This document provides an overview of spinal tuberculosis (TB), including: - Epidemiology statistics showing India has a high burden of spinal TB cases. - Pathophysiology involving hematogenous spread from a primary focus to the spine, where granulomas form and cause vertebral destruction. - Varied clinical presentations depending on location and severity, including back pain, abscesses, and deformity. - Investigations including imaging modalities like MRI and CT to identify bone destruction and soft tissue involvement, as well as laboratory tests and microbiological studies for diagnosis. - Management involving chemotherapy for uncomplicated cases and surgery plus chemotherapy for complicated cases with deformity, instability or neurological deficit.

1. FROM BASICS TO ADVANCES IN
SPINAL CORD TUBERCULOSIS
Dr. pramod meena
SR neurology
GMC kota

2. INTRODUCTION
• Evidence of spinal TB - in 5000-year-old mummies.
• In 1779, Percival Pott published -spinal TB.
• Tuberculosis is the chronic consumptive disease and
currently world’s leading cause of death.
• Tuberculous spondylitis is the most dangerous form
of skeletal TB.

3. EPIDEMIOLOGY
• One fifth of TB population is in India
• 3% are suffering from skeletal TB
• Vertebral TB - 50% of all cases of skeletal TB
• Almost 50% are from pediatric group
• Every day 1000 die of tuberculosis in India

4. SPINAL TUBERCULOSIS

5. Pathophysiology
• TB is caused by the Mycobacteriumtuberculosis complex -
It is a slow-growingfastidious
Aerobic bacillus
• The primary site of infections can be in the lungs, lymph nodes of the
mediastinum, mesentery, gastrointestinal tract, genitourinary system, or
any other viscera.
• Spinal infectionis always secondary
Caused by Hematogenousdisseminationof the bacillusfrom a primary
focus.

6. Pathophysiology
• Bacillus colonize the sub-chondral region of the vertebra
and forms granulomatous inflammation
• Characterized by lymphocytic infiltration and
epithelioid cells, which may merge to form the classical
Langhans-type giant cells and end up in caseating
necrosis of affectedtissues forming a cold abscess.
• With progressivedestructionof the vertebral body
leads to deformation of spine

7. Types of lesions
• Paradiscal - Commonest
• Central - Resulting in
vertebral body loss
• Posterior - Nonosseous abscess
formation

8. Clinical Presentation of Spinal TB
The clinical picture of spinal TB is extremely variegated.
The manifestation of spinal TB depends on the
1. Severity of the disease
2. Duration of the disease
3. Site of the disease
• Insidious in onset
• Slow progression

9. Clinical presentations
❑Backache
▪ Most common of all symptoms.
▪ During the active stage
▪ rarely can be radicular in nature.
❑ Constitutional symptoms
▪ loss of weight
▪ loss of appetite
▪ fever
▪ malaise
❑ Rest pain
The intensity is proportional
to the amount of bone
destruction and instability
❑ Cold Abscess
Cold abscess lacks inflammatory
features and initially forms in
the infective focus.

10. Clinical presentations
• The lumbar cold abscess
• usually presents as a swelling in
Petit’s triangle
• It can track down along the psoas
to cause pseudo-flexion
deformity of the hip.

11. • In the cervical spine, it can present as a retropharyngeal abscess or
as a swelling in the anterior or posterior triangle of the neck or
even in the axilla.
• The retropharyngeal abscess can produce dysphagia, hoarseness of
voice, and respiratory stridor.

12. Clinical presentations –
Cold abscess
• Thoracic region - the cold abscess usually
presents as a fusiform paravertebral swelling
• It can track along the intercostal vessels and
presents as a swelling in the chest wall.
• Thoracic cold abscess can track down through
the arcuate ligament, or via the openings in
the diaphragm.

13. Deformity
Owing to the involvement of the anterior
column, progressive destruction results in
kyphotic deformity of the spine most often.
The clinical appearance depends on the
number of vertebrae involved causing
1. Knuckle - (1 vertebra)
2. Gibbus - (2 vertebrae)
3. Rounded kyphosis - (>3 vertebral collapse)

14. Spine at risk signs
• The “spine at risk” signs to identify children at risk for severedeformity
(A) Separation of facet joints in lateral radiographs which indicates instability
(B) Retropulsionof the posterior part of the affected vertebra
(C) Lateral translation of vertebrae in the anteroposterior radiograph
(D) The toppling of one vertebra over the other vertebra.

15. Gibbus Deformity

16. Neurological Deficit
Neurological complications can occur
• Early active disease
• In the late healed stage
Early active disease – Acute direct compression due to
• Abscess
• Inflammatory tissue
• Retropulsion of the Sequestrum
• Instability and translation of spinal column
Late-onset neurological deficit due to
1. Ossification ligamentum flavum
2. Increasing deformity

17. Classification
Complicated TB - Pharmacological + Surgical
• Deformity
• Instability
• Neurological deficit
Uncomplicated spinal TB - Pharmacological management
• Diagnosis is made prior to development of such complications

18. Investigations
• Radiological investigations –
• None of the imaging options are reliable in distinguishing spinal
infection and neoplasm
• Immunoassays -
• Laboratory investigations –
• Microbiological investigation -
• Histological investigation –
• Genetic studies

19. Radiological Investigations
Plain radiographs
• Have no role in early diagnosis of spinal TB.
• Disc space narrowing
• rarefaction of vertebral end plates
• kyphosis
• instability can be made out only in late
stages.
• 60% to 70% of spinal TB may have an active
pulmonary lesion, and thus chest radiography
is essential

20. Radiological Investigations
Computed tomography (CT)
• CT is extremely useful in identifying extent of
bony destruction
• Posterior column involvement
• Junctional pathologies
• Joint involvement
• Regional stability
• Four types of destruction have been noticed

21. Fragmentary type
• Associated hypodense paravertebral
softtissue mass with bone fragments
causing spinal cord compression.
• Commonest pattern

22. Osteolytic type
• Second most common pattern
• Anterior and central parts of
vertebral body are completely
destroyed.
• Associated large paravertebral
soft-tissue mass.

23. Subperiostel type
• Anterior margin of vertebral
body has irregular ragged appearance.
• Characteristic hypodense abscesses
with rim calcification are seen in each
psoas muscle.

24. Localized sclerotic type
• Least common pattern
• Localized destruction with
Sclerotic margins.

25. Radiological Investigations
MRI
• It has been the imaging modality of choice as it has been able to detect
earliest changes.
• Gadolinium-enhancedMRI further helps in differentiating TB from other
causes of infectivespondylodiscitis.
• The extent of soft tissue involvement
• Spread of abscess
• Neural compression
• Whole spine screening aids in identifying skip lesions
• Assessing the response to treatment

26. Histopathology
• Demonstrating classical granulomas and staining of smears to
identify acid fast bacilli (AFB)
• Sensitivity - 50– 80%
• specificity - NA

27. Microbiological investigations
Culture and ABST
• Growth of Mycobacterium in culture specimens obtained from the
infected tissue is the single most confirmatory diagnostic test of
spinal TB and is considered the gold standard method.
• However, due to its very poor sensitivity - 47%
• Lowenstein Jensen media, 6-8 weeks, requires 101 to 10 2 bacilli/mL
(live bacilli)
• BACTEC radiometric culture takes 2 weeks

28. Laboratory investigations
Erythrocyte sedimentation rate (ESR) - sensitivity – 60-90%
• Usually in TB, ESR is >20 mm/ h and decreases as healing progresses
• Used to monitor therapeutic response,
• But its low specificity is a concern.
C- reactive protein (CRP) - Sensitivity - 71%
• is more specific for acute infection rather than TB

29. Immunoassays
• Immunoassays are high in active and chronic infective stages of TB
• Would not be able to differentiate between
1. active and healed disease
2. BCG vaccinated individuals
• Not recommended – WHO
Mantoux tuberculin skin test
• WHO recommendsusage in low-income countries
• It is of no diagnostic value in endemic areas
• It may also be false negative in immunodeficientindividuals
• Sensitivity - 40% to 55%
• Specificity - 75%

30. Interferon-g (IFN-g) releaseassaysand Wholeblood-based enzyme-
linked immunosorbentassays
Measuring the amount of IFN-g produced in response to
Mycobacterium tuberculosis antigens.
They are specific and differentiate between natural TB and BCG
vaccination, these tests cannot differentiate between latent TB and
active TB.
• Sensitivity - 50% to 65%
• Specificity - 85%

31. Genetic studies
Gene Xpert MTB/RIF - 2010
• It is an automated diagnostic test that can identify Mycobacterium
tuberculosis(MTB) DNA and resistanceto rifampicin (RIF).
• Sensitivity of 95.6% and specificityof 96.2%.
Xpert MTB/RIF Ultra -2017
• New generation
• More sensitivity and specificity
• Specimens with low numbers of bacilli, especially in smear-negative,
culture-positive specimens, in pediatric specimens and in extrapulmonary
specimens.

32. Summary of diagnosis
The diagnosis of spinal TB is based on
• Correlating clinical and classical imaging findings on MRI
• Confirmed by either
1. Culture and sensitivity,
2. Histopathological evidence.
3. Gene Xpert PCR test

33. Management
• Uncomplicated spinal TB -Chemotherapy only
• Complicated spinal TB -Chemotherapy + Surgery

34. UncomplicatedspinalTB is a medicaldiseaseandcanbe effectively managedby
chemotherapyalone

35. Surgical management
Indications of surgery
• Lack of response to chemotherapy or recurrence
• Severe weakness at presentation
• Static or worsening neural deficit even after initiating chemotherapy
• Instability
• Incapacitating pain
• Deformities

36. Surgical Management
Goals of treatment
The fundamentals of surgical management are
• Adequate decompression
• Debridement
• Maintenance and reinforcement of stability
• Correcting the deformity or halting the progress of deformity

37. The advantages of surgical treatment
1. Adequate sampling for histological confirmation of the diagnosis
2. Early and better healing by removal of the disease focus
3. Correction and prevention of the spinal deformity
4. Reducing the rates of recurrence
5. Promoting early neurological recovery

38. Approach
• Anterior Approach
• Spinal TB mainly affects anterior column
and thus anterior approaches enable
adequate exposure, debridement, and
reconstruction.
• Disadvantage
• Graft slippage – 50 -80%
• Fracture
• Absorption, or subsidence of graft.
• Mortality 4% morbidity 18%

39. Approach
Posterior approach
• Commonly used approach
• Easy, familiarity
• The ability to achieve adequate exposure for circumferential spinal cord
decompression, better deformity control through pedicle screws
• Possibility of extension of instrumentation
• Avoidance of thoracotomy-related complications
• Transpedicular decompression and posterior instrumentation facilitates
faster recovery and also prevents deformity progression and neurological
sequelae in early disease.

40. Completedestructionof L1 vertebrafixationby posterior
approach

41. PATHOLOGY
• Spinal tuberculosis is usually a secondary
• Hematogenous in origin
• Usually involves 2 adjacent vertebrae
• Delayed hypersensitivity immune reaction
• Initially : a pre-pus inflammatory reaction, with
Langerhan’s giant cells, epithelioid cells, and
lymphocyte
• The granulation tissue proliferates, producing
thrombosis of vessels

42. PATHOLOGY
• Tissue necrosis, tubercle formation result in paraspinal abscess
• The pus may be localized, or it may track along tissue planes
• Progressive necrosis of bone leads to a kyphotic deformity
• Typically, the infection begins in the anterior aspect of the
vertebral body adjacent to the disk
• The infection then spreads to the adjacent vertebral bodies under
the longitudinal ligaments
• Noncontiguous (skip) lesions are also seen occasionally

43. PATHOLOGY of spinal TB
• Can loose complete vertebrae
• Wedge shaped fractures are common

44. SIGNS & SYMPTOMS
A. Constitutional symptoms
B. Spine Deformity
▪ Kyphosis
▪ Scolosis
▪ Kypho Scoliosis

45. C. Neurological
• Pain
- Local /Radicular /both
• Motor deficits
• Spasticity
• Sensory deficits
• Bladder involvement
D. Local
• Cold abscess / Sinuses

46. Symptoms of Spinal TB
• Back pain (95%)
• 40-50% neurological symptoms –
weakness, paresthesia, bowel
symptoms
• 40-50% with systemic symptoms
–fever, night sweats, weight loss

47. DIAGNOSIS: Recent advance
• There are three diagnostic non- culture laboratory tests:
1. Immunological tests ( antigen & antibody)
2. Metabolic product detection test ( extra-corporeal IFN-y
test)
3. Amplification of DNA of M. Tuberculosis by PCR.
Other than these
• - ELISA technique & T- SPOT Using 6 kDa & 10 kDa.
• - Xene expert for MDR TB

48. Pott’s paraplegia
• The three main causes of Pott’s paraplegia are:
1) cord compression by abscess and granulation tissue;
2) cord compression by sequestrums and the posterior bony
edge of the vertebral body at the level of the kyphosis; and
3) Bony canal stenosis of the deformed spine above the level of the kyphosis.
• Factors affect recovery from Pott’s paraplegia.
1. Patient’s general physical condition and age;
2. Condition of the spinal cord; level and number of
vertebrae involved;
3. Duration and severity of the paraplegia;
4. Time to initiation of treatment.

49. Tuli and Kumar’s Staging of Pott’s Paraplegia :
• Stage I :Patient unaware of neural deficit, physician detects plantar extensor
and/or ankle clonus.
• Stage II : Patient aware of deficit but manages to walk
with support, clumsiness of gait.
• Stage III : Paralysis in extension, sensory deficit less than 50%
• Stage IV : III + flexor spasm/paralysis in flexion/ flaccid/ sensory deficit more
than 50%/ sphincters involved

50. INDICATION OF SURGERY:
A. Absolute indications:
1. Paraplegia with onset
2. Paraplegia getting worse
3. Complete loss of motor power
4.Paraplegia with spasticity
5. Severe paraplegia
B. Relative indications:
1. Recurrent paraplegia
2. Paraplegia in old age
3. Painful paraplegia
4. Complications
C. Rare indications:
1. Posterior spinal disease.
2. Spinal tumor syndrome.
3. Severe paralysis secondary
to cervical disease.
4.Severe cauda equine
syndrome.

51. Goals of Surgery
• Eradication of diseased vertebrae
• Decompression of spinal cord
• Correction of deformities
• Stabilization of spine & further protection of spinal cord

52. Surgical measures include:
1. Cold abscess drainage & Focal debridement
2. Decompressionsurgery
3.Decompressionsurgery and posterior instrumentation
4. Anterior radical surgery and anterior instrumentation;
5. Anterior radical surgery and posteriorinstrumentation
6. Corrective spinal osteotomy for healed rigid kyphosis
Posterior Surgery
• Long segment stabilization
• 360 degree decompression
• Three columnfixation is possible

53. Types of surgery
➢Cervical spine - Anterior approach
➢Thoracic spine - Anterior & anterolateral
➢ decompression by Thoraco-abdominal approach
➢Posterior - Costotransversectomy
➢ Laminectomy.
➢Lumbar - Posterior ,Anterior and Ant-lateral