Wernicke Encephalopathy
Thiamine Deficiency
Thyroid Crisis
Thyrotoxicosis
Hepatic Encephalopathy
Magnetic Resonance Imaging
Brain
Aphasia, Wernicke
Encephalopathy, Bovine Spongiform
Degeneration of anterior thalamic nuclei differentiates alcoholics with amnesia. (1/101)
The specific neural substrate underlying the amnesia in alcoholic Korsakoff's psychosis is poorly defined because of the considerable brain damage found in many non-amnesic alcoholics, particularly those with Wernicke's encephalopathy. Using operational criteria to identify alcoholics with and without Korsakoff's psychosis, we have shown that many of the cortical and subcortical regions involved in the encoding and retrieval of episodic memory are either unaffected (hippocampus) or damaged to the same extent (prefrontal cortex and the cholinergic basal forebrain) in both amnesic and non-amnesic alcoholics. In the present study we analysed the diencephalic regions involved in episodic memory to determine the neural substrate for the amnesia observed in alcoholic Korsakoff's psychosis. The number of neurons in spaced serial sections containing the hypothalamic mamillary nuclei and the anterior and mediodorsal thalamic nuclei was estimated using unbiased stereological techniques. Neurodegeneration of the hypothalamic mamillary nuclei and the mediodorsal thalamic nuclei was substantial in both non-amnesic and amnesic alcoholics with Wernicke's encephalopathy. However, neuronal loss in the anterior thalamic nuclei was found consistently only in alcoholic Korsakoff's psychosis. This is the first demonstration of a differentiating lesion in alcoholic Korsakoff's psychosis and supports previous evidence that degeneration of thalamic relays are important in this memory disorder. (+info)A survey of the current clinical practice of psychiatrists and accident and emergency specialists in the United Kingdom concerning vitamin supplementation for chronic alcohol misusers. (2/101)
Although it is well known that B-vitamin deficiencies directly affecting the brain are common in alcohol misuse, no concise guidelines on the use of vitamin supplements in alcohol misusers currently exist in the UK. The purpose of this study was to assess current practice and opinion among UK physicians. Questionnaires were completed by a total of 427 physicians comprising Accident and Emergency (A&E) specialists and psychiatrists, with a response rate of 25%. The main findings were that vitamin deficiency was perceived as being uncommon amongst alcohol misusers (<25%) and there was no consensus as to which B vitamins are beneficial in treatment or the best method of administration of B-vitamin supplementation. The majority of psychiatrists favoured oral administration for prophylaxis against the Wernicke-Korsakoff syndrome in chronic alcohol misusers and parenteral therapy in patients with signs of Wernicke-Korsakoff syndrome. Whilst only just over half the A&E specialists expressed a preference, most favoured parenteral therapy in both cases. Most respondents did not currently have a unit policy/protocol on the management of vitamin supplementation in chronic alcohol misusers. Overall, the findings suggest that there is wide variation in current practice and highlight the need for guidelines in this area. (+info)Neuropathological findings after bone marrow transplantation: an autopsy study of 180 cases. (3/101)
We prospectively evaluated the neuropathological complications of 180 patients who underwent autopsy studies following bone marrow transplantation (BMT) (177 allogeneic, three autologous). The most frequent underlying disorders included severe aplastic anemia (n = 55), chronic myelogenous leukemia (n = 53), acute myelogenous leukemia (n = 24) and Fanconi anemia (n = 16). There were 114 males and 66 females. Neuropathological findings were detected in 90.55% of the patients. The most frequent findings were subarachnoid hemorrhages (SAH) (n = 57), intraparenchymal hemorrhages (IHP) (n = 49), fungal infections (n = 16), Wernicke's encephalopathy (n = 10), microglial nodular encephalopathy (n = 10) and neurotoxoplasmosis (n = 8). In only 17 patients was the brain within normal limits. Survival time after BMT averaged 5.4 months and the majority of patients died in the first 3 months post BMT (n = 105). Central nervous system (CNS) pathology was the main cause of death in 17% of the patients (n = 31), with a predominance of IHP in this particular group. Furthermore, the survival time of these patients who died of CNS causes (96.3 days) was almost half of the survival time of those who died of extra-cerebral causes (177.8 days) (P = 0.0162). IHP (70. 96 vs27.22%) (P < 0.001), fungal infections (25.8 vs 8.88%) (P < 0. 001) and toxoplasmosis (9.67 vs 4.44%) (P < 0.001) were significantly more frequent in the group of patients who died due to CNS causes than in the control group. The findings of this work provide a possible guide to the possible causes of neurological syndromes following BMT. Bone Marrow Transplantation (2000) 25, 301-307. (+info)Gestational thyrotoxicosis with acute Wernicke encephalopathy: a case report. (4/101)
A 35-year-old hyperthyroid woman who developed nausea, vomiting, tachycardia, nystagmus and mental disturbance, was referred to our hospital with a suspected diagnosis of thyroid storm. However, the thyroid gland was only slightly palpable, bruits were not audible, and exophthalmos was not present. Serum levels of thyroid hormone were increased, but TSH receptor antibodies were negative. Echography and color flow doppler ultrasonography revealed a slightly enlarged thyroid gland and a slightly increased blood flow, both of which were much less milder than those expected for severe hyperthyroid Graves' disease. Under the diagnosis of hyperthyroidism due to gestational thyrotoxicosis associated with Wernicke encephalopathy, vitamin B1 was administered on the first day of admission. Her consciousness became nearly normal on the second day except for slight amnesia. Her right abducent nerve palsy rapidly improved, but horizontal and vertical nystagmus, diminished deep tendon reflexes and gait ataxia improved only gradually. MRI findings of the brain were compatible with acute Wernicke encephalopathy. We concluded that history taking and physical findings are important to make a differential diagnosis of gestational thyrotoxicosis with acute Wernicke encephalopathy from Graves' thyroid storm, and that Wernicke encephalopathy should be treated as soon as possible to improve the prognosis. (+info)High ethanol intake and malnutrition in alcoholic cerebellar shrinkage. (5/101)
To determine the influence of chronic ethanol intake and nutritional status on cerebellar shrinkage in alcoholism, we studied 12 undernourished patients with acute Wernicke's encephalopathy (WE), 12 undernourished and 24 well-nourished asymptomatic chronic alcoholics, and 24 age-matched well-nourished controls, using morphometric analysis of MRI scans with volumetry of the cerebellum. Alcoholics reported a mean daily intake of ethanol of 177+/-8 g over a period of 27+/-1 years. Most undernourished alcoholics and half of the well-nourished alcoholics, compared to one-tenth of the controls, showed a significant reduction in cerebellar volume (p< or =0.01, both). Alcoholics with cerebellar shrinkage (n=33) were older (p=0.05) and tended to report greater daily ethanol intake than alcoholics without cerebellar shrinkage (n=15), although not significantly so (p=0.09). Cerebellar volume correlated negatively with age in controls and asymptomatic alcoholics (r> or =0.52, p< or =0.01, both), with a significantly greater shrinkage for age in the latter (p=0.003). Logistic regression analysis showed that malnutrition (OR 6.6 [95%CI 1.7-25.6], p=0.005) and a daily ethanol intake of more than 140 g over ten years (OR 6.1 [95%CI 1.8-20.5], p=0.003) were independently associated with the development of cerebellar shrinkage. (+info)Wernicke's encephalopathy: atypical manifestation at MR imaging. (6/101)
SUMMARY: We report a case of atypical manifestation of hyperintense lesions in a 64-year-old female patient with Wernicke's encephalopathy. Fluid-attenuated inversion recovery and T2-weighted images demonstrated symmetrical distribution of hyperintense lesions in cerebellar dentate nuclei, tegmentum of the lower pons, red nuclei, and tectum of the midbrain, and T1-weighted sagittal images showed atrophy of the mamillary bodies. The hyperintense lesions were completely resolved on follow-up MR images. (+info)Diffusion-weighted imaging in a case of wernicke encephalopathy. (7/101)
In a chronic alcoholic patient with progressive confusion, which was consistent with the clinical diagnosis of Wernicke encephalopathy, T2-weighted, FLAIR and diffusion weighted (DWI) MR imaging depicted brain abnormalities located in both medial thalamic nuclei. Apparent Diffusion Coefficient (ADC) measurements in these regions shown unexpected normal values, referring to Wernicke pathological findings and DWI data. DWI may be helpful to diagnose early basal nuclei abnormalities, but may fail to compute ADC values in these locations. (+info)Wernicke's encephalopathy presenting with severe dysphagia: a case report. (8/101)
A 62-year-old man developed dysphagia 4 weeks before the classic symptoms and signs of Wernicke's encephalopathy appeared. Adequate treatment with parenteral thiamine resulted in complete recovery of all symptoms, including his dysphagia. This extraordinary presentation with dysphagia, and the unusual course of the disease, encouraged us to present this case history. (+info)Wernicke Encephalopathy is a neuropsychiatric disorder that is caused by a deficiency of thiamine (vitamin B1). It is characterized by a classic triad of symptoms: confusion, oculomotor dysfunction (such as nystagmus and ophthalmoplegia), and gait ataxia. Other symptoms can include memory loss, apathy, and hypothermia.
Wernicke Encephalopathy is most commonly seen in alcoholics due to poor nutrition, but it can also occur in people with conditions that cause malabsorption or increased thiamine requirements, such as AIDS, cancer, and chronic diarrhea. Immediate treatment with thiamine replacement therapy is necessary to prevent progression of the disease and potential permanent neurological damage. If left untreated, Wernicke Encephalopathy can lead to Korsakoff's syndrome, a chronic memory disorder.
Thiamine deficiency, also known as beriberi, is a condition that results from inadequate intake or impaired absorption of thiamine (vitamin B1), which is essential for energy metabolism and nerve function. This deficiency can lead to various symptoms such as peripheral neuropathy, muscle weakness, heart failure, and in severe cases, Wernicke-Korsakoff syndrome, a neurological disorder associated with alcoholism. Thiamine deficiency is commonly found in populations with poor nutrition, alcohol dependence, and gastrointestinal disorders affecting nutrient absorption.
Thiamine, also known as vitamin B1, is a water-soluble vitamin that plays a crucial role in certain metabolic reactions, particularly in the conversion of carbohydrates into energy in the body. It is essential for the proper functioning of the heart, nerves, and digestive system. Thiamine acts as a cofactor for enzymes involved in the synthesis of neurotransmitters and the metabolism of carbohydrates, lipids, and proteins. Deficiency in thiamine can lead to serious health complications, such as beriberi (a disease characterized by peripheral neuropathy, muscle wasting, and heart failure) and Wernicke-Korsakoff syndrome (a neurological disorder often seen in alcoholics due to chronic thiamine deficiency). Thiamine is found in various foods, including whole grains, legumes, pork, beef, and fortified foods.
A thyroid crisis, also known as thyrotoxic crisis or storm, is a rare but life-threatening condition characterized by an exaggerated response to the excess production of thyroid hormones (thyrotoxicosis). This condition can lead to severe hypermetabolic state, multi-organ dysfunction, and cardiovascular collapse if not promptly diagnosed and treated.
Thyroid crisis is often triggered by a stressful event, infection, or surgery in individuals with uncontrolled or poorly managed hyperthyroidism, particularly those with Graves' disease. The symptoms of thyroid crisis include high fever, tachycardia (rapid heart rate), hypertension (high blood pressure), agitation, confusion, delirium, vomiting, diarrhea, and sometimes coma.
The diagnosis of thyroid crisis is based on the clinical presentation, laboratory tests, and imaging studies. Treatment typically involves hospitalization in an intensive care unit, administration of medications to block the production and release of thyroid hormones, control heart rate and rhythm, correct electrolyte imbalances, and provide supportive care until the patient's condition stabilizes.
Thyrotoxicosis is a medical condition that results from an excess of thyroid hormones in the body, leading to an overactive metabolic state. It can be caused by various factors such as Graves' disease, toxic adenoma, Plummer's disease, or excessive intake of thyroid hormone medication. Symptoms may include rapid heart rate, weight loss, heat intolerance, tremors, and increased sweating, among others. Thyrotoxicosis is not a diagnosis itself but a manifestation of various underlying thyroid disorders. Proper diagnosis and management are crucial to prevent complications and improve quality of life.
Hepatic encephalopathy (HE) is a neuropsychiatric syndrome associated with liver dysfunction and/or portosystemic shunting. It results from the accumulation of toxic substances, such as ammonia and inflammatory mediators, which are normally metabolized by the liver. HE can present with a wide range of symptoms, including changes in sleep-wake cycle, altered mental status, confusion, disorientation, asterixis (flapping tremor), and in severe cases, coma. The diagnosis is based on clinical evaluation, neuropsychological testing, and exclusion of other causes of cognitive impairment. Treatment typically involves addressing the underlying liver dysfunction, reducing ammonia production through dietary modifications and medications, and preventing further episodes with lactulose or rifaximin therapy.
Medical Definition:
Magnetic Resonance Imaging (MRI) is a non-invasive diagnostic imaging technique that uses a strong magnetic field and radio waves to create detailed cross-sectional or three-dimensional images of the internal structures of the body. The patient lies within a large, cylindrical magnet, and the scanner detects changes in the direction of the magnetic field caused by protons in the body. These changes are then converted into detailed images that help medical professionals to diagnose and monitor various medical conditions, such as tumors, injuries, or diseases affecting the brain, spinal cord, heart, blood vessels, joints, and other internal organs. MRI does not use radiation like computed tomography (CT) scans.
The brain is the central organ of the nervous system, responsible for receiving and processing sensory information, regulating vital functions, and controlling behavior, movement, and cognition. It is divided into several distinct regions, each with specific functions:
1. Cerebrum: The largest part of the brain, responsible for higher cognitive functions such as thinking, learning, memory, language, and perception. It is divided into two hemispheres, each controlling the opposite side of the body.
2. Cerebellum: Located at the back of the brain, it is responsible for coordinating muscle movements, maintaining balance, and fine-tuning motor skills.
3. Brainstem: Connects the cerebrum and cerebellum to the spinal cord, controlling vital functions such as breathing, heart rate, and blood pressure. It also serves as a relay center for sensory information and motor commands between the brain and the rest of the body.
4. Diencephalon: A region that includes the thalamus (a major sensory relay station) and hypothalamus (regulates hormones, temperature, hunger, thirst, and sleep).
5. Limbic system: A group of structures involved in emotional processing, memory formation, and motivation, including the hippocampus, amygdala, and cingulate gyrus.
The brain is composed of billions of interconnected neurons that communicate through electrical and chemical signals. It is protected by the skull and surrounded by three layers of membranes called meninges, as well as cerebrospinal fluid that provides cushioning and nutrients.
Wernicke's aphasia is a type of fluent aphasia, also known as receptive or sensory aphasia. It is named after the neurologist Carl Wernicke. This type of aphasia is caused by damage to the posterior portion of the left superior temporal gyrus (Wernicke's area) in the dominant hemisphere of the brain, typically as a result of stroke or head injury.
Individuals with Wernicke's aphasia have difficulty understanding spoken or written language. They may speak in long, grammatically correct sentences that are filled with incorrect or made-up words (neologisms) and have little meaning. They are often unaware of their errors and have poor comprehension of both spoken and written language. This can lead to significant difficulties in communication and can be very frustrating for the person with aphasia and their communication partners.
Treatment for Wernicke's aphasia typically involves speech-language therapy, which may focus on improving comprehension, expression, reading, and writing skills. The prognosis for recovery varies depending on the severity of the brain injury and the individual's overall health and cognitive status.
Bovine spongiform encephalopathy (BSE), also known as "mad cow disease," is a progressive neurodegenerative disorder that affects cattle. It is caused by prions, which are misfolded proteins that can cause other proteins in the brain to also misfold and accumulate, leading to brain damage and degeneration. The disease is named for the sponge-like appearance of the brain tissue that results from this degenerative process.
BSE is a zoonotic disease, which means that it can be transmitted from animals to humans. In humans, BSE is known as variant Creutzfeldt-Jakob disease (vCJD) and is caused by consuming contaminated beef products. The symptoms of vCJD include rapidly progressing dementia, neurological symptoms such as muscle spasms and difficulty coordinating movements, and physical deterioration leading to death.
It's important to note that the use of certain growth promoters in cattle feed and the practice of feeding cattle meat and bone meal have been banned in many countries in order to prevent the spread of BSE. Additionally, strict controls on the inspection and testing of beef products have been implemented to ensure their safety.
Wernicke encephalopathy
Anaphe venata
Gastric bypass surgery
Nutritional neuroscience
Wernicke-Korsakoff syndrome
Thiamine
Korsakoff syndrome
Thiamine deficiency
Carl Wernicke
Ophthalmoparesis
Alcoholic ketoacidosis
2008 US beef protest in South Korea
Nystagmus
Thiamine transporter 2
Glossary of medicine
Vitamin B1 analogues
Confabulation
Biotin-thiamine-responsive basal ganglia disease
Psychopharmacology
Hepatic encephalopathy
Glial fibrillary acidic protein
Morning sickness
List of eponyms (L-Z)
Hyperemesis gravidarum
Rachel Levine
Long-term effects of alcohol
Anorexia nervosa
Hypothermia
Sam Sheppard
Encephalopathy
Wernicke encephalopathy - Wikipedia
Wernicke Encephalopathy: Practice Essentials, Etiology, Epidemiology
Wernicke Encephalopathy - Health Library
PRIME PubMed | Wernicke's encephalopathy: a predictable complication of hyperemesis gravidarum
Graded Brain Abnormalities in Alcoholics with and Without Signs of Wernicke Encephalopathy - SRI International
Wernicke Encephalopathy - Wernicke's Encephalopathy Summary Report | CureHunter
NDLI: Wernicke's encephalopathy and alcohol-related disease.
Wernicke Encephalopathy: Background, Etiology, Epidemiology
Dr Balaji Anvekar FRCR: Wernicke's Encephalopathy MRI
Wernicke Encephalopathy - Special Subjects - MSD Manual Professional Edition
Wernicke´s encephalopathy in hyperemesis gravidarum: rare case report
Wernicke's Encephalopathy: Expanding the Diagnostic Toolbox - information for practice
Failure to Diagnose Thiamine Deficiency/Wernicke's Encephalopathy | Harry S. Cohen
Wernicke Encephalopathy Mimicking MELAS. | Medicina (Kaunas);58(5)2022 May 13. | MEDLINE
Brainstem cranial nerve diffusion changes in Wernicke encephalopathy secondary to necrotizing pancreatitis
Acute cerebellar ataxia in a young woman: Wernicke's encephalopathy? | Dolgova | Neurology, Neuropsychiatry, Psychosomatics
Nonalcoholic Wernicke Encephalopathy in a Pediatric Patient with ...: The American Society of Neuroradiology
What Is Wet Brain? | Dual Diagnosis
Can the Ketogenic diet lead to Wernicke's encephalopathy?<...
Alcoholism - Wikipedia
DailyMed - ARSENIC TRIOXIDE injection, solution
Beriberi (Thiamine Deficiency) Treatment & Management: Approach Considerations, Activity
American Journal of Case Reports | Total parenteral nutrition caused Wernicke's encephalopathy accompanied by wet beriberi -...
Faris AA[au] - Search Results - PubMed
Nausea and vomiting of pregnancy and hyperemesis gravidarum | Nature Reviews Disease Primers
Selected Publications » Laboratory of Neuropsychology | Boston University
EEG in Dementia and Encephalopathy: Overview, Dementia, Vascular Dementia
A Case of Wernicke-Korsakoff Syndrome Treated 1 Year After the Onset of Symptoms | Psychiatrist.com
Wernicke's48
- Wernicke encephalopathy (WE), also Wernicke's encephalopathy, or wet brain is the presence of neurological symptoms caused by biochemical lesions of the central nervous system after exhaustion of B-vitamin reserves, in particular thiamine (vitamin B1). (wikipedia.org)
- Myths and misconceptions of Wernicke's encephalopathy: what every emergency physician should know. (medscape.com)
- The Royal College of Physicians report on alcohol: guidelines for managing Wernicke's encephalopathy in the accident and Emergency Department. (medscape.com)
- Azim W, Walker R. Wernicke's encephalopathy: a frequently missed problem. (medscape.com)
- Usefulness of CT and MR imaging in the diagnosis of acute Wernicke's encephalopathy. (medscape.com)
- Distinctive acid-base pattern in Wernicke's encephalopathy. (medscape.com)
- Wernicke's encephalopathy. (medscape.com)
- Metabolic syndromes such as Wernicke's encephalopathy may present with a sudden neurological deficit, thus mimicking acute onset stroke. (hindawi.com)
- The use of both clinical and radiological findings led to correctly diagnosing Wernicke's encephalopathy. (hindawi.com)
- Photophobia and bilateral pulvinar involvement in non-alcoholic Wernicke's encephalopathy. (nih.gov)
- Isolated abnormalities in the mamillary bodies on MRI in a patient with Wernicke's encephalopathy. (nih.gov)
- Mammillothalamic functional connectivity and memory function in Wernicke's encephalopathy. (nih.gov)
- Wernicke's encephalopathy: a more common disease than realised. (bmj.com)
- During a four year peirod, 51 cases of Wernicke's encephalopathy were diagnosed at necropsy, an incidence of 1.7% of all necropsies performed at the Royal Perth Hospital and by the Perth City coroner. (bmj.com)
- Many of the patients died suddenly and unexpectedly, apparently as a result of haemorrhagic brainstem lesions, typical of acute Wernicke's encephalopathy, since no other cause of death was found. (bmj.com)
- The diagnosis of Wernicke's encephalopathy may be missed at necropsy unless the brain is examined histologically. (bmj.com)
- It usually develops as symptoms of Wernicke's encephalopathy go away. (healthline.com)
- Serious and fatal encephalopathy, including Wernicke's, has occurred in patients treated with INREBIC. (nih.gov)
- Wernicke's encephalopathy is a neurologic emergency. (nih.gov)
- Wernicke's encephalopathy is an acute neurological disorder caused due to thiamine deficiency. (ruralneuropractice.com)
- Wernicke's encephalopathy can present with atypical clinical manifestations, particularly in setting of nonalcoholic background. (ruralneuropractice.com)
- The diagnosis of Wernicke's encephalopathy was entertained and he well responded to parental thiamine therapy. (ruralneuropractice.com)
- The clinician should be aware about atypical presentation of Wernicke's encephalopathy. (ruralneuropractice.com)
- 1 The diagnosis is frequently missed especially in patients having atypical clinical manifestations, as shown by multiple autopsy studies, where in the diagnosis of Wernicke's encephalopathy is made after post mortem. (ruralneuropractice.com)
- Serious encephalopathy, including Wernicke's, has occurred with arsenic trioxide. (nih.gov)
- If Wernicke's encephalopathy is suspected, immediately interrupt arsenic trioxide and initiate parenteral thiamine. (nih.gov)
- Wernicke's encephalopathy is an acute neurological disorder, caused by thiamine deficiency, which is clinically characterized by a triad of ophthalmoplegia, ataxia and disturbances of consciousness. (accjournal.org)
- We report a case of a 73-year-old man, who presented with recurred colon cancer, who was affected by Wernicke's encephalopathy while undergoing oral feeding and parenteral nutrition. (accjournal.org)
- In other reports of thiamine deficiency attributed to IV therapy containing insufficient or no thiamine supplementation, the deficiency was manifested by Wernicke's encephalopathy without lactic acidosis. (cdc.gov)
- and a chronically malnourished 22-year-old man with ulcerative colitis who developed Wernicke's encephalopathy 5 days after colectomy and 17 days after beginning a TPN regimen providing 300 g of carbohydrate (50 g on the last 3 days) and 3.2 mg of thiamine daily (6). (cdc.gov)
- Wernicke's encephalopathy in Crohn's disease and ulcerative colitis. (nih.gov)
- Preventing Wernicke's encephalopathy in anorexia nervosa: A systematic review. (nih.gov)
- Wernicke's encephalopathy represents the "acute" phase of the disorder and Korsakoff's amnesic syndrome represents the disorder progressing to a "chronic" or long-lasting stage. (nih.gov)
- Wernicke's encephalopathy is a degenerative brain disorder caused by the lack of vitamin B1. (nih.gov)
- In individuals with Wernicke's encephalopathy, it is very important to start thiamine replacement before beginning nutritional replenishment. (nih.gov)
- Most symptoms of Wernicke's encephalopathy can be reversed if detected and treated promptly and completely. (nih.gov)
- However, these supplements may not provide enough vitamin B1, which is essential for preventing a condition called Wernicke's encephalopathy (WE), a medical emergency. (medicalnewstoday.com)
- Wernicke's disease or encephalopathy, caused by a lack of vitamin B1, which leads to bleeding in the lower brain areas. (hubpages.com)
- The Wernicke-Korsakoff syndrome is a neuropathological term which encompasses two clinical syndromes in thiamine-deficient alcoholics, Wernicke's encephalopathy and Korsakoff's psychosis. (unboundmedicine.com)
- Wernicke's encephalopathy is characterised by eye and gait disorders and mental confusion, and can lead to the profound and permanent amnesia known as Korsakoff's psychosis. (unboundmedicine.com)
- To examine this, the number of chemically identified neurons in particular brain regions was quantified in patients with Wernicke's encephalopathy alone or in combination with Korsakoff's psychosis and compared with age- and sex-matched controls. (unboundmedicine.com)
- Our patients with either Wernicke's encephalopathy or additional Korsakoff's psychosis do not differ from controls in the distribution and number of these cells. (unboundmedicine.com)
- While patients with Wernicke's encephalopathy often had neuronal loss in the mediodorsal nucleus, only patients with Korsakoff's psychosis had cell loss in both medial thalamic nuclei. (unboundmedicine.com)
- Also referred to as Wernicke's encephalopathy, WKS affects a person's ability to retain and process information. (geisinger.org)
- Also, per medlineplus.gov , healthcare providers have been known to give thiamin shots to patients suffering from Wernicke's encephalopathy syndrome, which involves memory loss. (wonderlabs.com)
- This is also called Wernicke's encephalopathy (WE). (bluehillsrecovery.com)
- 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. (nih.gov)
- To evaluate alcohol's central nervous system effects, researchers distinguish "uncomplicated alcoholism" (i.e., alcohol use disorder [AUD]) from the various clinically diagnosable consequences of chronic alcohol consumption, including Wernicke's encephalopathy (WE), Korsakoff's syndrome (KS), hepatic encephalopathy (HE), central pontine myelinolysis (CPM), alcoholic cerebellar degeneration (ACD), alcohol-related dementia (ARD), and Marchiafava-Bignami disease (MBD). (nih.gov)
Thiamine deficiency5
- Thiamine deficiency and unexplained encephalopathy in hemodialysis and peritoneal dialysis patients. (medscape.com)
- Wernicke-Korsakoff syndrome is a brain disorder due to vitamin B1 (thiamine) deficiency . (medlineplus.gov)
- Wernicke encephalopathy (WE) is a medical emergency caused by thiamine deficiency. (thieme-connect.com)
- 9. Review of thiamine deficiency disorders: Wernicke encephalopathy and Korsakoff psychosis. (nih.gov)
- A brain disorder that is related to an acute and chronic phase of a vitamin B1 (thiamine) deficiency, which is known as wet brain or Wernicke-Korsakoff syndrome (WKS). (bluehillsrecovery.com)
Korsakoff23
- When it occurs simultaneously with alcoholic Korsakoff syndrome it is known as Wernicke-Korsakoff syndrome. (wikipedia.org)
- A very high percentage of patients with Wernicke-Korsakoff syndrome also have peripheral neuropathy, and many people who consume excess alcohol have this neuropathy without other neurologic signs or symptoms. (wikipedia.org)
- Wernicke encephalopathy and Korsakoff syndrome are different conditions that often occur together. (medlineplus.gov)
- Korsakoff syndrome, or Korsakoff psychosis, tends to develop as Wernicke encephalopathy as symptoms go away. (medlineplus.gov)
- But if Wernicke-Korsakoff syndrome is suspected, treatment should start immediately. (medlineplus.gov)
- Without treatment, Wernicke-Korsakoff syndrome gets steadily worse, and can be life threatening. (medlineplus.gov)
- Contact your health care provider or go to the emergency room if you have symptoms of Wernicke-Korsakoff syndrome, or if you have been diagnosed with the condition and your symptoms get worse or return. (medlineplus.gov)
- Not drinking alcohol or drinking in moderation and getting enough nutrition reduce the risk of developing Wernicke-Korsakoff syndrome. (medlineplus.gov)
- Wernicke-Korsakoff syndrome despite no alcohol abuse: A summary of systematic reports. (nih.gov)
- The disorder includes Wernicke encephalopathy and Korsakoff amnesic syndrome which are not different conditions but different stages of the same disease (Wernicke-Korsakoff syndrome). (nih.gov)
- How can I or my loved one help improve care for people with Wernicke-Korsakoff syndrome? (nih.gov)
- Consider participating in a clinical trial so clinicians and scientists can learn more about Wernicke-Korsakoff syndrome and related disorders. (nih.gov)
- 2. [Diagnostics and treatment of Wernicke-Korsakoff syndrome patients with an alcohol abuse]. (nih.gov)
- 16. Fetal demise and Wernicke-Korsakoff syndrome in a patient with hyperemesis gravidarum: a case report. (nih.gov)
- 18. B-complex vitamins in the prophylaxis and treatment of Wernicke-Korsakoff syndrome. (nih.gov)
- Halliday G, Cullen K, Harding A. Neuropathological correlates of memory dysfunction in the Wernicke-Korsakoff syndrome. (unboundmedicine.com)
- Additional similar terms include alcohol-related encephalopathy and Wernicke-Korsakoff syndrome. (thesaurus.net)
- Wet brain is formally called Wernicke-Korsakoff syndrome (WKS), and it is a severe life-threatening brain disorder. (bluehillsrecovery.com)
- The first component of Wernicke-Korsakoff syndrome (WKS) is a severe temporary condition that is characterized by loss of muscular coordination, confusion, and abnormal eye movements, along with vision changes. (bluehillsrecovery.com)
- The second component of Wernicke-Korsakoff syndrome (WKS) is Korsakoff's psychosis , which is a chronic condition that can induce a significant impairment in memory and learning. (bluehillsrecovery.com)
- Wernicke-Korsakoff syndrome (WKS) can sometimes be confused with symptoms of alcohol withdrawal and even other medical complications. (bluehillsrecovery.com)
- Before Sergei Sergeivich Korsakoff described the psychosis that bears his name, Carl Wernicke reported a closely related and often coexistent syndrome. (hekint.org)
- It is variously named Wernicke-Korsakoff encephalopathy, syndrome, or psychosis. (hekint.org)
Korsakoff's2
- In Wernicke Korsakoff's syndrome some single symptoms are present in about one-third. (wikipedia.org)
- 7. [Wernicke encephalopathy and Korsakoff's psychosis: clinical-pathophysiological correlation, diagnostics and treatment]. (nih.gov)
Bariatric surgery2
- Wernicke encephalopathy after bariatric surgery: a systematic review. (medscape.com)
- Preventing Wernicke Encephalopathy After Bariatric Surgery. (nih.gov)
Symptoms3
- Classically, Wernicke encephalopathy is characterised by a triad of symptoms: ophthalmoplegia, ataxia, and confusion. (wikipedia.org)
- The classic triad of symptoms found in Wernicke encephalopathy is: ophthalmoplegia (later expanded to other eye movement disorders, most commonly affecting the lateral rectus muscle. (wikipedia.org)
- Initial symptoms of ethylene glycol toxicity is typically a severe encephalopathy (similar clinically to acute basilar artery occlusion ) 1 . (radiopaedia.org)
Carl Wernicke1
- Wernicke encephalopathy (WE) was first described by Carl Wernicke in 1881. (nih.gov)
Beriberi1
- Glucose infusions may precipitate Wernicke disease or acute cardiovascular beriberi in a previously unaffected patient or cause rapid worsening of an early form of the disease. (medscape.com)
Ophthalmoplegia1
- Wernicke encephalopathy (WE) is characterized by a clinical triad of ataxia, ophthalmoplegia, and altered mental state. (thieme-connect.com)
Syndrome1
- Leukemic infiltration of the central nervous system, central nervous system infections in an immunocompromised state, drug toxicity-chemical meningitis, leukoencephalopathy, and posterior reversible encephalopathy syndrome were considered as probable differentials, and investigations were planned. (thieme-connect.com)
Ataxia1
- Some disease-specific therapies for ataxia exist, such as vitamin E for ataxia with vitamin E deficiency and thiamine for Wernicke encephalopathy, highlighting the importance of recognizing these forms of ataxia. (nih.gov)
Disease2
- citation needed] Because of the frequent involvement of heart, eyes and peripheral nervous system, several authors prefer to call it Wernicke disease rather than simply encephalopathy. (wikipedia.org)
- Variant Creutzfeldt-Jakob disease (vCJD) is a rare, fatal prion disease resulting from transmission to humans of the infectious agent of bovine spongiform encephalopathy. (cdc.gov)
20231
- and Stocker, Patrick J., "Wernicke Encephalopathy: Interplay Between Magnesium and Thiamine" (2023). (hcahealthcare.com)
Diagnosis2
- EFNS guidelines for diagnosis, therapy and prevention of Wernicke encephalopathy. (medscape.com)
- 3. Need for early diagnosis of mental and mobility changes in Wernicke encephalopathy. (nih.gov)
Parenteral3
- Wernicke encephalopathy: a complication of parenteral nutrition diagnosed by magnetic resonance imaging. (medscape.com)
- If encephalopathy is suspected, immediately discontinue INREBIC and initiate parenteral thiamine. (nih.gov)
- Most frequently, the encephalopathy is a consequence of chronic alcoholism, but it may occur in other forms of malnutrition or malabsorption, such as in prolonged parenteral nutrition without the addition of thiamine, total gastrectomy, gastrojejunostomy, severe anorexia or hyperemesis gravidarum. (accjournal.org)
Vitamin1
- Wernicke encephalopathy may result from other conditions that cause prolonged undernutrition or vitamin deficiencies. (msdmanuals.com)
Clinical1
- 8. Clinical Characteristics and Outcomes Associated With High-Dose Intravenous Thiamine Administration in Patients With Encephalopathy. (nih.gov)
Glucose1
- Why Thiamine before Glucose in Wernicke Encephalopathy? (medicinespecifics.com)
Severe1
- 6. Wernicke encephalopathy presenting in a patient with severe acute pancreatitis. (nih.gov)
Disorders1
- 1. Thiamine in the treatment of Wernicke encephalopathy in patients with alcohol use disorders. (nih.gov)
Medical emergency1
- Day GS, del Campo CM. Wernicke encephalopathy: a medical emergency. (medscape.com)
Brain damage1
- Wernicke encephalopathy causes brain damage in lower parts of the brain called the thalamus and hypothalamus. (medlineplus.gov)
Condition1
- Chronic traumatic encephalopathy is a brain condition associated with repeated blows to the head. (alzheimersresearchuk.org)
Sign1
- Mamillary body enhancement on MR as the only sign of acute Wernicke encephalopathy. (nih.gov)