INTRODUCTION
Tuberculosis (TB) of the central nervous system is rare, with an incidence of 0.5%–2% in patients with systemic TB.[1,2] The common manifestations of TB spine occur as Pott’s spine/tuberculous spondylitis (60%), arachnoiditis (20%), meningitis (12%), and intramedullary lesion (8%). The most common form of spinal intradural TB is meningitis. Intramedullary involvement is rare in TB and is usually present in the form of radiculomyelitis, transverse myelitis, intraspinal granulomas, or thrombosis of the anterior spinal artery.[1,2] Potts spine presenting as cauda equine syndrome has been suggested in the literature, however, the incidence is extremely rare. When diagnosed in time and managed appropriately, spinal TB with cauda equina syndrome has a good prognosis.
CASE REPORT
A 28-year-old female patient presented with weakness of both lower limbs associated with loss of bladder and bowel control for 1 day. She had a history of low backache for the past 2 months along with urinary urgency and precipitancy. There was no pain or any symptoms in the neck, upper limbs, chest, or trunk, or even any root pains. Past history was not suggestive for chronic cough, fever, weight loss, diabetes mellitus, other chronic illnesses, or exposure to toxins, alcohol, and TB. On examination, she was afebrile with normal vital signs. No organomegaly, lymphadenopathy, or spinal conditions such as deformity, swelling, tenderness, and ulcers/lesions were elicited on examination. Straight leg raising tests on both sides were positive at 60°. The extensors and flexors of the toes on both sides had Medical Research Council grade 4/5 power with decreased left-sided dorsi flexion (the patient was able to walk with support). Bilateral ankle jerk was absent and there were reduced sensory functions below the L5 dermatome on both sides along with perianal anesthesia. With these symptoms and signs, a clinical diagnosis of cauda equina syndrome was made. Except for the erythrocyte sedimentation rate, all routine hematological and biochemical parameters were within normal limits and the patient was seronegative for HIV. A magnetic resonance imaging (MRI) of the lumbosacral spine showed a T2 hyperintense lesion in the inferior end plate of L4 with surrounding edema and irregular end plate [Figure 1]. An urgent surgical decompression was performed following the MRI finding. Laminectomy performed at the L3-L5 levels revealed thick pus in the extradural space. This pus was aspirated which showed abundant acid-fast bacilli on Ziehl–Neelsen staining, which revealed as rifampicin-sensitive Mycobacterium tuberculosis in cartridge-based nucleic acid amplification test. The aerobic and anaerobic culture, Gram stain, and fungal stains did not reveal any findings. After a thorough general, radiological, and microbiological examination, no evidence of primary pulmonary illness could be elucidated. The patient was started on antituberculous therapy following this with gradual resolution of symptoms.
Figure 1: T2 hyperintense lesion in the inferior end plate of L4 with surrounding edema and irregular end plate suggestive of epidural abscess with cord compression (Red-arrow)
DISCUSSION
Cauda equina syndrome is a neurological condition, in which there is an acute loss of function of the neurological elements (sensory, motor, and autonomic) of the spinal canal below the termination of the spinal cord. Cauda equina syndrome of sudden onset is regarded as a medical emergency. Surgical decompression using laminectomy or other approaches may be undertaken on an urgent basis if a compressive lesion, for example., prolapsed disc, epidural abscess, tumor, or hematoma is demonstrated.[3,4] The most common cause of cauda equina syndrome is prolapsed intervertebral disc[5] and epidural collection due to infective cause is rarely reported as a cause. This is especially the case when the patient presents sudden-onset disease without any history of fever, weight loss, or an underlying immune-compromised status.[4]
Among extrapulmonary TB, about 10% have skeletal involvement and 50% of these skeletal TB are in the spine alone.[6] Segmental arteries bifurcate to supply two adjacent vertebrae, thus spinal TB, characteristically involves 2/ >2 vertebrae with subligamentous spread.[7,8] This results in intervertebral disk space destruction and collapse of the spinal elements leading to the characteristic angulation and gibbus (palpable deformity because of involvement of multiple vertebrae) formation along with back pain. In our patient, no such pain or deformity could be demonstrated. Constitutional symptoms such as fever and weight loss are seen in approximately 20%–30% of cases of osteoarticular TB (new) as seen in our case, thus high degree of suspicion is warranted for early diagnosis.
The upper lumbar and lower thoracic spine are the most frequently involved sites.[9] However, neurologic deficits are common with the involvement of thoracic and cervical regions. About 23%–76% of cases of spinal TB land into neurological deficits in some form.[10] Lumbosacral TB is reported generally have reduced reflexes, as was seen in our case, in contrast to other causes of cauda equina syndrome where hyperreflexia with bladder involvement is common. TB of the spine causes extramedullary compression and commonly presents with myelopathies.[11] Primary tubercular parenchymal involvement of the spinal cord is a very uncommon finding.[1,11]
Spinal involvement is usually a result of hematogenous spread of M. tuberculosis into the dense vasculature of cancellous bone of the vertebral bodies. The primary infection site is either a pulmonary lesion or an infection of the genitourinary system.[12] However, no primary lesion could be discerned in our case.
MRI is the preferred investigation to demonstrate the intramedullary lesions including tuberculomas and it can also demonstrate the extent of the disease with spread.[8] Smear, culture positivity, or histopathological evidence of granuloma may be only possible in a maximum 60% of cases. Thus, many a time, the diagnosis of spinal TB lies with radiological and clinical proof only without any corroborative laboratory evidence. Advent of polymerase chain reaction techniques narrows this gap to a large extent.
CONCLUSION
Surgical intervention is required in intraspinal TB with spinal abscesses with sudden-onset symptoms such as cauda equina syndrome. It will help in the confirmation of diagnosis and reduce compression and stabilization.[5] The results of surgical treatment together with antitubercular drugs are a preferred treatment of choice.
Limitation of study
Shorter period of follow-up is a minor limitation, but as of now, 11 months later, the patient has recovered and no new symptoms appeared.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient/family has given their consent for her images and other clinical information to be reported in the journal. The patient understands that her name and initials will not be published and due efforts will be made to conceal her identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
Acknowledgment
We acknowledge SOA University, Bhubaneswar, Odisha, for their help in doing this work.
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