# Wernicke's encephalopathy is attributed to:
A. Severe riboflavin deficiency
B. Severe thiamine deficiency
C. Excessive blood alcohol content
D. Excessive GGT levels
The correct answer is B. Severe thiamine deficiency.
Pathophysiology and Mechanism
Wernicke's encephalopathy (WE) is an acute, life-threatening neurological condition caused specifically by a deficiency in Thiamine (Vitamin B1).
Metabolic Role: Thiamine, in its active form thiamine pyrophosphate (TPP), is a crucial cofactor for several enzymes in the Krebs cycle and the pentose phosphate pathway, including:
Neuronal Injury: Deficiency leads to an inability to metabolize glucose, causing a decrease in ATP production and an accumulation of glutamate. This results in excitotoxicity, oxidative stress, and eventual neuronal cell death.
Targeted Areas: The lesions classically affect areas of high metabolic requirement, specifically the mammillary bodies, the dorsomedial thalamus, the locus coeruleus, the periaqueductal gray, and the ocular motor nuclei.
Why the other options are incorrect
A. Severe riboflavin deficiency (Vitamin B2): This typically presents with ariboflavinosis, characterized by cheilosis, angular stomatitis (relevant to dentistry), glossitis, and seborrheic dermatitis, not the acute neurological signs of WE.
C. Excessive blood alcohol content: While chronic alcohol abuse is the leading cause of thiamine deficiency (due to poor diet, impaired absorption, and reduced hepatic storage), alcohol itself does not directly trigger the specific neuropathology of WE. WE can occur in non-alcoholic contexts, such as hyperemesis gravidarum, starvation, or prolonged parenteral nutrition without supplementation. Therefore, the attribution of the disease is the vitamin deficiency, not the alcohol.
D. Excessive GGT levels: Gamma-glutamyl transferase (GGT) is a liver enzyme used as a marker of hepatobiliary disease and chronic alcohol consumption. It is a diagnostic marker, not a pathogenic cause of encephalopathy.
Clinical Relevance
WE is characterized by the classic clinical triad (though the complete triad is seen in only a minority of patients):
Ophthalmoplegia (nystagmus, lateral rectus palsy)
Ataxia (gait imbalance)
Confusion (mental status changes)
If untreated, Wernicke's encephalopathy can progress to Wernicke-Korsakoff syndrome, resulting in permanent anterograde and retrograde amnesia and confabulation.
