Pott's disease, or tuberculosis of the spine, is an extrapulmonary form of tuberculosis that infects the spine. It was first described in 1779 by Sir Percival Pott. Infection can spread to the spine hematogenously or contiguously from other sites. This leads to destruction of vertebral bodies and discs, causing spinal deformities like kyphosis. Advanced cases can cause paraplegia through cord compression. Diagnosis involves imaging and microbiological tests. Prompt treatment is needed to prevent neurological deficits and deformities.

1. POTT’S DISEASE

2. Historical aspects
• Sir Percival Pott
• Monograph in 1779
• Described tuberculous
infection of the spine

3. Introduction
• One of the oldest diseases known to mankind
• Found in Egyptian mummies dating back to
3400 BC
• Pott’s paraplegia - generally used for all cases
of paraplegia due to tuberculosis of the spine
• Frequently encountered extrapulmonary form
of TB

4. • Despite its common occurrence and the high
frequency of long-term morbidity, there are
no straightforward guidelines for the
diagnosis and treatment
• Early diagnosis and prompt treatment is
necessary to prevent permanent neurological
disability and to minimize spinal deformity

5. DEFINITION
• The classic destruction of the disk space and
the adjacent vertebral bodies, destruction of
other spinal elements, severe and progressive
kyphosis subsequently - Pott’s disease
• ‘Pott’s paraplegia’ - paraplegia resulting from
tuberculosis of the spine.

6. Epidemiology
• Exact incidence and prevalence of spinal
tuberculosis in most parts of the world are not
known
• more common in children and younger adults
• Osteoarticular tuberculosis accounts for 2-3%
of all cases of tuberculosis
• 50% of these are spinal tuberculosis.
• Incidence of paraplegia in spinal tuberculosis
varies between 10% and 40%

7. • The dorsal region is most frequently involved
In a study of 100 patients with Pott’s
paraplegia, the lesion was present
• middorsal region in 47%
• lower dorsal and lumbar region in 35%
• cervicodorsal in 16%
• cervical in 7%
• double lesions in 5%

8. Pathogenesis and pathology
• Predisposing factors - poverty, overcrowding,
illiteracy, malnutrition, alcoholism, drug
abuse, diabetes mellitus, immunosuppressive
treatment, and HIV infection
• Risk factors for tuberculous spondylitis –
older age, male gender, chronic peritoneal
dialysis, imprisonment, and previous
tuberculous infection.

9. Genetic susceptibility
• association between the Fok I polymorphism
in the vitamin-D receptor gene and spinal
tuberculosis in a Chinese population was
investigated
• gene was found to be associated with
susceptibility to spinal tuberculosis

10. Infection of Bone
• Usually secondary from a pulmonary lesion or
genitourinary system infection
• By hematogenous or lymphatic spread.
• Contiguous extension from a pulmonary
abscess can lead to thoracic spondylitis
• Hematogenous spread may occur via the
arterial or the venous route.

11. Arterial Extension
• An arterial arcade, in the subchondral region
of each vertebra - derived from anterior and
posterior spinal arteries
• forms a rich vascular plexus
• facilitates hematogenous spread of the
infection in the paradiskal regions.

13. Venous Extension
• Batson’s paravertebral venous plexus
• valve-less system
• allows free flow of blood in both directions
depending upon the pressure generated by
the intraabdominal and intrathoracic cavities
• Spread of the infection this venous system
may be responsible for central vertebral body
lesions.

15. Noncontiguous vertebral spread
• Spread via vertebral venous system - spreads
to multiple vertebrae
• Subligamentous extension of the tuberculous
abscess can also result in noncontiguous
spread

16. Classification
• Tubercular spondylitis, is classified into the
following varieties according to the
involvement of the vertebra:

17. Types of vertebral lesions
• 5 types:
1. Paradiscal- Arterial spread
2. Central – Venous spread
3. Anterior- Subperiosteal spread
4. Appendicular
5. Articular
Paradiskal, anterior, and central
are the common types

18. Paradiscal
• Commonest variety
• involves the adjacent margins of two
consecutive vertebrae
• The intervening disc space is reduced and the
vertebral margins appear fuzzy
• The infection is via the arterial blood supply,
which is segmental - supplies inferior half of
superior vertebra and superior half of inferior
vertebra

19. Central
• infection comes via the venous
• involves the central portion of a single
vertebra, the disk is not involved
• collapse of the vertebralbbody produces
vertebra plana - indicates complete
compression of the vertebral body

20. Anterior marginal
• The lesion begins as a destructive lesion in
one of the anterior margins of the body of a
vertebra
• minimally involving the disc space

21. Posterior/Appendicular
• The disease localizes itself in the posterior
elements i.e. the lamina, pedicle or the
spinous process.
• infection is via the arterial supply to these
structures
• no involvement of the body of the vertebra.
• may present primarily as neural deficit
without any lesion in the body

22. Synovial
• involves synovium of atlanto-axial and
atlanto-occipital joints
• infection starts with the hematogenous
seeding of the synovial tissue
• The synovitis involves the lateral masses and
articular surfaces
• The combination of bony and ligamentous
destruction leads to instability of the atlanto-
axial complex
• secondary basiliar invagination

23. • All the varieties can progress to other parts of
the same vertebra or to the adjoining
vertebrae if left untreated
• All varieties can ultimately lead to a
panvertebral disease and pathological
dislocation in advanced cases

24. Formation of Cold Abscess
• Vertebral TB develops as an exudative lesion
due to hypersensitivity to MTB
• Exudate consists of serum, leukocytes,
caseous material, bone fragments and
tubercle bacilli
• spreads under the anterior longitudinal
ligament, posterior longitudinal ligament and
available tissue planes for varying distances

25. • Spread of the disease beneath the anterior or
posterior longitudinal ligaments - involves
multiple contiguous vertebrae.
• Penetrates ligaments and follows the path of
least resistance along fascial planes, blood
vessels, and nerves to distant sites from the
original bony lesion and forms a swelling –
Cold Abscess

26. Cervical region
• exudate collects behind prevertebral fascia
and protrude as a retropharyngeal abscess
• Abscess may track down the mediastinum to
enter trachea, esophagus or pleural cavity
• May spread laterally into the sternomastoid
muscle and form an abscess in the neck

27. Thoracic spine
• exudate may remain confined locally for a
longtime
• Appear in radiographs as fusiform of bulbous
paravertebral abscess
• Tension may force the exudate to enter the
spinal canal and compress the cord
• The abscess enters the spinal canal either
through the intervertebral foramina or
through the posterior cortex of the vertebral
body

29. • In prevertebral region, the abscess may cause
prolonged pressure necrosis and
devascularization resulting in anterior
scalloping of the vertebrae
• Can penetrate the anterior longitudinal
ligament to form mediastinal abscess or pass
downwards through medial arcuate ligament
to form a lumbar abscess

30. Lumbar vertebrae
• most commonly enters the psoas sheath
• manifest radiologically as psoas abscess or
• clinically as a palpable abscess in the iliac
fossa
• Can gravitate beneath the inguinal ligament to
appear on the medial aspect of thigh

31. PATHOPHYSIOLOGY OF SEQUALE
OF POTT’S SPINE

32. Spinal Deformity
• deformity is an inevitable reality
• destruction of the intervertebral disk space
and the adjacent vertebral bodies
• anterior vertebral body destruction with
relatively intact posterior structures –
Collapse of the anterior column

33. • Local disease limited to one or two bodies -
knuckle
• Involvement of two to six bodies - gibbus
• More than six - kyphus.
• In active disease, deformity progresses until
diseased vertebrae attain autostabilization -
stage of stability is established with adequate
contact of two vertebral bodies

36. • In progressive kyphosis, the apical vertebrae
are slowly pushed towards the spinal canal
and eventually form an internal gibbus.
• This causes stretching of the cord over the
internal gibbus and leads to late onset
paraplegia

37. • Even after healing, progressive deformity may
occur in children below 10 years
• due to arrested anterior growth as a result of
tuberculous destruction of vertebral
endplates and continued posterior growth
• Destruction of only half of the vertebrae
results in unequal collapse and scoliosis

38. • Combined anterior and posterior element
involvement may result in pathologic
dislocation of the spinal column
• selective posterior element involvement –
spondylolisthesis, extremely rare

39. Paraplegia
• most serious complication of spinal
tuberculosis
• The risk of paraplegia is highest in the
cervicodorsal region
Space of spinal canal is smallest in the dorsal
region
Abscess remains confined under tension and is
forced into the spinal canal
Spinal cord terminates below L1

40. • prognosis depends
• Severity
• Duration
• level of deficit
• activity of disease
• general condition of the patient
• presence of associated disease and nature of
treatment

41. Classification
• Hodgson, in his classical paper on Pott’s
paraplegia, classified paraplegia into two
groups according to the activity of the
tuberculous infection
• paraplegia of active disease (early-onset
paraplegia) and paraplegia of healed disease
(late-onset paraplegia)

43. Paraplegia in Active Disease
• requires active treatment, has a better
prognosis
• due to compression of the cord by abscess,
sequestrae and granulation tissue
• Noncompressing causes are tuberculous
arachnoiditis, vasculitis and myelitis

44. • Destruction of the anterior vertebral column
leads to subluxation and subsequent
dislocation of the spine
• Concertina collapse - bulges into the
parenchyma of the spinal cord
• When both elements are involved, spinal
instability is responsible for paraplegia

45. Paraplegia without vertebral lesion
• epidural granuloma - 'spinal tumour
syndrome' type of spinal tuberculosis
• intradural and intramedullary spinal cord
abscess
• Tuberculous arachnoiditis

46. Paraplegia in Healed Spinal
Tuberculosis
• paraplegia occurs two to three decades after
active infection
• often associated with marked spinal
deformities
• Commonly, severe kyphosis causes stretching
of the relatively immobile spinal cord over the
internal gibbus
• The tough, fibrous membrane encircling the
cord (pachymeningitis externae) aggravates it

47. Mechanisms of paraplegia

48. Spinal artery thrombosis
• acute infective thrombosis of the anterior
spinal artery
• Sudden and acute onset paraplegia
• rapidly progressing paraplegia in either a
preexisting disease or without a preexisting
disease
• Has the poorest of prognosis as far as neural
recovery is concerned.

49. Abscess and Sinus
• Cold abscess and sinus formation have been
the hallmarks of tuberculosis in the past
• With the advent of multi-drug chemotherapy,
these have decreased

50. Clinical Features of Pott’s Spine
• The classical constitutional features of
tuberculosis signifying active disease are
malaise, loss of weight and appetite, night
sweats, evening rise of temperature
generalized body ache and fatigue
• History of tuberculosis in the family or close
relatives and past history of tuberculosis may
be important clues

51. • The progression of spinal tuberculosis is slow
and insidious.
• The total duration of the illness varies from
few months to few years, with average
disease duration ranging from 4 to 11 months.

52. Vertebral Disease
• local pain, tenderness, stiffness of the affected
part, spasm of the local muscles with
restricted mobility, a cold abscess, scars,
sinuses in the surrounding area and deformity
• Localised pain over the site of involvement –
most common early symptom and pain may
worsen with activity
• intensity of pain varies from constant mild dull
aching to severe disabling.

53. • pain may be aggravated by spinal motion,
coughing, and weight bearing
• Pain may be referred along spinal nerves –
misdiagnosed as neuralgia, sciatica, or
intraabdominal pathology
• As infection progresses, paraspinal muscle
spasm occurs
• obliterates normal spinal curves and all spinal
movements become restricted and painful

54. Spinal deformity
• hallmark feature of spinal tuberculosis
• Type of spinal deformity depends on the
location of the vertebral lesion
• Atlanto-axial tuberculosis presents as
torticollis
• Kyphosis, the most common spinal deformity,
occurs with lesions involving thoracic
vertebrae.

56. Cold Abscess
• The site of abscess depends on the region
affected
• Tuberculosis of the atlanto-axial region
presents as a retropharyngeal swelling in the
midline
• Lower cervical tuberculosis - prevertebral
abscess
• track into the mediastinum causing pressure
and displacement of the trachea leading to
respiratory stridor and dysphagia

57. • cervical abscess can track along the brachial
plexus producing an axillary swelling
• Similar swellings may be observed in the
anterior and posterior triangles of the neck
• thoracic spine, the cold abscess usually
presents as a fusiform or bulbous
paravertebral swellings and may produce
posterior mediastinal lumps

58. • In the thoracic region, the abscess tracks
along the neuro-vascular bundle and presents
itself in the chest wall or the paraspinal region
• Psoas and iliacus abscesses always represent
dorsolumbar tuberculosis
• may also present as an abdominal lump or a
flexion deformity of the hip (pseudo-hip)

59. • Posteriorly, extension of the abscess causes a
swelling in the petits’ triangle overlying the
posterior iliac crest

60. Paraplegia
• Paraplegia may occur at any time and during
any stage of the vertebral disease.
may present as:
• paraplegia developing in a known case of
spinal tuberculosis
• paraplegia as a primary presenting symptom
• paraplegia presenting like a spinal tumor
• paraplegia due to tuberculosis of posterior
neural arch

61. • Motor functions are always affected before
and to a greater extent than the sensory
functions
• diseased area in the spine lies anterior to the
cord thus being nearer to the motor tracts
• high sensitivity of motor tracts to the
compression of cord

62. Tuli’s classification
• Grade-I - Negligible - Patient unaware of
neurological deficit, clinician detects signs of
upper motor neuron lesion
• Grade-II Mild Patient aware of deficit but
manages to walk with support
• Grade-III Moderate Nonambulatory because
of paralysis (in extension), sensory deficit less
than 50%

63. • Grade-IV Severe III+flexor spasms/paralysis in
flexion/flaccidity/sensory deficit more than
50%/sphincters involved.

64. References
• Tropical neurology U. K. Misra, J. Kalita, R. A.
Shakir
• Garg, Ravindra Kumar, and Dilip Singh
Somvanshi. “Spinal Tuberculosis: A
Review.” The Journal of Spinal Cord
Medicine 34.5 (2011): 440–454.
• Tandon PN, Pathak SN. Tuberculosis of central
nervous system. In: Spillaine JD ed. Tropical
Neurology. London: Oxford University Press,
1973:37-62.

65. • Tuli S. Tuberculosis of the Skeletal System.
New Delhi: Jaypee Brothers, 1991:268.