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Diagnosis of Dementia
Published in Dawn Brooker, Sue Lillyman, Mary Bruce, Dementia Care, 2023
Dawn Brooker, Sue Lillyman, Mary Bruce
There are several specific types of ARBD. The two most common types are: alcohol-related ‘dementia’ caused from damage of excessive drinking over a period of time;Wernicke–Korsakoff syndrome (Korsakoff Syndrome) caused specifically by the lack of thiamine normally through drinking over a period of time. Wernicke–Korsakoff syndrome has two stages. Firstly, there will be intense inflammation (swelling) of their brain. known as ‘Wernicke’s encephalopathy’. If not treated as an emergency this can lead to long term brain damage and ‘Korsakoff’s syndrome’ or possibly death.
Nutritional Diseases
Published in Ayşe Serap Karadağ, Lawrence Charles Parish, Jordan V. Wang, Roxburgh's Common Skin Diseases, 2022
Chelsea Kesty, Madeline Hooper, Erin McClure, Emily Chea, Cynthia Bartus
Management: Oral thiamine supplementation is used to manage beriberi with 5–30 mg per dose daily to 3 times daily (TID) depending on severity of illness. Wernicke encephalopathy is immediately managed with 500 mg IV thiamine TID in combination with other B vitamins. Glucose administration must follow thiamine supplementation in severely malnourished patients. Korsakoff encephalopathy is treated with oral vitamin B1 supplementation to help prevent further deterioration of mental status. Lifetime abstinence from alcohol is crucial in Wernicke-Korsakoff syndrome.
Central nervous system lesions
Published in Ibrahim Natalwala, Ammar Natalwala, E Glucksman, MCQs in Neurology and Neurosurgery for Medical Students, 2022
Ibrahim Natalwala, Ammar Natalwala, E Glucksman
FALSE – These are described as being part of the hypothalamus and the limbic system and thus are implicated in the function of memory. Pathology of the mammillary bodies is associated with amnesic syndromes. Also, damage as a result of Wernicke-Korsakoff syndrome may lead to anterograde memory loss.
Resveratrol impairs acquisition, reinstatement and precipitates extinction of alcohol-induced place preference in mice
Published in Neurological Research, 2021
Alcohol addiction, also known as alcohol-use disorder is defined as a ‘chronic relapsing brain disease’ that produces a person to drink compulsively notwithstanding adverse results to daily life and overall health [1,2]. There are numerous neurological disorders and diseases that can be produced by alcohol dependence and misuse, including dementia, cerebellar degeneration, fetal alcohol syndrome, Wernicke-Korsakoff syndrome, Marchiafava‐Bignami disorder, amblyopia, and alcohol absence symptoms [1]. These negative effects of alcohol change with the brain area, age, sex, dose, developmental stage, and duration of exposures [1,3]. Relapse after lengthened periods of abstinence is a common feature of drug addiction and remains the principal problem in treating alcohol-use disorder [2]. In fact, excessive alcohol consumption is the cause of an ongoing public health crisis and is estimated to comprise ~5% of the global disease costs [2]. Evidence suggests that alcohol influences the brain’s reward regions by interacting with various neurotransmitter and reward pathways [4–6].
Low rates of thiamine prescribing in adult patients with alcohol-related diagnoses in the emergency department
Published in The American Journal of Drug and Alcohol Abuse, 2021
Nathan M. Peck, Theodore C. Bania, Jason Chu
Alcohol use disorder (AUD) is a pervasive issue in the United States with recent estimates at a 13.9% twelve-month prevalence for the entire population aged 18 or older (1). AUD is defined by the Diagnostic and Statistical Manual of Mental Disorders, 5th Edition (DSM-5) as an alcohol consumption pattern that produces significant impairment or distress and is diagnosed by identifying specific complications of alcohol use or manifestations of alcohol dependence in a given patient (2). Wernicke encephalopathy and Korsakoff’s psychosis are neurologic disorders that most frequently develop in the setting of AUD and are due to thiamine deficiency (3). Given the common etiology of thiamine deficiency for both Wernicke encephalopathy and Korsakoff’s psychosis, and because patients with Wernicke encephalopathy often progress to Korsakoff’s psychosis, these two conditions are often referenced together as Wernicke-Korsakoff Syndrome (WKS). The prevalence of WKS, based on autopsy, is estimated between 0.8% and 2.8% for the entire population and 12.5% among individuals with AUD (4–6).
Thiamine administration to all patients with alcohol use disorder: why not?
Published in The American Journal of Drug and Alcohol Abuse, 2021
Roberta Agabio, Lorenzo Leggio
In the United States (US), there are almost 5 million alcohol-related visits to Emergency Departments (EDs) per year (1). Many of these visits involve patients with alcohol use disorder (AUD) who have, or are at risk for, thiamine deficiency. These individuals should receive thiamine supplementation (2–4). However, thiamine deficiency is difficult to identify because initial symptoms are often nonspecific, e.g., headaches, fatigue, irritability, and abdominal discomfort (5,6). The lack of thiamine supplementation in patients with thiamine deficiency can contribute to heart failure and sudden death, Wernicke’s encephalopathy, and irreversible brain damage. The latter includes Korsakoff’s psychosis, which is characterized by anterograde amnesia, an inability to remember recent events, and confabulation (5,6). Because Wernicke’s encephalopathy and Korsakoff’s psychosis have a shared etiology and often co-occur, they are often referred to as Wernicke–Korsakoff syndrome (WKS).