A physician-validated, board-style question from the Active Transport QBank. Try it, then check the reasoning for every option.
A man appearing to be in his mid-50s is brought in by ambulance after he was seen walking on railroad tracks. On further questioning, the patient does not recall being on railroad tracks and is only able to provide his name. Later on, he states that he is a railroad worker, but this is known to be false. On exam, his temperature is 99.9°F (37.7°C), blood pressure is 128/86 mmHg, pulse is 82/min, and respirations are 14/min. He appears disheveled, and his clothes smell of alcohol. The patient is alert, is only oriented to person, and is found to have abnormal eye movements and imbalanced gait when attempting to walk. Which of the following structures in the brain likely has the greatest reduction in the number of neurons?
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A
Cerebellar vermisIncorrect. Cerebellar vermis atrophy explains the truncal ataxia of chronic alcohol use but not the dense amnesia and confabulation, which localize to mammillary bodies.
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B
Frontal eye fieldsIncorrect. Frontal eye field damage causes contralateral gaze deviation, not the abducens/oculomotor palsies seen in Wernicke encephalopathy.
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C
Mammillary bodiesCorrect. Wernicke-Korsakoff syndrome from thiamine deficiency causes hemorrhagic necrosis and neuronal loss in the mammillary bodies, producing confabulation, amnesia, and the classic confusion/ophthalmoplegia/ataxia triad.
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D
Parietal-temporal cortexIncorrect. Parietal-temporal cortex atrophy is characteristic of Alzheimer disease (early memory loss with cortical signs) — not the Wernicke-Korsakoff pattern.
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E
Substantia nigra pars compactaIncorrect. Substantia nigra neuronal loss defines Parkinson disease (resting tremor, bradykinesia, rigidity), not the dense amnesia, confabulation, and ophthalmoplegia of Wernicke-Korsakoff syndrome localized to mammillary bodies.
↑ Tap an answer to reveal the reasoning
Answer: C. A disheveled middle-aged man with alcohol odor presenting with confusion, confabulation (claiming false occupational history), ophthalmoplegia (abnormal eye movements), and ataxia (imbalanced gait) has Wernicke-Korsakoff syndrome. The classic triad of Wernicke encephalopathy — confusion, ophthalmoplegia, and ataxia — is caused by thiamine (vitamin B1) deficiency from chronic alcohol use and inadequate nutrition; Korsakoff syndrome is the chronic memory-impairment/confabulation phase that follows untreated Wernicke encephalopathy.
The neuropathologic lesions of Wernicke-Korsakoff specifically involve the MAMMILLARY BODIES (most characteristic), as well as periaqueductal gray, dorsomedial nucleus of the thalamus, and cerebellar vermis. Atrophy of the mammillary bodies is visible on MRI in chronic Korsakoff and produces the dense anterograde amnesia and confabulation seen here.
Treatment is immediate IV thiamine BEFORE glucose administration — giving glucose first to a thiamine-deficient patient can precipitate or worsen Wernicke encephalopathy.
Key distinction: cerebellar vermis degeneration (option A) causes the truncal ataxia seen in chronic alcohol use, but the CONFABULATION and amnesia in this case is mediated by mammillary body and thalamic damage — the BEST single answer is mammillary bodies.
**Why each option:**
**A.** Cerebellar vermis atrophy explains the truncal ataxia of chronic alcohol use but not the dense amnesia and confabulation, which localize to mammillary bodies.
**B.** Frontal eye field damage causes contralateral gaze deviation, not the abducens/oculomotor palsies seen in Wernicke encephalopathy.
**C.** Correct. Wernicke-Korsakoff syndrome from thiamine deficiency causes hemorrhagic necrosis and neuronal loss in the mammillary bodies, producing confabulation, amnesia, and the classic confusion/ophthalmoplegia/ataxia triad.
**D.** Parietal-temporal cortex atrophy is characteristic of Alzheimer disease (early memory loss with cortical signs) — not the Wernicke-Korsakoff pattern.