symptoms remaining beyond the acute treatment with thiamine are thought to be irreversible. Whether neurorehabilitation may be an effective route to help recovery of those persistent symptoms is an open question. At our neurorehabilitation center, which specializes in the treatment of severe chronic deficits after brain injury, the opportunity arose to treat a 35 year old male with WKS, and to conduct follow-up assessments 3- and 7-years post discharge, respectively. Initially MK was admitted to emergency care with suspected postconcussive syndrome, alcohol-related thiamine deficiency, and TAON. Thiamin, cobalamin, and folate substituion improved TAON but major cognitive deficits remained. When admitted to our center 4 months later, he was fully reliant on care staff for all activities of daily living (ADL). Through intensive neurocognive training and psychological treatment he improved gradually and, after 26 months, was well enough to be discharged into the community and pursue work in a sheltered setting. Neuropsychological tests, as well as patient reports obtained at the follow-ups showed that the benefits apparent at discharge had been sustained, and for some scores, improved further. This was particularly evident in the Rey-Osterrieth Complex Figure Test which improved from percentage ranges <1 for immediate recognition and recall at discharge to rank 16 for immediate recognition and rank 5 for recall at the 7-year follow-up. This case study illustrates the immense benefits neurorehabilitation can have for WKS induced by alcohol misuse. It further demonstrates how skills and strategies, learned in the inpatient setting, translate into living well and independently, and how the latter promotes further improvement long after discharge. [ABSTRACT FROM AUTHOR]

Introduction: Thiamine deficiency, also known as beriberi, is a nutritional disorder caused by a lack of thiamine (vitamin B 1 ) in the diet. It can occur in 2 forms: dry beriberi, which affects the nervous system, and wet beriberi, which affects the cardiovascular system. Gastrointestinal beriberi is a subtype that affects the digestive system and can lead to multisystem involvement. In the United States (US), thiamine deficiency often arises from chronic malnutrition secondary to alcoholism, known as Wernicke-Korsakoff Syndrome., Case Presentation: A 45-year-old female with no known past medical history or alcohol use disorder came to the emergency department with an altered mental status and with a history of intractable nausea and vomiting for several months prior to presentation. During intake, the medical team discovered she had bilateral lower extremity weakness and an anion gap metabolic acidosis. Her inpatient workup ruled out meningitis, encephalitis, peritonitis, diabetic ketoacidosis, and cerebrovascular accident. A thiamine deficiency was the most probable cause of her presentation, secondary to her protracted history of vomiting and poor oral medication intake. Refeeding syndrome complicated her hospitalization. After replenishing thiamine, the patient experienced significant improvement in mental status and lower extremity weakness. The healthcare team later discharged her with home physical therapy rehabilitation and nutritional counseling., Conclusion: Thiamine deficiency is not common in the US. However, this case highlights the importance of including this deficiency in the differential when a patient arrives with a history of malnourishment secondary to a gastrointestinal illness with signs of altered mental status and neurological symptoms., Competing Interests: Conflicts of Interest: The authors declare they have no conflicts of interest., (© 2024 HCA Physician Services, Inc. d/b/a Emerald Medical Education.)

Alcohol misuse is often a hidden problem and alcohol-related brain damage is thought to account for around 10% of cases of dementia (Gupta and Warner, 2008; Brust, 2010). In England, an estimated 589 101 adults are alcohol-dependent and 24% of adults in England and Scotland regularly drink more than Department of Health and Social Care (DHSC) guidelines (Burton et al, 2016). Alcohol misuse can affect many aspects of health and can lead to alcohol-related brain damage (ARBD). This article explains about the pathophysiology and clinical features of ARBD, and how it is diagnosed, treated and managed. [ABSTRACT FROM AUTHOR]

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Alcohol misuse is often a hidden problem and alcohol-related brain damage is thought to account for around 10% of cases of dementia (Brust, 2010; Gupta and Warner, 2008). In England, an estimated 589 101 adults are alcohol-dependent and 24% of adults in England and Scotland regularly drink more than Department of Health and Social Care (DHSC) guidelines (Burton et al, 2016). Alcohol misuse can affect many aspects of health and can lead to alcohol-related brain damage (ARBD). This article, the fifth in a series on dementia, explains about the pathophysiology and clinical features of ARBD, and how it is diagnosed, treated and managed. [ABSTRACT FROM AUTHOR]

Hemorrhage inside the mammillary bodies (MMBs) is known to be one of the findings of Wernicke encephalopathy. Brain MRI of two patients with Wernicke-Korsakoff syndrome (WKS) demonstrated high susceptibility values representing hemosiderin deposition in MMBs by using quantitative susceptibility mapping (QSM). QSM provided additional information of susceptibility values to susceptibility-weighted imaging in diagnosis of WKS.

Aim To offer an estimate of the incidence of anaphylactic reactions to parenteral products containing thiamine used in the treatment of Wernicke's encephalopathy (WE) and make recommendations. Method Review of previously released data on some older products and parenteral thiamine use in some other countries; analysis of sales and adverse incident data on anaphylaxis for a contemporary parenteral product used in the UK, Pabrinex. Results It was difficult to estimate the incidence of related anaphylactic reactions to Pabrinex in the UK because the number of doses given is unknown. Sales data are only an approximation to doses given because for products with a limited shelf life not all product sold is administered. However, available data indicate that there have been 10 anaphylactic reactions to Pabrinex from between 5,431,235–6,651,947 patient-days (14,880–16,080 years) of treatment. Conclusion It is reasonable to assume that the risk of anaphylaxis is low, and lower than for many other drugs. The risk-benefit ratio for administration is favourable given the potential severity of brain damage in Wernicke–Korsakoff (WK) syndrome. There is a need for international agreement on the reporting of anaphylaxis and on the optimum thiamine therapy for the treatment of WK syndrome. We make recommendations on how this might be achieved. [ABSTRACT FROM AUTHOR]

Prion diseases are a phenotypically diverse set of disorders characterized by protease-resistant abnormally shaped proteins known as prions. There are three main groups of prion diseases, termed sporadic (Creutzfeldt-Jakob disease [CJD], sporadic fatal insomnia, and variably protease-sensitive phonopathy), genetic (genetic CJD, fatal familial insomnia, and Gerstmann-Straussler-Scheinker syndrome), and acquired (kuru, variant CJD, and iatrogenic CJD). This article will review the pathophysiology, genetics, clinical presentations, and diagnostic challenges in patients with prion disease. Case discussions, images, and tables will be used to highlight important characteristics of prion disease and prion mimics. [ABSTRACT FROM AUTHOR]

Aims Prior research has been mainly concerned with the ability of patients with Korsakoff syndrome (KS) to project themselves into the past. Little is known about the patients' ability to project themselves into the future. We therefore compared past and future thinking in patients with KS. Methods We invited patients with KS and control participants to retrieve past events and reconstruct future events. Participants were also invited to rate subjective characteristics (i.e. time travel, emotional feeling, and visual imagery) of the past and future events. Results Patients with KS demonstrated low specificity, time travel, and emotional experience during past and future thinking. However, while lower emotional experience was observed in patients with KS than in the control participants during future thinking, no significant differences were observed between the two populations during past thinking. Regarding within-group comparisons, patients with KS demonstrated no significant differences between past and future thinking in terms of specificity, time travel, and visual imagery; however, they demonstrated higher emotional experience during past than during future thinking. Regarding control participants, they demonstrated no significant differences between past and future thinking in terms of specificity, time travel, emotional experience, and visual imagery. Conclusion Our findings demonstrate a diminished ability to construct specific future scenarios as well as a diminished subjective experience during future thinking in KS. [ABSTRACT FROM AUTHOR]

Vitamins are either fat-soluble or water-soluble micronutrients that are derived from a healthy, well-balanced diet. The B-complex vitamins are well-known examples of such water-soluble nutrients that are readily absorbed from a healthy gut, and easily eliminated via renal excretion. They are required for their vital physiological functions and are significant contributors towards maintaining optimal health. Multiple B-vitamin deficiencies are quite commonly seen and therefore a balanced diet, including a full spectrum of B-vitamins, is usually needed when any of them is found to be deficient. Conversely, their therapeutic value will be limited to supplementation during states of deficiency, since they have no additional benefits in the presence of an adequate dietary intake. In general, their active supplementation should only be used to correct deficiencies. This article provides an overview of such B-complex vitamin deficiencies and their supplementation. [ABSTRACT FROM AUTHOR]

Wernicke-Korsakoff syndrome and Wernicke's encephalopathy are both progressive illnesses that result from thiamine deficiency. To assess and screen for thiamine levels, clinical staff have traditionally relied on the triad of ophthalmoplegia, cerebellar dysfunction and either an altered mental state or mild memory impairment. However, these symptoms are late signs of illness, and treatment efficacy may be limited due to permanent thalamus damage. This is costly in terms of both healthcare resources and the patient's health. The signs of thiamine deficiency are similar to those of early sepsis, and they can only be identified after prolonged assessment and testing. Patients who have significant illness that results in gastrointestinal imbalance or periods of malnutrition, malabsorption or protracted vomiting may present to hospital many days after the symptoms have commenced. This can result in patients missing life-improving treatment due to diagnostic overshadowing or treatment only being offered to those identified as having a history of alcohol misuse. [ABSTRACT FROM AUTHOR]