Wernicke-Korsakoff syndrome - Revision history

Danbot: Strip excess bold

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	==Background==		==Background==
	*Wernicke's Encephalopathy (WE): ~~'''~~acute~~'''~~ neurologic syndrome caused by [[thiamine deficiency]]		*Wernicke's Encephalopathy (WE): acute neurologic syndrome caused by [[thiamine deficiency]]
	*Korsakoff's Psychosis (KS): ~~'''~~chronic~~'''~~ neuropsychiatric syndrome caused by thiamine deficiency		*Korsakoff's Psychosis (KS): chronic neuropsychiatric syndrome caused by thiamine deficiency
	*Wernicke-Korsakoff Syndrome (WKS): presence of Wernicke's Encephalopathy + Korsakoff's Psychosis simultaneously		*Wernicke-Korsakoff Syndrome (WKS): presence of Wernicke's Encephalopathy + Korsakoff's Psychosis simultaneously
	*First described by Carl Wernicke in 1881; remains one of the most underdiagnosed and undertreated neurologic emergencies		*First described by Carl Wernicke in 1881; remains one of the most underdiagnosed and undertreated neurologic emergencies
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	*Autopsy prevalence ~2% in the general population; up to 12.5% in patients with alcohol use disorder<ref>Donnino MW, Vega J, Miller J, Walsh M. Myths and misconceptions of Wernicke's encephalopathy: what every emergency physician should know. Ann Emerg Med. 2007;50(6):715-21.</ref>		*Autopsy prevalence ~2% in the general population; up to 12.5% in patients with alcohol use disorder<ref>Donnino MW, Vega J, Miller J, Walsh M. Myths and misconceptions of Wernicke's encephalopathy: what every emergency physician should know. Ann Emerg Med. 2007;50(6):715-21.</ref>
	*Only ~20% of cases are identified before death; failure of diagnosis leads to ~20% mortality and ~75% permanent neurologic damage		*Only ~20% of cases are identified before death; failure of diagnosis leads to ~20% mortality and ~75% permanent neurologic damage
	*Classic triad (encephalopathy, oculomotor dysfunction, ataxia) is present in ~~'''~~only ~10% of patients~~'''~~<ref>Sinha S, Kataria A, Kolla BP, et al. Wernicke Encephalopathy-Clinical Pearls. Mayo Clin Proc. 2019;94(6):1065-1072.</ref>		*Classic triad (encephalopathy, oculomotor dysfunction, ataxia) is present in only ~10% of patients<ref>Sinha S, Kataria A, Kolla BP, et al. Wernicke Encephalopathy-Clinical Pearls. Mayo Clin Proc. 2019;94(6):1065-1072.</ref>
	*~80% of patients with untreated WE progress to Korsakoff syndrome		*~80% of patients with untreated WE progress to Korsakoff syndrome
	*Not limited to alcoholics — increasingly recognized post-bariatric surgery (~10% prevalence), in hyperemesis gravidarum, cancer, and critically ill patients		*Not limited to alcoholics — increasingly recognized post-bariatric surgery (~10% prevalence), in hyperemesis gravidarum, cancer, and critically ill patients
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	*Classic triad: [[encephalopathy]], oculomotor dysfunction, gait [[ataxia]]		*Classic triad: [[encephalopathy]], oculomotor dysfunction, gait [[ataxia]]
	**Classic triad present in only ~10% of cases — do NOT rely on complete triad to make diagnosis		**Classic triad present in only ~10% of cases — do NOT rely on complete triad to make diagnosis
	*~~wer'''NIC'''ke~~ mnemonic:		*werNICke mnemonic:
	**[[nystagmus\|~~'''N'''ystagmus~~]]/ophthalmoplegia		**[[nystagmus\|Nystagmus]]/ophthalmoplegia
	***Horizontal nystagmus is the ~~'''~~most common~~'''~~ ocular finding (not complete ophthalmoplegia)		***Horizontal nystagmus is the most common ocular finding (not complete ophthalmoplegia)
	***Other ocular findings: bilateral 6th nerve palsy, conjugate gaze palsy, pupillary abnormality, retinal hemorrhage, ptosis		***Other ocular findings: bilateral 6th nerve palsy, conjugate gaze palsy, pupillary abnormality, retinal hemorrhage, ptosis
	***May progress to complete ophthalmoplegia		***May progress to complete ophthalmoplegia
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	***Legs affected more than arms (vestibular + cerebellar dysfunction)		***Legs affected more than arms (vestibular + cerebellar dysfunction)
	***Primarily affects gait; arms and speech usually spared		***Primarily affects gait; arms and speech usually spared
	**[[confusion\|~~'''C'''onfusion~~]]/memory impairment		**[[confusion\|Confusion]]/memory impairment
	***Delirium/encephalopathy is the ~~'''~~most consistent~~'''~~ clinical feature		***Delirium/encephalopathy is the most consistent clinical feature
	***May present as apathy, inattention, disorientation, or progress to coma		***May present as apathy, inattention, disorientation, or progress to coma
	*Other symptoms:		*Other symptoms:
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	*Confusion, disorientation, apathy		*Confusion, disorientation, apathy
	*Lack of insight into deficits		*Lack of insight into deficits
	*Largely ~~'''~~irreversible~~'''~~		*Largely irreversible

	==Differential Diagnosis==		==Differential Diagnosis==
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	**[[BMP]]— electrolytes, glucose, renal function, hepatic function		**[[BMP]]— electrolytes, glucose, renal function, hepatic function
	**[[CBC]]		**[[CBC]]
	**[[Magnesium]] level — ~~'''~~critical~~'''~~; hypomagnesemia causes resistance to thiamine therapy		**[[Magnesium]] level — critical; hypomagnesemia causes resistance to thiamine therapy
	**[[Lactate]] — may be elevated (thiamine is a cofactor for pyruvate dehydrogenase)		**[[Lactate]] — may be elevated (thiamine is a cofactor for pyruvate dehydrogenase)
	**Blood alcohol level		**Blood alcohol level
	**Serum thiamine level (whole blood thiamine preferred over serum/plasma):		**Serum thiamine level (whole blood thiamine preferred over serum/plasma):
	***Draw '''before''' administering thiamine if possible, but '''never delay treatment''' to obtain		***Draw '''before''' administering thiamine if possible, but '''never delay treatment''' to obtain
	***Normal range generally 70-180 nmol/L, but sensitivity and specificity are ~~'''~~poorly defined~~'''~~		***Normal range generally 70-180 nmol/L, but sensitivity and specificity are poorly defined
	***A normal thiamine level does ~~'''~~NOT~~'''~~ exclude WE<ref>Ono K, Hayano S, Kashima M. Wernicke encephalopathy: limitations in a laboratory and radiological diagnosis. BMJ Case Rep. 2023;16(12):e254786.</ref>		***A normal thiamine level does NOT exclude WE<ref>Ono K, Hayano S, Kashima M. Wernicke encephalopathy: limitations in a laboratory and radiological diagnosis. BMJ Case Rep. 2023;16(12):e254786.</ref>
	**Other labs as clinically indicated: [[TSH]], [[ammonia]], [[lipase]], toxicology screen, blood cultures		**Other labs as clinically indicated: [[TSH]], [[ammonia]], [[lipase]], toxicology screen, blood cultures
	*Consider [[lumbar puncture]] if [[meningitis]]/[[encephalitis]] suspected — CSF in WKS typically shows normal or mildly elevated protein without pleocytosis		*Consider [[lumbar puncture]] if [[meningitis]]/[[encephalitis]] suspected — CSF in WKS typically shows normal or mildly elevated protein without pleocytosis
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	*MRI brain (best imaging modality if obtained):		*MRI brain (best imaging modality if obtained):
	**Sensitivity ~53%, specificity ~93%, positive predictive value ~89%		**Sensitivity ~53%, specificity ~93%, positive predictive value ~89%
	***MRI is better at ~~'''~~confirming~~'''~~ the diagnosis than ~~'''~~ruling it out~~'''~~		***MRI is better at confirming the diagnosis than ruling it out
	***A '''normal MRI does NOT exclude WE''' — do not withhold treatment based on normal imaging		***A '''normal MRI does NOT exclude WE''' — do not withhold treatment based on normal imaging
	**Classic findings: bilateral, symmetric T2/FLAIR hyperintensities in:		**Classic findings: bilateral, symmetric T2/FLAIR hyperintensities in:
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	**Cerebellar dysfunction (ataxia)		**Cerebellar dysfunction (ataxia)
	**Altered mental status or mild memory impairment		**Altered mental status or mild memory impairment
	*Per EFNS guidelines, clinical diagnosis of WE in alcoholics requires ~~'''~~at least 2 of the following~~'''~~<ref>Galvin R, Bråthen G, Ivashynka A, et al. EFNS guidelines for diagnosis, therapy and prevention of Wernicke encephalopathy. Eur J Neurol. 2010;17(12):1408-18.</ref>:		*Per EFNS guidelines, clinical diagnosis of WE in alcoholics requires at least 2 of the following<ref>Galvin R, Bråthen G, Ivashynka A, et al. EFNS guidelines for diagnosis, therapy and prevention of Wernicke encephalopathy. Eur J Neurol. 2010;17(12):1408-18.</ref>:
	**Dietary deficiencies		**Dietary deficiencies
	**Ocular findings (ophthalmoplegia, nystagmus)		**Ocular findings (ophthalmoplegia, nystagmus)
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	===Acute Treatment===		===Acute Treatment===
	*[[Thiamine]] — ~~'''~~IV administration is critical; oral absorption is unreliable in at-risk patients~~'''~~		*[[Thiamine]] — IV administration is critical; oral absorption is unreliable in at-risk patients
	**Royal College of Physicians / UK guideline (widely adopted):		**Royal College of Physicians / UK guideline (widely adopted):
	***500 mg IV over 30 min TID x 2-3 days → then 250 mg IV/IM once daily x 3-5 days → then 100 mg PO daily until patient no longer at risk		***500 mg IV over 30 min TID x 2-3 days → then 250 mg IV/IM once daily x 3-5 days → then 100 mg PO daily until patient no longer at risk
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	===Treatment Response (Expected Timeline)===		===Treatment Response (Expected Timeline)===
	*Oculomotor dysfunction: often begins improving within ~~'''~~hours to days~~'''~~		*Oculomotor dysfunction: often begins improving within hours to days
	*Confusion/encephalopathy: may take ~~'''~~days to weeks~~'''~~		*Confusion/encephalopathy: may take days to weeks
	*Ataxia: ~~'''~~slowest to improve~~'''~~; may be permanent		*Ataxia: slowest to improve; may be permanent
	*Korsakoff psychosis: largely ~~'''~~irreversible~~'''~~ once established		*Korsakoff psychosis: largely irreversible once established

	===Common Pitfalls===		===Common Pitfalls===

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 | Confusing WE with cerebellar stroke || Both present with ophthalmoplegia, ataxia, AMS — always consider WE in differential
 |}
 ==Disposition==

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	===Pathophysiology===		===Pathophysiology===
	*Thiamine (vitamin B1) is a cofactor for enzymes critical to cerebral energy metabolism:		*Thiamine (vitamin B1) is a cofactor for enzymes critical to cerebral energy metabolism:
	**~~'''~~Energy production pathways~~'''~~: pyruvate dehydrogenase, alpha-ketoglutarate dehydrogenase, transketolase (Krebs cycle, pentose phosphate pathway)		**Energy production pathways: pyruvate dehydrogenase, alpha-ketoglutarate dehydrogenase, transketolase (Krebs cycle, pentose phosphate pathway)
	***Deficiency leads to impaired ATP production → [[lactic acidosis]], neuronal/astrocytic injury, and altered brain metabolism		***Deficiency leads to impaired ATP production → [[lactic acidosis]], neuronal/astrocytic injury, and altered brain metabolism
	***Brain regions with high metabolic demand are most vulnerable		***Brain regions with high metabolic demand are most vulnerable
	**~~'''~~Lipid metabolism~~'''~~ (including myelin sheath formation)		**Lipid metabolism (including myelin sheath formation)
	***Alterations in myelination leads to peripheral neuropathy		***Alterations in myelination leads to peripheral neuropathy
	*Thiamine half-life is only ~96 minutes; body stores are depleted within 2-3 weeks without intake		*Thiamine half-life is only ~96 minutes; body stores are depleted within 2-3 weeks without intake
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	===Causes===		===Causes===
	*Thiamine (vitamin B1) deficiency caused by:		*Thiamine (vitamin B1) deficiency caused by:
	**~~'''~~Insufficient intake~~'''~~		**Insufficient intake
	***Chronic [[alcoholism]] (most common cause in Western countries)		***Chronic [[alcoholism]] (most common cause in Western countries)
	***Starvation/[[anorexia]]/eating disorders		***Starvation/[[anorexia]]/eating disorders
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	***Unbalanced or thiamine-deficient TPN		***Unbalanced or thiamine-deficient TPN
	***Self-imposed dietary restriction		***Self-imposed dietary restriction
	**~~'''~~Malabsorption~~'''~~		**Malabsorption
	***Post-bariatric surgery (especially Roux-en-Y gastric bypass)		***Post-bariatric surgery (especially Roux-en-Y gastric bypass)
	***Post-gastrectomy		***Post-gastrectomy
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	***[[Pancreatitis]]		***[[Pancreatitis]]
	***Intestinal obstruction		***Intestinal obstruction
	**~~'''~~Increased metabolic requirements~~'''~~		**Increased metabolic requirements
	***Malignancy/cancer chemotherapy		***Malignancy/cancer chemotherapy
	***[[Thyrotoxicosis]]		***[[Thyrotoxicosis]]
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	***Refeeding syndrome		***Refeeding syndrome
	***Carbohydrate loading (iatrogenic — can unmask subclinical deficiency)		***Carbohydrate loading (iatrogenic — can unmask subclinical deficiency)
	**~~'''~~Thiamine losses~~'''~~		**Thiamine losses
	***[[Hemodialysis]]/peritoneal dialysis		***[[Hemodialysis]]/peritoneal dialysis
	**~~'''~~Miscellaneous~~'''~~: [[AIDS]], chronic liver disease, prolonged ICU admission, magnesium depletion (magnesium is a cofactor for thiamine-dependent enzymes)		**Miscellaneous: [[AIDS]], chronic liver disease, prolonged ICU admission, magnesium depletion (magnesium is a cofactor for thiamine-dependent enzymes)
	{{Thiamine deficiency types}}		{{Thiamine deficiency types}}

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	===Wernicke's Encephalopathy===		===Wernicke's Encephalopathy===
	*Classic triad: [[encephalopathy]], oculomotor dysfunction, gait [[ataxia]]		*Classic triad: [[encephalopathy]], oculomotor dysfunction, gait [[ataxia]]
	**~~'''~~Classic triad present in only ~10% of cases~~'''~~ — do NOT rely on complete triad to make diagnosis		**Classic triad present in only ~10% of cases — do NOT rely on complete triad to make diagnosis
	*wer'''NIC'''ke mnemonic:		*wer'''NIC'''ke mnemonic:
	**[[nystagmus\|'''N'''ystagmus]]/ophthalmoplegia		**[[nystagmus\|'''N'''ystagmus]]/ophthalmoplegia
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	***Other ocular findings: bilateral 6th nerve palsy, conjugate gaze palsy, pupillary abnormality, retinal hemorrhage, ptosis		***Other ocular findings: bilateral 6th nerve palsy, conjugate gaze palsy, pupillary abnormality, retinal hemorrhage, ptosis
	***May progress to complete ophthalmoplegia		***May progress to complete ophthalmoplegia
	**~~'''I'''ncoordination~~/[[ataxia]]		**Incoordination/[[ataxia]]
	***Legs affected more than arms (vestibular + cerebellar dysfunction)		***Legs affected more than arms (vestibular + cerebellar dysfunction)
	***Primarily affects gait; arms and speech usually spared		***Primarily affects gait; arms and speech usually spared
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	===Imaging===		===Imaging===
	*~~'''~~CT head~~'''~~: sensitivity only ~13% for WE; primary role is to exclude other pathology (hemorrhage, mass, infarct)<ref>Medscape. Wernicke Encephalopathy Workup. Available at: https://emedicine.medscape.com/article/794583-workup</ref>		*CT head: sensitivity only ~13% for WE; primary role is to exclude other pathology (hemorrhage, mass, infarct)<ref>Medscape. Wernicke Encephalopathy Workup. Available at: https://emedicine.medscape.com/article/794583-workup</ref>
	*~~'''~~MRI brain~~'''~~ (best imaging modality if obtained):		*MRI brain (best imaging modality if obtained):
	**Sensitivity ~53%, specificity ~93%, positive predictive value ~89%		**Sensitivity ~53%, specificity ~93%, positive predictive value ~89%
	***MRI is better at '''confirming''' the diagnosis than '''ruling it out'''		***MRI is better at '''confirming''' the diagnosis than '''ruling it out'''
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	===Diagnosis===		===Diagnosis===
	*~~'''~~Clinical diagnosis~~'''~~ — maintain high index of suspicion		*Clinical diagnosis — maintain high index of suspicion
	*~~'''~~Caine criteria~~'''~~ (operational diagnostic criteria; ~85% sensitive when ≥2 present)<ref>Caine D, Halliday GM, Kril JJ, Harper CG. Operational criteria for the classification of chronic alcoholics: identification of Wernicke's encephalopathy. J Neurol Neurosurg Psychiatry. 1997;62(1):51-60.</ref>:		*Caine criteria (operational diagnostic criteria; ~85% sensitive when ≥2 present)<ref>Caine D, Halliday GM, Kril JJ, Harper CG. Operational criteria for the classification of chronic alcoholics: identification of Wernicke's encephalopathy. J Neurol Neurosurg Psychiatry. 1997;62(1):51-60.</ref>:
	**Nutritional deficiency (any state, not just alcoholism)		**Nutritional deficiency (any state, not just alcoholism)
	**Ocular findings (ophthalmoplegia, nystagmus)		**Ocular findings (ophthalmoplegia, nystagmus)
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	===Acute Treatment===		===Acute Treatment===
	*~~'''~~[[Thiamine]]~~'''~~ — '''IV administration is critical; oral absorption is unreliable in at-risk patients'''		*[[Thiamine]] — '''IV administration is critical; oral absorption is unreliable in at-risk patients'''
	**Royal College of Physicians / UK guideline (widely adopted):		**Royal College of Physicians / UK guideline (widely adopted):
	***~~'''~~500 mg IV over 30 min TID x 2-3 days~~'''~~ → then 250 mg IV/IM once daily x 3-5 days → then 100 mg PO daily until patient no longer at risk		***500 mg IV over 30 min TID x 2-3 days → then 250 mg IV/IM once daily x 3-5 days → then 100 mg PO daily until patient no longer at risk
	**EFNS guideline:		**EFNS guideline:
	***200 mg IV TID (diluted in 100 mL NS or D5W, infused over 30 min)		***200 mg IV TID (diluted in 100 mL NS or D5W, infused over 30 min)
	**~~'''~~100 mg/day (e.g., banana bag dose) is likely insufficient~~'''~~ — especially in patients with alcohol use disorder		**100 mg/day (e.g., banana bag dose) is likely insufficient — especially in patients with alcohol use disorder
	**Thiamine has a short half-life (~96 min); multiple daily doses are more effective than once-daily dosing		**Thiamine has a short half-life (~96 min); multiple daily doses are more effective than once-daily dosing
	**Overall safety of thiamine is very good; anaphylaxis risk with IV thiamine is rare		**Overall safety of thiamine is very good; anaphylaxis risk with IV thiamine is rare

	===Key Principles===		===Key Principles===
	*~~'''~~Give thiamine BEFORE glucose~~'''~~ in any at-risk patient requiring dextrose		*Give thiamine BEFORE glucose in any at-risk patient requiring dextrose
	**Glucose without thiamine can precipitate or worsen WE by driving remaining thiamine intracellularly		**Glucose without thiamine can precipitate or worsen WE by driving remaining thiamine intracellularly
	**If both are urgently needed (e.g., symptomatic hypoglycemia), give them simultaneously — do not withhold glucose to wait for thiamine		**If both are urgently needed (e.g., symptomatic hypoglycemia), give them simultaneously — do not withhold glucose to wait for thiamine
	*~~'''~~Give [[magnesium]]~~'''~~		*Give [[magnesium]]
	**Magnesium is a cofactor for thiamine-dependent enzymes		**Magnesium is a cofactor for thiamine-dependent enzymes
	**Hypomagnesemia may cause resistance to thiamine therapy		**Hypomagnesemia may cause resistance to thiamine therapy
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	==Disposition==		==Disposition==
	*~~'''~~Admit~~'''~~ (inpatient medicine or neurology service)		*Admit (inpatient medicine or neurology service)
	**Ensures continued IV thiamine and magnesium administration		**Ensures continued IV thiamine and magnesium administration
	**Observation for development of Korsakoff syndrome		**Observation for development of Korsakoff syndrome

Ostermayer at 17:20, 16 March 2026

2026-03-16T17:20:10Z

Show changes

Rossdonaldson1: /* Video */

2024-04-17T20:13:41Z

Video

← Older revision		Revision as of 20:13, 17 April 2024
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	==See Also==		==See Also==
	{{Ethanol DDX}}		{{Ethanol DDX}}

	~~==Video==~~
	~~{{#widget:YouTube\|id=6MhVkxiZdck}}~~

	==References==		==References==

Rossdonaldson1: /* Evaluation */

2023-10-18T22:46:52Z

Evaluation

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	==Evaluation==		==Evaluation==
	[[File:MRI FLAIR sequence Wernicke Encephalopathy.jpg\|thumb\|Axial MRI FLAIR image showing hyperintense signal in the mesial dorsal thalami, a common finding in Wernicke encephalopathy		[[File:MRI FLAIR sequence Wernicke Encephalopathy.jpg\|thumb\|Axial MRI FLAIR image showing hyperintense signal in the mesial dorsal thalami, a common finding in Wernicke encephalopathy]]
	===Workup===		===Workup===

Rossdonaldson1: /* Evaluation */

2023-10-18T22:45:52Z

Evaluation

← Older revision		Revision as of 22:45, 18 October 2023
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	==Evaluation==		==Evaluation==
			[[File:MRI FLAIR sequence Wernicke Encephalopathy.jpg\|thumb\|Axial MRI FLAIR image showing hyperintense signal in the mesial dorsal thalami, a common finding in Wernicke encephalopathy
	===Workup===		===Workup===

Elcatracho: /* Causes */

2021-02-23T19:31:26Z

Causes

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	===Causes===		===Causes===
	*Thiamine (vitamin B1) deficiency caused by		*Thiamine (vitamin B1) deficiency caused by
	**Insufficient intake (e.g. chronic alcoholism, starvation/anorexia, severe vomiting/diarrhea, unbalanced TPN)		**Insufficient intake (e.g. chronic [[alcoholism]], starvation/[[anorexia]], severe [[vomiting]]/[[diarrhea]], unbalanced TPN)
	**Malabsorption (post-gastrectomy, [[IBD]], [[pancreatitis]]		**Malabsorption (post-gastrectomy, [[IBD]], [[pancreatitis]])
	**Increased metabolic requirements (malignancy, [[thyrotoxicosis]])		**Increased metabolic requirements (malignancy, [[thyrotoxicosis]])
	**Thiamine losses ([[hemodialysis]])		**Thiamine losses ([[hemodialysis]])

Rossdonaldson1: /* Background */

2020-10-27T21:12:25Z

Background

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	**Thiamine losses ([[hemodialysis]])		**Thiamine losses ([[hemodialysis]])
	**Miscellaneous: [[AIDS]], liver disease		**Miscellaneous: [[AIDS]], liver disease

			{{Thiamine deficiency types}}

	==Clinical Features==		==Clinical Features==

Rossdonaldson1: /* Evaluation */

2019-11-16T11:58:03Z

Evaluation

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	==Evaluation==		==Evaluation==
			===Workup===

			===Diagnosis===
	*Clinical diagnosis		*Clinical diagnosis
	*Wernicke's Encephalopathy - at least 2 of the following:<ref>Isenberg-Grzeda E, Kutner HE, Nicolson SE. Wernicke-Korsakoff-syndrome: under-recognized and under-treated. Psychosomatics. 2012 Nov-Dec;53(6):507-16.</ref>:		*Wernicke's Encephalopathy - at least 2 of the following:<ref>Isenberg-Grzeda E, Kutner HE, Nicolson SE. Wernicke-Korsakoff-syndrome: under-recognized and under-treated. Psychosomatics. 2012 Nov-Dec;53(6):507-16.</ref>: