Wernicke Syndrome

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Wernicke syndrome is an acute/chronic ?

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acute

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neurological /psychiatric ?

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neuropsych

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classic triad of

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ophthalmoplegia, ataxia, and disturbances of mental activity or consciousness

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due to a deficiency of

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thiamine

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deficiency of thiamine often associated with.

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chronic alcoholism

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Genetics• Biochemical studies in 111111 from patients with WE show 22222-dependent enzyme, 333333, to have a decreased affinity for 444444.

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1 fibroblasts

2 thiamine

3 transketolase

4 thiamine pyrophosphate

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Thiamine deficiency causes wet 1111 beriberi more commonly in the Asian population and dry beriberi 2222 in the European population.

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1 (cardiovascular)

2 (polyneuropathy and WE)

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Risk Factors

#1

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Alcohol abuse/misuse•

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Diet○

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Malnutrition/unbalanced nutrition/infant formulas○ Intravenous hyperalimentation without thiamine supplementation○

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xxxx depletion–cofactor required by enzymes: transketolase and thiamine pyrophosphokinase

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Magnesium

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• Gastrointestinal disorders including recurrent vomiting or chronic diarrhea such as 1111

• Gastrointestinal surgical procedures (gastrointestinal resection) that cause malabsorption secondary to reduced surface area of gastric and duodenal mucosa such as xxxx•

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1hyperemesis gravidarum

x bariatric surgery

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Systemic cancers○ Most common underlying disorder onset for WE in xxxx

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Children

Consumption of thiamine by fast-growing neoplastic cells•

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Chemical compounds/drugs or chemotherapeutic treatments

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no example

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Systemic diseases

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○ Peritoneal or hemodialysis

○ Hypermetabolic states

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Thyroid dysfunction?

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Thyrotoxicosis

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Infections

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1 HIV/AIDS

2 Prolonged infectious febrile disease

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Etiology• The biologically active form of vitamin B 1 , thiamine pyrophosphate (TP), a coenzyme for several important biochemical pathways involved in (3 pathways)

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1 energy production,

2 lipid metabolism,

3 production of amino acids and glucose-derived neurotransmitters.

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• Body’s reserve for thiamine is sufficient for xx days.

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18

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• Malnutrition for xxx or a diet disproportionately high in carbohydrates and low in thiamine intake can lead to an impaired function of enzymes requiring TP.

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2 to 3 wk

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Differential Diagnosis

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Syndrome/Clinical Setting

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Administration of intravenous glucose to a thiamine-deficient alcoholic patient

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Wernicke-Korsakoff syndrome

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Intractable vomiting due to hyperemesis gravidarum or gastroplasty

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Wernicke-Korsakoff syndrome

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Intractable vomiting and severe weight loss in patients following weight reduction surgical procedures

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Postgastroplasty neuropathy

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Nitrous oxide administration in cobalamin-deficient patients

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Vitamin B 12 myeloneuropathy

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Sudden change in tissue osmolarity in critically ill patients or alcoholics

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Central pontine myelinolysis

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Thalamus

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Paramedian thalamic infarction

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Encephalitis (3 types)

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Ventriculoencephalitis, paraneoplastic encephalitis, herpes simplex encephalitis

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Ophthalmoplegia

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Miller-Fisher syndrome

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Lymphoma

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Primary cerebral lymphoma

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Demyelinating lesions

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Multiple sclerosis,

Behcet’s disease,

Leigh’s disease

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Virion

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Variant Creutzfeldt-Jakob disease

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Workup• WE is a xxx diagnosis based on the triad of features listed above.

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clinical

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Laboratory Tests

• Blood xxx concentration.

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thiamine

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• Functional measurement of erythrocyte thiamine transketolase (ETKA) before and after administration of parenteral thiamine. A diagnosis may be confirmed if

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ETKA is low followed by a 25% increase after thiamine supplementation.

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xxxx for assessment of thiamine, thiamine mono- and di-phosphate in human erythrocytes.

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High-performance liquid chromatography

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Serum xxxx concentration (depletion of magnesium may mimic features of WE).

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magnesium

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Imaging StudiesMRI of brain may show bilaterally symmetric increase in xxx signal at the paraventricular regions of the thalamus and mammillary bodies.

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T2

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Other areas include xxxx, periaqueductal region, floor of the fourth ventricle, and midline xxxx.

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hypothalamus

cerebellum

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Treatment Acute General Rx• Treatment should be initiated in all patients with clinical suspicion of WE. Thiamine supplementation should precede xxxx administration in all patients at risk for WE.

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glucose

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Alcoholics with WE: treat with 1111 of thiamine hydrochloride (dissolved in 100 ml of 4444) infused intravenously over 2222 min, 3 times daily for 33333 days.

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1 500 mg of thiamine hydrochloride (dissolved in 100 ml of normal saline)

2 infused intravenously over 30 min, 3 times daily for

3 2 to 3 days.

4 normal saline

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• If a response is observed, continue with 111 of thiamine hydrochloride intravenously or intramuscularly daily until clinical improvement ceases.

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1 250 mg

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• Nonalcoholics with WE: treat with xxxx mg of thiamine hydrochloride (dissolved in 100 ml of normal saline) infused intravenously over 30 min, 3 times daily for 2 to 3 days.

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200

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• Parenteral side effects may include (3)

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1 generalized pruritus,

2 transient local irritation, or

3 rarely, anaphylactic or anaphylactoid reactions.

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Parenteral xxx must be infused concurrently with thiamine.

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Magnesium

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Chronic RxRecommended oral dose after treatment for WE: thiamine xxx twice daily

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30 to 100 mg

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Disposition• If not treatmented with thiamine is not administered during reversible stages of WE, xxx may develop

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Korsakoff’s syndrome

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Korsakoff’s syndrome

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memory loss emerging after the acute global confusional state of WE

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• Approximately xxx% who survive WE develop Korsakoff’s syndrome.

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80

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Prevention• Prophylactic treatment for patient with severe alcohol withdrawal, poor nourishment, or signs of malnutrition: thiamine xxxx mg intramuscular daily for 3 to 5 days.

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250

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• In individuals susceptible to WE, xxx mg of intravenous thiamine should precede any glucose infusion.

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100

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• Recommended daily dose of thiamine for an average, healthy adult: xxx mg or yy mg per 1000 kcal of carbohydrates consumed.

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x 1.4

y 0.5

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Higher dose recommended for

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1 children,

2 critically ill conditions

3 pregnancy

4 lactation.