Charcot spinal arthropathy presenting as adjacent segment disease after lumbar spinal fusion surgery in Parkinson's disease: A case report. (March 2019)

• Record Type: Journal Article
• Authors: Miura, Kousei; Koda, Masao; Tatsumura, Masaki; Shiina, Itsuo; Mammoto, Takeo; Hirano, Atsushi; Abe, Tetsuya; Funayama, Toru; Noguchi, Hiroshi; Yamazaki, Masashi
• Is Part Of: Journal of clinical neuroscience. Volume 61(2019)
• Page Start: 281
• Page End: 284
• Publication Date: 2019-03
• Subjects: Charcot spinal arthropathy -- Neuroarthropathic change -- Parkinson's disease -- Adjacent segment disease; Brain -- Surgery -- Periodicals; Neurosciences -- Periodicals; Nervous system -- Surgery -- Periodicals; Brain -- surgery -- Periodicals; Neurosurgical Procedures -- Periodicals; Neurosciences -- Periodicals; Electronic journals; 616.8
• DOI: 10.1016/j.jocn.2018.11.013
• Languages: English
• ISSNs: 0967-5868

Abstract

Highlights: Charcot spinal arthropathy (CSA) associated with Parkinson's disease (PD) is rare. We encountered a case of CSA presenting as adjacent segment disease (ASD) in PD. The possible causes of CSA in this case were severe PD, strong opioid analgesics. Concentration of mechanical stress by the long lever arm might cause CSA. We recommend vigilance for CSA after spinal fusion surgery in patients with PD. Abstract: Charcot spinal arthropathy (CSA) is a rare spinal disorder presenting neuropathic osteoarthropathy of facet joints leading to progressive destruction. After L4-5 PLIF, a 63-year-old woman with Parkinson's disease (PD) underwent L3-4 and L5-S1 PLIF for primary adjacent segment disease caused by degenerative change, which was found as facet joint osteophytes and a vacuum disc phenomenon with endplate sclerosis. However, her postural disorder from PD deteriorated, and strong opioid analgesics were administered for severe recurring low back pain. Anterior subluxation at L2-3 occurred because of destructive secondary adjacent segment disease, which was found as destruction of the endplate and the facet without degenerative change, and formation of paravertebral osteophytes and fluid collection in the intervertebral space. The appearance on imaging met that for neuroarthropathic change, which was previously reported as CSA. L2-3 PLIF following extension of posterior fusion to T10 was additionally performed, and the postoperative course was uneventful with symptomatic improvement. In this case, the important finding was in the different appearance of the disease between adjacent segments on imaging. It is possible that deterioration of PD and administration of the analgesics inhibited deep pain sensation, and concentration of mechanical stress in the proximal adjacent segment by the long lever arm because of extension of the fusion level resulted in neuroarthropathic change of the facets in the secondary adjacent segments. The pathophysiology of association of CSA and PD remains unknown. However, we recommend vigilance for destructive neuroarthropathic facet change as CSA after spinal surgery in patients with severe PD.