eMedicine Specialties > Emergency Medicine > Neurology

Wernicke Encephalopathy

Philip N Salen, MD, Clinical Professor, Department of Emergency Medicine, PA Program, Desales University; Adjunct Clinical Associate Professor, Department of Emergency Medicine, Temple University Medical School; Research Director, Emergency Medicine Education, Saint Luke's Hospital

Updated: Jan 13, 2009

Introduction

Background

Thiamine (vitamin B-1) deficiency can result in Wernicke encephalopathy, a serious neurologic disorder. Dr Carl Wernicke, a Polish neurologist, described it in 1881 as a triad of acute mental confusion, ataxia, and ophthalmoplegia. Korsakoff amnestic syndrome is a late neuropsychiatric manifestation of Wernicke encephalopathy with memory loss and confabulation; sometimes, the condition is referred to as Wernicke-Korsakoff syndrome or psychosis. It is most often seen in alcoholics, but it can be seen in persons with disorders associated with malnutrition and also in patients on long-term hemodialysis or with AIDS. Frequently unrecognized, Wernicke encephalopathy is more prevalent than commonly supposed.

Pathophysiology

Thiamine plays a vital role in the metabolism of carbohydrates. Thiamine is a cofactor for several essential enzymes in the Krebs cycle and the pentose phosphate pathway, including alpha-ketoglutarate dehydrogenase, pyruvate dehydrogenase, and transketolase.¹  In the setting of thiamine deficiency, thiamine-dependent cellular systems begin to fail, resulting eventually in cell death. Because thiamine-dependent enzymes play an essential role in cerebral energy utilization, thiamine deficiency may propagate brain tissue injury by inhibiting metabolism in brain regions with higher metabolic demands and high thiamine turnover.¹

Both pyruvate dehydrogenase and alpha-ketoglutarate are essential enzymes in the Krebs cycle and lack of these enzymes alters cerebral energy utilization. If cells with high metabolic requirements have inadequate stores of thiamine to draw from, energy production drops, and neuronal damage ensues. Increased cell death then feeds the localized vasogenic response.² Additionally, the reduced production of succinate, which plays a role in gamma-aminobutyric acid (GABA) metabolism and the electrical stimulation of neurons, leads to further central nervous system injury.

Increased lactic acid production ensues in the absence of pyruvate dehydrogenase function, as the reduced conversion of pyruvate to acetyl coenzyme A results in less efficient oxidative phosphorylation.³

Thiamine pyrophosphate is also essential for nucleotide synthesis, production of nicotinamide adenine dinucleotide phosphate (NADPH), and maintenance of reduced glutathione within erythrocytes.³

Frequency

United States

Autopsy series identifying typical brainstem lesions of Wernicke encephalopathy have placed the incidence between 0.8% and 2.8% of the general population. However, the incidence can be as high as 12.5% in a population of alcoholics.⁴ It has been described in many other situations where nutrition has been compromised. These cases include patients with AIDS, individuals receiving hemodialysis, those with hyperemesis gravidarum, and those with malignancy with or without chemotherapy.

International

Although it may not be diagnosed as frequently in third and fourth world nations, the incidence is probably higher in areas where there is more malnutrition and less vitamin supplementation.

Mortality/Morbidity

Studies suggest that up to 80% of patients with Wernicke encephalopathy may not be diagnosed, which makes estimates of mortality rates unreliable.⁵ Wernicke encephalopathy is a significantly disabling and potentially lethal condition that can be prevented or reversed if treated early. Established Wernicke encephalopathy can have major long-term consequences among patients requiring permanent institutional care.

Race

No racial predilection is known to exist for Wernicke encephalopathy.

Sex

The male-to-female ratio is 1.7:1, likely owing to alcoholism being 3-4 times more frequent in men than in women.

Age

Average age at onset is 50 years. However, Wernicke encephalopathy can occur in small numbers in unusual situations such as in total parenteral nutrition-dependent patients during a multivitamin shortage, in persons with hyperemesis gravidarum, or in infants who are fed thiamine-deficient infant formula.⁶

Clinical

History

The 3 components of the classic triad of Wernicke encephalopathy are encephalopathy, ataxic gait, and some variant of oculomotor dysfunction. All 3 features of the triad are recognized in only about one third of cases.

• Consideration for Wernicke encephalopathy should be given to patients with any evidence of long-term alcohol abuse or malnutrition and any of the following: acute confusion, decreased conscious level, ataxia, ophthalmoplegia, memory disturbance, hypothermia with hypotension, and delirium tremens.
• A high proportion of patients with acute Wernicke encephalopathy who survive develop Korsakoff psychosis, also called Korsakoff syndrome, characterized by retrograde and anterograde amnesia with varying degrees of other cognitive deficits.⁷
• Wernicke encephalopathy should be considered when any patient with long-term malnutrition presents with confusion or altered metal status. Significant overlap exists between Wernicke encephalopathy and Korsakoff psychosis, in which patients experience delayed and potentially irreversible anterograde and retrograde amnesia. For this reason, the two entities have been described together as Wernicke-Korsakoff syndrome.
• Alcohol abuse, AIDS, malignancy, hyperemesis gravidarum, prolonged total parenteral nutrition, iatrogenic glucose loading in any predisposed patient, and other disorders associated with grossly impaired nutritional status have been associated with Wernicke-Korsakoff syndrome.
• Recent reports of Wernicke encephalopathy in patients who have undergone bariatric surgery illustrate that advances in medicine may predispose new groups of patients to this syndrome.¹
• Epidemics of Wernicke encephalopathy can occur as evidenced by a recent report of Israeli infants with infantile thiamine deficiency who were fed formula deficient in thiamine.⁶

Physical

• Ocular abnormalities are the hallmarks of Wernicke encephalopathy. The oculomotor signs are nystagmus, bilateral lateral rectus palsies, and conjugate gaze palsies reflecting cranial nerve involvement of the oculomotor, abducens, and vestibular nuclei. Less frequently noted are pupillary abnormalities such as sluggishly reactive pupils, ptosis, scotomata, and anisocoria. The most common ocular abnormality is nystagmus, not complete ophthalmoplegia.¹
• Encephalopathy is characterized by a global confusional state, disinterest, inattentiveness, or agitation. The most constant symptoms of Wernicke encephalopathy are the mental status changes.¹ Stupor and coma are rare.
• Gait ataxia is often a presenting symptom.³  Ataxia is likely to be a combination of polyneuropathy, cerebellar damage, and vestibular paresis. Vestibular dysfunction, usually without hearing loss, is universally impaired in the acute stages of Wernicke encephalopathy.³ In less severe cases, patients walk slowly with a broad-based gait. However, gait and stance may be so impaired as to make walking impossible. Cerebellar testing in bed with finger-to-nose and heel-to-shin tests may not illicit any notable deficit; thus, it is important to test for truncal ataxia with the patient sitting or standing. Other symptoms that may occur in addition to, or in place of, the classic triad include vestibular dysfunction, hypothermia, hypotension, and coma.⁷
• In addition to ophthalmoplegia and ataxia, 80% of adults will have some degree of peripheral neuropathy, which may include weakness, foot drop, and decreased proprioception.
• Thiamine deficiency has recently been shown to possibly cause a gastrointestinal syndrome of nausea, vomiting, abdominal pain, and lactic acidosis.⁸
• Thiamine deficiency often affects the temperature-regulating center in the brainstem, which can result in hypothermia.
• Hypotension can be secondary to thiamine deficiency either through cardiovascular beriberi or thiamine deficiency–induced autonomic dysfunction.³ Hypotension can also be the result of significant alcoholic liver disease.  
• Coma is rarely the sole manifestation of Wernicke encephalopathy.
• Of patients surviving Wernicke encephalopathy, a large percentage have Korsakoff psychosis, characterized by the following: retrograde amnesia (inability to recall information), anterograde amnesia (inability to assimilate new information), decreased spontaneity and initiative, and confabulation.
• Other manifestations of thiamine deficiency involve the cardiovascular system (wet beriberi) and peripheral nervous system (nutritional polyneuropathy).
• Manifestations of thiamine deficiency in infants are constipation, agitation, apathy, vomiting, lack of appetite, and later, diarrhea, grunting, nystagmus, convulsions, unconsciousness, and cardiomyopathy.⁶

Causes

• Long-term alcohol abuse is the most common cause of Wernicke encephalopathy. In long-term alcoholics, malnutrition can reduce intestinal thiamine absorption by 70%, decreasing serum levels of thiamine from between 30% and 98% below the lower level established for normal subjects. Alcohol alone can also decrease thiamine absorption by 50% in one third of patients who are not malnourished.
• Other less common etiologies are forced or self-imposed starvation, protein-energy malnutrition resulting from inadequate diet or malabsorption (from sprue), conditions associated with protracted vomiting (eg, hyperemesis gravidarum), chronic renal failure, carbohydrate loading in the presence of marginal thiamine stores (feeding after starvation), bariatric surgery and other gastric bypass surgeries, absence of thiamine from the diet (in the case of infants fed formula without the addition of thiamine), and congenital transketolase function abnormalities.
• The most common inciting factor contributing to Wernicke encephalopathy in the setting of thiamine deficiency is infection. Concomitant illnesses, such as pneumonia or even meningitis, do not exclude a codiagnosis of Wernicke encephalopathy.¹
• Iatrogenic exacerbation of Wernicke encephalopathy can occur with prolonged glucose or carbohydrate loading in the setting of thiamine deficiency. A single acute administration of glucose does not appear to cause this effect. Nutritionally deficient patients receiving glucose should also receive thiamine, but urgent administration of glucose should not be delayed pending thiamine administration.¹

Differential Diagnoses

Alcohol and Substance Abuse Evaluation
Alcoholic Ketoacidosis
Delirium Tremens
Delirium, Dementia, and Amnesia
Stroke, Ischemic
Withdrawal Syndromes

Other Problems to Be Considered

Psychosis
Normal pressure hydrocephalus
Cerebrovascular accident
Chronic hypoxia
Closed-head injury
Hepatic encephalopathy
Postictal state

Workup

Laboratory Studies

Patients with Wernicke encephalopathy present with altered mental status and other neurologic abnormalities. Careful history, physical examination, laboratory workup, and radiographic evaluation are essential to exclude other causes of CNS dysfunction. No specific laboratory test is available for diagnosing Wernicke encephalopathy. Wernicke encephalopathy is a clinical diagnosis, and normal electrolyte levels may only give false reassurance and delay therapy. This is particularly the case where malnutrition is likely to be present. The motto should be "If in doubt, treat," as administration of thiamine does not pose potential harm.

• The history and initial evaluation guide selection of laboratory and radiographic tests. Although Wernicke encephalopathy remains a clinical diagnosis with no characteristic abnormalities in diagnostic studies, it remains important to exclude alternate or coexisting medical conditions.
• Biomarkers, including an assay for thiamine, are not typically available for timely diagnostic purposes. Further, no study has clearly described the sensitivity, specificity, and accuracy of thiamine levels in relation to active disease.⁹  However, the thiamine levels can help the clinician assuming care of the patient in ambiguous cases, and obtaining a thiamine level can be considered for diagnostic dilemmas.¹
• Complete blood cell (CBC) count rules out severe anemias and leukemias as causes of altered mental status.
• Alterations in serum electrolyte levels, such as hypernatremia or hypercalcemia, can cause altered mental status and must be excluded.
• A recent case series suggested that patients with Wernicke encephalopathy may exhibit a distinctive acid-base pattern consisting of a primary metabolic acidosis in conjunction with a primary respiratory alkalosis. The primary metabolic acidosis is secondary to thiamine's role in aerobic metabolism and the Krebs cycle; without thiamine, aerobic metabolism cannot progress and metabolic products, including lactate and pyruvate, are produced, which result in an anion gap acidosis. The role of thiamine in causing a primary respiratory alkalosis is unclear.⁹
• Obtain serum glucose levels to exclude hypoglycemia and hyperglycemia.
• Obtain pulse oximetry and/or arterial blood gases (ABGs) measurement to exclude hypoxia and hypercarbia.
• Perform toxic drug screening to exclude some causes of drug-induced altered mental status.
• Consider lumbar puncture (LP) to exclude CNS infections if indicated.
• Erythrocyte transketolase levels reliably detect thiamine deficiency but are not necessary for the diagnosis of Wernicke encephalopathy. In the erythrocyte transketolase activity assay, the extent of thiamine deficiency is expressed in percentage stimulation compared with baseline levels (the thiamine pyrophosphate effect). Normal values range from 0-15%; a value of 15-25% indicates thiamine deficiency, and greater than 25% indicates severe deficiency.⁶
• Blood pyruvate and lactate measurements, although not specific for thiamine deficiency illnesses, are sensitive and helpful, as thiamine is a cofactor of the pyruvate dehydrogenase enzyme, an important enzyme in aerobic metabolism.⁶

Imaging Studies

• A head computed tomography (CT) scan is a vital initial test for emergency diagnosis of focal neurologic disease such as intracerebral hemorrhage. In patients who are comatose, CT scan can detect not only intracranial lesions but also fractures of the skull and minute amounts of blood. However, CT of the head does not appear to be useful in screening for Wernicke-Korsakoff syndrome.⁷
• Magnetic resonance imaging (MRI) offers the best way to make a definitive diagnosis antemortem, but the sensitivity is poor and obtaining an MRI for this indication is typically impractical and unnecessary in the ED.¹  Although the clinical evidence for the utility of MRI is based on a study in which the sample size was small, the reported sensitivity of MRI was 53% and specificity was 93% for both acute and chronic Wernicke-Korsakoff syndrome. The same study reported 13% sensitivity for CT scanning.⁷  Because of the low sensitivity of MRI for Wernicke encephalopathy, particularly an acute presentation, and because many patients with Wernicke encephalopathy may not exhibit diagnostic features on MRI, means that normal MRI results should not be used to exclude the diagnosis of acute illness. The low sensitivity of CT scan for Wernicke encephalopathy means that CT does not have a role in the routine screening for this typeofencephalopathy.⁷   
• The appearance of acute Wernicke encephalopathy on MRI demonstrates abnormal hyperdensity of the mammillary bodies and periaqueductal gray matter with associated abnormal enhancement on T1-weighted images.¹⁰ In chronic Wernicke encephalopathy and Korsakoff syndrome, radiographic imaging, especially MRI, may be normal or may show symmetric low-density abnormalities in periventricular areas, the diencephalon, the midbrain, excessive mamillary body, cerebellar, and cerebral shrinkage.⁷ Such symmetric lesions are uncommon in other cerebral encephalopathic disorders and are suggestive of Wernicke-Korsakoff syndrome.⁷  
• Morphometric studies of MRI imaging confirm that patients with Wernicke-Korsakoff syndrome show excessive mamillary body and cerebellar shrinkage indicating that these are highly specific MRI findings for this kind of encephalopathy.⁷

Other Tests

• Consider an electroencephalogram (EEG) if nonconvulsive status epilepticus is suspected as a potential cause of coma and altered mental status.

Treatment

Prehospital Care

Because patients with Wernicke encephalopathy present with altered mental status in the prehospital setting, focus prehospital care on stabilizing the airway, ensuring oxygenation, and maintaining blood pressure and euvolemia.

Emergency Department Care

Wernicke encephalopathy must be viewed as a medical emergency, even if other competing diagnoses of CNS processes are being considered. Because the condition is potentially reversible, institution of treatment is indicated in patients exhibiting any combination of symptoms and signs, particularly if the patient is in a high-risk population. Onset of the disease may be acute, subacute, or chronic.

Although as little as 2 mg of thiamine may be enough to reverse symptoms, the dose of thiamine required to prevent or treat Wernicke encephalopathy in most alcoholic patients may be as high as greater than 500 mg given once or, preferably, twice or thrice daily parenterally. With a short half-life, multiple daily administrations may be necessary to replete levels and allow for optimal blood-brain diffusions.¹  Thiamine solution should be fresh, since old solutions may be inactive. Ataxia and acute confusional state may resolve dramatically, although improvement may not be noted for days or months.

• Treat all poorly nourished patients with large doses of parenteral thiamine, particularly if intravenous glucose administration is necessary, even in the absence of symptoms and signs of Wernicke encephalopathy. Administering dextrose in a thiamine-deficient state exacerbates the process of cell death by providing more substrate for biochemical pathways that lack sufficient amounts of coenzymes.²
• Start thiamine prior to or concurrently with treatment of intravenous glucose solutions, and continue until the patient resumes a normal diet. The administration of dextrose or other carbohydrates in this setting can be hazardous, because glucose oxidation is a thiamine-intensive process that may drive the last reserves of circulating vitamin B-1 toward the intracellular compartment, thereby aggravating the neurologic damage.⁶
• Patients with Wernicke encephalopathy are likely hypomagnesemic and should be treated empirically with parenteral magnesium sulfate, as they may be unresponsive to parenteral thiamine in the presence of hypomagnesemia. After correction of hypomagnesemia in conjunction with thiamine repletion, the blood transketolase activity can return to normal and clearing of the clinical signs may occur.

Consultations

• Consult a neurologist for further evaluation and treatment of altered mental status or other neurologic deficit.
• A psychiatrist may be helpful in evaluating comorbid psychiatric conditions.

Medication

The cornerstone of therapy for prevention or treatment of Wernicke encephalopathy in most alcoholic patients is thiamine until the patient resumes a normal diet.

Nutrients

The primary objective is to replenish vitamin B-1 stores. In adults, 60-180 mEq of potassium, 10-30 mEq of magnesium, and 10-40 mmol/L of phosphate per day appear necessary to achieve optimum metabolic balance.

Thiamine (Thiamilate)

Begin thiamine administration prior to treating with IV glucose solutions. 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.

Dosing

Adult

100-200 mg IV; followed by 50-100 mg/bid up to 5 times/d IV

Pediatric

50 mg IV; followed by 10-25 mg/d IV/IM

Interactions

None reported

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

A - Fetal risk not revealed in controlled studies in humans

Precautions

Sensitivity reactions can occur (intradermal test dose recommended in suspected sensitivity); deaths have resulted from IV use; sudden onset or worsening of Wernicke encephalopathy following glucose administration may occur in patients who are thiamine deficient; administer before or with dextrose-containing fluids in suspected thiamine deficiency

Magnesium sulfate

Cofactor in a number of enzyme systems; also involved in neurochemical transmission and muscular excitability. Persons with long-term alcoholism and patients who are malnourished usually have inadequate magnesium stores.

Dosing

Adult

2-4 g IV mixed with initial IV fluid bolus; followed by 1-4 g IV q4h prn
Alternatively: 1-4 g/h continuous infusion

Pediatric

25-50 mg/kg/dose IV q4-6h mixed with initial fluid bolus for 3-4 h; not to exceed single dose of 2 g; also may be administered and repeated if hypomagnesemia persists

Interactions

Concurrent use with nifedipine may cause hypotension and neuromuscular blockade; may increase neuromuscular blockade seen with aminoglycosides and potentiate neuromuscular blockade produced by tubocurarine, vecuronium, and succinylcholine; may increase CNS effects and toxicity of CNS depressants, betamethasone, and cardiotoxicity of ritodrine

Contraindications

Documented hypersensitivity; heart block; Addison disease; myocardial damage; severe hepatitis

Precautions

Pregnancy

A - Fetal risk not revealed in controlled studies in humans

Precautions

May alter cardiac conduction leading to heart block in digitalized patients; monitor respiratory rate, deep tendon reflex, and renal function when electrolyte is administered parenterally; caution when administering, since may produce significant hypertension or asystole; in overdose, 10% calcium gluconate solution 10-20 mL IV can be administered as antidote for clinically significant hypermagnesemia

Follow-up

Further Inpatient Care

• Depending on mental status and ability to protect his or her airway, admit patients with suspected or confirmed Wernicke encephalopathy to an internal medicine or neurology service.
• Admission ensures that the patient receives continued intravenous thiamine and magnesium administration, observation for possible development of Korsakoff psychosis, and evaluation for possible cardiovascular beriberi.

Further Outpatient Care

• Refer patients with alcoholism to alcohol-cessation programs and monitor for signs of alcohol withdrawal.
• Patients who are malnourished, whether from alcohol or other causes, should continue to receive thiamine supplementation on an outpatient basis.

Inpatient & Outpatient Medications

• Administer daily oral thiamine (100 mg) on a long-term outpatient basis.
• Inpatient therapy of infants with thiamine deficiency involves administration of high-dose thiamine 50 mg/day for 2 weeks.⁶

Deterrence/Prevention

• Patients should avoid alcohol consumption and other behaviors that predispose to thiamine deficiency.
• In the United States, many foods (but not alcoholic beverages) are supplemented with multiple vitamins and minerals. Some health policy experts have hypothesized that fortifying alcoholic beverages with thiamine would lower healthcare costs.

Complications

• Korsakoff psychosis
• Alcohol withdrawal
• Acute precipitation of Wernicke encephalopathy
• Congestive heart failure
• The administration of dextrose in the setting of thiamine deficiency can be harmful because glucose oxidation is a thiamine-intensive process that may drive the insufficient circulating vitamin B-1 intracellularly, thereby precipitating neurologic injury.⁶
• Gastrointestinal beriberi⁸
• Lactic acidosis⁹

Prognosis

• Administration of thiamine improves disease to some degree in almost all cases; however, persistent neurologic dysfunction is common.¹ Ophthalmoplegia usually resolves briskly; the initial presentation of global confusion often improves within hours or days.
• Patients with Wernicke encephalopathy have a significant morbidity and mortality rate, especially if no early signs of neurologic improvement are present after repletion of thiamine.
• Of patients surviving Wernicke encephalopathy, a percentage will develop Korsakoff psychosis.
• Typical residual findings from Wernicke encephalopathy include nystagmus, gait ataxia, and Korsakoff syndrome.¹
• Of patients with Korsakoff psychosis, a significant number do not recover and require long-term institutionalization. Only about 20% eventually recover completely during long-term follow-up care.

Miscellaneous

Medicolegal Pitfalls

• Failure to consider Wernicke encephalopathy as a cause of altered mental status is a pitfall. Acute Wernicke encephalopathy should be ruled out in all alcoholic patients with any neurologic symptoms, especially in those with evidence of caloric or protein malnutrition or of peripheral neuropathy.⁷
• Acute Wernicke encephalopathy may be precipitated rapidly in high-risk patients after instituting intravenous therapy with glucose-containing solutions, resulting in rapid changes in cognitive function and ocular characteristics.
• Because Wernicke encephalopathy is reversible, the diagnosis of subclinical cases would permit treatment and probably cure the patient.⁷
• Neither a normal CT scan of the brain nor a normal MRI do not exclude or rule out either acute or chronic Wernicke-Korsakoff syndrome.⁷

References

1. Donnino MW, Vega J, Miller J, et al. Myths and misconceptions of Wernicke's encephalopathy: what every emergency physician should know. Ann Emerg Med. Dec 2007;50(6):715-21. [Medline].

2. Buscaglia J, Faris J. Unsteady, unfocused, and unable to hear. Am J Med. Nov 2005;118(11):1215-7. [Medline].

3. Decker MJ, Isaacman DJ. A common cause of altered mental status occurring at an uncommon age. Pediatr Emerg Care. Apr 2000;16(2):94-6. [Medline].

4. Thomson AD, Cook CC, Touquet R, et al. The Royal College of Physicians report on alcohol: guidelines for managing Wernicke's encephalopathy in the accident and Emergency Department. Alcohol Alcohol. Nov-Dec 2002;37(6):513-21. [Medline].

5. Azim W, Walker R. Wernicke's encephalopathy: a frequently missed problem. Hosp Med. Jun 2003;64(6):326-7. [Medline].

6. Fattal-Valevski A, Kesler A, Sela BA, et al. Outbreak of life-threatening thiamine deficiency in infants in Israel caused by a defective soy-based formula. Pediatrics. Feb 2005;115(2):e233-8. [Medline].

7. Antunez E, Estruch R, Cardenal C, et al. Usefulness of CT and MR imaging in the diagnosis of acute Wernicke's encephalopathy. AJR Am J Roentgenol. Oct 1998;171(4):1131-7. [Medline].

8. Donnino M. Gastrointestinal beriberi: a previously unrecognized syndrome. Ann Intern Med. Dec 7 2004;141(11):898-9. [Medline].

9. Donnino MW, Miller J, Garcia AJ, et al. Distinctive acid-base pattern in Wernicke's encephalopathy. Ann Emerg Med. Dec 2007;50(6):722-5. [Medline].

10. Kaineg B, Hudgins PA. Images in clinical medicine. Wernicke's encephalopathy. N Engl J Med. May 12 2005;352(19):e18. [Medline].

11. Blass JP, Gibson GE. Abnormality of a thiamine-requiring enzyme in patients with Wernicke-Korsakoff syndrome. N Engl J Med. Dec 22 1977;297(25):1367-70. [Medline].

12. Henry GL. Coma and altered states of consciousness. In: Emergency Medicine. 4^th ed. 1996:225-233.

13. Hoffman RS. Thiamine hydrochloride. In: Goldfrank's Toxicologic Emergencies. 5^th ed. 1994:825-6.

14. Hung SC, Hung SH, Tarng DC, et al. Thiamine deficiency and unexplained encephalopathy in hemodialysis and peritoneal dialysis patients. Am J Kidney Dis. Nov 2001;38(5):941-7. [Medline].

15. Marx JA. The varied faces of Wernicke's encephalopathy. J Emerg Med. 1985;3(5):411-3. [Medline].

16. Reuler JB, Girard DE, Cooney TG. Current concepts. Wernicke's encephalopathy. N Engl J Med. Apr 18 1985;312(16):1035-9. [Medline].

17. Victor M. Persistent altered mentation due to ethanol. Neurol Clin. Aug 1993;11(3):639-61. [Medline].

18. Willett WC, Stampfer MJ. Clinical practice. What vitamins should I be taking, doctor?. N Engl J Med. Dec 20 2001;345(25):1819-24. [Medline].

Keywords

Wernicke encephalopathy, Wernicke's encephalopathy, Wernicke-Korsakoff syndrome, thiamine deficiency, vitamin B-1 deficiency, Wernicke's disease, Wernicke-Korsakoff psychosis, mental confusion, ataxia, ophthalmoplegia, Korsakoff's amnestic syndrome, Korsakoff amnestic syndrome, memory loss, confabulation, vitamin B deficiencies, alcoholism, malnutrition, AIDS

Contributor Information and Disclosures

Author

Philip N Salen, MD, Clinical Professor, Department of Emergency Medicine, PA Program, Desales University; Adjunct Clinical Associate Professor, Department of Emergency Medicine, Temple University Medical School; Research Director, Emergency Medicine Education, Saint Luke's Hospital
Philip N Salen, MD is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Medical Editor

Peter MC DeBlieux, MD, Professor of Clinical Medicine and Pediatrics, Section of Pulmonary and Critical Care Medicine, Program Director, Department of Emergency Medicine, Louisiana State University Health Sciences Center
Peter MC DeBlieux, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, Radiological Society of North America, and Society of Critical Care Medicine
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

J Stephen Huff, MD, Associate Professor, Emergency Medicine and Neurology, Department of Emergency Medicine, University of Virginia Health Sciences Center
J Stephen Huff, MD is a member of the following medical societies: American Academy of Emergency Medicine, American Academy of Neurology, American College of Emergency Physicians, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

Rick Kulkarni, MD, Medical Director, Assistant Professor of Surgery, Section of Emergency Medicine, Yale-New Haven Hospital
Rick Kulkarni, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: WebMD Salary Employment

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