PURPOSE: A case of cauda equina lesion as a result of recurrent adjacent segment degeneration (ASD) after multiple lumbar fusions is reported. ASD might be a consequence of biomechanical overload or simply a normal degenerative process. The reported clinical relevance of ASD is rather low. We describe an unusual case of cauda equina compression at L1-L2 in a patient who had undergone L2-L4 fusion 8 years previously and 2 decompression-fusion surgeries 16 years before. MATERIALS AND METHODS: A 72-year-old man, who had two previous lumbar fusion-decompression procedures, underwent a third lumbar surgery in December 2000 to treat symptomatic spinal canal stenosis associated with L3-L4 pseudoarthrosis. After a symptom-free period of 8 years, the patient experienced low back pain radiating to both legs while standing, associated with saddle sensory disturbances and incontinence. Physical examination ruled out significant motor deficits. Plain radiographs showed solid fusion from L2 to L4, good spinal alignment, and low-grade L1-L2 retrolisthesis. Stainless steel pedicular instrumentation distorted magnetic resonance imaging, preventing adequate spinal canal evaluation. Electromyography demonstrated signs of cauda equina compression (bilateral L3-S2). CT myelography showed a stop at L1-L2, due to a severe spinal canal stenosis. L1-L2 decompression and fusion were performed. RESULTS: After an uneventful surgery with no complications, the symptoms abated and incontinence recovered. CONCLUSIONS: Even if the reported clinical relevance of ASD is very low, fused patients with a constitutional narrow spinal canal are at risk of developing severe neural compression at the level adjacent to the fusion.
PURPOSE: A case of cauda equina lesion as a result of recurrent adjacent segment degeneration (ASD) after multiple lumbar fusions is reported. ASD might be a consequence of biomechanical overload or simply a normal degenerative process. The reported clinical relevance of ASD is rather low. We describe an unusual case of cauda equina compression at L1-L2 in a patient who had undergone L2-L4 fusion 8 years previously and 2 decompression-fusion surgeries 16 years before. MATERIALS AND METHODS: A 72-year-old man, who had two previous lumbar fusion-decompression procedures, underwent a third lumbar surgery in December 2000 to treat symptomatic spinal canal stenosis associated with L3-L4 pseudoarthrosis. After a symptom-free period of 8 years, the patient experienced low back pain radiating to both legs while standing, associated with saddle sensory disturbances and incontinence. Physical examination ruled out significant motor deficits. Plain radiographs showed solid fusion from L2 to L4, good spinal alignment, and low-grade L1-L2 retrolisthesis. Stainless steel pedicular instrumentation distorted magnetic resonance imaging, preventing adequate spinal canal evaluation. Electromyography demonstrated signs of cauda equina compression (bilateral L3-S2). CT myelography showed a stop at L1-L2, due to a severe spinal canal stenosis. L1-L2 decompression and fusion were performed. RESULTS: After an uneventful surgery with no complications, the symptoms abated and incontinence recovered. CONCLUSIONS: Even if the reported clinical relevance of ASD is very low, fused patients with a constitutional narrow spinal canal are at risk of developing severe neural compression at the level adjacent to the fusion.
Authors: Gary Ghiselli; Jeffrey C Wang; Nitin N Bhatia; Wellington K Hsu; Edgar G Dawson Journal: J Bone Joint Surg Am Date: 2004-07 Impact factor: 5.284
Authors: Paul Park; Hugh J Garton; Vishal C Gala; Julian T Hoff; John E McGillicuddy Journal: Spine (Phila Pa 1976) Date: 2004-09-01 Impact factor: 3.468