BACKGROUND: This study sought to describe a patient with a slowly progressive cauda equina syndrome (CES) who had imaging findings of the CES that occurs as a rare complication of ankylosing spondylitis (AS), but whose spinal fusion was due to thoracolumbosacral instrumentation, not spondyloarthropathy. METHODS: A 53-year-old woman presented with a 5-year history of slowly progressive CES affecting sensory and sphincter more than motor function many years after sequential instrumented fusions of her thoracic and then lumbosacral spine. Imaging studies showed enlargement of the caudal sac and dorsal arachnoid diverticula eroding into posterior elements of the lumbar spine similar to findings reported in patients with CES in longstanding AS. Despite extensive evaluation, no other cause for her CES was found. We postulate that our patient's CES is on the same pathophysiologic basis as that proposed for patients with longstanding AS (fibrosis of peridural tissues with increase in transmitted cerebrospinal fluid pulse pressure). Because of reports that patients with CES due to longstanding AS are helped by placement of a lumboperitoneal shunt, our patient underwent this procedure. RESULTS: Seventeen months postoperatively, the patient's symptoms and neurologic examination are unchanged, and her previous slow progression has been halted. CONCLUSIONS: This case strongly suggests that extensive surgical thoracolumbosacral fusion can, rarely and after many years, be associated with lumbosacral nerve root damage and a slowly progressive CES that is similar to that seen in patients with spinal fusion due to longstanding AS.
BACKGROUND: This study sought to describe a patient with a slowly progressive cauda equina syndrome (CES) who had imaging findings of the CES that occurs as a rare complication of ankylosing spondylitis (AS), but whose spinal fusion was due to thoracolumbosacral instrumentation, not spondyloarthropathy. METHODS: A 53-year-old woman presented with a 5-year history of slowly progressive CES affecting sensory and sphincter more than motor function many years after sequential instrumented fusions of her thoracic and then lumbosacral spine. Imaging studies showed enlargement of the caudal sac and dorsal arachnoid diverticula eroding into posterior elements of the lumbar spine similar to findings reported in patients with CES in longstanding AS. Despite extensive evaluation, no other cause for her CES was found. We postulate that our patient's CES is on the same pathophysiologic basis as that proposed for patients with longstanding AS (fibrosis of peridural tissues with increase in transmitted cerebrospinal fluid pulse pressure). Because of reports that patients with CES due to longstanding AS are helped by placement of a lumboperitoneal shunt, our patient underwent this procedure. RESULTS: Seventeen months postoperatively, the patient's symptoms and neurologic examination are unchanged, and her previous slow progression has been halted. CONCLUSIONS: This case strongly suggests that extensive surgical thoracolumbosacral fusion can, rarely and after many years, be associated with lumbosacral nerve root damage and a slowly progressive CES that is similar to that seen in patients with spinal fusion due to longstanding AS.