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
- Granulation tissue
- Tubercular debris
- Tuberculous caseous tissue
- Localized pressure due to salient (internal gibbus)
- Pathological subluxation/dislocation of vertebrae.
- Inflammatory edema
- The affection of meninges and cord by tuberculous inflammation
- Infective thrombosis/endarteritis of spinal vessels
In Healed Disease
- A transverse ridge of bone anterior to spinal cord producing localized pressure.
- Constricting scarring around/or dura.
- 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.
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)
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)
The patient is bedridden (severe motor weakness) with signs of upper motor neuron paraplegia, sensory loss less than 50 percent.
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.
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.
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.
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 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 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.
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.
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
- 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°.
- 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.
- 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
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.
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).
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.
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.
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