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\begin{document}

\title{NON-OSSEOUS INTRADURAL TUBERCULOMA OF THE THORACIC SPINE WITH
COMPRESSIVE MYELOPATHY}



\author[1]{Shyam Duvuru}%
\author[2]{Vivek Sanker}%
\author[3]{Naureen Syed}%
\author[4]{Prakash  Gupta}%
\author[5]{Sanjana Rajurkar}%
\author[6]{Tirth Dave}%
\affil[1]{Apollo Speciality Hospitals Madurai}%
\affil[2]{Noorul Islam Institute of Medical Science and Research Foundation Medicity}%
\affil[3]{UTMDACC}%
\affil[4]{Virgen Milagrosa University Foundation}%
\affil[5]{Datta Meghe Institute of Higher Education \& Research}%
\affil[6]{Bukovinian State Medical University}%


\vspace{-1em}



  
  \date{May 27, 2024}


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\sloppy


\textbf{INTRODUCTION:}

Tuberculosis remains a significant global health burden, with central
nervous system (CNS) involvement being a rare but serious manifestation.
While pulmonary tuberculosis is the most common form, extrapulmonary
manifestations can affect various organs and systems. The CNS
involvement in developing countries constitutes nearly 10\% of all
tuberculosis patients {[}1{]}. Tuberculomas with compressive
myelopathies without bone involvement are an even rarer occurrence. In
the differential diagnosis of extensive spinal cord injuries,
particularly in young patients with a history of pulmonary tuberculosis
or tuberculous meningitis, it is important to consider the possibility
of an intradural extramedullary tuberculoma {[}2{]}.

Here we will be discussing a case of intradural extramedullary
tuberculosis of the thoracic spine, with progressive neurological
dysfunction. Surgery aims to decompress the spinal cord and remove the
tuberculoma, thereby relieving the pressure on the neural tissues and
preventing further neurological deterioration {[}3-5{]}. The specific
surgical technique employed depends on the location and extent of the
tuberculoma.

Following surgery, anti-tubercular therapy is initiated to target the
underlying tuberculosis infection. This typically involves a combination
of multiple anti-tuberculosis medications, such as isoniazid,
rifampicin, ethambutol, and pyrazinamide {[}2{]}. The duration of
anti-tubercular therapy may vary but generally lasts several months to
ensure complete eradication of the infection. Continual postoperative
monitoring assumes paramount importance in assessing neurological
recovery and treatment response. Concurrently, physiotherapy and
rehabilitation assume significance in facilitating the functional
restoration and enhancing the overall quality of life {[}1{]}.

This report aims to discuss the diagnostic challenges, treatment
strategy, and clinical outcomes, highlighting the importance of a
multidisciplinary approach in managing this uncommon condition.

\textbf{CASE REPORT:}

A 29-year-old man, who had been under treatment for disseminated
tuberculosis for seven months, was admitted with progressive weakness of
both lower limbs leading to difficulty in walking. There was no history
of fever, cough, palpitations, or breathlessness. Physical examination
revealed a palpable spleen but no lymphadenopathy. He had spastic
paraparesis with involvement of right side more than the left. There was
severe girdle pain at T5 level. The patient underwent a computed
tomography (CT) chest, which revealed multiple patchy resolving ground
glass opacities and interlobular septal thickening in bilateral lower
lobes, predominantly superior and posterior basal segments, suggesting
resolving tuberculosis. Also, mild centrilobular emphysema in bilateral
upper lobes with sub-centimeter right paratracheal and left paraaortic
lymph nodes, the largest measuring 7 mm, were present. Other findings
included splenomegaly measuring 17.6 cm and calcified hepatic granulomas
(segment VII).

Magnetic Resonance Imaging (MRI) thoracic spine revealed a single 2.1
*1.7 * 1.45 cm intradural/juxta medullary and extramedullary mass
appearing as well-defined T1-weighted low signal/ T2-weighted FLAIR
bright signal with central necrosis and marginal enhancement after
gadolinium (Gd) suggestive of immature tuberculoma at T5 level with
surrounding edema \textbf{(Figure 1: A, B, \& C} ).\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image1/image1}

\end{center}
\end{figure}

\textbf{Figure 1: A, B, \& C: The MRI images of the thoracic spine. A)
Coronal T1-weighted MRI image shows a ring-like enhancing intradural
lesion after gadolinium. B) Sagittal T1-weighted MRI image shows a 2.1
X1.7 X 1.45 cm intradural/juxta medullary and extramedullary mass with
central necrosis and marginal enhancement after gadolinium suggestive of
immature tuberculoma at T5 level. C) Axial T2-weighted image.}

No evidence of vertebral TB, spinal tract infiltration, or engulfment
was noted. A diagnosis of D5 Intra-dural extra medullary space-occupying
lesion (SOL) with spastic paresis, cord compression, compressive
myelopathy, disseminated tuberculosis, and post-tuberculous
medication-induced hepatic granuloma was made. D4-D6 laminectomy and
microsurgical excision under IONM was planned to remove the lesion.
After pre-anesthetic assessment and consent, the patient underwent the
procedure with the head held in a horseshoe, subperiosteal muscle
dissection made, and laminae exposed. Durotomy was performed under a
microscope and the lesion was visualized. A grayish-white, firm lesion
with a central necrotic area was exposed (\textbf{Figure 2} ).\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image2/image2}

\end{center}
\end{figure}

\textbf{Figure 2. The capsule and necrotic component is seen which is
densely adherent to spinal cord}\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image3/image3}

\end{center}
\end{figure}

The pus was aspirated, followed by internal bulking using ultrasonic
surgical aspirator (\textbf{Figure 3, 4, 5} ). The thin rim of the
capsule was left behind but was coagulated well. Homeostasis was
achieved, and the dura was closed using a 5-0 proline continuous suture.
The patient tolerated the procedure well. After surgery, he was treated
with antibiotics, anti-diabetics, steroids, anti-tubercular drugs,
anti-inflammatory, gastro protectives, antiemetics, and other supportive
measures. Physiotherapy measures were instituted. The neurologist was
involved in his paraparesis care, and an endocrinologist for glycemic
control. He gradually improved symptomatically, able to walk with
minimal support.

\textbf{Figure 3. Intraoperative picture showing a densely adherent
lesion with neovascularization}\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image4/image4}

\end{center}
\end{figure}

\textbf{Figure 4. The capsule is incised and pus is delivered off the
lesion}\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image5/image5}

\end{center}
\end{figure}

\textbf{Figure 5. Post-excision status with decompression of the spinal
cord}

\textbf{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 \emph{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-\selectlanguage{greek}α\selectlanguage{english}) is a critical cytokine in \emph{M.
tuberculosis}neuropathogenesis. Although it helps in granuloma formation
and control of mycobacterial infections, local production of TNF-\selectlanguage{greek}α \selectlanguage{english}in
the central nervous system can alter the permeability of the blood-brain
barrier and promote the progression of TBM {[}13{]}.

\emph{M. tuberculosis} has a unique ability to enter and multiply in
macrophages. Human microglia are selectively infected by \emph{M.
tuberculosis} and the CD14 receptor facilitates engulfment of
unopsonized bacilli by microglia. Microglia infected with \emph{M.
tuberculosis} produce a variety of cytokines and chemokines, including
TNF-\selectlanguage{greek}α, \selectlanguage{english}IL-6, IL-1\selectlanguage{greek}β, \selectlanguage{english}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 \textbf{Table 1:}\selectlanguage{english}
\begin{longtable}[]{@{}llllll@{}}
\toprule
\begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Case Report\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Case age/Sex\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Symptoms\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Radiographic Findings\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Treatment Plan\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Outcome\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Kim et al, 2000 {[}34{]}\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
49/F\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Seizure, facial palsy, left upper extremity weakness, paraparesis,
hypesthesia below the T6 dermatome, urine incontinence\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
IDEM mass between the T1 and T2 spinal levels\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Surgery and antituberculous drugs\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Paraparesis has improved, and urine function is normal\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
Muthukumar et al, 2006 {[}35{]}\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
14/F\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
Tonic-clonic seizure\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
Lesion in the spinal cord\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
T7-T12 Laminectomy\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
Power gradually increased during a three-month period\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
45/F\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
Numbness, sphincter problems, and lower extremity inability\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
T1-weighted~scans~show~an~isointense~lesion~spreading~the~cord,~whereas~T2-weighted~images~show~hypointensity~with~a~central~region~of~hyperintensity.\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
T2-T5 Laminectomy\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
The patient's neurological condition had not improved\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Hristea et al, 2008 {[}36{]}\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
20/M\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Lower-limb weakness and disorientation\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Obliterated thoracic and lumbar subarachnoid space\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
IV dexamethasone and intrathecal methylprednisolone\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
when supported, walk\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
40/M\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Right-leg paresthesia, walking difficulties, and bladder
incontinence\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Multiple intramedullary lesions at D4, D5---6, D8, D10, and D11\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
IV dexamethasone and intrathecal methylprednisolone\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
The patient was able to walk without assistance, had modest sensory
loss, moderate spasticity, and no sphincter problems\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
29/M\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Sensory loss, paresthesia, gradual lower limb weakness, and walking
difficulties\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
At T8-9, a solitary intramedullary mass suggests tuberculoma\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
IV dexamethasone and intrathecal methylprednisolone\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
The patient was able to walk on his own\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
Ding et al, 2012 {[}37{]}\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
63/M\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
Weak hands and arms neck and thoracic discomfort\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
A shuttle-like mass with low signal intensity extending from C2 to C4 in
the posterior epidural region, an intraspinal extradural mass, and a
compressed and edematous spinal cord\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
C2-C4 laminectomy was used to decompress the spinal cord and remove the
tumor\strut
\end{minipage} & \begin{minipage}[t]{0.16\columnwidth}\raggedright\strut
The patient recovered completely neurologically\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Verma et al, 2013 {[}38{]}\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
68/M\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Low back discomfort, left-sided lower-extremity weakness, and
radiculopathy\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
A lobulated enhancing intrathecal mass at L1\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Bilateral~laminectomy~and~medial~facetectomy\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Reported minor discomfort, independent walking, and persistent weakness
in just the left tibialis anterior muscle\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Venkatesh et al, 2018 {[}39{]}\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
31/M\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Mid-backache with growing weakening of both lower limbs, urgent
micturition\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
T1 hypointense and T2 heterointense lesion seen posterior to the
thoracic spinal cord, ranging from C7 to D5 vertebral levels\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
D1-D5 laminectomy\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
The patient showed normal bladder function and increased strength in
both lower limbs (Grade 4-5)\strut
\end{minipage}\tabularnewline
\bottomrule
\end{longtable}

\textbf{Table 1:} List of case reports having similar presentation

\textbf{CONCLUSIONS:}

Intradural extramedullary (IDEM) tuberculoma is a rare manifestation of
central nervous system (CNS) tuberculosis, often arising as a result of
paradoxical reactions to antitubercular medication. When patients on
antitubercular therapy develop new-onset neurological deficits
indicative of compressive myelopathy, IDEM tuberculoma should be
considered as one of the potential causes. Early and accurate diagnosis,
along with timely initiation of appropriate medical or surgical
interventions, is crucial to prevent irreversible dysfunction. Excision
plays a pivotal role in the treatment of this uncommon condition.

\textbf{CONFLICTS OF INTEREST:}

None declared.

\textbf{AUTHOR CONTRIBUTION:}

All the authors contributed equally in drafting, editing, revising and
finalizing the case report.

\textbf{ETHICAL APPROVAL:~}

The ethical approval was not required for the case report as per the
country's guidelines.

\textbf{CONSENT:}

Written informed consent was obtained from the patient to publish this
report.

\textbf{DATA AVAILABILITY STATEMENT:}

The data that support the findings of this article are available from
the corresponding author upon reasonable request.

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\end{enumerate}

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