THE CASE
A 64-year-old woman with a history of late-onset type 1 diabetes mellitus, Hashimoto thyroiditis, and scoliosis presented to the sports medicine clinic with acute-onset, sharp, nonradiating right lower back pain that began when she bent forward to apply lotion. At presentation, she denied fever, chills, numbness, tingling, aggravation of pain with movement, weakness, and incontinence. Her neuromuscular examination was unremarkable except for left-side paraspinal tenderness. She was prescribed cyclobenzaprine for symptomatic relief.
Two days later, she was seen for worsening pain. Her physical exam was unchanged. She was prescribed tramadol and advised to start physical therapy gradually. As the day progressed, however, she developed anterior thigh sensory loss, which gradually extended distally.
The following day, she was brought to the emergency department with severe left-side weakness without urinary incontinence. Her mental status and cranial nerve exams were normal. On examination, strength of the iliopsoas and quadriceps was 1/5 bilaterally, and of the peroneal tendon and gastrocnemius, 3/5 bilaterally. Reflexes of triceps, biceps, knee, and Achilles tendon were symmetric and 3+ with bilateral clonus of the ankle. The Babinski sign was positive bilaterally. The patient had diminished pain sensation bilaterally, extending down from the T11 dermatome (left more than right side) with diminished vibration sensation at the left ankle. Her perianal sensation, bilateral temperature sensation, and cerebellar examination were normal.
Magnetic resonance imaging (MRI) without contrast of the lumbar spine demonstrated ischemia findings corresponding to T12-L1. Degenerative changes from L1-S1 were noted, with multiple osteophytes impinging on the neural foramina without cord compression.
THE DIAGNOSIS
The initial presentation was consistent with mechanical low back pain with signs of anterior spinal artery infarction and medial lemniscus pathway involvement 48 hours after initial presentation. Spinal cord infarction occurs more commonly in women and in the young than does cerebral infarction,1 with better reemployment rates.1,2 Similar to other strokes, long-term prognosis is primarily determined by the initial severity of motor impairment, which is linked to long-term immobility and need for bladder catheterization.3
Neurogenic pain developing years after spinal cord infarction is most often observed in anterior spinal artery infarction4 without functional limitations.
Initial treatment. Our patient was started on aspirin 325 mg/d and clopidogrel 75 mg/d. Her mean arterial blood pressure was maintained above 80 mm Hg. Computed tomography angiography of the abdomen and pelvis was negative for aortic dissection. Lumbar puncture for cerebrospinal fluid analysis was unremarkable. Results of antineutrophil cytoplasmic antibody testing, antinuclear antibody testing, a hepatitis panel, and an antiphospholipid panel were all negative. The patient was started on IV steroids with a plan for gradual tapering. The neurosurgical team agreed with medical management.
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