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Tuberculosis of spine: neurological deficit - PubMed

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Tuberculosis of spine: neurological deficit

Anil K Jain et al. Eur Spine J. 2013 Jun.

Abstract

The most dreaded neurological complications in TB spine occur in active stage of disease by mechanical compression, instability and inflammation changes, while in healed disease, these occur due to intrinsic changes in spinal cord secondary to internal salient in long standing kyphotic deformity. A judicious combination of conservative therapy and operative decompression when needed should form a comprehensive integrated course of treatment for TB spine with neurological complications. The patients showing relatively preserved cord with evidence of edema/myelitis with predominantly fluid collection in extradural space on MRI resolve on non-operative treatment, while the patients with extradural compression of mixed or granulomatous nature showing entrapment of spinal cord should be undertaken for early surgical decompression. The disease focus should be debrided with removal of pus caseous tissue and sequestra. The viable bone should only be removed to decompress the spinal cord and resultant gap should be bridged by bone graft. The preserved volume of spinal cord with edema/myelitis and wet lesion on MRI usually would show good neural recovery. The spinal cord showing myelomalacia with reduced cord volume and dry lesion likely to show a poor neural recovery. The internal kyphectomy is indicated for paraplegia with healed disease. These cases are bad risk for surgery and neural recovery. The best form of treatment of late onset paraplegia is the prevention of development of severe kyphosis in initial active stage of disease.

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Figures

Fig. 1
Fig. 1

a Pre-operative lateral X-ray of dorsal spine (a) show healed TB of spine (D2–4) showing severe kyphotic deformity. Similar post operative X-ray (b) after surgery shows adequate decompression and minimal correction of kyphosis. b T1WI (a) and T2WI (b) midsagittal MRI shows healed vertebral body (D2–4) with severe kyphosis and showing internal salient indenting the spinal cord. The bright signal intensity (T2WI) on spinal cord at apex of kyphosis is suggestive of cord edema. c Axial T1WI (a) and T2WI (b) MRI images show shrunken cord with a cord edema at apex of deformity. d Post-operative reconstructed right parasagittal (a) and left parasagittal (c) image of CT scan show adequate anterior decompression with bone graft in situ. Obliteration of posterior facet joints (solid arrow) suggestive of spontaneous posterior fusion. Similar mid sagittal (b) CT scan image show adequate anterior decompression and interbody bone graft

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