DISCUSSION:
Tuberculosis (TB) remains a common health issue in developing countries
even though TB has not been seen widely as before [6]. Osseous TB
involvement may account for up to 35% of patients with extrapulmonary
TB, and vertebral osteomyelitis infections (Pott’s disease) account for
25–60% of all osseous infections caused by TB [7-9]. Approximately
10% of patients with extrapulmonary tuberculosis (TB) experience
central nervous system (CNS) involvement, typically resulting from the
bacteremic stage of the disease. During this stage, tuberculous lesions
known as Rich foci may develop in the meninges or within the brain or
spinal cord tissue [10,11]. After several months or even years,
these foci can rupture into the cerebrospinal fluid, leading to
meningitis, or they can enlarge and form tuberculomas within the brain
or spinal cord parenchyma,
The Mycobacterium bacilli can also spread hematogenously to
various parts of the body, including the brain, due to minor bacteremia.
The pathogenesis of central nervous system tuberculosis involves the
development of small foci of tuberculosis, known as Rich foci, in the
brain, spinal cord or meninges [10]. Earlier studies by Rich and
McCordock showed that TBM requires direct inoculation of the bacilli
through a meningeal focus in the central nervous system. However, later
studies showed that disseminated tuberculosis plays a crucial role in
the development of tuberculosis [12]. Tumor necrosis factor alpha
(TNF-α) is a critical cytokine in M. tuberculosisneuropathogenesis. Although it helps in granuloma formation and control
of mycobacterial infections, local production of TNF-α in the central
nervous system can alter the permeability of the blood-brain barrier and
promote the progression of TBM [13].
M. tuberculosis has a unique ability to enter and multiply in
macrophages. Human microglia are selectively infected by M.
tuberculosis and the CD14 receptor facilitates engulfment of
unopsonized bacilli by microglia. Microglia infected with M.
tuberculosis produce a variety of cytokines and chemokines, including
TNF-α, IL-6, IL-1β, CCL2, CCL5, and CXCL10. Microglia play a central
role in the neuropathogenesis of tuberculosis, and their infection can
lead to immunosuppressive effects, especially in more virulent strains
[14].
Tuberculous meningitis is the most common form of central nervous system
(CNS) tuberculosis (TB) compared to tuberculomas. Similarly, among
various forms of spinal TB involvement such as Pott disease, non-osseous
spinal TB, tuberculous spinal meningitis, and tuberculous arachnoiditis,
non-osseous spinal tuberculoma is infrequent. In a review conducted by
Dastur, 74 cases of spinal tuberculomas were analyzed, revealing that
65% were located extra-durally, 8% were intramedullary, 5% were
intradural extramedullary, and 20% were arachnoidal [15-17].
Non-osseous spinal tuberculomas typically originate from a primary
pulmonary focus, spreading hematogenously or through direct extension
from hilar lymph nodes [18]. In our case, a rare and unexpected
involvement occurred in the form of a non-osseous intradural
extramedullary (IDEM) tuberculoma of the spinal cord, resulting in
paraparesis despite the patient receiving antitubercular therapy (ATT).
To our knowledge, this is the first reported case of a tuberculoma at
the juxta-medullary location in the thoracic region.
The clinical presentation of the case aligns with the findings reported
in the literature, which often show a higher prevalence among males
[19]. The most common presentation in our case was spastic
paraplegia, post-ATT liver failure, and respiratory problems associated
with tuberculosis and COVID-19. Nevertheless, tuberculomas are slow
growing with areas of necrosis that are encapsulated, avascular, and
infrequently calcification. Our patient exhibited involvement of the
thoracic spinal cord, which aligns with the reported incidence of up to
70% of cases in the literature. The thoracic spine is the most
frequently affected site in Pott’s syndrome [20]. The radiological
imaging findings of tuberculomas can vary depending on the stage of the
lesion. On MRI, tuberculomas may present with non-caseating granulomas
or caseating granulomas characterized by a solid or liquid center
[21]. The tuberculous lesion typically appears isointense on T1W
images, isointense to hypointense on T2Wimages, and exhibits ring
enhancement with a hypointense center on gadolinium-enhanced MR scans.
As the lesion undergoes caseation, the center becomes bright and gives
rise to a target sign, as observed in our case [22-24].
A combination of surgical intervention and medical treatment has shown
excellent outcomes. While some authors argue that anti-tuberculous
therapy alone is sufficient when a paradoxical reaction develops into a
tuberculoma [25,26], a literature review on intradural
extramedullary spinal tuberculoma confirms the limited effectiveness of
medical therapy alone and highlights the need for surgical intervention
[27-33]. The reason for the poor response to chemotherapy in this
condition remains unclear. Therefore, we believe that surgery is
warranted when intradural extramedullary spinal tuberculoma arises as a
paradoxical response to therapy.
The list of similar published cases is mentioned in Table 1: