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Wernicke’s encephalopathy


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Wernicke’s encephalopathy

  1. 1. 1 Wernicke’s Encephalopathy AMITESHWAR SINGH INTERN, KMC MANIPAL.
  2. 2. 2 Dr Carl Wernicke A Polish neurologist, who described this neuropsychiatric syndrome in 1881 as a triad of acute mental confusion, ataxia, and ophthalmoplegia.
  3. 3. Etiopathogenesis 3  Deficiency of vitamin B1 (thiamine)  An essential coenzyme in several biochemical pathways in the brain,  Krebs cycle and the pentose phosphate pathway  α-ketoglutarate dehydrogenase, pyruvate dehydrogenase, and transketolase.  Mainly involved in the glucose metabolism and cerebral energy utilization
  4. 4. 4 THIAMINE DEFICIENCY Failure of thiamine-dependent cellular systems Inhibition of metabolism in brain regions with higher metabolic demands and high thiamine turnover. Energy production drops, and neuronal damage ensues BRAIN TISSUE INJURY Reduced production of succinate Failure of GABA metabolism
  5. 5. Causes  Chronic alcoholism – Malnutrition – reduced thiamine uptake and utilization  Prolonged starvation  Hyperemesis Gravidarum  Bariatric Surgery (Bariatric BeriBeri)  Malabsorption Syndromes  Infants on formula diet deficient in thiamine 5
  6. 6. Epidemiology  The 6 incidence can be as high as 12.5% in a population of alcoholics.  The prevalence approximately 2%.  The male-to-female ratio is 1.7 : 1  Average age at onset is 50 years.
  7. 7. History  The classical triad of symptoms – only 1/3rd of cases  Evidence of long-term alcohol abuse or malnutrition  Other symptoms could include memory disturbance, hypothermia with hypotension, and delirium tremens.  Special clinical scenarios as previously mentioned 7
  8. 8. Physical examination 8  Ocular abnormalities – nystagmus , bilateral lateral rectus palsies, conjugate gaze palsies, sluggish pupils, ptosis, and anisocoria  Encephalopathy – global confusional state, disinterest, inattentiveness, or agitation; Coma is rare.  Gait ataxia – cerebellar damage, and vestibular paresis  Peripheral neuropathy – foot drop, and decreased proprioception
  9. 9. Differential Diagnosis  Psychosis  Normal pressure hydrocephalus  Cerebrovascular accident  Chronic hypoxia  Closed-head injury  Hepatic encephalopathy  Postictal state 9
  10. 10. Work-Up 10  CBC – R/o severe anemias and leukemias as causes of altered mental status  Blood glucose levels hypoglycemia/ hyperglycemia  O2 Saturation and ABG - Exclude hypoxia/ hypercarbia; Metabolic Acidosis may be+  Toxic drug screening - Excludes some causes of drug-induced altered mental status.  Lumbar puncture (LP) infections, if indicated - Exclude Exclude CNS
  11. 11. 11  CT/MRI – exclude ICSOLs etc.  No particular Changes in acute presentation  Chronic encephalopathy - excessive mamillary body and cerebellar shrinkage  Erythrocyte transketolase activity assay, Thiamine assay – very specific tests – not widely available – reserved for diagnostic dilemmas
  12. 12. Treatment 12  Emergency department care – Parenteral thiamine – Requirement in chronic alcoholics may be as high as 500mg single dose or multiple daily doses.  Never start on Dextrose  Parenteral magnesium sulfate as thiamine therapy ineffective in presence of hypomagnesemia  In-Patient care – Watch for complications – Korsakoff psychosis – Alcohol withdrawal – Congestive heart failure – Lactic acidosis  Out-Patient Care – Thiamine 100 mg PO daily, start alcohol cessation program, Advise on importance of balanced diet.
  13. 13. Wernicke-Korsakoff Syndrome 13  85% of the survivors of the acute phase of Wernicke encephalopathy who remain untreated go on to develop WernickeKorsakoff syndrome.  It manifests with confabulation.  About 20% eventually recover completely during long-term follow-up care. memory loss and
  14. 14. Conclusion 14  Wernicke encephalopathy must be considered as a medical emergency, as it is associated with significant morbidity and mortality.  Because the condition is potentially reversible, early diagnosis is important.  The diagnosis is clinical and is mainly supported by the dramatic improvement of neurological signs on parenteral thiamine therapy.