Vascular Anatomy, Human Anatomy, USMLE Step 1 - Full Vignette with Extended Explanations

Описание: A 59-year-old woman experiences months of worsening gait difficulty, urinary urgency progressing to retention, heavy and tight legs, and nocturnal calf cramps. Neurologic exam reveals spastic paraparesis, sensory changes to T10, hyperreflexia, sustained clonus, and a stiff, scissoring gait. MRI shows long-segment thoracic hyperintensity with perimedullary flow-voids. How should you interpret the evolving clinical and imaging findings? What clues from her history and exam inform your understanding of this pathologic process?

VIDEO INFO
Category: Vascular Anatomy, Human Anatomy, USMLE Step 1
Difficulty: Hard - Advanced level - Challenges experienced practitioners
Question Type: Natural History
Case Type: Rare Presentation

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QUESTION
A 59-year-old woman presents with 7 months of insidiously progressive gait difficulty and urinary urgency that has progressed to intermittent retention requiring occasional self-catheterization. She reports legs that feel heavy and tight by late afternoon, worse after prolonged standing or stair climbing, and transient nocturnal calf cramps. She has no fever, weight loss, night sweats, or recent infections. She denies alcohol use; she stopped methamphetamine use 18 years ago....

OPTIONS
A. Without definitive fistula disconnection, venous hypertensive congestive myelopathy typically progresses in a stepwise fashion to severe, often irreversible paraparesis with sphincter failure; longer pre-treatment symptom duration strongly predicts incomplete recovery even after cure.
B. Untreated course is a relapsing-remitting inflammatory myelitis with near-complete recovery between attacks after corticosteroids or plasmapheresis; durable disability is uncommon if immunotherapy is used early.
C. Natural history reflects anterior spinal artery arterial-steal ischemia that stabilizes spontaneously within weeks; bladder function is usually spared and most patients recover baseline strength without intervention.
D. Most cases follow a monophasic demyelinating trajectory triggered by infection; cerebrospinal fluid oligoclonal bands persist and long-term outcome depends primarily on steroid responsiveness rather than timing of any vascular procedure.

CORRECT ANSWER
A. Without definitive fistula disconnection, venous hypertensive congestive myelopathy typically progresses in a stepwise fashion to severe, often irreversible paraparesis with sphincter failure; longer pre-treatment symptom duration strongly predicts incomplete recovery even after cure.

EXPLANATION
This patient s examination and thoracic MRI point to venous hypertensive congestive myelopathy from a spinal dural arteriovenous fistula. The key natural-history teaching point is that, without definitive disconnection of the fistula, symptoms generally progress in a stepwise manner to severe, often irreversible paraparesis with sphincter dysfunction. Stepwise dips after exertion or prolonged upright posture reflect dynamic worsening of cord venous congestion and reduced arteriovenous perfusion gradient. CSF is typically bland or shows only mild protein elevation, oligoclonal bands are usually absent, and MRI often demonstrates long-segment central T2 cord hyperintensity with perimedullary serpiginous flow voids. Longer time from symptom onset to treatment predicts worse functional recovery even after anatomical cure, because chronic venous ischemia leads to irreversible cord injury....


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