Spine

Spinal tumor syndrome is not a condition in itself. It is a clinical label for the patient’s condition with many differentials in the offering.

Most often, the term is used in cases of spine tuberculosis where there is no apparent osseous lesion.

To understand spinal tumor syndrome one must first know about the typical presentation of tuberculosis of the spine.

Most of the typical cases involve anterior bodies or posterior elements of a vertebra. Back pain is the most common presenting feature which lingers on for a long time. There would be spine deformity and slow appearance and worsening of neural deficits.

Most of the tubercular lesion present this way and lesions are visible on x-rays.

However, tuberculosis is known to involve just soft tissue of the spine without any involvement of bony lesions.

It was earlier thought to be extremely rare. But with new imaging, more and more cases are being labeled as extraosseous spinal tuberculosis.

These lesions may present with sudden onset neural deficit to the extent of paraplegia or quadriplegia [very unusual].

Now a patient presents with the neural deficit and gives no prior history of back pain. Moreover, there is no deformity in the spine, the back is absolutely normal.

This patient has a mass lesion in the spinal cord leading to a neural deficit. Spinal cord tumors behave this way – no back pain, back normal on examination and even normal x-rays [except when calcified].

Could it be a tumor?

Could it be tuberculosis?

We cannot know that clinically though patient’s other parameters and endemicity might point to the later. So we label the condition as spinal tumor syndrome.

The differential diagnoses include extraosseous tuberculosis like localized tuberculoma or a diffuse granuloma and spinal cord tumors.

In the endemic region, the patient would turn out to have tubercular lesions, mostly.

Evaluation of Patient with Spinal Tumor Syndrome

An atypical spinal tuberculosis is difficult to identify on plain radiographs. X-rays even fail to identify bony lesions <1cm.

Advanced imaging techniques like CT and MRI are required to delineate the lesion clearly.

MRI is the gold standard in imaging of these lesions.

CT-Myelography is another option.

Treatment

As these lesions present with spinal compression and neural deficit, the treatment is surgical.

A cover of antitubercular medications is started and the patient is operated at the earliest.

Early surgical intervention gives good results and sometimes dramatic.

Importance  of the Term

The term spinal tumor syndrome is a confusing term. It is a clinical or rather academic label which wants to convey the uncertainty of the findings. Any tubercular spinal lesion that does not have the typical clinical features is referred to as atypical spinal tuberculosis which is a better term than spinal tumor syndrome.

The patients of spinal tuberculosis who present with the features of compressive myelopathy and radiculopathy both, without any radiologically evident bony lesion are described as spinal tumor syndrome. The differential diagnoses are neurofibroma, meningioma, lipoma, astrocytoma and other neural tissue tumors too.

These lesions are difficult to diagnose clinically and radiographically. The reported incidence of atypical spinal tuberculosis is about 2.1%.

References

• Hasengawa K, Hideyuki M et al. Spinal tuberculosis. Clin Orthop. 2002; 403: 100-103.
• Martin RJ, Yuan HA. Neurosurgical care of spinal, epidural, subdural, and intramedullary abscess and arachnoiditis. Spinal infection. Orthop Clin North Am. 1996; 27(1): 125-136.
• Pande KC, Babhulkar SS. Atypical spinal tuberculosis. Clin Orthop. 2002; 398: 67-74.

Pyogenic vertebral osteomyelitis is a type of spinal infection which may result from direct trauma, the spread of infection from adjacent structures or hematogenous spread from the distant focus of infection. It can have devastating complications if untreated which could be a pathological fracture, epidural infection, and compression of the neural structures.

Vertebral osteomyelitis is considered uncommon, there is a suggested increase in spinal infections because of increased use of vascular devices, other instrumentation and increasing rates of IV drug abuse.

Pathophysiology of Vertebral Osteomyelitis

The spine is column formed by stacking of vertebrae, intervertebral discs and associated joints stabilized by muscles, tendons, and ligaments. Cord and roots are contained in the vertebral column and it serves to protect them.

The spine starts below the skull and forms articulations with the skull for neck motion. It ends at the coccyx, a point palpable below the beginning of gluteal cleft posteriorly.

It has the following regions –

• Cervical spine – First seven vertebrae in the spinal column (C1-7)
• Thoracic – Next 12 vertebrae (T1-12) and is stabilized by the attached rib cage and intercostal musculature.
• Lumbar spine – Next five vertebrae (L1-5), located between the relatively immobile segments of the thoracic and sacral segments.

95% of pyogenic spinal infections involve the vertebral body, and only 5% involve the posterior elements of the spine. The difference of involvement is due to blood supply which is more in vertebral bodies.

A distant focus of infection provides an infective nidus from which bacteria spread by the bloodstream to the spinal column. The skin and the genitourinary tract are sites. Septic arthritis, sinusitis, subacute bacterial endocarditis, and respiratory, oral, or gastrointestinal infection could be other sources of infective agents.

[Approximately 30-70% of patients with vertebral osteomyelitis have no obvious prior infection.]

Circulating bacteriae may enter the vertebra or a disc space via small metaphyseal arteries arising from larger primary periosteal arteries that, or venous system.

Bone infarct may result from blockage of metaphyseal arteries by septic thrombi. The sequestrum facilitates colonization.

The disc is avascular and is secondarily invaded by bacteria from the endplate region after the metaphyseal bone is infected.

Retrograde seeding of venous blood via the Batson plexus can also cause the infection. During periods of increased intra-abdominal pressure, venous blood is shunted toward the vertebral venous plexus.

Spread of contiguous infection into the vertebrae and disc from a retropharyngeal abscess or a retroperitoneal abscess may cause resulting in osteomyelitis and discitis.

Pyogenic infection can affect any vertebra but most vertebral body infections occur in the lumbar spine because of the blood flow to this region of the spine. Tuberculosis has a predilection for the thoracic spine, and IV drug abusers are more likely to contract an infection of the cervical spine.

The combination of mechanical compression of the spinal cord by pus or granulation tissue can result in ischemia with spinal cord infarction, which accounts for the rapid neurologic progression.

Patients with a spinal epidural abscess may progress to complete paralysis within minutes to hours, even while receiving optimal antibiotic therapy.

Pathological fractures can occur due to the softening of the bone, and present with acute spinal cord compression.

Risk Factors for Vertebral Osteomyelitis

Risk factors for developing osteomyelitis include conditions that compromise the immune system, such as the following:

• Advanced age
• Intravenous (IV) drug use
• Diabetes mellitus  
• Organ transplantation
• Malnutrition
• Congenital immunodepression
• Long-term systemic administration of steroids
• Cancer
• Surgical site infection

The common microorganisms that cause vertebral osteomyelitis are

• Staphylococci
• Enterococcus species
• Enterococcus species
• Pseudomonas aeruginosa
• Enterobacteriaceae
• Beta-hemolytic streptococci
• Propionibacterium acnes
• Tuberculosis
• Fungus
• Yeast
• Parasitic organisms

Clinical Presentation

Adult patients usually present with insidious onset back pain. There is often a history of back pain several weeks or months of gradually progressing neck or back pain that increases with movement.

The pain gradually increases in intensity and eventually becomes severe and unrelieved by medication and rest.

Neural signs are often not present until late.

The children present with more acute symptoms and discitis. [More about that here]

In most of the patients, there is only mild tenderness over the spinous process of the involved vertebra, and minimal spasm may be present.

The range of motion may be decreased. Fever is not present in 50% of the patients.

In advanced disease, bony collapse, the spread of the infection underneath the posterior longitudinal ligament, or frank epidural abscess may cause compression of the spinal cord or nerve roots.

Radicular signs followed by neural deficit suggests epidural abscess. [Spinal epidural abscess occurs in 5-18% of cases]

It may be noted that cervical vertebral osteomyelitis is associated with paralysis more commonly than either thoracic or lumbar infection.

A detailed motor and sensory examination should be performed

Sensorimotor examination suggests the level of the affliction of the spinal cord. [Neural deficits occur in about 15%]

Secondary sepsis may occur in uncontrolled infections.

Lab Studies

• Elevated ESR and CRP
• A minimal increase of leucocytes [Unlike other infections]
• Blood cultures for establishing the diagnosis
• Aspiration biopsy for cytology, culture, and sensitivity
  • CT guided
  • Positive only 60-70% of the time.
  • Trocar Biopsy/open biopsy when does not yield material

Imaging Studies

X-rays

• Normal in the first 2-4 weeks
• Reduced disc space
• Destruction of the endplates around the disc
• Rarefaction, loss of bony trabeculation close to the cartilaginous plate, and an irregular narrowing of the vertebral disk space
• Vertebral body collapse
• Evidence of rapid bone regeneration
  • Bone spurs
  • Dense new bone
• Paravertebral soft-tissue shadow

CT

• Depicts osteomyelitis earlier
• Hypodensity at the site of infected discs
• Lytic fragmentation of the involved bone,
• Gas within an involved vertebra
• Decreased density of adjacent vertebrae
• Epidural and paraspinal extension of infection

MRI

• Destructive and expansile lesions involving two adjacent vertebrae and the in-between disc
• Low-density changes in bone and disc on T1- weighted images
• High-density changes are seen in these structures on T2-weighted images,
• Gadolinium enhancement shows the involved structures.
• Soft tissue infections are visualized better
  • Paravertebral infection
  • Collections under the posterior longitudinal ligament
  • Epidural abscesses

Radionuclide scanning

Radionuclide scan findings become positive long before plain film changes are evident.

Treatment of Vertebral Osteomyelitis

Most patients with pyogenic vertebral osteomyelitis respond to medical management. Surgery is indicated where medical treatment is not successful.

Medical Treatment

The treatment of vertebral osteomyelitis must be individualized according to the patient’s condition. Underlying infections (eg, retropharyngeal, pelvic, decubital) require simultaneous treatment.

Initially, broad-spectrum antibiotics are given covering both gram-positive and gram-negative organisms, aerobes and anaerobes, including methicillin-resistant S aureus.

As S aureus is the most common agent, it should be covered by most of the antibiotics. Specific antibiotics can be instituted when culture and sensitivity reports are available.

With lack of response to antibiotics and negative cultures, less common organisms should be considered.

Antibiotics are given for 6-8 weeks.

Choice of antibiotics as per agent is given in the table below, as per IDSA guidelines

ESR and CRP are markers of the disease. Antibiotics can be withdrawn when the patient is without fever and pain, ESR has fallen to at least two-thirds of the pretherapy level, and there are not as neurologic deficits.

A persistent high ESR demands additional antibiotics. Repeat biopsy can be taken from the infected vertebra to see if organisms not susceptible to the chosen antibiotics.

Bracing is recommended for 6-12 weeks. It provides rest to spine, restrict motion and allows fusion of the vertebrae. A rigid brace is preferred.

A residual kyphosis after healing, if severe, may require corrective surgery later.

Surgical Treatment

Indications for surgery include the following:

• Significant bony involvement requiring debridement and stabilization
• Neural deficits
  • Significant kyphosis
  • Compression due to abscess/collapse
  • Infection in the epidural space
• Infection not responding to antibiotics

Goals of surgery are the preservation of neural function and achievement of stable bony fusion without deformity.

The anterior disease is best addressed by an anterior or anterolateral surgical decompression and debridement. Debridement and drainage should be followed by extensive irrigation with antibiotic solution. In most cases, the closure can be done primarily, with a surgical drain left in place.

Patients with extensive vertebral destruction usually require instrumentation and fusion.

Postoperatively orthosis for a variable period is given. The antibiotics are adjusted according to the culture results.

The patient should be watched for decubitus ulcers, lung problems, and deep vein thrombosis.

Once the correct treatment is implemented, patients require neurologic monitoring to exclude progressive neurologic deterioration.

The guidelines are published by the Infectious Disease Society of America. These guidelines include evidence and opinion-based recommendations for the diagnosis and management of patients with native vertebral osteomyelitis treated with antimicrobial therapy, with or without surgical intervention.

Native vertebral osteomyelitis in adults is often the result of hematogenous seeding of the adjacent disc space from a distant focus.

It is a rare spinal condition, native vertebral osteomyelitis is the most common form of hematogenous osteomyelitis for patients 50 to 70 years of age.^.

Native vertebral osteomyelitis (NVO) can be a difficult disease to diagnose as the symptoms are non-specific. These symptoms could be a back pain that does not relieve, fever, and elevated inflammation markers.

The new guidelines present a comprehensive framework for proper clinical diagnostics and treatment of the condition.

Here are the recommendations.

When to Suspect Native Vertebral Osteomyelitis

NVO should be suspected in patients with

• New or worsening back or neck pain and fever
•  New or worsening back or neck pain + elevated ESR or CRP
• new or worsening back or neck pain and bloodstream infection or infective endocarditis (strong, low).
• Fever and new neurologic symptoms with or without back pain
• New neck or back pain, following a recent episode of Staphylococcus aureus bloodstream infection

Recommendations for Diagnostic Work Up

• Medical and motor/sensory neurologic examination

• Obtain bacterial (aerobic and anaerobic) blood cultures (2 sets) and baseline ESR and CRP
• Spine MRI

• If MRI is contraindicated (eg, implantable cardiac devices, cochlear implants, claustrophobia, or unavailability) or unavailable, consider one of the following

• • Spine gallium/Tc99 bone scan
  • Computed tomography scan
  • Positron emission tomography when MRI cannot be obtained
• Special tests
  • Consider blood cultures and serologic tests for Brucella species in patients from endemic areas for brucellosis
  • Fungal blood cultures in patients at risk for fungal infection
  • Tuberculin test purified protein derivative test or an interferon alpha release assay in patients at risk for Mycobacterium tuberculosis NVO (endemic areas, low immunity, HIV)

• Aspiration/Biopsy
  • When clinical, laboratory and imaging studies suggest NVO and microbiologic diagnosis has not been established by blood cultures or serologic tests.

• • In patients with S. aureus, S. lugdunensis, or Brucella species bloodstream infection
  • Not recommended in patients with suspected subacute NVO (high endemic setting) and strongly positive Brucella serology (strong, low).
  • Addition of fungal, mycobacterial, or brucella cultures on image-guided biopsy and aspiration specimens should be done in patients with suspected NVO if epidemiologic, host risk factors, or characteristic radiologic clues are present (weak, low).
  • Histopathology/cytology if sufficient sample is available

• Repeat Aspiration Biopsy/ percutaneous endoscopic discectomy and drainage/Excisional Biopsy
• Growth of skin concomitants from previous aspiration and the absence of concomitant bloodstream infection
• To exclude difficult-to-grow organisms (eg, anaerobes, fungi, Brucella species, or mycobacteria) in negative first image-guided aspiration biopsy

Treatment Recommendation for Non-Vertebral Osteomyelitis

If the patient is normal, stable hemodynamics and stable neurologic examination  – wait for culture and sensitivity before starting antibiotic therapy.

Empirical antibiotic therapy should be started in cases of hemodynamic instability, sepsis, or severe or progressive neurologic symptoms. The antibiotics can be switched to specific antibiotics.

Antibiotics are recommended for a period of six weeks.

In case of  Brucella species infection, antibiotics are given for 3 months.

Antibiotic agents that can be onsidered are given in the table

Indications for Surgery

• Progressive neurologic deficits, progressive deformity, and spinal instability with or without pain despite adequate antimicrobial therapy.

• Surgical debridement with or without stabilization in patients with persistent or recurrent bloodstream infection  if another source without alternative source has been ruled out
• Worsening pain despite appropriate medical therapy

It is advised to refrain from surgery in with worsening bony imaging findings at 4–6 weeks in the setting of improvement in clinical symptoms, physical examination, and inflammatory markers.

Follow Up

• Monitoring systemic inflammatory markers (ESR and or CRP) after approximately 4 weeks of antimicrobial therapy, in conjunction with a clinical assessment.
• A follow-up MRI to assess spinal tissues in patients with  are judged to have a poor clinical response

Treatment Failure

Unchanged or increasing values of serum markers [ESR and CRP] after 4 weeks of treatment along with clinical assessment should bring suspicion of treatment failure.

• Obtain a follow-up MRI
• Obtain additional tissue samples for microbiologic either by aspiration biopsy or by open surgery.
•  surgical sampling

Samples should be for histopathology, aerobic and anaerobic bacterial cultures, and fungal, brucella, and mycobacterial cultures. In select circumstances, serologic assays for uncommon causes should be considered as well.

Source

Spinal tuberculosis  with neural deficit can occur in the lesions when disease comrpresses the cord. Potts paraplegia is term for this deficit in TB spine

Spinal tuberculosis  is the most common form of skeletal tu­berculosis accounting for 50 percent of osteoarticular tuberculosis. Neural compression in spinal tuberculosis may lead to tetraparesis-tetraplegia or paraparesis-paraplegia.

Pathology of Neurological Complications in Spinal Tuberculosis

A neurological complication is observed mostly with dorsal spine affection because

• Most commonly affected
• Narrow canal
• Anterior longitudinal ligaments contain the abscess which produces cord compression unlike in lumbar spine where it trickles down in psoas muscle.

Pott’s paraplegia is of two types

• Paraplegia of early-onset – found in the early and active stage of the disease usually within the first 2 years
• Paraplegia of late onset-found late in the course of the disease usually many years after the apparent quiescence of the disease

Causes of Pott’s paraplegia are discussed below

During Active Disease

Extrinsic causes

• Abscess
• Granulation tissue
• Tubercular debris
• Tuberculous caseous tissue
• Localized pressure due to salient (internal gibbus)
• Pathological subluxation/dislocation of vertebrae.

Intrinsic causes

• Inflammatory edema
• The affection of meninges and cord by tu­berculous inflammation
• Infective thrombosis/endarteritis of spinal vessels

In Healed Disease

Extrinsic causes

• A transverse ridge of bone anterior to spinal cord producing localized pressure.
• Constricting scarring around/or dura.

Intrinsic causes

• Inflammatory edema.
• Stretching of cord over the internal salient leading of interstitial gliosis.

More than one cause may be acting at the same time.

Extrinsic causes of paraplegia causing compression on the spinal cord can be demonstrated objec­tively on imaging like myelography or MRI.

It has been found that up to 75 percent canal occu­pancy can occur without affecting neural status.

But, when other causative factors such as a vascular cause or mechanical instability can add to produce paraplegia at lesser canal compromise.

With magnetic resonance imaging, the cord and soft tissue could be visualized directly and the patient showing relatively preserved cord size with evidence of myelitis/edema respond well to chemotherapy with or without surgical decompression.

Predominantly fluid collection in extradural space resolves well with antitubercular chemotherapy alone, and a conservative trial is likely to be rewarding in cases who along with this finding have apparently normal cord parenchyma at the inception of treatment.

In patients with an extradural collection of mixed or granulomatous (dry) nature showing en­trapment of a normal size cord or a constric­tion of the cord with features suggestive of myelitis shows improvement in neural deficit if taken up for surgical decompression early.

Patients have significant cord compression/constriction showing strangulation with evidence of myelomalacia are those in which irreversible changes have already set in and are not likely to show a favorable response even after surgical decompression

Mild cord atrophy was observed in all patients who had excellent neural recovery after non-operative/operative treatment. In paraplegia with the healed disease, the cord was found atrophied with edema in patients having a mild neural deficit.

Staging of Neural Deficit

Frankel’s classification and ASIA Score classify the severity of neu­ral deficit in cases of acute spinal trauma. But these do not classify all types of neural deficit.

Following classification is by Tuli seems most rational, and it classifies all cases of paraplegia.

Stage I

The patient does not appreciate weakness but clinician notices clumsiness of gait and signs sug­gestive of upper motor neuron lesion (planter ex­tensor and ankle clonus)

Stage II

Patient has motor weakness, signs of upper motor neuron lesion, but power is sufficient that he/she manages to walk (motor power grade 3 or above)

Stage III

The patient is bedridden (severe mo­tor weakness) with signs of upper motor neuron paraplegia, sensory loss less than 50 percent.

Stage IV

The complete motor weakness with loss of sensation more than 50 percent and/or bladder bowel in­volvement and/or flaccid paraplegia and/or paraplegia with flexor spasm.

Lesions around conus and cauda equina present with sphincter involvement very early in the disease process and also have upper/lower motor neuron presentation.

Deficit associated with Intraspinal granuloma and with the atypical location of lesions may not always fit in the classification which accounts for less than 5 % of tuberculosis lesions.

Clinical Presentation

The patient has pain which aggravates on the movement of the spine. The pain is acute and stabbing,. Sometimes the patient may present with acute neural deficit f especially in cases of intraspinal granuloma or posterior complex disease.

Imaging

X-rays

Plain radiography can provide adequate information about a number of vertebrae involved, the level of bone destruction and the angle of kyphosis particularly in a paradiscal tuberculous lesion. The lesion is seen as rarefaction of the affected vertebrae, the fuzziness of the adjacent disc margin to complete obliteration of intervertebral disk space, the collapse of ver­tebrae leading to kyphosis of the vertebral column.

The paravertebral shadows are seen as a fusiform shadow in the Dorsal spine and increased prevertebral soft tissue shadow in the cervical spine.

The involvement of the neural arch is not well seen in a plain radiograph if the lesion is less than 1.5 cm in diameter.

Therefore the lesion is visualized on x-ray after some progression of the disease.

CT

CT scan detects bone destruction earlier than an x-ray. It can define the site and extent of bony involvement and soft tissue affection.

It is very useful in the detection of neural arch disease which could often be missed on x-rays.

CT scan shows bone destruction earlier than plain X-Rays. It helps in early detection of the tuberculous lesion and helps in evaluating the healing of the lesion. It is a good imaging tool in such location of disease which can’t be appreciated on plain x-ray such as in the junctional area of the spine.

CT guided fine needle aspiration cytology is a useful and minimally invasive method ascertaining the histological diagnosis of the ver­tebral lesion.

MRI

MRI is more sensitive for detection of the presence of musculoskeletal infection. It possesses high tissue contrast resolution with multiplanar capabilities. The lesion seen hence is more extensive than seen on plain x-ray. The better soft tissue resolution helps in evaluating the spinal cord and pre-paravertebral abscesses.

MRI can detect cord health and surrounding fluid, therefore has overtaken myelo, CT myelo to check continuity of the space.

Ultrasound

Ultrasonography can differentiate between the solid or cystic nature of abscesses.

Treatment of Pott’s Paraplegia

The best treatment of neurological complica­tions in the tuberculous spine is the prevention of para/quadriplegia by early identification and treatment.

A detailed discussion of the treatment of tuberculosis of the spine

Paraplegia of early onset (with active disease)

Tuberculosis of spine with neurological complications warrants urgent and meticu­lous care. Any delay in establishing the diagnosis and in instituting appropriate treatment is a major contributory factor to incomplete neural recovery, increased morbidity, and even mortality. Three definite methodologies has been described.

Earlier, most surgeons preferred non-operative treatment and rarely performed surgery for fear of worsening the already existing neural deficit.

Then emerged the second school of thought which advocated uni­versal surgical extirpation in all cases of tu­berculous paraplegia with the advantage of good quality and speedy neural recovery. The improved drug penetration was achieved since surgical decompression removes a fibrous barrier to drugs and the diagnosis is established beyond doubt.

Both method­ology of management are extreme. An absolute non-operative approach to Pott’s paraplegia is considered unjustifiable because very valuable time may be lost, while at the same time, surgery in every patient also seems to be unnecessary for every patient.

This has been very well achieved by Middle Path Regime [named so because it stands somewhere in the middle of the above two approaches.

A judicious combination of conservative therapy and operative decom­pression when needed should form a comprehensive integrated course of treatment for tuberculosis of the spine with neurologi­cal complications.

The approach of this treatment is shown in the diagram above.

The rationale of Middle Path Regime

Tubercular liquid pus, granulation tissue, caseous tissue causing compression and inflammatory edema are amenable to non-operative treatment.

In middle path regimen, 3 to 4 weeks delay will give a chance for above-mentioned reasons of neural deficit to subside for the patient to show a neural recovery, thus, to avoid surgical de­compression in those cases which would otherwise show neural improvement.

The patient showing relatively preserved cord with evidence of edema/myelitis with the predominantly fluid collection in extradural space will resolve well on non-operative treatment.

The compression in the tu­berculous spine and thus neurological complication is a slowly developing process (exception vascular catastrophe and pathological subluxation/ dislocation). A short delay in surgical decompression does not significantly alter the long-term recovery of neurological function.

Indications of surgery in Tuberculous Para/quadriplegia

Clinical factors

• Paraplegia with rapid onset [Indicates unusually severe paralysis from the mechanical accident]
• Severe paraplegia
  • Flaccid paraplegia
  • Paraplegia in flexion
  • Complete sensory loss
  • Complete loss of motor power for more than 6 months.
• Spinal tumor syndrome [the condition shows neural deficit without any local clinical signs or changes on x-ray images]
• Recurrent paraplegia.
• Paraplegia accompanied by uncontrolled spasticity of such severity that reasonable rest and immobilization are impossible.
• Patient with massive prevertebral abscess [ Neurological signs are associated with the difficulty of swallowing/ respiration.]
• Pretreatment Kyphosis more than 60°.

Treatment factors

• Neurological complications developing during conservative treatment.
• Neural complications not showing signs of improvement after a fair trial of conservative treatment (3-4 weeks).
• Neural deficit getting worse on non-operative treatment.

Patient factors

• Painful paraplegia
  • Pain resulting from severe spasm or root compression.
• Paraplegia with onset in old age
  • Hazards of immobilization.

Surgery for Pott’s Paraplegia

The surgery aims to decompress the spinal cord. As the vertebral body is affected in almost 98% cases of tuberculosis of the spine, the surgical decompression should include full exposure of the front of the dura mater at the apex of Kyphosis.

The decompression is done by an anterior approach or anterolateral approach. Anterior decompression allows direct access to the focus of disease to expose the duramater.

Laminectomy as surgical decompression is indicated in isolated neural arch affection and in the compressive myelopathy by intraspinal tuberculous granuloma presenting as spinal tumor syndrome.

Prognosis in Tuberculous Para/ Quadriplegia with Active Disease

Factors affecting neurological recovery in tuberculous para/quadriplegia are

Age

Young patients show good neural recovery as compared to elderly patients. The children show the best neural improvement.

General Condition of the Patient.

Patients with the good nutritional state show better neural recovery. The disease in nutritionally poor patients is more aggressive as immune status is poor. Such patients tolerate surgery poorly.

Region of Spine

Cervicodorsal junction and upper dorsal spine show poor neural recovery as the canal is narrowest here.

Type of Paraplegia

The patients of neurological complications with the active disease show better neurological recovery as compared to with healed disease.

Kyphosis

he patient with severe Kyphosis show poor neural recovery. so is the case of the patients with loss of more than two vertebrae.

Duration of Paraplegia

Neurological complications of shorter duration show better neurological recovery than of longer duration because permanent changes in the cord develop in long-standing cases.

Similarly, decompression after 12 months of neurological deficit is unlikely to respond.

Progression of Neurological Complications

Rapidly developing neurological complications show poor recovery as compared to slowly developing paraplegia.

Rapidly progressive paraplegia signifies more chances of compression by disc/ sequestrae or pathological subluxation/dislocation or vascular catastrophe and permanent cord damage is more likely.

Severity of Neurological Complications

Patient presenting with severe paraplegia as stage IV paraplegia or paraplegia with flexor spasm or with sphincter involvement or with complete sensory loss show poor neural improvement whereas less severe grade of neural deficits shows a partial cord involvement thus better chances of neural recovery.

Type of compression

• Extradural compression of fluid nature resolve well on treatment, and patients show a good neural recovery.
• A preserved cord with edema/myelitis of cord on MRI would show a good neural recovery whereas the cord showing myelomalacia or syringomyelia would show a poor neural recovery.
• During surgery, if pus is drained out (wet lesion) along with extradural compression of granulation tissue, the patient is likely to show better neural recovery in comparison to thick inspissated pus, caseous tissue, fibrous tissue, bony sequestrae and disc (dry lesion).

Late-onset Paraplegia

The patient usually has a history of extensive spinal tuberculosis but made an apparent recovery. The patient has been asymptomatic apart from increasing kyphosis. The paraplegia sets after a long asymptomatic period [4-40 years]

This type of paraplegia is usually seen in patients with severe kyphosis.

Usually, dorsal and dorsolumbar spine are involved as the kyphosis does not progress so severely in the cervical and lumbar spine.

It is attributed to

• Stretching of spinal cord over internal salient.  [often on a sharp ridge at the angle of kyphosis]
• Prolonged anterior impingement from constriction caused by fibrosis around the neural element.

It is always associated with severe kyphosis.

Management

It is important to differentiate paraplegia of healed disease from a reactivation or recrudescence.

Clinically paraplegia because of reactivation/recrudescence is severe and relatively rapidly developing as compared to late-onset paraplegia with the healed lesion.

Paraplegia with reactivation/recrudescence responds early and better to treatment than paraplegia with healed lesions.

In absence of reactivation/recrudescence, anterior decompression with removal of internal gibbus. But the treatment is fraught with the complication of deterioration of neural deficit.

The risk involved is high as severe kyphosis, with costovertebral impingement makes these patients have a poor pulmonary reserve.

The pognosis in this type of paraplegia is guarded and the prospects of recovery from treatment are not very bright. Yet it is advised to attempt removal of the internal gibbus and full anterior decompression of the cord in cases of paraplegia in healed disease. There is always the danger of worsening of neurological status following and due to surgery.

Therefore, it is suggested that internal gibbus should be removed only in cases with moderate to severe paraplegia, while mild paraplegics should not be decompressed.

The best form of treatment of late-onset paraplegia is the prevention of development of severe kyphosis.