To prevent Wernicke-Korsakoff syndrome, it is extremely important that thiamine should be given preventively to all persons with an alcohol use disorder even if they don’t show any signs of the syndrome.
Full Answer
Can thiamine be used to treat Wernicke-Korsakoff syndrome?
Thiamine for prevention and treatment of Wernicke-Korsakoff Syndrome in people who abuse alcohol Evidence from randomised controlled clinical trials is insufficient to guide clinicians in determining the dose, frequency, route or duration of thiamine treatment for prophylaxis against or treatment of WKS due to alcohol abuse.
What is thiamine used for?
Thiamine for prevention and treatment of Wernicke-Korsakoff syndrome in people who abuse alcohol. Wernicke-Korsakoff syndrome (WKS) is a disorder of the brain caused by a deficiency of vitamin B 1 (thiamine).
Does thiamine have a role in the treatment of alcohol‐induced WKS?
One study ( Ambrose 2001) set out to investigate the therapeutic effects of thiamine in a sample of alcohol‐dependent people without the clinical triad of acute WKS, whereas the other study ( Nichols unpublished) assessed the cognitive effects of thiamine in participants with memory impairment associated with chronic alcohol abuse.
Is Wernicke‐Korsakoff syndrome a rare disorder?
Autopsy studies suggest that Wernicke‐Korsakoff syndrome (WKS) is not a rare disorder, particularly in individuals who abuse alcohol. Thiamine has been established as the treatment of choice for over 50 years, but uncertainty remains about appropriate dosage and duration.
What is thiamine used for?
Thiamine for prevention and treatment of Wernicke-Korsakoff syndrome in people who abuse alcohol. Wernicke-Korsakoff syndrome (WKS) is a disorder of the brain caused by a deficiency of vitamin B 1 (thiamine).
What is a randomised trial of thiamine?
Any randomised trials comparing thiamine with alternative interventions or comparing different thiamine regimens (varying in formulation, dose or duration of administration).
Is Wernicke Korsakoff syndrome rare?
Autopsy studies suggest that Wernicke-Korsakoff syndrome (WKS) is not a rare disorder, particularly in individuals who abuse alcohol. Thiamine has been established as the treatment of choice for over 50 years, but uncertainty remains about appropriate dosage and duration.
Does drinking thiamine help with WKS?
Heavy drinking may lead to particular problems with uptake of thiamine from the diet. When recognised, WKS is treated with thiamine, but it is not clear how effective this is, particularly in managing the mental features. Recommendations about dosage and duration of thiamine treatment are acknowledged to be arbitrary.
What is the difference between Wernicke and Korsakoff syndrome?
Wernicke–Korsakoff syndrome refers to a life-threatening encephalopathy due to inadequate supply of thiamine (vitamin B1) to the brain. It is a combination of Wernicke encephalopathy (WE), an acute neuropsychiatric disorder fully responsive to prompt and adequate thiamine replacement, and Korsakoff syndrome (KS), the chronic, irreversible form of WE that does not remit with thiamine treatment. Thiamine deficiency can occur in any condition of unbalanced nutrition that lasts for 2–3 weeks. These include poor nutrition, chronic alcohol misuse, loss of thiamine owing to recurrent vomiting or malabsorption, increased thiamine requirements owing to chronic diseases, prolonged and excessive carbohydrate intake and gastrointestinal surgical procedures, in particular, patients after bariatric surgery. The diagnosis is clinical and is mainly supported by the dramatic improvement of neurological signs to parenteral thiamine. Neuroimaging studies are useful to confirm the diagnosis of both WE and KS. Patients with suspected thiamine deficiency should be treated immediately with parenteral thiamine at the doses deemed to be effective in the treatment of WE and prevention of KS.
What is Korsakoff syndrome?
In this review, we present a survey on Korsakoff’s syndrome (KS), a residual syndrome in patients who suffered from a Wernicke encephalopathy (WE) that is predominantly characterized by global amnesia, and in more severe cases also by cognitive and behavioral dysfunction. We describe the history of KS and its definition, its epidemiology, and the lack of consensus criteria for its diagnosis. The cognitive and behavioral symptoms of KS, which include anterograde and retrograde amnesia, executive dysfunction, confabulation, apathy, as well as affective and social-cognitive impairments, are discussed. Moreover, recent insights into the underlying neurocognitive mechanisms of these symptoms are presented. In addition, the evidence so far on the etiology of KS is examined, highlighting the role of thiamine and alcohol and discussing the continuity hypothesis. Furthermore, the neuropathology of KS is reviewed, focusing on abnormalities in the diencephalon, including the mammillary bodies and thalamic nuclei. Pharmacological treatment options and nonpharmacological interventions, such as those based on cognitive rehabilitation, are discussed. Our review shows that thiamine deficiency (TD) is a crucial factor in the etiology of KS. Although alcohol abuse is by far the most important context in which TD occurs, there is no convincing evidence for an essential contribution of ethanol neurotoxicity (EN) to the development of WE or to the progression of WE to KS. Future research on the postmortem histopathological analysis of brain tissues of KS patients is crucial for the advancement of our knowledge of KS, especially for associating its symptoms with lesions in various thalamic nuclei. A necessary requirement for the advancement of studies on KS is the broad acceptance of a comprehensive definition and definite diagnostic criteria. Therefore, in this review, we propose such a definition of KS and draft outlines for prospective diagnostic criteria.
What is Wernicke's encephalopathy?
Introduction: Wernicke's encephalopathy (WE) is a severe neuropsychiatric disorder, which results from a nutritional deficiency of thiamine. The occurrence of WE is rarely reported in patients with cerebral infarction, who often have complications of malnutrition. Cerebral infarction is a neurological disease, patients with cerebral infarction may show symptoms such as disturbance of consciousness and gait instability, which is difficult to differentiate from WE. Thus, early recognition and differential diagnosis of WE are important. We report a rare case of cerebral infarction patient who developed WE due to malnutrition and parenteral nutrition. Patient concerns: A 65-year-old woman was admitted to our hospital with cerebral infarction. She had lost 15 kg of weight in the past month or so and was diagnosed with malnutrition. In order to correct malnutrition, parenteral nutrition and intravenous glucose without thiamine were administered. Cognitive dysfunction, laloplegia, sleep rhythm inversion, somnolence and bilateral lower limbs weakness were presented 20 days after admission. Diagnosis: Brain magnetic resonance imaging confirmed the diagnosis of WE. Interventions: The patient was given thiamine and nutrition support therapy. Outcomes: The patient's cognitive impairment, laloplegia and sleep condition improved within 4 days. Neurological status continued to improve and physical activity recovered gradually within 2 weeks. She received rehabilitation training when her condition was relatively stable, and her muscle strength of limbs and physical function gradually improved. Conclusion: Infarction-related malnutrition may result in nutrient deficiency-related neurological complications, such as WE. Thus, it is important to pay close attention to the nutritional status of patients with cerebral infarction. In addition, early recognition and differential diagnosis of WE in patients with infarction-related malnutrition are necessary, early treatment of replete thiamine supplementation and nutrition support therapy can reduce the risk of WE and improve the prognosis.
What is neuropsychological assessment?
Background: Neuropsychological assessment is central to identifying and determining the extent of Alcohol-Related Cognitive Impairment (ARCI). The present systematic review aimed to synthesize and discuss the evidence appraising the neuropsychological tests used to assess ARCI in order to support clinicians and researchers in selecting appropriate tests for use with this population. Methods: We searched for studies investigating the psychometric, diagnostic and practical values of tools used in the screening, diagnosis, and assessment of Korsakoff's Syndrome (KS), Alcohol-Related Dementia (ARD), and those with a specific diagnosis of Alcohol-Related Brain Damage (ARBD). The following databases were searched in March 2016 and again in August 2018: MEDLINE, EMBASE, Psych-INFO, ProQuest Psychology, and Science Direct. Study quality was assessed using a checklist designed by the authors to evaluate the specific factors contributing to robust and clearly reported studies in this area. A total of 43 studies were included following the screening of 3646 studies by title and abstract and 360 at full-text. Meta-analysis was not appropriate due to heterogeneity in the tests and ARCI samples investigated in the studies reviewed. Instead, review findings were narratively synthesized and divided according to five domains of assessment: cognitive screening, memory, executive function, intelligence and test batteries, and premorbid ability. Effect sizes (d) were calculated to supplement findings. Results: Overall, several measures demonstrated sensitivity to the cognitive deficits associated with chronic alcoholism and an ability to differentiate between gradations of impairment. However, findings relating to the other psychometric qualities of the tests, including those important for the accurate assessment and monitoring of ARCI (e.g., test-retest reliability), were entirely absent or limited. Additionally, the synthesis of neuropsychological outcomes presented here supports the recent impetus for a move away from discrete diagnoses (e.g., KS, ARD) and the distinctions between them toward more broad and inclusive diagnostic conceptualizations of ARCI, thereby recognizing the heterogeneity in presentation. Conclusions: Based on the evidence reviewed, provisional recommendations for appropriate tests in each domain of assessment are presented, though further validation of most tests is warranted. Review findings can support efficient and evidenced-based test-selection and guide future research in this area.
How does brain imaging help with alcoholism?
Brain imaging technology has allowed researchers to conduct rigorous studies of the dynamic course of alcoholism through periods of drinking, sobriety, and relapse and to gain insights into the effects of chronic alcoholism on the human brain. Magnetic resonance imaging (MRI) studies have distinguished alcohol-related brain effects that are permanent from those that are reversible with abstinence. In support of postmortem neuropathological studies showing degeneration of white matter, MRI studies have shown a specific vulnerability of white matter to chronic alcohol exposure. Such studies have demonstrated white-matter volume deficits as well as damage to selective gray-matter structures. Diffusion tensor imaging (DTI), by permitting microstructural characterization of white matter, has extended MRI findings in alcoholics. MR spectroscopy (MRS) allows quantification of several metabolites that shed light on brain biochemical alterations caused by alcoholism. This article focuses on MRI, DTI, and MRS findings in neurological disorders that commonly co-occur with alcoholism, including Wernicke’s encephalopathy, Korsakoff’s syndrome, and hepatic encephalopathy. Also reviewed are neuroimaging findings in animal models of alcoholism and related neurological disorders. This report also suggests that the dynamic course of alcoholism presents a unique opportunity to examine brain structural and functional repair and recovery.
What is the WKS syndrome?
Background: Wernicke-Korsakoff syndrome (WKS) is a triad of ophthalmoplegia, ataxia and memory deficits due to thiamine insufficiency resulting from under- or untreated Wernicke’s encephalopathy (WE), which may be associated with hyperemesis gravidarum (HEG). Case presentation: We present a case of a 36-year-old Filipino woman in her first trimester with HEG, along with the WKS triad and abnormal hyperintense signals in the bilateral thalami and midbrain, left occipital lobe, periaqueductal gray matter and pontine periventricular areas. Neurologic deficits partially improved but persisted despite intravenous thiamine administration. Evidence review: A review of current treatments for WE, and the prevention and neurocognitive recovery of WKS was done. The beneficial effects of thiamine for acute WKS are supported by several case reports and clinical experience. Evidence from one randomized controlled trial wherein thiamine was given in various doses for treating WE or preventing WKS in an alcohol-dependent population is limited by methodological issues. Rehabilitation and pharmacotherapy for neurocognitive recovery seems promising, but they have inadequate evidentiary support. More robust studies on multi-modal strategies are warranted to facilitate the neurocognitive recovery of patients with WKS.
Why are vitamins and minerals important for oral health?
Nutritional deficiencies occur when bodily metabolic requirements are not matched by intake and absorption. Reasons for this discrepancy are numerous, but often social, economic, medical, and even psychiatric factors may play a role. Vitamins and minerals are required for appropriate rapid cell turnover of the oral mucosa. The oral cavity is a unique anatomic environment that may manifest early signs of nutritional disorders as well as other indicators of systemic disease. Knowledge of these oral manifestations and associated findings will allow a practitioner to consider a nutritional disorder when evaluating oral changes, and in turn, initiate appropriate therapy. A systematic approach to examination of the mouth and perioral skin is suggested. A detailed medical and social history complements the physical exam in identifying patients at risk for nutritional disorders and heightening the clinical suspicion to warrant additional nutritional screening. The rising prevalence of anorexia and bulimia, as well as fad diets, add to the population of patients at risk for vitamin and mineral deficiencies that a clinician must now consider.
How long has thiamine been used?
Thiamine has been established as the treatment of choice for over 50 years, but there is uncertainty about appropriate dosage and duration. Current practice guidelines are based on case reports and clinical experience.
Is Wernicke Korsakoff Syndrome rare?
Background: Autopsy studies suggest that Wernicke-Korsakoff Syndrome (WKS) is not a rare disorder, particularly in individuals who abuse alcohol. Thiamine has been established as the treatment of choice for over 50 years, but there is uncertainty about appropriate dosage and duration. Current practice guidelines are based on case reports and clinical experience.
Author information
1. Department of Psychiatry, Birmingham and Solihull Mental Health NHS Foundation Trust, Birmingham, UK.
Abstract
BACKGROUND:Autopsy studies suggest that Wernicke-Korsakoff syndrome (WKS) is not a rare disorder, particularly in individuals who abuse alcohol. Thiamine has been established as the treatment of choice for over 50 years, but uncertainty remains about appropriate dosage and duration.
Abstract
Autopsy studies suggest that Wernicke‐Korsakoff syndrome (WKS) is not a rare disorder, particularly in individuals who abuse alcohol. Thiamine has been established as the treatment of choice for over 50 years, but uncertainty remains about appropriate dosage and duration.
Plain language summary
Wernicke‐Korsakoff syndrome (WKS) is a disorder of the brain caused by a deficiency of vitamin B 1 (thiamine). It is characterised by an acute onset of some or all of an eye movement disorder, lack of voluntary coordination of muscle movement (ataxia) and confusion.
Background
Alcohol abuse is associated with a variety of neuropsychiatric problems, and the Wernicke‐Korsakoff syndrome (WKS) is one of the most serious.
Discussion
Although the use of thiamine or thiamine‐containing products for prophylaxis against and treatment of WKS in individuals who misuse alcohol is well established, only two small randomised controlled trials were identified by our search.
Authors' conclusions
WKS is a fairly common condition, and effective recognition and treatment of this disorder have important human and economic consequences. The use of thiamine in the treatment of acute WKS is well established and is supported by a series of published case reports ( Cook 1998; Victor 1989; NCGCACC 2010 ).
What is the Korsakoff psychosis?
In 1887 Sergei Korsakoff gave the first comprehensive account ofthe amnestic syndrome now known as Korsakoff psychosis (KP).He described a range of features including delirium, but the disor-der came to be characterised by recent memory loss with confabu-lation but with relative preservation of other intellectualfunctions.The two disorders were brought together by Victor and colleaguesin 1971 (Victor 1971). WKS is now considered to be a unitarydisorder comprising acute WE, which proceeds in a proportion ofcases to KP. From a case series of 245 patients, Victor et al con-cluded that the clinical triad of ophthalmoplegia, ataxia and men-tal confusion ’needs to be amplified to include the characteristicmemory disorder’ as well as peripheral neuropathy (Victor 1971).A major complicating factor is that the pathology of WE may notbe associated with the classical clinical triad in up to 90% of pa-tients (Harper 1986). The full triad of symptoms is recognised injust 0.05% of all hospital admissions, whereas the whole popula-tion prevalence of WKS based on autopsy studies in Western coun-tries has been estimated at 1% to 2% (Harper 1995;Torvik 1991).Autopsy studies suggest that WE is not a rare disorder, particularlyamong abusers of alcohol. Therefore it has been suggested thata presumptive diagnosis of WE should be made for any patientwith a history of alcohol abuse who may be at risk. This includesanyone showing evidence of ophthalmoplegia, ataxia, acute con-fusion, memory disturbance, unexplained hypotension, hypother-mia, coma or unconsciousness (Cook 2000). Operational criteriafor the diagnosis of WE have been proposed (Caine 1997), andalthough they are not yet widely used, they can help in distinguish-ing this problem from other potentially coexisting conditions suchas alcohol withdrawal or hepatic encephalopathy.
What is the most serious disorder of alcohol abuse?
Alcohol abuse is associated with a variety of neuropsychiatricprob-lems, and the Wernicke-Korsakoff syndrome ( WKS) is one ofthe most serious. Wernicke’s encephalopathy (WE) is tradition-ally thought of as a disorder of acute onset characterised by nys-tagmus, abducent and conjugate gaze palsies, ataxia of gait and aglobal confusional state, which may occur together or in variouscombinations (Victor 1989). It is due to deficiency of the B vita-min thiamine (vitamin B1, also known asaneurin). Carl Wernickefirst described the disorder in 1881 in three cases, two associatedwith chronic alcohol dependence and one with persistent vomit-ing after sulphuric acid poisoning. The symptoms that Wernickerecorded included disturbances of eye movement, ataxia of gait,polyneuropathy and mental changes including apathy, decreasedattention span and disorientation in time and space. He notedsim-ilar pathological changes in all three cases, in particular numerouspunctate haemorrhages in the grey matter around the third andfourth ventricles and the aqueduct of Sylvius. Work by Alexander(1939) and then Jolliffe (1941) established the role of thiaminedeficiency in development and potential treatment of the disorder
What is WKS in alcohol?
All participants with, or at risk of developing, WKS as the resultof any diagnosis of alcohol use disorder or ’alcoholism’, includingharmful use, abuse and dependence. Participants who developedWKS after thiamine deficiency secondary to causes other thanalcohol abuse were excluded.
Is Wernicke Korsakoff syndrome rare?
Autopsy studies suggest that Wernicke-Korsakoff syndrome (WKS) is not a rare disorder, particularly in individuals who abuse alcohol.Thiamine has been established as the treatment of choice for over 50 years, but uncertainty remains about appropriate dosage andduration. Current practice guidelines are based on case reports and clinical experience. This is an update of a review first published in2004 and last updated in 2008.