Wernicke encephalopathy

Last updated

Wernicke encephalopathy
Other namesWernicke's disease
Hypothalamus image.png
Hypothalamus
Specialty Neurology   OOjs UI icon edit-ltr-progressive.svg
Symptoms Ataxia, ophthalmoplegia, confusion
CausesThiamine deficency
Risk factors Alcohol use disorder, malnutrition

Wernicke encephalopathy (WE), also Wernicke's encephalopathy, [1] 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). [2] The condition is part of a larger group of thiamine deficiency disorders that includes beriberi, in all its forms, and alcoholic Korsakoff syndrome. When it occurs simultaneously with alcoholic Korsakoff syndrome it is known as Wernicke–Korsakoff syndrome. [3] [4]

Contents

Classically, Wernicke encephalopathy is characterised by a triad of symptoms: ophthalmoplegia, ataxia, and confusion. Around 10% of patients exhibit all three features, and other symptoms may also be present. [5] While it is commonly regarded as a condition particular to malnourished people with alcohol misuse, it can be caused by a variety of diseases. [3] [6] It is treated with thiamine supplementation, which can lead to improvement of the symptoms and often complete resolution, particularly in those where alcohol misuse is not the underlying cause. [7] Often other nutrients also need to be replaced, depending on the cause. Medical literature notes how managing the condition in a timely fashion can avoid worsening symptoms. [6] [8] [9]

Wernicke encephalopathy may be present in the general population with a prevalence of around 2%, and is considered underdiagnosed; probably, many cases are in patients who do not have commonly-associated symptoms. [10]

Signs and symptoms

The classic triad of symptoms found in Wernicke encephalopathy is: [11]

Other symptoms found in patients with this condition include:

Although hypothermia is usually diagnosed with a body temperature of 35 °C (95 °F), or less, incipient cooling caused by deregulation in the central nervous system (CNS) needs to be monitored because it can promote the development of an infection. [18] The patient may report feeling cold, followed by mild chills, cold skin, moderate pallor, tachycardia, hypertension, tremor or piloerection. External warming techniques are advised to prevent hypothermia.[ citation needed ]

Among the frequently altered functions are the cardio circulatory. There may be tachycardia, dyspnea, chest pain, orthostatic hypotension, changes in heart rate and blood pressure. [29] The lack of thiamine sometimes affects other major energy consumers, the myocardium, and also patients may have developed cardiomegaly. [30] Heart failure with lactic acidosis syndrome has been observed. [31] Cardiac abnormalities are an aspect of the WE, which was not included in the traditional approach, [4] [32] and are not classified as a separate disease. Infections have been pointed out as one of the most frequent triggers of death in WE. [33] [32] Furthermore, infections are usually present in pediatric cases. [34] [35]

In the last stage other symptoms may occur: hyperthermia, increased muscle tone, spastic paralysis, choreic dyskinesias and coma.[ 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. [4] [36]

Early symptoms are nonspecific, [37] [38] and it has been stated that WE may present nonspecific findings. [39] In Wernicke Korsakoff's syndrome some single symptoms are present in about one-third. [40]

Location of the lesion

Depending on the location of the brain lesion different symptoms are more frequent:[ citation needed ]

Mamillary lesion are characteristic-small petechial hemorrhages are found.

Korsakoff syndrome

Korsakoff syndrome, characterised by memory impairment, confabulation, confusion and personality changes, has a strong and recognised link with WE. [3] [42] 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. [43] Korsakoff's occurs much more frequently in WE due to chronic alcoholism. [42] It is uncommon among those who do not consume excessive amounts of alcohol. Up to 80% of WE patients who misuse alcohol develop Korsakoff's syndrome. [39] In Korsakoff's, is usually observed atrophy of the thalamus and the mammillary bodies, and frontal lobe involvement. [39] In a study, half of Wernicke–Korsakoff cases had good recovery from the amnesic state, which may take from 2 months to 10 years. [2]

Risk factors

Wernicke encephalopathy has classically been thought of as a disease solely of people who drink excessive amounts of alcohol, but it is also found in the chronically undernourished, and in recent years has been discovered post bariatric surgery. [11] [39] Without being exhaustive, the documented causes of Wernicke encephalopathy have included:

Pathophysiology

Thiamine deficiency and errors of thiamine metabolism are believed to be the primary cause of Wernicke encephalopathy. Thiamine, also called B1, helps to break down glucose. Specifically, it acts as an essential coenzyme to the TCA cycle and the pentose phosphate shunt. Thiamine is first metabolised to its more active form, thiamine diphosphate (TDP), before it is used. The body only has 2–3 weeks of thiamine reserves, which are readily exhausted without intake, or if depletion occurs rapidly, such as in chronic inflammatory states or in diabetes. [11] [39] Thiamine is involved in: [39] [47]

  1. Metabolism of carbohydrates, releasing energy.
  2. Production of neurotransmitters including glutamic acid and GABA.
  3. Lipid metabolism, necessary for myelin production.
  4. Amino acid modification. Probably linked to the production of taurine, of great cardiac importance. [48] [49]

Neuropathology

The primary neurological-related injury caused by thiamine deficiency in WE is three-fold: oxidative damage, mitochondrial injury leading to apoptosis, and directly stimulating a pro-apoptotic pathway. [50] Thiamine deficiency affects both neurons and astrocytes, glial cells of the brain. Thiamine deficiency alters the glutamate uptake of astrocytes, through changes in the expression of astrocytic glutamate transporters EAAT1 and EAAT2, leading to excitotoxicity. Other changes include those to the GABA transporter subtype GAT-3, GFAP, glutamine synthetase, and the Aquaporin 4 channel. [51] Focal lactic acidosis also causes secondary oedema, oxidative stress, inflammation and white matter damage. [52]

Pathological anatomy

Cerebellum Cerebellum small.gif
Cerebellum

Despite its name, WE is not related to Wernicke's area, a region of the brain associated with speech and language interpretation.

Brain lesions in WE are usually credited to focal lactic acidosis. An absence of thiamine can lead to too much pyruvate within the cells since it is not available to help convert pyruvate through the TCA cycle. An increase in pyruvate causes an increase in lactate concentration leading to focal lactic acidosis. [53]

Lesions can be reversed in most cases with immediate supplementation of thiamine.[ citation needed ]

Lesions are usually symmetrical in the periventricular region, diencephalon, the midbrain, hypothalamus, and cerebellar vermis. Brainstem lesions may include cranial nerve III, IV, VI and VIII nuclei, the medial thalamic nuclei, and the dorsal nucleus of the vagus nerve. Oedema may be found in the regions surrounding the third ventricle, and fourth ventricle, also appearing petechiae and small hemorrhages. [54] Chronic cases can present the atrophy of the mammillary bodies. [55]

In 1949, the idea that WE lesions are a result of a disruption to the blood-brain barrier was introduced. [53] Large proteins passing into the brain can put neurological tissue at risk of toxic effects. The blood-brain barrier junctions are typically found to have WE lesions located at that region of the brain. [53]

An altered blood–brain barrier may cause a perturbed response to certain drugs and foods. [56]

Diagnosis

Diagnosis of Wernicke encephalopathy or disease is made clinically. [6] [57] Caine et al. in 1997 established criteria that Wernicke encephalopathy can be diagnosed in any patient with just two or more of the main symptoms noted above. [58] The sensitivity of the diagnosis by the classic triad was 23% but increased to 85% taking two or more of the four classic features. These criteria are challenged because all the cases he studied were people who drank excessive amounts of alcohol. Some consider it sufficient to suspect the presence of the disease with only one of the principal symptoms. [5] Some British hospital protocols suspect WE with any one of these symptoms: confusion, decreased consciousness level (or unconsciousness, stupor or coma), memory loss, ataxia or unsteadiness, ophthalmoplegia or nystagmus, and unexplained hypotension with hypothermia. The presence of only one sign should be sufficient for treatment. [59]

The sensitivity of magnetic resonance imaging (MR) was 53% and the specificity was 93%. The reversible cytotoxic edema was considered the most characteristic lesion of WE. The location of the lesions were more frequently atypical among people who drank appropriate amounts of alcohol, while typical contrast enhancement in the thalamus and the mammillary bodies was observed frequently associated with alcohol misuse. [55] These abnormalities may include: [11]

There appears to be very little value for CT scans. [6]

Thiamine can be measured using an erythrocyte transketolase activity assay, [6] or by activation by measurement of in vitro thiamine diphosphate levels. [6] Normal thiamine levels do not necessarily rule out the presence of WE, [6] as this may be a patient with difficulties in intracellular transport.

Prevention

There are hospital protocols for prevention, supplementing with thiamine in the presence of: history of alcohol misuse or related seizures, requirement for IV glucose, signs of malnutrition, poor diet, recent diarrhea or vomiting, peripheral neuropathy, intercurrent illness, delirium tremens or treatment for DTs, and others. [59] [61] [62]

Some experts advise parenteral thiamine should be given to all at-risk patients in the emergency department. [6]

In the clinical diagnosis should be remembered that early symptoms are nonspecific, [37] [38] and it has been stated that WE may present nonspecific findings. [39] There is consensus to provide water-soluble vitamins and minerals after gastric operations. [63]

In some countries certain foods have been supplemented with thiamine, and have reduced WE cases. Improvement is difficult to quantify because they applied several different actions. Avoiding or moderating alcohol consumption and having adequate nutrition reduces one of the main risk factors in developing Wernicke–Korsakoff syndrome.[ citation needed ].

Treatment

Most symptoms will improve quickly if deficiencies are treated early. Memory disorder may be permanent. [43]

In patients suspected of WE, thiamine treatment should be started immediately. [39] Blood should be immediately taken to test for thiamine, other vitamins and minerals levels. Following this an immediate intravenous or intramuscular dose of thiamine should be administered [36] two or three times daily. Thiamine administration is usually continued until clinical improvement ceases. [6]

Considering the diversity of possible causes and several surprising symptomatologic presentations, and because there is low assumed risk of toxicity of thiamine, because the therapeutic response is often dramatic from the first day, some qualified authors indicate parenteral thiamine if WE is suspected, both as a resource for diagnosis and treatment. [6] The diagnosis is highly supported by the response to parenteral thiamine, but is not sufficient to be excluded by the lack of it. [64] Parenteral thiamine administration is associated with a very small risk of anaphylaxis. [65]

People who consume excessive amounts of alcohol may have poor dietary intakes of several vitamins, and impaired thiamine absorption, metabolism, and storage; they may thus require higher doses. [37]

If glucose is given, such as in people with an alcohol use disorder who are also hypoglycaemic, thiamine must be given concurrently. If this is not done, the glucose will rapidly consume the remaining thiamine reserves, exacerbating this condition. [39]

The observation of edema in MR, and also the finding of inflation and macrophages in necropsied tissues, [54] has led to successful administration of antiinflammatories. [66] [67]

Other nutritional abnormalities should also be looked for, as they may be exacerbating the disease. [33] [32] In particular, magnesium, a cofactor of transketolase which may induce or aggravate the disease. [39]

Other supplements may also be needed, including: cobalamin, ascorbic acid, folic acid, nicotinamide, zinc, [68] [69] phosphorus (dicalcium phosphate) [70] and in some cases taurine, especially suitable when there cardiocirculatory impairment. [71] [72] Patient-guided nutrition is suggested. In patients with Wernicke–Korsakoff syndrome, even higher doses of parenteral thiamine are recommended. Concurrent toxic effects of alcohol should also be considered. [42] [70]

Epidemiology

There are no conclusive statistical studies, all figures are based on partial studies.

Wernicke's lesions were observed in 0.8 to 2.8% of the general population autopsies, and 12.5% of people with an alcohol use disorder. This figure increases to 35% of such individuals if including cerebellar damage due to lack of thiamine. [73]

Most autopsy cases were from people with an alcohol use disorder. Autopsy series were performed in hospitals on the material available which is unlikely to be representative of the entire population. Considering the slight affectations, previous to the generation of observable lesions at necropsy, the percentage should be higher. There is evidence to indicate that Wernicke encephalopathy is underdiagnosed. [17] [74] For example, in one 1986 study, 80% of cases were diagnosed postmortem. [17] Is estimated that only 5–14% of patients with WE are diagnosed in life. [73] [75]

In a series of autopsy studies held in Recife, Brazil, it was found that only 7 out of 36 had consumed excessive amounts of alcohol, and only a small minority had malnutrition. [76] In a reviewed of 53 published case reports from 2001 to 2011, the relationship with alcohol was also about 20% (10 out of 53 cases). [11]

WE related to alcohol misuse is more common in males and is more common in females when not related to alcohol misuse. [53] In alcohol-related cases, WE patients average the age of 40, and non-alcohol-related cases typically occur in younger people. [53]

History

WE was first identified in 1881 by the German neurologist Carl Wernicke, although the link with thiamine was not identified until the 1930s.[ citation needed ]

Carl Wernicke discovered the sensory center of speech. Wernicke figured out that Broca's area was not the only center of speech, it was also able to distinguish motor aphasia from sensory aphasia. [77] He also pointed to the possibility of conduction aphasia since he came to understand the arrangement of the brain's extrinsic and intrinsic connections. He demonstrated that the sensory information reached its corresponding area in the cerebral cortex through projection fibers. From there, this information, following the association system, would be distributed to different regions of the cortex, integrating sensory processing. [77]

He reported three patients with WE, including two men (aged 33 and 36) who were alcoholics and one woman (aged 20) who ingested sulfuric acid, leading to pyloric stenosis. All three had ocular motor abnormalities and he performed an autopsy on each, providing a clinical-pathological correlation. [78]

A similar presentation of this disease was described by the Russian psychiatrist Sergei Korsakoff in a series of articles published 1887–1891; [11] where the chronic version of WE was described as Korsakoff's Syndrome, involving symptoms of amnesia. [79] [80] [9]

Related Research Articles

<span class="mw-page-title-main">Central pontine myelinolysis</span> Medical condition

Central pontine myelinolysis is a neurological condition involving severe damage to the myelin sheath of nerve cells in the pons. It is predominately iatrogenic (treatment-induced), and is characterized by acute paralysis, dysphagia, dysarthria, and other neurological symptoms.

<span class="mw-page-title-main">Brain injury</span> Destruction or degeneration of brain cells

Brain injury (BI) is the destruction or degeneration of brain cells. Brain injuries occur due to a wide range of internal and external factors. In general, brain damage refers to significant, undiscriminating trauma-induced damage.

<span class="mw-page-title-main">Wernicke–Korsakoff syndrome</span> Combined presence of Wernickes encephalopathy (WE) and Korsakoffs syndrome

Wernicke-Korsakoff syndrome (WKS) is the combined presence of Wernicke encephalopathy (WE) and alcoholic Korsakoff syndrome. Due to the close relationship between these two disorders, people with either are usually diagnosed with WKS as a single syndrome. It mainly causes vision changes, ataxia and impaired memory.

<span class="mw-page-title-main">Korsakoff syndrome</span> Mental illness caused by a lack of thiamine in the brain

Korsakoff syndrome (KS) is a disorder of the central nervous system characterized by amnesia, deficits in explicit memory, and confabulation. This neurological disorder is caused by a deficiency of thiamine (vitamin B1) in the brain, and it is typically associated with and exacerbated by the prolonged, excessive ingestion of alcohol. Korsakoff syndrome is often accompanied by Wernicke encephalopathy; this combination is called Wernicke–Korsakoff syndrome.

Encephalopathy means any disorder or disease of the brain, especially chronic degenerative conditions. In modern usage, encephalopathy does not refer to a single disease, but rather to a syndrome of overall brain dysfunction; this syndrome has many possible organic and inorganic causes.

<span class="mw-page-title-main">Leigh syndrome</span> Metabolic disease

Leigh syndrome is an inherited neurometabolic disorder that affects the central nervous system. It is named after Archibald Denis Leigh, a British neuropsychiatrist who first described the condition in 1951. Normal levels of thiamine, thiamine monophosphate, and thiamine diphosphate are commonly found, but there is a reduced or absent level of thiamine triphosphate. This is thought to be caused by a blockage in the enzyme thiamine-diphosphate kinase, and therefore treatment in some patients would be to take thiamine triphosphate daily. While the majority of patients typically exhibit symptoms between the ages of 3 and 12 months, instances of adult onset have also been documented.

<span class="mw-page-title-main">Asymptomatic</span> Patient is a carrier for a disease or infection but experiences no symptoms

Asymptomatic is an adjective categorising the medical conditions that patients carry but without experiencing their symptoms, despite an explicit diagnosis.

<span class="mw-page-title-main">Carl Wernicke</span> German physician and neuropathologist (1848–1905)

CarlWernicke was a German physician, anatomist, psychiatrist and neuropathologist. He is known for his influential research into the pathological effects of specific forms of encephalopathy and also the study of receptive aphasia, both of which are commonly associated with Wernicke's name and referred to as Wernicke encephalopathy and Wernicke's aphasia, respectively. His research, along with that of Paul Broca, led to groundbreaking realizations of the localization of brain function, specifically in speech. As such, Wernicke's area has been named after the scientist.

<span class="mw-page-title-main">Alcoholic polyneuropathy</span> Medical condition

Alcoholic polyneuropathy is a neurological disorder in which peripheral nerves throughout the body malfunction simultaneously. It is defined by axonal degeneration in neurons of both the sensory and motor systems and initially occurs at the distal ends of the longest axons in the body. This nerve damage causes an individual to experience pain and motor weakness, first in the feet and hands and then progressing centrally. Alcoholic polyneuropathy is caused primarily by chronic alcoholism; however, vitamin deficiencies are also known to contribute to its development. This disease typically occurs in chronic alcoholics who have some sort of nutritional deficiency. Treatment may involve nutritional supplementation, pain management, and abstaining from alcohol.

<span class="mw-page-title-main">Transketolase</span> Enzyme involved in metabolic pathways

Transketolase is an enzyme that, in humans, is encoded by the TKT gene. It participates in both the pentose phosphate pathway in all organisms and the Calvin cycle of photosynthesis. Transketolase catalyzes two important reactions, which operate in opposite directions in these two pathways. In the first reaction of the non-oxidative pentose phosphate pathway, the cofactor thiamine diphosphate accepts a 2-carbon fragment from a 5-carbon ketose (D-xylulose-5-P), then transfers this fragment to a 5-carbon aldose (D-ribose-5-P) to form a 7-carbon ketose (sedoheptulose-7-P). The abstraction of two carbons from D-xylulose-5-P yields the 3-carbon aldose glyceraldehyde-3-P. In the Calvin cycle, transketolase catalyzes the reverse reaction, the conversion of sedoheptulose-7-P and glyceraldehyde-3-P to pentoses, the aldose D-ribose-5-P and the ketose D-xylulose-5-P.

<span class="mw-page-title-main">MELAS syndrome</span> Mitochondrial disease

MELAS is one of the family of mitochondrial diseases, which also include MIDD, MERRF syndrome, and Leber's hereditary optic neuropathy. It was first characterized under this name in 1984. A feature of these diseases is that they are caused by defects in the mitochondrial genome which is inherited purely from the female parent. The most common MELAS mutation is mitochondrial mutation, mtDNA, referred to as m.3243A>G.

<span class="mw-page-title-main">Thiamine deficiency</span> Human disease

Thiamine deficiency is a medical condition of low levels of thiamine (vitamin B1). A severe and chronic form is known as beriberi. The name beriberi was possibly borrowed in the 18th century from the Sinhalese phrase බැරි බැරි (bæri bæri, “I cannot, I cannot”), owing to the weakness caused by the condition. The two main types in adults are wet beriberi and dry beriberi. Wet beriberi affects the cardiovascular system, resulting in a fast heart rate, shortness of breath, and leg swelling. Dry beriberi affects the nervous system, resulting in numbness of the hands and feet, confusion, trouble moving the legs, and pain. A form with loss of appetite and constipation may also occur. Another type, acute beriberi, found mostly in babies, presents with loss of appetite, vomiting, lactic acidosis, changes in heart rate, and enlargement of the heart.

<span class="mw-page-title-main">Marchiafava–Bignami disease</span> Medical condition

Marchiafava–Bignami disease (MBD) is a progressive neurological disease of alcohol use disorder, characterized by corpus callosum demyelination and necrosis and subsequent atrophy. The disease was first described in 1903 by the Italian pathologists Amico Bignami and Ettore Marchiafava in an Italian Chianti drinker. In this autopsy, Marchiafava and Bignami noticed that the middle two-thirds of the corpus callosum were necrotic. It is very difficult to diagnose and there is no specific treatment. Until 2008 only around 300 cases had been reported. If caught early enough, most patients survive.

The Great Imitator is a phrase used for medical conditions that feature nonspecific symptoms and may be confused with a number of other diseases. The term connotes especially difficult differential diagnosis (DDx), increased potential for misdiagnosis, and the protean nature of some diseases. Most great imitators are systemic in nature or have systemic sequelae, and an aspect of nonspecific symptoms is logically almost always involved. In some cases, an assumption that a particular sign or symptom, or a particular pattern of several thereof, is pathognomonic turns out to be false, as the reality is that it is only nearly so.

Alcohol-related dementia (ARD) is a form of dementia caused by long-term, excessive consumption of alcohol, resulting in neurological damage and impaired cognitive function.

<span class="mw-page-title-main">Nystagmus</span> Dysfunction of eye movement

Nystagmus is a condition of involuntary eye movement. People can be born with it but more commonly acquire it in infancy or later in life. In many cases it may result in reduced or limited vision.

<span class="mw-page-title-main">Nutritional neuroscience</span> Scientific discipline

Nutritional neuroscience is the scientific discipline that studies the effects various components of the diet such as minerals, vitamins, protein, carbohydrates, fats, dietary supplements, synthetic hormones, and food additives have on neurochemistry, neurobiology, behavior, and cognition.

In psychology, confabulation is a memory error consisting of the production of fabricated, distorted, or misinterpreted memories about oneself or the world. It is generally associated with certain types of brain damage or a specific subset of dementias. While still an area of ongoing research, the basal forebrain is implicated in the phenomenon of confabulation. People who confabulate present with incorrect memories ranging from subtle inaccuracies to surreal fabrications, and may include confusion or distortion in the temporal framing of memories. In general, they are very confident about their recollections, even when challenged with contradictory evidence.

Alcohol-related brain damage alters both the structure and function of the brain as a result of the direct neurotoxic effects of alcohol intoxication or acute alcohol withdrawal. Increased alcohol intake is associated with damage to brain regions including the frontal lobe, limbic system, and cerebellum, with widespread cerebral atrophy, or brain shrinkage caused by neuron degeneration. This damage can be seen on neuroimaging scans.

Biotin-thiamine-responsive basal ganglia disease (BTBGD) is a rare disease that affects the nervous system, particularly the basal ganglia in the brain. It is a treatable neurometabolic disorder with autosomal recessive inheritance. First described in 1998 and then genetically distinguished in 2005, the disease is characterized by progressive brain damage that, if left untreated, can lead to coma and/or death. Commonly observed in individuals with BTBGD is recurring subacute encephalopathy along with confusion, seizures, and disordered movement (hypokinesia).

References

  1. ↑ "Wernicke Encephalopathy". MeSH Browser. U.S. National Library of Medicine.
  2. 1 2 Oudman E, Oey MJ, Batjes D, van Dam M, van Dorp M, Postma A, Wijnia JW (December 2022). "Wernicke-Korsakoff syndrome diagnostics and rehabilitation in the post-acute phase". Addiction Neuroscience. 4: 100043. doi:10.1016/j.addicn.2022.100043. ISSN   2772-3925. S2CID   253296206.
  3. 1 2 3 [ unreliable medical source? ]Sullivan EV, Fama R (June 2012). "Wernicke's encephalopathy and Korsakoff's syndrome revisited". Neuropsychology Review. 22 (2): 69–71. doi:10.1007/s11065-012-9205-2. PMC   4723427 . PMID   22588370.
  4. 1 2 3 Ropper A, Brown R. Princ. of Neurology, Adams & Victor. 8º ed. McGraw Hill 2007.
  5. 1 2 Cook CC (2000). "Prevention and treatment of Wernicke-Korsakoff syndrome". Alcohol and Alcoholism. 35 (1): 19–20. doi:10.1093/alcalc/35.Supplement_1.19. PMID   11304070. S2CID   45726575.
  6. 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 Galvin R, Bråthen G, Ivashynka A, Hillbom M, Tanasescu R, Leone MA (December 2010). "EFNS guidelines for diagnosis, therapy and prevention of Wernicke encephalopathy". European Journal of Neurology. 17 (12): 1408–1418. doi:10.1111/j.1468-1331.2010.03153.x. PMID   20642790. S2CID   8167574.
  7. ↑ Sechi G, Serra A (May 2007). "Wernicke's encephalopathy: new clinical settings and recent advances in diagnosis and management". The Lancet. Neurology. 6 (5): 442–455. doi:10.1016/s1474-4422(07)70104-7. PMID   17434099. S2CID   15523083.
  8. ↑ Arts NJ, Pitel AL, Kessels RP (1 January 2021), Swaab DF, Kreier F, Lucassen PJ, Salehi A (eds.), "Chapter 29 – The contribution of mamillary body damage to Wernicke's encephalopathy and Korsakoff's syndrome", Handbook of Clinical Neurology, The Human Hypothalamus, 180, Elsevier: 455–475, doi:10.1016/b978-0-12-820107-7.00029-x, ISBN   9780128201077, PMID   34225949, S2CID   235746125 , retrieved 18 November 2022
  9. 1 2 Oudman E, Wijnia JW, Oey MJ, van Dam M, Postma A (July 2021). "Wernicke-Korsakoff syndrome despite no alcohol abuse: A summary of systematic reports". Journal of the Neurological Sciences. 426: 117482. doi: 10.1016/j.jns.2021.117482 . PMID   34000679. S2CID   234769882.
  10. ↑ Isenberg-Grzeda E, Kutner HE, Nicolson SE (2012). "Wernicke-Korsakoff-syndrome: under-recognized and under-treated". Psychosomatics. 53 (6): 507–516. doi:10.1016/j.psym.2012.04.008. PMID   23157990.
  11. 1 2 3 4 5 6 7 8 9 10 Lough ME (June 2012). "Wernicke's encephalopathy: expanding the diagnostic toolbox". Neuropsychology Review. 22 (2): 181–194. doi:10.1007/s11065-012-9200-7. PMID   22577001. S2CID   18884274.
  12. ↑ Mumford CJ (June 1989). "Papilloedema delaying diagnosis of Wernicke's encephalopathy in a comatose patient". Postgraduate Medical Journal. 65 (764): 371–373. doi:10.1136/pgmj.65.764.371. PMC   2429353 . PMID   2608577.
  13. ↑ Chitra S, Lath KV (May 2012). "Wernicke's encephalopathy with visual loss in a patient with hyperemesis gravidarum". The Journal of the Association of Physicians of India. 60: 53–56. PMID   23029727.
  14. 1 2 Truswell AS (June 2000). "Australian experience with the Wernicke-Korsakoff syndrome". Addiction. 95 (6): 829–832. doi:10.1046/j.1360-0443.2000.9568291.x. PMID   10946433.
  15. ↑ Flabeau O, Foubert-Samier A, Meissner W, Tison F (August 2008). "Hearing and seeing: Unusual early signs of Wernicke encephalopathy". Neurology. 71 (9): 694. doi: 10.1212/01.wnl.0000324599.66359.b1 . PMID   18725598.
  16. ↑ Jethava A, Dasanu CA (2012). "Acute Wernicke encephalopathy and sensorineural hearing loss complicating bariatric surgery". Connecticut Medicine. 76 (10): 603–605. PMID   23243762.
  17. 1 2 3 Harper CG, Giles M, Finlay-Jones R (April 1986). "Clinical signs in the Wernicke-Korsakoff complex: a retrospective analysis of 131 cases diagnosed at necropsy". Journal of Neurology, Neurosurgery, and Psychiatry. 49 (4): 341–345. doi:10.1136/jnnp.49.4.341. PMC   1028756 . PMID   3701343.
  18. 1 2 3 Puiggros C (1994). Tratado de Neurología. Madrid: Editorial Libro del Año. pp. 823–824. ISBN   9788487748547.
  19. ↑ Meierkord H, Boon P, Engelsen B, Göcke K, Shorvon S, Tinuper P, Holtkamp M (March 2010). "EFNS guideline on the management of status epilepticus in adults". European Journal of Neurology. 17 (3): 348–355. doi:10.1111/j.1468-1331.2009.02917.x. PMID   20050893. S2CID   1032139.
  20. ↑ Kondo K, Fujiwara M, Murase M, Kodera Y, Akiyama S, Ito K, Takagi H (August 1996). "Severe acute metabolic acidosis and Wernicke's encephalopathy following chemotherapy with 5-fluorouracil and cisplatin: case report and review of the literature". Japanese Journal of Clinical Oncology. 26 (4): 234–236. doi: 10.1093/oxfordjournals.jjco.a023220 . PMID   8765181.
  21. ↑ Becker JT, Furman JM, Panisset M, Smith C (1990). "Characteristics of the memory loss of a patient with Wernicke-Korsakoff's syndrome without alcoholism". Neuropsychologia. 28 (2): 171–179. doi:10.1016/0028-3932(90)90099-A. PMID   2314572. S2CID   41693535.
  22. ↑ Zhang G, Ding H, Chen H, Ye X, Li H, Lin X, Ke Z (January 2013). "Thiamine nutritional status and depressive symptoms are inversely associated among older Chinese adults". The Journal of Nutrition. 143 (1): 53–58. doi:10.3945/jn.112.167007. PMC   3521461 . PMID   23173173.
  23. ↑ Worden RW, Allen HM (2006). "Wernicke's encephalopathy after gastric bypass that masqueraded as acute psychosis: a case report". Current Surgery. 63 (2): 114–116. doi:10.1016/j.cursur.2005.06.004. PMID   16520112.
  24. ↑ Jiang W, Gagliardi JP, Raj YP, Silvertooth EJ, Christopher EJ, Krishnan KR (January 2006). "Acute psychotic disorder after gastric bypass surgery: differential diagnosis and treatment". The American Journal of Psychiatry. 163 (1): 15–19. doi:10.1176/appi.ajp.163.1.15. PMID   16390883.
  25. ↑ Lindberg MC, Oyler RA (April 1990). "Wernicke's encephalopathy". American Family Physician. 41 (4): 1205–1209. PMID   2181837.
  26. ↑ Mann MW, Degos JD (1987). "[Hypothermia in Wernicke's encephalopathy]" [Hypothermia in Wernicke's encephalopathy]. Revue Neurologique (in French). 143 (10): 684–686. PMID   3423584. INIST   7514445.
  27. ↑ Reinhard R (2004). Color Atlas of Neurology. Thieme. ISBN   978-1-58890-191-0.[ page needed ]
  28. ↑ Biller J (2008). The Interface of Neurology & Internal Medicine. Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins. ISBN   978-0-7817-7906-7.[ page needed ]
  29. ↑ Rohkamm R (2004). "Hemodynamic abnormalities". Color Atlas of Neurology. Thieme. p. 148. ISBN   978-1-58890-191-0.
  30. ↑ Ishiko T, Taguchi T, Takeguchi M, Saito H, Nanri K (September 2009). "[Case of Wernicke's encephalopathy and subacute combined degeneration of the spinal cord due to vitamin deficiency showing changes in the bilateral corpus striatum and cardiac arrest due to beriberi heart disease]" [Case of Wernicke's encephalopathy and subacute combined degeneration of the spinal cord due to vitamin deficiency showing changes in the bilateral corpus striatum and cardiac arrest due to beriberi heart disease]. Brain and Nerve = Shinkei Kenkyu No Shinpo (in Japanese). 61 (9): 1069–1073. PMID   19803406.
  31. ↑ Harper C, Fornes P, Duyckaerts C, Lecomte D, Hauw JJ (March 1995). "An international perspective on the prevalence of the Wernicke-Korsakoff syndrome". Metabolic Brain Disease. 10 (1): 17–24. doi:10.1007/BF01991779. PMID   7596325. S2CID   9751459.
  32. 1 2 3 Zarranz JJ (2007). Neurologia (in Spanish) (4th ed.). Madrid, España: Harcourt Brace De Espana SA. p. 821. ISBN   978-8480862288.
  33. 1 2 Brown AH, Ropper RH (2007). Principios de neurología de Adams y Victor (in Spanish) (8th ed.). México: McGraw-Hill. p. 1132. ISBN   978-9701057070.
  34. ↑ Vasconcelos MM, Silva KP, Vidal G, Silva AF, Domingues RC, Berditchevsky CR (April 1999). "Early diagnosis of pediatric Wernicke's encephalopathy". Pediatric Neurology. 20 (4): 289–294. doi:10.1016/s0887-8994(98)00153-2. PMID   10328278.
  35. ↑ Fattal-Valevski A, Kesler A, Sela BA, Nitzan-Kaluski D, Rotstein M, Mesterman R, et al. (February 2005). "Outbreak of life-threatening thiamine deficiency in infants in Israel caused by a defective soy-based formula". Pediatrics. 115 (2): e233 –e238. doi:10.1542/peds.2004-1255. PMID   15687431. S2CID   2230681.
  36. 1 2 Hauser S (2010). Harrison's Neurology in Clinical Medicine (2nd ed.). New York: McGraw-Hill Publishing. ISBN   978-0-07-174123-1.
  37. 1 2 3 Current Medical Diagnosis & Treatment 2012 (48th ed.). New York: McGraw-Hill Medical. 2009. ISBN   978-0-07-176372-1.
  38. 1 2 Johnson LE (November 2022). "Thiamin Deficiency". Merk Manuals.
  39. 1 2 3 4 5 6 7 8 9 10 11 12 13 14 Sechi G, Serra A (May 2007). "Wernicke's encephalopathy: new clinical settings and recent advances in diagnosis and management". The Lancet. Neurology. 6 (5): 442–455. doi:10.1016/S1474-4422(07)70104-7. PMID   17434099. S2CID   15523083.
  40. ↑ Shand F, Gates J, Fawcett J, Mattick R (October 2003). "Wernicke Korsakoff's syndrome". Guidelines for the Treatment of Alcohol Problems (PDF). National Drug and Alcohol Research Centre, Commonwealth of Australia. p. 48. ISBN   978-0-642-82383-0. Archived from the original (PDF) on 14 February 2014.
  41. ↑ Haberland C (2007). Clinical neuropathology: text and color atlas. Demos Medical Publishing. p. 200. ISBN   978-1-888799-97-2.
  42. 1 2 3 Thomson AD, Guerrini I, Marshall EJ (June 2012). "The evolution and treatment of Korsakoff's syndrome: out of sight, out of mind?". Neuropsychology Review. 22 (2): 81–92. doi:10.1007/s11065-012-9196-z. PMC   3545191 . PMID   22569770.
  43. 1 2 Goldman L, Ausiello DA, Arend W, Armitage JO, Clemmons D, Drazen J, et al., eds. (2007). "Chapter 443". Cecil Medicine (23rd ed.). Saunders, Elsevier. ISBN   978-1-4160-4478-9.
  44. 1 2 3 4 5 MedlinePlus Encyclopedia : Wernicke-Korsakoff syndrome
  45. ↑ Ng KL, Nguyễn LT (April 2013). "The role of thiamine in HIV infection". International Journal of Infectious Diseases. 17 (4): e221 –e227. doi: 10.1016/j.ijid.2012.11.019 . PMID   23274124.
  46. ↑ Rosen A, van Kuilenburg A, Assmann B, Kuhlen M, Borkhardt A (May 2011). "Severe encephalopathy, lactic acidosis, vegetative instability and neuropathy with 5-Fluorouracil treatment – pyrimidine degradation defect or beriberi?". Case Reports in Oncology. 4 (2): 371–376. doi:10.1159/000328803. PMC   3177792 . PMID   21941485.
  47. ↑ Martin PR, Singleton CK, Hiller-Sturmhöfel S (2003). "The role of thiamine deficiency in alcoholic brain disease". Alcohol Research & Health. 27 (2): 134–142. PMC   6668887 . PMID   15303623.
  48. ↑ Soukoulis V, Dihu JB, Sole M, Anker SD, Cleland J, Fonarow GC, et al. (October 2009). "Micronutrient deficiencies an unmet need in heart failure". Journal of the American College of Cardiology. 54 (18): 1660–1673. doi: 10.1016/j.jacc.2009.08.012 . PMID   19850206.
  49. ↑ Lee JH, Jarreau T, Prasad A, Lavie C, O'Keefe J, Ventura H (2011). "Nutritional assessment in heart failure patients". Congestive Heart Failure. 17 (4): 199–203. doi:10.1111/j.1751-7133.2011.00239.x. PMID   21790970.
  50. ↑ Hirsch JA, Parrott J (2012). "New considerations on the neuromodulatory role of thiamine". Pharmacology. 89 (1–2): 111–116. doi:10.1159/000336339. PMID   22398704. S2CID   22555167.
  51. ↑ Hazell AS (2009). "Astrocytes are a major target in thiamine deficiency and Wernicke's encephalopathy". Neurochemistry International. 55 (1–3): 129–135. doi:10.1016/j.neuint.2009.02.020. PMID   19428817. S2CID   12615886.
  52. ↑ Hazell AS, Todd KG, Butterworth RF (June 1998). "Mechanisms of neuronal cell death in Wernicke's encephalopathy". Metabolic Brain Disease. 13 (2): 97–122. doi:10.1023/A:1020657129593. PMID   9699919. S2CID   25130884.
  53. 1 2 3 4 5 Kohnke, Sara; Meek, Claire L (January 2021). "Don't seek, don't find: The diagnostic challenge of Wernicke's encephalopathy". Annals of Clinical Biochemistry: International Journal of Laboratory Medicine. 58 (1): 38–46. doi:10.1177/0004563220939604. ISSN   0004-5632. PMC   7791272 . PMID   32551830.
  54. 1 2 Powell SZ, Schochet Jr SS (March 2003). "Intoxications and Metabolic Diseases of the Central Nervous System". In Nelson JS, Mena H, Parisi JE, Schochet SS (eds.). Principles and Practice of Neuropathology. Oxford University Press. p. 193. ISBN   978-0-19-802907-6.
  55. 1 2 Zuccoli G, Pipitone N (February 2009). "Neuroimaging findings in acute Wernicke's encephalopathy: review of the literature". AJR. American Journal of Roentgenology. 192 (2): 501–508. doi:10.2214/AJR.07.3959. PMID   19155417. S2CID   32749934.
  56. ↑ Cernicchiaro L (September 2017). "Wernicke's Disease (or Wernicke's Encephalopathy). Symptoms and new treatments. Clinical and practical approach. Daily monitoring for twelve years of a reversed severe case".[ self-published source? ][ unreliable medical source? ]
  57. ↑ McPhee SJ, Papadakis MA, Rabow MW, eds. (12 September 2011). Current medical diagnosis & treatment 2012 (51st ed.). New York: McGraw-Hill Medical. ISBN   978-0-07-176372-1.[ page needed ]
  58. ↑ Caine D, Halliday GM, Kril JJ, Harper CG (January 1997). "Operational criteria for the classification of chronic alcoholics: identification of Wernicke's encephalopathy". Journal of Neurology, Neurosurgery, and Psychiatry. 62 (1): 51–60. doi:10.1136/jnnp.62.1.51. PMC   486695 . PMID   9010400.
  59. 1 2 Protocol for: The management of the alcohol withdrawal syndrome and Wernicke encephalopathy (Report). East Kent Hospitals NHS Trust.
  60. ↑ Hegde AN, Mohan S, Lath N, Lim CC (2011). "Differential diagnosis for bilateral abnormalities of the basal ganglia and thalamus". Radiographics. 31 (1): 5–30. doi:10.1148/rg.311105041. PMID   21257930. S2CID   207707771.
  61. ↑ Attard A, Torrens N, Holvey C (June 2012). "Clinical Guideline: The Management of Wernicke's Encephalopathy (WE)" (PDF). Guy's and St. Thomas Hospitals. Archived from the original (PDF) on 9 July 2015.
  62. ↑ Wood VM (June 2006). "Guidelines for the Management of Alcohol Issues in the Acute Hospital Setting" (PDF). Doncaster and Bassetlaw Hospitals. Archived from the original (PDF) on 21 September 2013.
  63. ↑ Habas, Elmukhtar; Farfar, Kalifa; Errayes, Nada; Rayani, Amnna; Elzouki, Abdel-Naser (2023). "Wernicke Encephalopathy: An Updated Narrative Review". Saudi Journal of Medicine & Medical Sciences. 11 (3): 193–200. doi: 10.4103/sjmms.sjmms_416_22 . ISSN   1658-631X. PMC   10393093 . PMID   37533659.
  64. ↑ Thomson AD, Cook CC, Guerrini I, Sheedy D, Harper C, Marshall EJ (2008). "Wernicke's encephalopathy revisited. Translation of the case history section of the original manuscript by Carl Wernicke 'Lehrbuch der Gehirnkrankheiten fur Aerzte and Studirende' (1881) with a commentary". Alcohol and Alcoholism. 43 (2). Oxford, Oxfordshire: 174–9. doi: 10.1093/alcalc/agm144 . PMID   18056751.
  65. ↑ Thomson A, Guerrini I, Marshall EJ. "Incidence of Adverse Reactions to Parenteral Thiamine in the Treatment of Wernicke's Encephalopathy, and Recommendations." Alcohol and Alcoholism. 2019 Nov;54(6):609-614. doi:https://doi.org/10.1093/alcalc/agy091
  66. ↑ Iwamoto Y, Okuda B, Miyata Y, Tachibana H, Sugita M (June 1994). "[Beneficial effect of steroid pulse therapy on Wernicke-Korsakoff syndrome due to hyperemesis gravidarum]". Rinsho Shinkeigaku = Clinical Neurology. 34 (6): 599–601. PMID   7955722.
  67. ↑ Warot P, Lesage R, Dupuys P (February 1962). "[Corticotherapy of the severe forms of the Gayet-Wernicke encephalopathy]". Lille Medical. 7: 123–124. PMID   14005025. (article in French)
  68. ↑ Harrison TR, Braunwald E, Agud Aparicio JL (2002). Medicina Interna. p. 2462.
  69. ↑ Kelley WN, DeVita VT, DuPont HL, Harris ED, Hazzard WR (1990). Medicina Interna (1st ed.). Buenos Aires: Médica Panamericana. pp. 621, 974. ISBN   9789500612401.
  70. 1 2 Thomson AD, Cook CC, Touquet R, Henry JA (2002). "The Royal College of Physicians report on alcohol: guidelines for managing Wernicke's encephalopathy in the accident and Emergency Department". Alcohol and Alcoholism. 37 (6): 513–521. doi:10.1093/alcalc/37.6.513. PMID   12414541.
  71. ↑ Lourenço R, Camilo ME (2002). "Taurine: a conditionally essential amino acid in humans? An overview in health and disease" (PDF). Nutricion Hospitalaria. 17 (6): 262–270. PMID   12514918.
  72. ↑ Iwamoto Y, Okuda B, Miyata Y, Tachibana H, Sugita M (June 1994). "[Beneficial effect of steroid pulse therapy on Wernicke-Korsakoff syndrome due to hyperemesis gravidarum]". Rinsho Shinkeigaku = Clinical Neurology (in Japanese). 34 (6): 599–601. PMID   7955722.
  73. 1 2 Torvik A, Lindboe CF, Rogde S (November 1982). "Brain lesions in alcoholics. A neuropathological study with clinical correlations". Journal of the Neurological Sciences. 56 (2–3): 233–48. doi:10.1016/0022-510x(82)90145-9. PMID   7175549. S2CID   26100578.
  74. ↑ Harper C (March 1979). "Wernicke's encephalopathy: a more common disease than realised. A neuropathological study of 51 cases". Journal of Neurology, Neurosurgery, and Psychiatry. 42 (3): 226–231. doi:10.1136/jnnp.42.3.226. PMC   490724 . PMID   438830.
  75. ↑ Blansjaar BA, Van Dijk JG (July 1992). "Korsakoff minus Wernicke syndrome". Alcohol and Alcoholism (Oxford, Oxfordshire). 27 (4): 435–7. doi:10.1093/oxfordjournals.alcalc.a045269. PMID   1418116.
  76. ↑ Lana-Peixoto MA, Dos Santos EC, Pittella JE (September 1992). "Coma and death in unrecognized Wernicke's encephalopathy. An autopsy study". Arquivos de Neuro-Psiquiatria. 50 (3): 329–333. doi: 10.1590/S0004-282X1992000300012 . PMID   1308411.
  77. 1 2 Bem Junior, Luiz Severo; Lemos, Nilson Batista; de Lima, Luís Felipe Gonçalves; Dias, Artêmio José Araruna; Neto, Otávio da Cunha Ferreira; de Lira, Carlos Cezar Sousa; Diniz, Andrey Maia Silva; Rabelo, Nicollas Nunes; Barroso, Luciana Karla Viana; Valença, Marcelo Moraes; de Azevedo Filho, Hildo Rocha Cirne (28 June 2021). "The anatomy of the brain – learned over the centuries". Surgical Neurology International. 12: 319. doi:10.25259/SNI_200_2021. ISSN   2152-7806. PMC   8326080 . PMID   34345460.
  78. ↑ Isen, Danielle R.; Kline, Lanning B. (30 June 2020). "Neuro-ophthalmic Manifestations of Wernicke Encephalopathy". Eye and Brain. 12: 49–60. doi: 10.2147/EB.S234078 . PMC   7335288 . PMID   32636690.
  79. ↑ Isenberg-Grzeda E, Kutner HE, Nicolson SE (1 November 2012). "Wernicke-Korsakoff-syndrome: under-recognized and under-treated". Psychosomatics. 53 (6): 507–516. doi:10.1016/j.psym.2012.04.008. PMID   23157990.
  80. ↑ Sechi G, Serra A (May 2007). "Wernicke's encephalopathy: new clinical settings and recent advances in diagnosis and management". The Lancet. Neurology. 6 (5): 442–455. doi:10.1016/S1474-4422(07)70104-7. PMID   17434099. S2CID   15523083.
This page is based on this Wikipedia article
Text is available under the CC BY-SA 4.0 license; additional terms may apply.
Images, videos and audio are available under their respective licenses.