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TB Spine and Management of Kyphosis deformity

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Page 1: Tb spine

TB Spine and Management of Kyphosis deformity

Page 2: Tb spine

Introduction

• Described first by Sir Percival Pott in 1779.

• The classic destruction of the disk space and the adjacent vertebral bodies, destruction of other spinal elements, severe and progressive kyphosis subsequently became known as Pott’s disease.

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• Approx. 10% of patients with extrapulmonary tuberculosis have skeletal involvement.

• The spine is the most common skeletal site affected, followed by the hip and knee.

• Spinal tuberculosis accounts for almost 50% cases of skeletal tuberculosis.

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• Higher incidence in concomitant HIV infections.

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Predisposing factors

• Poverty• Overcrowding• Illiteracy• Malnutrition• Alcoholism

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• Drug abuse• Diabetes mellitus• Immunosuppressive treatment• HIV infection• FokI polymorphism in the vitamin-D receptor

gene.

Zhang HQ, Deng A, Guo CF, Wang YX, Chen LQ, Wang YF, et al. Association betweenFokI polymorphism in vitamin D receptor gene and susceptibility to spinal tuberculosis inChinese Han population. Arch Med Res 2010;41(1):46–9.

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Spinal involvement

• Hematogenous spread of M. tuberculosis into the dense vasculature of cancellous bone of the vertebral bodies.

• Pulmonary lesion, Genitourinary system infection as primary source.

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Spread

• Subchondral arterial arcade derived from anterior and posterior spinal arteries.

• Batsons paravertebral venous plexus.

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• Anterior inferior portion of vertebral body Spread to central part of disk.

• Common sites-– Paradiscal– Anterior– Central

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Vertebra plana

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• In younger patients, the disk is primarily involved because it is more vascularized.

• In old age, the disk is not primarily involved because of its age-related avascularity.

• Segmental arteries bifurcate to supply two adjacent vertebrae.

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• Multiple contigous vertebrae involved if spread occurs below the anterior or posterior longitudnal vertebrae.

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• Destruction of the intervertebral disk space and the adjacent vertebral bodies.

• Collapse of the spinal elements.

• Anterior wedging.

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Early onset paraplegiaProblem Cause of involvement

Mechanical pressure Mechanical pressure by tuberculous debris, sequestrum of bone or disk, abscess, subluxation and dislocations, concertina collapse, and internal gibbus.

Tuberculous granuloma Tuberculoma in extradural, intradural, or intramedullary regions.

Tuberculous myelitis Uncommon. May involve spinal cord parenchyma

Spinal artery thrombosis Infective thrombosis of anterior spinal artery

Tuberculous arachnoiditis Meningeal inflammation andFibrosis.

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Late onset paraplegiaProblem Cause of involvement

Transection of spinal cord by bony bridge Transverse ridge of bone produced by severe kyphosis

Fibrosis of dura (pachymeningitis) Formation of tough, fibrous membrane encircling the cord

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Clinical Features

• Local pain, local tenderness, stiffness and spasm of the muscles.

• Cold abscess, gibbus.• Slow and insidous progression.• 4-11 months average duration.• Constitutional symptoms.

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• Pain may be aggravated by spinal motion, coughing, and weight bearing due toadvanced disk disruption and spinal instability, nerve root compression, or pathological fracture.

• Neurological deficits common with cervical and thoracic segment involvement.

• Can occur during any stage.

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Cold Abcess

• Dysphagia, respiratory distress or hoarseness of voice due to retropharyngeal abcess.

• Extension into pleural cavity, mediastinum and oesophagus.

• Paravertebral abcess• Psoas abcess.

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‘SADDER’ Spine

• Sclerosis• Abcess• Disc space reduction• Destruction• Erosion of vertebrae• Rarefaction

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Type ofinvolvement

Mechanisms of involvement Radiological appearances

Paradiskal Spread of disease via the arteries

adjacent margins of two consecutive vertebrae. Theintervening disk space is reduced

Central Spread of infection along Batson’s plexusof veins

Involves central portion of a single vertebra; proximal and distal diskspaces intact

Anteriormarginal

Abscess extension beneath the anteriorlongitudinal ligament and the periosteum

Begins as destructive lesion in one of the anterior margins of the bodyof a vertebra, minimally involving the disk space but sparing thevertebrae on either side

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Type ofinvolvement

Mechanisms of involvement

Radiological appearances

Skipped lesions Spread of infection along Batson’s plexusof veins

circumferentially involvement of two noncontiguous vertebral levelswithout destruction of the adjacent vertebral bodies andintervertebral disks

Posterior Spread via the posterior external venousplexus of vertebral veins or direct spread

Involves posterior arch without involvement of vertebral body

Synovial Hematogenous spread through subsynovialvessels

Involves synovial membrane of atlanto-axial and atlanto-occipital joints

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• Paravertebral soft tissue shadows- calcifications presence due to lack of proteolytic enzymes.

• 50 and 75% of patients with osteoarticular tuberculosis and up to 67% of patients with spinal tuberculosis have an associated primary lung focus or have a reported history of pulmonary tuberculosis.

Schirmer P, Renault CA, Holodniy M. Is spinal tuberculosis contagious?Int J Infect Dis 2010;14(8):e659–66.

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CT

• CT demonstrates abnormalities earlier than plain radiography.

• Delineation of encroachment of the spinal canal by posterior extension of inflammatory tissue, bone or disk material

• CT-guided biopsy

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MRI

• Rapid determination of the mechanism for neurologic involvement.– Involvement of the vertebral bodies– Disk destruction– Cold abscess– Vertebral collapse– Spinal deformities

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Lab

• Demonstration of acid-fast bacilli on pathological specimen

• Histological evidence of a tubercle.• Presence of epithelioid cells on the biopsy

material

Skaf GS, Kanafani ZA, Araj GF, Kanj SS. Non-pyogenic infections of the spine. Int J Antimicrob Agents 2010;36(2): 99–105.

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• Neuroimaging guided-needle biopsy from the affected site is the gold standard technique for early histopathological diagnosis.

• Open biopsy of the spine is usually performed when either closed techniques have proved insufficient or other procedures, such as decompression and possibly arthrodesis, are planned.

Jain R, Sawhney S, Berry M. Computed tomography of tuberculosis: patterns of bone destruction. Clin Radiol 1993;47(3): 196–9

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• Smear positivity for acid-fast bacilli may be seen in up to 52% of cases and culture positivity in about 83% of cases.

Cytopathology 1999;10(6):390–401

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Histology

• Epithelioid cell granulomas• Granular necrotic background• Lymphocytic infiltration.• Scattered multinucleated and Langhans’ giant

cells.

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PCR

• Detects as few as 10-50 bacilli; faster and more sensitive.

• Sensitivity ranging from 61 to 90%.• Specificity of 80–90%.

Colmenero JD, Morata P, Ruiz-Mesa JD, Bautista D, Bermúdez P, Bravo MJ, et al. Multiplex real-time polymerase chain reaction: a practical approach for rapid diagnosis of tuberculous and brucellarvertebral osteomyelitis. Spine (Phila Pa 1976) 2010;35(24):E1392–6.

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QuantiFERON-TB Gold assay

• Cell-mediated inflammatory responses in vitro to tuberculosis infection

• Measures interferon-gamma harvested in plasma from whole blood incubated with the M. tuberculosis-specific antigens.

• Sensitivity- 84% • Specificity- 95%

Kumar R, Das RK, Mahapatra AK. Role of interferon gamma release assay in the diagnosis of Pott disease. J Neurosurg Spine 2010;12(5):462–6.

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Treatment

• WHO recommendation- 9 months(2 HRZE+ 7HR)

• Middle path regime:• Supportive therapy-– Multivitamins– Hematinics– High protein diet

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• X rays and ESR at 3-6 months interval.• Gradual mobilisation with help of spinal

braces.• Aspiration of abcesses• Sinuses excision• Decompression• Surgical stabilisation

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Indications

• Without neurological complaints– Progressive destruction

inspite of ATT– No response to

conservative therapy– Increase in size of

paravertebral abcess– Mechanical :Kyphosis,

Deformity

• With neurological complaints– New or worsening

neurological deficits– Paraplegia of rapid onset

or severe paraplegia.– Neural arch disease– Spinal tumor disease.

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The Hong- Kong Operation

• First reported by Ito and later popularised by Hogsdon and Stock in 1956.

• Thorough excision( extirpation) of the tuberculous focus.

• Posteriorly- dura mater. • Cephalad and caudad till healthy, bleeding

cancellous bone was exposed.

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• Create surfaces suitable for docking of the strut graft.(Rib/ Tricortical illiac crest)

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• Aim : Study the progress of interbody union, the extent of correction of the kyphosis and its maintenance with early mobilisation.

• Incidence of graft and implant-related problems.

• The American Spinal Injury Association (ASIA) score was used to assess the neurological status.

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• Mean preoperative vertebral loss was highest (0.96) in the dorsal spine.

• The maximum correction of the kyphosis in the dorsolumbar spine was 17.8°.

• Loss of correction maximal in the lumbosacral spine at 13.7°.

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• All patients had firm anterior fusion at a mean of five months.

• The incidence of infection was 3.9% and of graft-related problems 6.5%.

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• Adjuvant posterior stabilisation allows early mobilisation and rehabilitation.

• Graft related problems were fewer and the progression and maintenance of correction of the kyphosis were better than with anterior surgery alone.

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• There is no additional risk relating to the use of an implant either posteriorly or anteriorly even when large quantities of pus are present

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• Few mycobacteria adhere to the stainless steel, whereas Staphylococcus heavily colonizes on stainless steel.

• Pyogenic organisms form a thick biofilm, whereas mycobacteria show a scanty biofilm.

• Hence, the use of implant in the presence of TB infection is theoretically safe.

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Indications for stabilisation

• Pan vertebral disease, in which all three columns are diseased.

• Long-segment disease, in which after surgical decompression a bone graft >5 cm is inserted with instrumentation to prevent graft-related complications and consequent progression of kyphosis and neural complications

International Orthopaedics (SICOT) (2012) 36:285–292

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• Surgical correction of a kyphosis is performed when both anterior decompression and posterior column shortening is required.

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Kyphosis

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• Problems of progressive deformity and correction of residual severe deformity are current challenges.

• Patients with spinal tuberculosis treated conservatively have an average increase of 15 deg in deformity.

• 3–5 % of the patients develop with a deformity greater than 60 deg.

Korean Orthop Assoc 6:203–208

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Problems

• Cosmetic and psychological disturbance.• Costo-pelvic impingement.• Secondary cardiorespiratory problems.• Late onset paraplegia.• Correction difficult with high rate of

complications.

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• Affects the anterior column in more than 90% of patients.

• Vertebral collapse can continue until the healthy vertebral bodies in the region of the kyphosis approximate anteriorly and consolidate.

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Factors affecting the progression

• Age- Children have more severe deformity and more rapid progression to collapse and variable outcome after healing.

• Changes in healed phase.

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Kyphosis In Adults

• Structural weakness of the vertebral column lead to pathological fracture in the diseased vertebrae and it can collapse into a kyphosis.

• Even after diagnosis and ambulant chemotherapy, kyphosis continues to grow despite being treated.

• Progression of kyphosis can be minimized by prescribing suitable braces.

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• Patients treated nonoperatively have an average increase of 15° in deformity and three to five per cent end up with a deformity greater than 60°.

• Kyphosis also continues to grow in a TB spine lesion which is surgically decompressed and bridged by bone graft with associated complications of slippage and breakage.

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• Kyphosis, once healed, with osseous fusion does not grow alarmingly in adults in later life.

• When the lesion heals with fibrous or fibro-osseous healing it may progresses further.

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Kyphosis in Children

• The TB spine lesion in children causes more destruction as most of the vertebral bodies are cartilaginous.

• Even when a TB lesion heals by nonoperative treatment kyphosis continues to increase with growth.

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• The anterior growth potential of the vertebral body is destroyed:– The disease itself– Surgical excision of disease focus– Alteration in the growth resulting from the effect

of biomechanical forces on the growth plate of both the fusion mass and the vertebral segments within the kyphosis.

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• Patients treated with radical resection and anterior fusion showed the worst results with respect to progression of kyphosis particularly when the lesion was in thoracic spine and several segments were involved.

• Posterior elements contribute to growth and as far as possible anterior radical resection should be avoided in children.

Schulitz KP, Kothe R, Leong JC, Wehling P. Growth changes of solidly fused kyphotic bloc after surgery for tuberculosis-comparison of four procedures. Spine. 1997;22:1150–5

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• Type I -increase in deformity until growth had ceased. – Ia-continuous – Ib-After a lag period of three to five

• Type II-decrease in deformity with growth. – IIa- occur immediately after the active phase – IIb- after a lag period of three to five years.

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• Type-III progression showed minimal change during either the active or healed phases and was seen only in those with limited disease.

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Influence of level of lesion

• Thoracic and thoracolumbar lesions have a greater deformity at presentation.

• Natural thoracic kyphosis allows progression of deformity and lumbar lordosis protects against the deformity.

• In the thoracic spine, the more horizontally oriented articular facets allow earlier subluxation of the facet joints leading to a rapid collapse.

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Buckling Collapse

• Complete destruction of more than two vertebral bodies.

• Dislocation of facet joints occurred at multiple levels leading to a kyphosis of more than 120 deg.

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• Longitudinal overgrowth of vertebral segments is noted leading to stretching of the spinal cord at the apex of the kyphosis with possible secondary late onset paraplegia.

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Risk factors for buckling collapse

• Age of less than 7 years at the time of the disease

• Thoracolumbar involvement • Loss of more than two vertebral bodies• Presence of radiographic spine-at-risk signs

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Risk factors for severe progression

• Age below 10 years.• Vertebral body loss of more than 1–1.5• A pre-treatment deformity angle of greater

than 30 deg, especially in children.• Cervical thoracic and thoracolumbar

junctional lesions.• The presence of ‘spine-at-risk’ radiological

signs.

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Spine ‘at risk’ signs

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Separation of the facet joint

• The facet joint separates at the apex of the curve

• Instability and loss of alignment

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Retropulsion

• The posterior retropulsion of the diseased vertebral segment is identified by drawing two lines along the posterior surfaces of the first upper and lower normal vertebra.

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Lateral translation

• A line drawn through the middle of the pedicle of the lower vertebra does not touch the pedicle of the superior vertebra.

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Toppling• In the initial stages of

collapse, the line drawn along the anterior surface of the lower normal vertebra intersects the inferior surface of the upper normal vertebra.

• Toppling has occurred when the line intersects above the middle of the anterior surface of the upper vertebra.

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• Each sign is given a score of 1 with a maximum possible score of 4.

• A spinal instability score of more than 2 is associated with a significantly larger final deformity.

• A score of 3 or more accurately predicts an increase in the angles of deformity and kyphosis of more than 30 and a final deformity of more than 60.

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Prediction of deformity progression

• y= a+ bx• Y= final angle of gibbus deformity.• X= measurement of initial loss of vertebral

body.• A and B are constants 5.5 and 30.5

respectively.

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Patients reporting with classical disease

• In adult patients, three or more vertebral body affection with initial vertebral body loss of one to 1.5 vertebral body height in a dorsal or dorsolumbar spine, need to be taken up for kyphosis correction.

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• Children younger than seven years of age with three or more vertebral body affection in dorsal or dorsolumbar spine.

• Two or more spine at risk segment will have a progressive kyphosis with growth.

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Correction in active disease

• Correction of the kyphosis without opening the disease area and without anterior decompression will produce more prominent spinal cord indentation by retropulsed fragment (internal salient) and consequently neural deficit.

• Hence internal salient should be removed by anterior debridement and corpectomy

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• Moderate to severe kyphosis which needs correction is a long standing problem.

• Abrupt correction of kyphosis with a column that is shortened anteriorly will produce lengthening of anterior column, which will stretch the spinal cord with consequent neural deficit.

• Thus it is desirable to shorten the vertebral column posteriorly.

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• Instrumented stabilization with anterior gap grafting and posterior fusion is needed as the spine becomes unstable following anterior corpectomy and posterior column fusion.

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Methods

• Single stage transpedicular approach.• Single or two-staged anterior decompression

with bone grafting followed by correction of kyphosis and posterior instrumentation.

• Single stage kyphosis correction by extra pleural anterolateral approach.

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Correction in healed lesion

• Transpedicular decancellation osteotomy.

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Late onset paraplegia/ Paraplegia with healed disease

• Long standing severe kyphosis with a history of being treated for spinal TB 10 or more years ago and now present with signs of upper motor neuron spinal cord injury or paraplegia.

• The cause may be a reactivation of old healed lesion at kyphus or intrinsic changes in spinal cord due to continued stretch on internal salient

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• Anterior decompression and fusion.• Internal salient is removed either by

transthoracic transpleural anterior approach or by the extrapleural anterolateral approach.

• Costotransversectomy/ Extrapleural anterolateral.

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• Posterior vertebral column resection and intraoperative manual traction to correct severe post-tubercular rigid spinal deformities incurred during childhood: minimum 2-year follow-up.

Eur Spine J. 2015 Mar;24(3):586-93

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• Aim: evaluate the clinical and radiographic outcomes of posterior vertebral column resection (PVCR) and intraoperative manual traction to correct severe post-tubercular spinal deformity incurred during childhood.

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• Retrospective study of 11 patients (4M+7F)• Clinical outcome assesment with Oswestry

index and Visual Analog scale.• Imaging measurements and fusion status

were assessed using plain radiography and CT.

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• Kyphosis improved from a preoperative average of 93.4° to a postoperative average of 18.7° for a correction of 80.1 %.

• The Cobb angle in the coronal plane improved from an average of 48.1° to 10.3° postoperatively for a correction of 76.3 %.

• At the last follow-up, two patients improved neurologically from ASIA grade C to grade D, and one patient improved from grade C to grade E.

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• Perioperative complications occurred in 4 of the 11 cases.

• One patient had a dural tear. • Three patients had temporary degradation of

intraoperative neuromonitoring, and one experienced transient paralysis of the left lower extremity postoperatively.