A physician-validated, board-style question from the Active Transport QBank. Try it, then check the reasoning for every option.
A 37-year-old man presents to his primary care provider complaining of bilateral arm numbness. He was involved in a motor vehicle accident 3 months ago. His past medical history is notable for obesity and psoriatic arthritis. He takes adalimumab. His temperature is 99.3°F (37.4°C), blood pressure is 130/85 mmHg, pulse is 90/min, and respirations are 18/min. On exam, superficial skin ulcerations are found on his fingers bilaterally. His strength is 5/5 bilaterally in shoulder abduction, arm flexion, arm extension, wrist extension, finger abduction, and thumb flexion. He demonstrates loss of light touch and pinprick response in the distal tips of his 2nd and 5th fingertips and over the first dorsal web space. Vibratory sense is intact in the bilateral upper and lower extremities. Which of the following nervous system structures is most likely affected in this patient?
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A
Ventral white commissureCorrect. The ventral white commissure carries decussating spinothalamic fibers; central cord syrinx damages this structure first, producing bilateral suspended pain/temperature loss with preserved dorsal column function.
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B
Cuneate fasciculusIncorrect. Cuneate fasciculus damage would cause loss of vibration and proprioception in the upper limbs; this patient has PRESERVED vibratory sense.
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C
Anterior corticospinal tractIncorrect. Anterior corticospinal tract injury causes upper motor neuron weakness; this patient has full 5/5 strength.
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D
Spinocerebellar tractIncorrect. Spinocerebellar tract injury causes ataxia and incoordination, not the dissociated sensory loss seen here.
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E
Lateral corticospinal tractIncorrect. Lateral corticospinal tract damage produces upper motor neuron weakness with hyperreflexia and a positive Babinski sign; this patient retains full 5/5 strength, and central cord syrinx involving the ventral white commissure better explains the bilateral dissociated sensory loss.
↑ Tap an answer to reveal the reasoning
Answer: A. This patient has bilateral, dissociated sensory loss (loss of pain and light touch in C6, C7, and C8 dermatomes bilaterally) with PRESERVED vibration/proprioception and intact motor strength, occurring after a motor vehicle accident. This 'cape distribution' suspended sensory loss with sparing of dorsal columns is the hallmark of syringomyelia, a fluid-filled cavity (syrinx) in the central spinal cord.
The syrinx expands within the central cord and first damages the ventral white commissure, where second-order spinothalamic neurons cross to ascend in the contralateral spinothalamic tract. Because crossing fibers from both sides traverse this commissure, a central cavity produces BILATERAL loss of pain and temperature sensation in the dermatomes of the affected cord segments. Dorsal column fibers (vibration, proprioception, fine touch) run posteriorly and are spared until late disease. As the syrinx expands laterally, it can later affect anterior horn motor neurons (causing lower motor neuron weakness in the hands) or corticospinal tracts.
Syringomyelia is commonly post-traumatic or associated with Chiari I malformation. Diagnosis is by MRI; treatment is surgical decompression when symptomatic.
**Why each option:**
**A.** Correct. The ventral white commissure carries decussating spinothalamic fibers; central cord syrinx damages this structure first, producing bilateral suspended pain/temperature loss with preserved dorsal column function.
**B.** Cuneate fasciculus damage would cause loss of vibration and proprioception in the upper limbs; this patient has PRESERVED vibratory sense.
**C.** Anterior corticospinal tract injury causes upper motor neuron weakness; this patient has full 5/5 strength.
**D.** Spinocerebellar tract injury causes ataxia and incoordination, not the dissociated sensory loss seen here.