Wernicke's encephalopathy

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:

Wernicke encephalopathy
Thiamine-2D-skeletal.png
Thiamine
ICD-10 E51.2
ICD-9 265.1
eMedicine emerg/642 

Overview

Wernicke encephalopathy is a severe syndrome characterised by ataxia, ophthalmoplegia, confusion and loss of short-term memory.[1][2] It is linked to damage to the medial thalamic nuclei, mammillary bodies, periaqueductal, and periventricular brainstem nuclei , and superior cerebellar vermis. In the brain, it is the result of inadequate intake or absorption of thiamine (Vitamin B)[1] coupled with continued carbohydrate ingestion.[1] The most common cause of an onset is prolonged alcohol consumption that is sufficient enough to cause a thiamine deficiency. Alcoholics are therefore particularly at risk, but it may also occur due to other causes of malnutrition. Other causes of thiamine deficiency may be found in patients with carcinoma, chronic gastritis, or continuous vomiting.[3][4]

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Wernicke's encephalopathy from Other Diseases

Wernicke's encephalopathy must be differentiated from other causes of headache, altered mental status and seizures such as brain tumors and delirium trmemns.

Diseases Diagnostic tests Physical Examination Symptoms Past medical history Other Findings
Na+, K+, Ca2+ CT /MRI CSF Findings Gold standard test Neck stiffness Motor or Sensory deficit Papilledema Bulging fontanelle Cranial nerves Headache Fever Altered mental status
Brain tumour[5][6] ? Cancer cells[7] MRI ? ? ?  ? ? ? Cachexia, gradual progression of symptoms
Delerium Tremens ? Clinical diagnosis ? ?  ?  ? ? ? Alcohal intake, sudden witdrawl or reduction in consumption Tachycardia, diaphoresis, hypertension, tremors, mydriasis, positional nystagmus, tachypnea
Subarachnoid hemorrhage[8] ? Xanthochromia[9] CT scan without contrast[10][11] ? ? ? ?  ? ? ? ? Trauma/fall Confusion, dizziness, nausea, vomiting
Stroke ? Normal CT scan without contrast ? ? ? ? ? TIAs, hypertension, diabetes mellitus Speech difficulty, gait abnormality
Neurosyphilis[12][13] ? ? Leukocytes and protein CSF VDRL-specifc

CSF FTA-Ab -sensitive[14]

? ? ? ? ? ? Unprotected sexual intercourse, STIs Blindness, confusion, depression,

Abnormal gait

Viral encephalitis ? Increased RBCS or xanthochromia, mononuclear lymphocytosis, high protein content, normal glucose Clinical assesment ? ? ?  ? ? ? ? Tick bite/mosquito bite/ viral prodome for several days Extreme lethargy, rash hepatosplenomegaly, lymphadenopathy, behavioural changes
Herpes simplex encephalitis ? Clinical assesment ? ? ? ? ? History of hypertension Delirium, cortical blindness, cerebral edema, seizure
Wernicke’s encephalopathy Normal ? ? ? History of alcohal abuse Ophthalmoplegia, confusion
CNS abscess ? ? leukocytes >100,000/ul, ? glucose and ? protien, ? red blood cells, lactic acid >500mg Contrast enhanced MRI is more sensitive and specific,

Histopathological examination of brain tissue

? ? ? ? ? ? ? History of drug abuse, endocarditis, ? immune status High grade fever, fatigue,nausea, vomiting
Drug toxicity ? ? Lithium, Sedatives, phenytoin, carbamazepine
Conversion disorder Diagnosis of exclusion ? ?  ? ? ? Tremors, blindness, difficulty swallowing
Electrolyte disturbance ? or ? Depends on the cause ? ? Confusion, seizures
Febrile seizures Not performed in first simple febrile seizures Clinical diagnosis and EEG  ? ? ? ? Family history of febrile seizures, viral illness or gastroenteritis Age > 1 month,
Subdural empyema ? Clinical assesment and MRI ? ? ? ? ? ? History of relapses and remissions Blurry vision, urinary incontinence, fatigue
Hypoglycemia ? or ? Serum blood glucose

HbA1c

?  ? ? History of diabetes Palpitations, sweating, dizziness, low serum, glucose

Wernicke's encephalopathy must be differentiated from other causes of headache,seizures and loss of consciousness.

Diseases Symptoms Physical Examination Past medical history Diagnostic tests Other Findings
Headache LOC Motor weakness Abnormal sensory Motor Deficit Sensory deficit Speech difficulty Gait abnormality Cranial nerves CT /MRI CSF Findings Gold standard test
Meningitis + - - - - + + - - History of fever and malaise - Leukocytes,

Protein

↓ Glucose

CSF analysis[15] Fever, neck

rigidity

Encephalitis + + +/- +/- - - + +/- + History of fever and malaise + Leukocytes, ↓ Glucose CSF PCR Fever, seizures, focal neurologic abnormalities
Brain tumor[16] + - - - + + + - + Weight loss, fatigue + Cancer cells[7] MRI Cachexia, gradual progression of symptoms
Hemorrhagic stroke + + + + + + + + - Hypertension + - CT scan without contrast[10][11] Neck stiffness
Subdural hemorrhage + + + + + - - - + Trauma, fall + Xanthochromia[9] CT scan without contrast[10][11] Confusion, dizziness, nausea, vomiting
Neurosyphilis[12][13] + - + + + + - + - STIs + Leukocytes and protein CSF VDRL-specifc

CSF FTA-Ab -sensitive[14]

Blindness, confusion, depression,

Abnormal gait

Complex or atypical migraine + - + + - - + - - Family history of migraine - - Clinical assesment Presence of aura, nausea, vomiting
Hypertensive encephalopathy + + - - - - + + - Hypertension + - Clinical assesment Delirium, cortical blindness, cerebral edema, seizure
Wernicke’s encephalopathy - + - - - + + + + History of alcohal abuse - - Clinical assesment and lab findings Ophthalmoplegia, confusion
CNS abscess + + - - + + + - - History of drug abuse, endocarditis, immunosupression + leukocytes, glucose and protien MRI is more sensitive and specific High grade fever, fatigue,nausea, vomiting
Drug toxicity - + - + + + - + - - - - Drug screen test Lithium, Sedatives, phenytoin, carbamazepine
Conversion disorder + + + + + + + + History of emotional stress - - Diagnosis of exclusion Tremors, blindness, difficulty swallowing
Metabolic disturbances (electrolyte imbalance, hypoglycemia) - + + + + + - - + - - Hypoglycemia, hypo and hypernatremia, hypo and hyperkalemia Depends on the cause Confusion, seizure, palpitations, sweating, dizziness, hypoglycemia
Multiple sclerosis exacerbation - - + + - + + + + History of relapses and remissions + CSF IgG levels

(monoclonal bands)

Clinical assesment and MRI [17] Blurry vision, urinary incontinence, fatigue
Seizure + + - - + + - - + Previous history of seizures - Mass lesion Clinical assesment and EEG [18] Confusion, apathy, irritability,

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications, and Prognosis

Natural History

Complications

Prognosis

Diagnosis

Diagnostic Criteria

History and Symptoms

Physical Examination

Wernicke encephalopathy onsets acutely, and usually presents with nystagmus, gaze palsies, ophthalmoplegia (especially of the abducens nerve, CN VI), gait ataxia, confusion, and short-term memory loss.

The classic triad for this disease is encephalopathy, ophthalmoplegia, and ataxia. Untreated, this condition may progress to Korsakoff's psychosis or coma.[1][2] Despite its name, Wernicke's encephalopathy is not related to damage of the speech and language interpretation area named Wernicke's area (see Wernicke's aphasia). Instead the pathological changes in Wernicke's encephalopathy are concentrated in the mammillary bodies, cranial nerve nuclei III, IV, VI and VIII, as well as the thalamus, hypothalamus, periaquiductal grey, cerebellar vermis and the dorsal nucleus of the vagus nerve. The ataxia and ophthalmoparesis relate to lesions in the oculomotor (ie IIIrd, IVth, and VIth nerves) and vestibular (ie VIIIth nerve) nuclei.

Laboratory Findings

Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Treatment includes an intravenous (IV) or intramuscular (IM) injection of thiamine, prior to the assessment of other central nervous system (CNS) diseases or other metabolic disturbances. Patients are usually dehydrated, and so rehydration to restore blood volume should be started. If the condition is treated early, recovery may be rapid and complete.

In individuals with sub-clinical thiamine deficiency, a large dose of glucose (either as sweet food etc or glucose infusion), can precipitate the onset of overt encephalopathy. Glucose loading results in metabolic disturbances in the brain that exacerbate the signs and symptoms of encephalopathy, and may trigger cellular processes leading to brain damage. [19]. If the patient is hypoglycemic (common in alcoholism), a thiamin injection should always precede the glucose infusion.

Surgery

Prevention

See also

External links

References

  1. 1.0 1.1 1.2 1.3 Aminoff, Michael J, Greenberg, David A., Simon, Roger P. (2005) Clinical Neurology (6th ed.). page 113 Lange Medical Books/McGraw-Hill. ISBN 0-07-142360-5
  2. 2.0 2.1 Beers, Mark H. et al (2006), The Merck Manual of Diagnosis and Therapy (18th ed.), pages 1688-1689, Merk Research Laboratories 2006, ISBN 0911910-18-2
  3. Kumar, Vinay, Abbas, Abul K., Fausto, Nelson (2005), Pathologic Basis of Disease (7th ed.), page 1399, Elsevier Saunders. ISBN 0-8089-2302-1
  4. Sullivan, Joseph; Hamilton, Roy; Hurford, Matthew; Galetta, Steven L; Liu Grant T (2006), "Neuro-Opthalmic Findings in Wernicke's Encephalopathy after Gastric Bypass Surgery", Neuro-Ophthalmology, Jul/Aug2006, Vol. 30 Issue 4, p85-89
  5. Soffer D (1976) Brain tumors simulating purulent meningitis. Eur Neurol 14 (3):192-7. PMID: 1278192
  6. 7.0 7.1 Weston CL, Glantz MJ, Connor JR (2011). "Detection of cancer cells in the cerebrospinal fluid: current methods and future directions.". Fluids Barriers CNS. 8 (1): 14. PMC 3059292Freely accessible. PMID 21371327. doi:10.1186/2045-8118-8-14. 
  7. Yeh ST, Lee WJ, Lin HJ, Chen CY, Te AL, Lin HJ (2003) Nonaneurysmal subarachnoid hemorrhage secondary to tuberculous meningitis: report of two cases. J Emerg Med 25 (3):265-70. PMID: 14585453
  8. 9.0 9.1 Lee MC, Heaney LM, Jacobson RL, Klassen AC (1975). "Cerebrospinal fluid in cerebral hemorrhage and infarction.". Stroke. 6 (6): 638–41. PMID 1198628. 
  9. 10.0 10.1 10.2 Birenbaum D, Bancroft LW, Felsberg GJ (2011). "Imaging in acute stroke.". West J Emerg Med. 12 (1): 67–76. PMC 3088377Freely accessible. PMID 21694755. 
  10. 11.0 11.1 11.2 DeLaPaz RL, Wippold FJ, Cornelius RS, Amin-Hanjani S, Angtuaco EJ, Broderick DF; et al. (2011). "ACR Appropriateness Criteria® on cerebrovascular disease.". J Am Coll Radiol. 8 (8): 532–8. PMID 21807345. doi:10.1016/j.jacr.2011.05.010. 
  11. 12.0 12.1 Liu LL, Zheng WH, Tong ML, Liu GL, Zhang HL, Fu ZG; et al. (2012). "Ischemic stroke as a primary symptom of neurosyphilis among HIV-negative emergency patients.". J Neurol Sci. 317 (1-2): 35–9. PMID 22482824. doi:10.1016/j.jns.2012.03.003. 
  12. 13.0 13.1 Berger JR, Dean D (2014). "Neurosyphilis". Handb Clin Neurol. 121: 1461–72. PMID 24365430. doi:10.1016/B978-0-7020-4088-7.00098-5. 
  13. 14.0 14.1 Ho EL, Marra CM (2012). "Treponemal tests for neurosyphilis--less accurate than what we thought?". Sex Transm Dis. 39 (4): 298–9. PMC 3746559Freely accessible. PMID 22421697. doi:10.1097/OLQ.0b013e31824ee574. 
  14. Carbonnelle E (2009). "[Laboratory diagnosis of bacterial meningitis: usefulness of various tests for the determination of the etiological agent].". Med Mal Infect. 39 (7-8): 581–605. PMID 19398286. doi:10.1016/j.medmal.2009.02.017. 
  15. Morgenstern LB, Frankowski RF (1999). "Brain tumor masquerading as stroke.". J Neurooncol. 44 (1): 47–52. PMID 10582668. 
  16. Giang DW, Grow VM, Mooney C, Mushlin AI, Goodman AD, Mattson DH; et al. (1994). "Clinical diagnosis of multiple sclerosis. The impact of magnetic resonance imaging and ancillary testing. Rochester-Toronto Magnetic Resonance Study Group.". Arch Neurol. 51 (1): 61–6. PMID 8274111. 
  17. Manford M (2001). "Assessment and investigation of possible epileptic seizures.". J Neurol Neurosurg Psychiatry. 70 Suppl 2: II3–8. PMC 1765557Freely accessible. PMID 11385043. 
  18. Zimitat C, Nixon P, (2000). "Glucose loading precipitates encephalopathy in thiamine-deficient rats.". Metabolic Brain Disease. 14 (1): 1–10. 
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