This document provides information on spinal tuberculosis, including its history, types of lesions, clinical presentation, imaging findings, treatment, and indications for surgery. It discusses how spinal tuberculosis is usually secondary to a primary infection elsewhere in the body that spreads hematogenously to the spine. The most common type of spinal lesion is a paradiscal lesion that begins in the vertebral body. Clinical presentation varies from asymptomatic to paraplegia. Imaging like CT and MRI are useful to identify bone destruction and abscesses. Treatment involves anti-tuberculosis medications for 18 months along with rest. Surgery is indicated for neurological deterioration, advanced disease, or diagnostic uncertainty.

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SURESH BISHOKARMA, MS
MCH RESIDENT, NEUROSURGERY
NINAS
SPINAL TUBERCULOSIS

2. *The classical paper by Pott entitled, “Remarks on that kind of Palsy of the
lower limbs which is frequently found to accompany a curvature of the
spine, and is supposed to be caused by it, together with the Method of Cure”,
has led to paraplegia of tuberculous origin being named Pott’s paraplegia.
HISTORY

3. *The spinal disease is always secondary to a primary lesion, usually from a
visceral focus, and occurs due to haematogenous spread.
*Involvement of different parts of the spine and the presence of associated
visceral lesions imply a bacteremia. Infection may reach the spine due to a
bacillaemia or through the Batson’s plexus of veins.
*The primary focus may be active or quiescent and may be in the lungs,
mediastinal lymph nodes, kidneys or other viscera.
*Simultaneous involvement of the paradiscal part of two contiguous vertebrae
suggests spread of infection via the common blood supply to the region
Route of infection

5. *Classically, four types of involvement of
the spinal column have been described
in spinal tuberculosis:
*(i) Para-discal lesion which arises from
arterial spread of the infection
*(ii) Central type of vertebral body
involvement of one or more distant or
adjacent vertebrae (this is o en
associated with tuberculous meningitis
as the spread of the infection is via the
Batson’s plexus of veins);
*(iii) Anterior type with cortical bone
destruction
*(iv) appendiceal type
Types of Lesions

6. *The paradiscal lesion begins in the vertebral
metaphysis, erodes the cartilage plate and destroys
the disc.
*The cartilaginous end plate acts as a barrier, but
once invaded, destruction of the disc progresses
rapidly due to its relative avascularity, and the
infection goes on to involve the adjacent vertebrae.
*The early resorption of the disc leads to narrowing
of the disc space, although with progressive
involvement of the body and accumulation of
debris, the space may sometimes be widened.
PARADISCAL LESION

7. *In the central type of lesion the infection begins in the midsection of the
body instead of the metaphysis.
*It extends centrifugally to involve the whole body.
*Following the infection, marked hyperaemia and osteoporosis occur.
*The body, which is thus softened, easily yields under gravity and muscle
action, leading to compression, collapse and bony deformation.
CENTRAL TYPE

8. *Anterior lesions lead to cortical bone
destruction beneath the anterior
longitudinal ligament.
*Spread of the infection in the subperiosteal
and subligamentous planes, allows
extension of the infection to adjacent
bodies without involvement of the
intervening disc space.
*Stripping of the periosteum results in loss
of the periosteal blood supply to the body.
*This, along with thromboembolic
phenomena, periarteritis and endarteritis
can lead to ischemic reactions of the bone
contributing to the vertebral collapse.
ANTERIOR LESIONS

9. *In the appendiceal type the pedicle, the lamina, the articular process or the
spinous process is affected primarily
APPENDICEAL TYPE

10. Appendicular dorsal caries at D3 with dorsal epidural collection
causing cord compression

13. *Infection and infarction lead to the formation of bone and cartilage
sequestrae.
*The granulomatous debris and infective material may be compressed
between normal bony and ligamentous structures, and get pushed along
tissue planes, resulting in lateral extension, retropulsion into the spinal canal
or propulsion anteriorly.
Patho-anatomical consequences

14. *Tuberculous spondylitis
*thoracic spine>> lumbar >> cervical spines. (Commonst in children Tuli et
al.)

15. The cause of paraplegia in most cases is compression of the spinal cord
due to one of the following mechanisms:
Compressive paraplegia
Mechanism
In healed disease:
(a) Transverse ridge or bone anterior
to the spinal cord;
(b) Stretching or attrition of the cord
due to spinal deformity;
(c) Fibrosis of the dura
In active disease:
(a) Abscess (fluid or caseous);
(b) Granulation tissue;
(c) Sequestrated bone and disc;
(d) Pathological subluxation or
dislocation of vertebrae.

16. *Infective thrombosis of the cord, and the spinal tumour syndrome.
*Non-compressive pathologies may rarely lead to neurological deficits.
*There is no proof that the paraplegia can be caused by toxic or vascular
reactions in the cord secondary to the presence of active tuberculosis in close
relationship to the dura as was proposed by Butler.

17. *The extradural mass, caused by an abscess, sequestrae or granulation tissue,
fills the epidural space and spreads around the dural sac, thus compressing
the spinal cord.
*It may get adherent to the dura, which becomes thickened by the formation
of new fibrous tissue on its outer surface.
*The granulation tissue causes loss of function by not only direct
compression of the cord, but also by impeding venous drainage, thus causing
cord oedema.
*As a rule the dura constitutes a very good barrier against the spread of
infection.
*Rarely, the barrier is broken and the infection spreads intradurally to result in
focal or di use meningitis, arachnoiditis or a granuloma.
Pathology

18. * The usual pathological lesion in the cord, in the early stages, is a vacuolar type of myelin
degenera- tion seen in the lateral or anterolateral columns.
* This is more diffuse than seen in ischaemic lesions and may be secondary to venous
obstruction.
* Wallerian degeneration above or below the lesion is uncommon in spite of considerable
myelin damage at that level.
* Autopsy findings in chronic cases show vacuolisation and myelin degeneration.
* Acute severe lesions of the cord may be produced where there is rapid collapse of a
vertebral body with the cord stretched over a relatively intact intervertebral disc or when
sequestrae are pushed backwards into the spinal canal by a sudden angulation.
* Infarction of the spinal cord may occur due to endarteritis, periarteritis or thrombosis of
the arterial supply of the cord. An important radicular supply to the cord may be
compromised occasionally at the intervertebral foramen before it enters the dura.
* Angulation of the spine on healing may lead to the formation of a bony ridge or spur
called ‘an internal gibbus’ on the anterior wall of the spinal canal, resulting in a slow and
progressive paraparesis.

19. *Stage 1 :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.
Neurological assessment staging :
Tuli’s classification

20. *Jain and Sinha, on evaluating the ASIA scoring system and Tuli’s
classication for assessment of the neurological status of patients with
tuberculosis of the spine, found both systems wanting.
*In their study they found the Tuli system insensitive to early detection of
improvement or deterioration, while the ASIA system failed to score all
types of neurological involvement.
*They have suggested a new staging system for Pott’s spine.
Critics of classification system
Jain AK, Sinha S. Evaluation of systems of grading of neurological deficit in
tuberculosis of the spine. Spinal Cord. 2005;43:375−80.

21. *The incidence of associated visceral lesions (of the lung, kidney or lymph
nodes) varies between 40% and 50% in different series.
*Outside the nervous system in 33% (Bahemuka and Murungi)
*Pulmonary tuberculosis in 25% (Chan et al.)
*Simultaneous involvement of other bones and joints : 12% and 15%
Associated Lesions

22. *Weakness of the legs (69%), gibbus (46%), pain (21%) and a palpa- ble
mass (10%) were the most common clinical features seen in 694 cases
reported by Turgut
Clinical presentaion

23. *While usually the onset of symptoms is slow and progressive, in a small
percentage of cases the paraplegia may be of sudden onset and nearly
complete from the beginning.
*Tandon and Pathak have divided the clinical picture of Pott’s disease into
four groups:
(1) Paraplegia arising in a known case of spinal tuberculosis;
(2) Paraplegia as the presenting symptom of spinal tuberculosis;
(3) Spinal tumour syndrome and
(4) Paraplegia due to tuberculosis of the posterior neural arch.
Neurological deficit
Tandon PN, Pathak SN. Tuberculosis of the central nervous system. In: Spillane JD (Ed). Tropical
Neurology. London: Oxford University Press;1973. pp. 37−62.

24. *Lesions of the posterior neural arch, including the lamina and pedicle, while
reported to be rare by orthopaedic surgeons are more frequently seen in
neuro- surgical practice.
*This is probably due to increasing use of the CT scan and the magnetic
resonance (MR) in neurologically compromised patitents.
Posterior element involvement in Pott’s
spine

25. *The paradiscal lesion is the commonest lesion seen.
*Narrowing of the disc space is the earliest radiological finding on plain X-
rays, and when associated with a loss of definition of the paradiscal margins
of the vertebra, the diagnosis of tuberculosis is obvious.
*Lytic areas in the metaphyseal regions of the body may not be seen early, as
foci less than 1.5 cm in diameter are not demonstrable on a conventional
radiograph.
*At least 30−40% of calcium should be lost before a radiolucent area is
visible on a plain X-ray.
*Sclerosis may be seen in up to 50% of patients at presentation.
Imaging

26. Paraspinal and psoas abscess with bony destruction causing
dislocation

27. Significant pre- and paravertebral cold abscess along with compression of the
thecal sac and the exiting nerve roots

28. *The central type of disease arises from the centre of the vertebral body,
which loses the normal bony trabeculae and may show as areas of
destruction.
*Occasionally, and especially in children, the body may be ballooned out as a
result of the accumulation of inflammatory debris which expands the
weakened cortical bone.
*Towards the later stages, the diseased vertebral body may show a
“concertina” collapse and may resemble a collapse due to secondary
deposits.

29. *In the anterior type of lesion, the infection begins beneath the anterior
longitudinal ligament.
*This results in erosion of the peripheral parts of the vertebral body (in front
and on the sides), which is seen well in the lateral or oblique views as
shallow excavations.
*Destruction of the anterior surface of the vertebral body due to a tense
paravertebral abscess may simulate scalloping due to an aneurysm of the
abdominal aorta
* The tendency for erosion is greater when the aorta is in close proximity to
the paravertebral abscess as the transmitted pulsations compound the
pressure caused by the abscess.
*Stripping of the periosteum deprives the bone of its blood supply, making
the bone more liable to the destructive and scalloping effects of the lesion

30. *Lesions of the pedicle, transverse process and the spinous process appear as
erosion of the region involved and may be missed in the plain X-rays unless
speci cally looked for.

31. *A paravertebral shadow is seen on the plain X-rays due to the presence
either of an abscess or extension of tuberculous granulation tissue.
*An abscess produces typical radiological findings depending on its size and
location:
*Cervical Absces: widening of the space between the pharynx and the
vertebral body and
*Upper thoracic:
• Small size: squaring of the superior mediastinal shadow
• Large size: V-shaped shadow shifting the apices of the lungs laterally
and downwards
*Abscesses below D4 take up a typical fusiform shape;
*those below the diaphragm produce a widening of the psoas shadow.
Paravertebral abscess in pott’s

32. *CT scan is useful in assessing the destructive lesions in the vertebral column.
*classi ed the ndings on CT scan into fragmentary, osteolytic, subperiosteal,
and localised and sclerotic types.
*The fragmentary type was most com mon followed by the osteolytic variety.
*Vertebral body destruction, intraspinal extension, paravertebral so tissue
masses, extension of involvement into the neural arches and calcification
can be seen on plain scans.
COMPUTED TOMOGRAPHY

33. *With contrast, rim enhancement may be seen around a multiloculated fluid
collection.
*Calcification, representing retained bone fragments, seen with paraspinal
collections and in regions of bone destruction, is said to be pathognomic of
tuberculous infection.

34. *Early detection of marrow infiltration and dural invasion.
MRI

35. *MR is also helpful in revealing associated lesions like intraosseous
abscesses, paraspinal cold abscess, vertebral body and disc collapse, spinal
deformity, skip lesions, epidural and intraspinal extension, involvement and
compression of the cord or nerve roots and appen- dicular lesions

36. *Response to therapy may be seen as an increase in the signal intensity on
T1-weighted images from the affected vertebra.
*This has been found to correlate well with clinical signs and symptoms.
*However, radiologically evidenced progression of bone destruction may be
seen up to 14 months after the initiation of anti-tubercular therapy.
*This should not be taken as an indication of treatment failure.
MRI to follow up

37. *Distinguishing spinal tuberculosis from other spinal diseases, especially
pyogenic and fungal spondylitis and also metastatic disease of the spine is
important. Features that are indicative of a tuberculous infection are:
(1) calcification within a paravertebral abscess,
(2) presence of a large paravertebral abscess,
(3) involvement of more than two vertebral levels,
(4) involvement of the posterior elements,
(5) multicentric disease, (6) subligamentous spread and
(7) heteroge- neous MR signal.
*MRI can distinguish tuberculous from pyogenic infection in most instances
D/D

38. *While bone scans are useful in delineating osteomyelitis
*In spinal caries, Technetium scans may be negative in one-third of cases and
gallium scans negative in two- thirds.
* Their diagnostic value is limited and of historic interest only.
Radioisotope Bone Scans

39. *The orthodox conservative treatment in modern times was entirely
constitutional and included recumbency and immobilisation by body casts,
plaster beds and braces, but the results were often unsatisfactory.
*This led surgeons to attempt direct surgical procedures. Unfortunately, these
had disastrous results.
*SO THAT CALOT IN 1930 REMARKED,
* “the surgeon who, so far as tuberculosis is concerned, swears to remove the evil from the very
root, will nd only one result awaiting him—the death of his patient”.
Treatment

40. *Our policy is to advise our patients on chemotherapy to have bed rest
without immobilisation for 4−6 weeks till the pain and spasm disappear and
the general health improves. They are then allowed to get up, but wear
braces which can be discarded after a period of 6−8 weeks.
*The chemotherapy is continued for 18 months.
*The family members and contacts are checked for the presence of
tuberculous infection at the beginning of the treatment

41. 1. Neurological signs not improving or worsening within 4 weeks of
adequate conservative and drug therapy
2. Development of neurological signs with progression while on adequate
therapy.
3. Recurrence of neurological signs after improvement.
4. Rapid onset paraplegia.
5. Paraplegia with flexor or painful spasms.
6. Posterior spinal disease with spinal tumour syndrome.
7. Pre vertebral cervical abscess with difficulty in deglutition.
8. When the diagnosis is in doubt.
9. Late onset paraplegia.
10.Correction of kyphosis.
Indications of Surgical Therapy

42. *Surgery to decompress the spinal cord is indicated in patients:
(i) Failure to respond to conservative treatment;
(ii) Develop paraplegia while on appropriate chemotherapy;
(iii) Patients in an advanced stage of disease when delay in decompression
is risky;
(iv) If the diagnosis is in doubt : Diseases affecting the posterior element.
(v) Patients with posterior neural arch disease;
(vi) Those with “spinal tumour syndrome” and
Surgical indication for paraplegia

43. *Relief of pressure on the spinal cord by the most appropriate technique is the
aim of treatment when parapare-sis starts to appear. Bed rest and anti-
tubercular therapy alone have been found su cient in mild paraparesis.
*However, if there is no obvious improvement within wo or three weeks,
surgical decompression becomes necessary. Simple drainage of the cold
abscess would
*Be sufficient in those cases where the tension inside the abscess is the cause
of cord compression. In cases where the cord is compressed due to debris,
sequestra or granulation tissue, a direct approach becomes necessary.
*Laminectomy is an unsatisfactory procedure except in a few cases when the
compressing element is posterior, as in tuberculous disease of the neural
arch, or in spinal tumour syndrome.

44. 1. Pathological fractures,
2. Involvement of the anterior and posterior spinal elements,
3. Translation or dislocation of the destroyed vertebrae, and
4. Long segment disease with kyphosis
Sign of instability in pott’s spine

45. *Delaying surgical decompression for too long in the presence of paraplegia
may lead to problems, like extradural fibrosis, which may be difficult to
eradicate.
Risk of delay in surgery decompression in
spinal paraplegia

46. *Urgent early surgical intervention in the treatment of Pott’s paraplegia may
have been overstated. (Pattison).
*a series of 89 consecutive cases of Pott’s disease, out of which 85 were
treated conservatively.
*Around 83% of these returned to normal life and full activity.
*Of 41 patients, who deteriorated neurologically in the rest 3 months, 37
recovered completely. (Pattison).
Conservative treatment
Pattison recommend that the conservative regime be used confidently, especially in less privileged countries
where adequate facilities for hospital treatment may not be available

47. *The aims of treatment are to confirm diagnosis, achieve bacteriological cure,
prevent and/or treat deformity and neural compression
*With technological advancements in the field of spinal imaging, early
diagnosis of spinal tuberculosis is possible. With better chemotherapeutic
drugs available that reach pus, granulation, caseous material and bone, non-
operative management has become more effective, especially in cases
diagnosed early.
RECENT TRENDS IN THE
MANAGEMENT OF SPINAL
TUBERCULOSIS

48. *6 and 9 months courses of isoniazid plus rifampicin was excellent and
similar to that of the 18 months course of ethambutol plus PAS.
*They, however, found the 9 months ethambutol plus PAS regime inferior to
the others.
The fourteenth report of the MRC working party on tuberculosis of the spine

49. *Radical resection has been de ned as excision of the disease focus to uncover
the dura mater as completely as possible until healthy bleeding bone is
reached.
*Debridement, on the other hand, has been defined as removal of pus,
granulation tissue, caseous tissue and loose sequestrated bone from lesions
and also part of the viable bone needed to decompress the spinal cord
leaving a relatively stable spine.
*It is now recommended that radical excision is not necessary for infective
spinal lesions, like tuberculosis, where effective anti-tubercular
chemotherapy is available.
Terminology

50. *In cases of tuberculous infection of the lumbosacral region, surgery is
indicated in the group who are younger than 10 years old, as they have a
tendency to a greater kyphosis. (Rajasekharan et al.)
*Instable pott’s spine
Indication of surgery

51. *Lesions affecting the vertebral body should be decompressed anteriorly.
*Performing a posterior decompression like a laminectomy is not recommended
as it removes the healthy segment of the spinal column and renders the spine
unstable
*In the cervical spine the anterior approach is presently established as the
approach of choice.
*In the case of thoracic tuberculosis, a transthoracic transpleural approach gives
an excellent exposure of the diseased segments. However, in the presence of
compromised pulmonary function, systemic morbidity factors and extensive
disease, the risk of surgery increases and one may opt for an extrapleural
anterolateral exposure.
*Jain et al. reported that the extrapleural anterolateral approach provides the
surgeon the exposure to perform anterior decompression as well as a posterior
instrumentation at the same sitting with decreased morbidity.
*The lumbar and lumbosacral spine may be approached retroperitonially.
APPROACH

52. *Single level disease with no major substance loss, anterior debridement and
grafting alone was adequate.
(Klockner and Valencia,retrospective)
*Instrumentation is recommended in the presence of multi-level disease and
extensive kyphotic deformity
Instrumentation

53. *Years afer the primary disease of the spine, paraplegia may develop due to
recrudescence of active disease at the original site or as a result of chronic
compression and ischaemia of the cord due to pronounced kyphosis.
*Anterior decompression is helpful for these patients
Late onset Paraplegia

54. *Craniovertebral tuberculosis is rare, forming less than 1% of spinal tuberculosis
*Karapurkardescribed five types of clinical presentations:
1. The commonest was that of progressive pain in the neck, restriction of
movement and torticollis. The pain radiates to the occipital region.
Neurological deficit is usually progressive, but may be stuttering or
sudden. Some patients in this group had no neurological deficit.
2. Low grade fever, progressive neck pain and stiffness without any
neurological deficit.
3. Fever, neck pain, difficulty in swallowing and an orpharyngeal bulge.
4. Neck pain and stiffness associated with dysphagia and involvement of the
lower cranial nerves.
5. Fever, neck pain and progressive quadriparesis starting in one leg,
successively followed by the other and then the upper limbs.
Craniovertebral tuberculosis

55. *Tuberculosis of the craniovertebral junction may
*cause atlantoaxial dislocation, upward translocation of the dens,
cervicomedullary compression by tubercu- lar abscess or direct invasion by
tuberculous disease

56. *Traction and anti-tubercular drugs are the principal modes of therapy and
stability may be achieved within 3−6 months.
*The neck may be immobilised by a halo vest or a four post-cervical collar
and the patient is allowed normal activities.
*Surgical decompression is indicated in patients who do not stabilise
spontaneously or if there are progressive neurological signs.
*Following such a transoral decompression, halo traction is used till
radiological union (8−17 weeks) becomes apparent, or else a posterior
fusion and internal stabilisation may be done as second stage surgery.
Treatment

57. Thank you
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