• Kee-Yong Ha and Young-Hoon Kim.
• Department of Orthopaedic Surgery, Seoul St. Mary's Hospital, College of Medicine, The Catholic University of Korea, 222 Banpodae-ro, Seocho-Gu, Seoul, 137-701, Korea. kyh@catholic.ac.kr.
• Eur Spine J. 2016 Apr 1; 25 (4): 1039-46.

PurposeTo investigate the causes of late-onset, progressive neurological deficits in patients with severe angular kyphosis caused by spondylitis secondary to tuberculosis (TB spondylitis).MethodsFrom 2000 to 2011, 36 patients with severe angular kyphosis secondary to TB spondylitis (TB kyphosis) were enrolled in the study. All patients had late-onset, progressive neurological deficits. The causes of these deficits were classified with respect to the level of the causative lesion. Group A (n = 25, 69.4%) comprised patients whose neurological deficits resulted from the kyphosis itself. Patients in group B (n = 11, 30.6%) had developed neurological symptoms related to a lesion cephalad or caudal from the kyphosis. Surgical intervention was performed in 23 patients; 13 patients were treated conservatively. Clinical outcomes were evaluated using the American Spinal Injury Association (ASIA) impairment scale.ResultsThe late onset of neurological deficits was attributed to cord compression, pure cord distraction, stenosis, and instability above or below the level of the angular kyphosis. An improvement of the neurological symptoms at the cord level after surgical intervention, as indicated by a change from a non-ambulatory (ASIA impairment scale A/C) to an ambulatory (ASIA D/E) status, occurred in four of nine (44.4%) surgically treated patients. However, only 2 of 10 (20.0%) patients treated conservatively showed cord level improvement, as assessed using the ASIA impairment scale.ConclusionsIn their evaluation of paraplegic patients, spine surgeons should consider the many potential causes of late-onset neurological deficits in TB spondylitis to avoid performing unnecessary surgery. A simpler procedure may yield equivalent results.

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