Imaging intracranial and spinal tuberculosis features are nonspecific and often challenging, making diagnosing tuberculous myelitis difficult even in TB-endemic regions. The term ‘tuberculous radiculomyelitis’ (TBRM), coined by Dastur and Wadia [6], includes spinal cord complications of TB myelitis, such as arachnoiditis or spinal granulomas. They described the findings as a comparison between operative findings and histopathology. The changes were seen as dense exudates with thick septae adherent to the spinal cord. Areas of cord hemorrhage with associated arterial thrombosis were also seen. Tuberculomas were seen as well-defined circular structures. The histopathological manifestation was the presence of tuberculomas with surrounding reactive giant cells, lymphocytes, and plasma cells, as well as exudates containing microcysts. The earliest description of spinal tuberculosis was given in 1988 by Rhoton et al. [7].
Fever, weight loss, and generalized weakness commonly present constitutional symptoms [8]. Pain or tenderness in the spine is usually not present [9]. CNS involvement can manifest as altered sensorium or vomiting, with associated hydrocephalus being a partial contributor for latter [9]. Depending on the segment cord involved, upper and lower limbs mixed motor and sensory involvement manifest as mono, para, quadriplegia, or paresis. Similar segmental involvement was seen in the case of radiculopathy [10]. Bladder and bowel involvement usually occurs late in the disease [8, 9].
CSF examination findings may include high protein, lymphocytic pleocytosis, and culture infrequently favorable for acid-fast bacilli [8,9,10].
The commonly encountered imaging manifestation in a series of 15 cases included cord expansion, T1 hypointense, and T2 hyperintense intramedullary signal abnormality with or without heterogeneous or ring enhancement pattern attributable to the presence of a necrotic component in the latter [8,9,10]. Similar T1 and T2 signal changes showing no appreciable enhancement with relatively well-defined margins are attributed to changes in syrinx [10]. The thoracic cord is the most frequently affected segment.
Another review citing ten cases of TB myelitis confirmed similar T1 and T2 signal abnormalities, with cervical and thoracic cord segments frequently involved. In addition, cord expansion and enhancement features were also seen, consistent with our case. There may be cases showing T2 hypointense signal abnormality, explained by caseous necrosis as opposed to T2 hyperintensity of edema. A study also proposed cavitation as a marker for a worse prognosis, with another study stating incomplete recovery in cases of syrinx formation [9].
Tuberculous radiculomyelitis manifests as thick inflammatory exudates within subarachnoid space and granuloma formation in or on the surface of the spinal cord. This granuloma eventually ruptures into subarachnoid space and incites an exudative inflammatory response. With time, the tenacious exudates organize themselves to produce adhesions between dura and cord, indistinct cord outline, and formation of CSF loculations [11]. Adhesive Arachnoiditis manifests on imaging as an empty thecal sac sign with a T2 hyperintense signal of CSF occupying a large cross-section area of thecal sac due to clumping of nerve roots centrally or peripherally with or without associated tethering [10]. Abnormal postcontrast enhancement of nerve roots is almost always seen, as in our case. Obliterative endarteritis eventually leads to ischemia, myelomalacia, and syrinx formation of long cord segments [12]. The same cord changes are also observed in our case, portraying the chronic nature of the ailment. The decrease in the postcontrast enhancement of spinal meninges post-treatment indicates treatment response [11]. There can be associated changes of vertebral changes in the form of altered marrow signal, discal or paradiscal abscess formation, vertebral collapse, or paraspinal collections.
A case report of LETM encountered in the past emphasized poor penetration of antitubercular medication into CSF post-subsidence of the inflammatory response [13]. In our case, the probable mechanism of LETM was an immune-mediated inflammatory response to degraded tubercular proteins exacerbated by antitubercular drugs [14]. Another possibility can be a delayed-type hypersensitivity reaction to tubercular proteins [15].
Our patient developed LETM despite good adherence to antitubercular treatment. It may be related to the paradoxical response of antitubercular therapy, characterized by clinical worsening or the appearance of new lesions on imaging following a period of initial significant clinical response [16]. Interestingly, despite this pseudoprogression, Dynamic Contrast-Enhanced Magnetic Resonance Imaging (DCE-MRI) trans (permeability) and ve (leakage) values representing blood–brain barrier (BBB) dynamics confirmed therapeutic response to medication [15, 16].
Neuromyelitis optica spectrum disorder (NMOSD) is the most common cause of LETM, although less specific for the pediatric age group, seen as the second most common manifestation after optic neuritis. LETM can be coexistent with tuberculosis, with myelin essential protein being postulated common antigen as tubercular exposed lymphocytes showed a propensity to affect myelin [15]. Studies have shown clinical improvement after administering antitubercular treatment in NMOSD cases, establishing an association between the two [17, 18]. NMOSD lesional morphology corresponds to T2 high signal/bright spotty lesions, corresponding T1 low signal abnormality, and characteristic lenticular enhancing morphology on the sagittal plane. The cervical cord central gray matter is the site of predilection with invariable involvement of area postrema [19, 20]. The involvement of the dorsolumbar cord was a rare occurrence, as stated in one study [21]. One of the critical considerations when diagnosing NMOSD is the timing of acquiring a scan, as brain lesions are often forerunners of spinal abnormality, and a follow-up scan invariably reveals new onset spinal lesions [20, 21].
Although, in our case, the diagnosis of LETM was based on combined clinical, laboratory, and imaging inputs, it is sometimes difficult to reach a unifying diagnosis. A broad differential category must be considered, such as infective, inflammatory disorders, demyelinating disease, autoimmune and paraneoplastic etiology. The mainstay of treatment is antitubercular therapy and corticosteroids to combat inflammatory response and supportive care.
