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Ecr2019 C-1497
Ecr2019 C-1497
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Page 1 of 25
Learning objectives
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Background
The spectrum of central nervous system tuberculosis is wide but can be classified into two
main groups non parenchymal or meningeal, which constitutes 70-80% of all cases, and
parenchymal forms. The hallmark of parenchymal involvement is parenchymal infection
with central caseating necrosis known as TB granuloma or tuberculoma. Tuberculous
spondylodiscitis and spinal meningitis are the most common forms of spinal TB.
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Diagnosis is made based on clinical features, abnormal cerebrospinal fluid (CSF),
imaging and tissue smear, culture or biopsy characteristics. Smear and culture is
difficult and possible only in a small number of patients [3,7]. CSF shoes low glucose,
elevated protein, lymphocitic pleocytosis and in some cases acid-fast bacilli can be
identified in smears. CSF culture and polymerase chain reaction (PCR) provide definite
diagnosis [3,7,8]. Radiographic examination of suspected CNS TB begins with computed
tomography Fig. 1 on page 5 (CT) and magnetic resonance imaging (MRI), and up
to 30% of patients have TB features on conventional chest radiography [3] Fig. 2 on page
5.
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Images for this section:
© IMSS, Hospital de Especialidades del Centro Médico Nacional Siglo XXI - Ciudad de
México/MX
Page 5 of 25
Fig. 2: 28 year old female with chronic use of adalimumab for rheumatoid arthritis
presented with neurological deterioration and was diagnosed with CNS TB. Chest
radiography shows cavitation in left upper lobe and nodular opacity in right middle lobe.
© IMSS, Hospital de Especialidades del Centro Médico Nacional Siglo XXI - Ciudad de
México/MX
Page 6 of 25
Findings and procedure details
Early diagnosis and treatment are essential for prognosis, this makes noninvasive
imaging modalities cornerstone in the approach of suspected CNS TB. We review the
most common spectrum of imaging findings in patients that have presented in our
institution in 2018. These presented with the following:
Parenchymal involvement:
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homogeneous enhancement on contraste (Gadolinium) administration. Solid caseating
lesions are the most common finding appearing as iso to hypointense in T1WI and
hypointense on T2WI. Caseating lesions with liquefaction show similar T1 findings but
appear hyperintense on T2WI. Both show rim enhancement on contrast administration
Fig. 12 on page 15 Fig. 13 on page 15 [7, 9, 10, 11]. Vasogenic edema seen on
T2WI and FLAIR is variable and can be seen in all lesions.
Miliary brain TB is defined as multiple lesions measuring less than 2-3 mm spread
throughout the parenchyma usually in the corticomedullary junction and can be
associated with meningeal involvement. They are a result of hematogenous spread
usually seen in severely immunocompromised patients. They appear hyperintense on
T2WI with homogenous enhancement on gadolinium enhanced T1WI Fig. 14 on page
16 [6, 11].
TB brain abscess is an infrequent complication arising in less than 10% of patients with
TB. They present as large (>3 cm) multiloculated ring enhancing lesions with important
perilesional edema Fig. 15 on page 17 Fig. 16 on page 17 , presenting restricted
diffusion on diffusion weighted imaging [6, 11].
Spinal involvement:
Spinal involvement is the most common osseous manifestation of TB, it usually affects
the lower thoracic and upper lumbar spine. The disease begins in the anterior part of
the vertebral body with progressive vertebral body destruction but relative sparing of the
intervertebral disc [11, 13]. Posterior vertebral elements are rarely affected [2]. Paraspinal
involvement and paravertebral abscess are common findings, usually affecting the psoas
muscles Fig. 17 on page 18 [6]. CT is recommended in evaluation of osseous
destruction and demonstration of bone fragments in adjacent soft tissue Fig. 18 on page
19 . MRI is more sensitive seen as hypointense with reduced disk height on T1WI,
increased signal intensity on T2WI/STIR, and rim enhancement Fig. 19 on page 20
[5, 6, 10, 11].
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Images for this section:
Fig. 3: Hydrocephalus with ventricular dilation in patient with known CNS TB.
© IMSS, Hospital de Especialidades del Centro Médico Nacional Siglo XXI - Ciudad de
México/MX
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Fig. 4: Hyperdense exudates in basal cisterns. Nodular hyperdense lesion in relation to
a tuberculoma is also observed.
© IMSS, Hospital de Especialidades del Centro Médico Nacional Siglo XXI - Ciudad de
México/MX
Page 10 of 25
Fig. 5: Dilation of supra and infra tentorial ventricular system and tonsillar herniation.
Meningeal enhancement is appreciated on contrast enhanced T1WI.
© IMSS, Hospital de Especialidades del Centro Médico Nacional Siglo XXI - Ciudad de
México/MX
Fig. 6: Axial magnetic resonance imaging shows increased signal intensity on T2WI
and FLAIR along the basal cisterns and marked meningeal enhancement on Gadolinium
enhanced T1WI.
© IMSS, Hospital de Especialidades del Centro Médico Nacional Siglo XXI - Ciudad de
México/MX
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Fig. 7: Gadolinium enhanced T1WI demonstrates pia-arachnoid enhancement extending
into the subarachnoid spaces between the cerebellar folia in a patient with miliary CNS
TB.
© IMSS, Hospital de Especialidades del Centro Médico Nacional Siglo XXI - Ciudad de
México/MX
Page 12 of 25
Fig. 8: Focal dural enhancement adjacent to tuberculous abscess.
© IMSS, Hospital de Especialidades del Centro Médico Nacional Siglo XXI - Ciudad de
México/MX
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Fig. 9: Mixed meningeal enhancement comparison of contrast enhanced T1WI and
FLAIR. Post contrast FLAIR has been proposed as superior to contraste enhanced T1WI
in defining and detecting meningeal disease.
© IMSS, Hospital de Especialidades del Centro Médico Nacional Siglo XXI - Ciudad de
México/MX
Fig. 10: Post contrast FLAIR aids in diagnosis of meningeal disease. It is routinely used
in our institution in patients with suspected CNS TB.
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© IMSS, Hospital de Especialidades del Centro Médico Nacional Siglo XXI - Ciudad de
México/MX
Fig. 11: NECT shows round hyperdense lesions with perilesional edema. Contrast
enhanced CT demonstrates ring like enhancement. Meningeal involvement is also
appreciated.
© IMSS, Hospital de Especialidades del Centro Médico Nacional Siglo XXI - Ciudad de
México/MX
Fig. 12: Multiple nodular lesions show ring enhancement. Adjacent dural enhancement
is also observed. T2WI shows important edema and mass effect of lesions.
© IMSS, Hospital de Especialidades del Centro Médico Nacional Siglo XXI - Ciudad de
México/MX
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Fig. 13: DWI and ADC in same patient show diffusion restriction.
© IMSS, Hospital de Especialidades del Centro Médico Nacional Siglo XXI - Ciudad de
México/MX
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Fig. 14: Patient with multiple lesions spread throughout the brain parenchyma with
associated with meningeal involvement. They appear hyperintense on T2WI with
homogenous enhancement on gadolinium enhanced T1WI.
© IMSS, Hospital de Especialidades del Centro Médico Nacional Siglo XXI - Ciudad de
México/MX
Fig. 15: Multiloculated ring enhancing lesions with important perilesional edema.
© IMSS, Hospital de Especialidades del Centro Médico Nacional Siglo XXI - Ciudad de
México/MX
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Fig. 16: FLAIR imaging of multiloculated ring enhancing lesions with important
perilesional edema.
© IMSS, Hospital de Especialidades del Centro Médico Nacional Siglo XXI - Ciudad de
México/MX
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Fig. 17: Coronal and sagital contrast enhanced CT images show large left psoas abscess
in patient with tuberculous spondylitis.
© IMSS, Hospital de Especialidades del Centro Médico Nacional Siglo XXI - Ciudad de
México/MX
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Fig. 18: Same patient with bone window shows vertebral destruction of T12.
Heterogeneous left psoas abscess is observed.
© IMSS, Hospital de Especialidades del Centro Médico Nacional Siglo XXI - Ciudad de
México/MX
Fig. 19: Same patient MRI T1WI, STIR, CET1WI show T12 vertebral collapse, abnormal
signal intensity in STIR and rim enhancement.
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© IMSS, Hospital de Especialidades del Centro Médico Nacional Siglo XXI - Ciudad de
México/MX
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Conclusion
Tuberculosis is a multi-spectrum disease in all its presentations and the CNS this is no
exception. Clinical history and presentation of disease is important in differentiating from
multiple differential diagnosis. CT and MRI are the imaging modalities of choice, at first
to come to a diagnosis then to define the limits of tuberculous extension.
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Personal information
Email: quinn_bere_nice@hotmail.com
Email: jaimeiuit@gmail.com
Email:adriana_paola@hotmail.com
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Email: abrilele_maciel@hotmail.com
Email: macruz1988@gmail.com
Email:aracelihdzt@gmail.com
Email: zmichelle2101@gmail.com
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References
1. Global tuberculosis report 2017. Geneva. World Health Organization; 2017. License
CC BY - NCSA 2.0 IGO.
2. Burrill, J., Williams, C., et al. (2007). Tuberculosis: A radiologic review. Radiographics,
27 (5), 1255-1273.
3. Rock, R., et al. (2008). Central Nervous System Tuberculosis: Pathogenesis and
Clinical Aspects. Clinical Microbiology Reviews, 21 (2), 243-261.
5. Patkar, D., Narang, J., et al. (2012). Central Nervous System Tuberculosis
Pathophysiology and Imaging Findings. Neuroimag Clin N Am. 22, 677-705. Doi:
10.1016/j.nic.2012.05.006.
8. Aher, A., et al. (2018). Study of Central Nervous System Tuberculosis. Journal of the
Association of Physicians of India. 66, 41-44.
9. Chou, P., et al. (2012). Central Nervous System Tuberculosis: A Forgotten Diagnosis.
The Neurologist. 18 (4), 219-222.
10. Torres, C., et al. (2014). Central Nervous System Tuberculosis. Topics in Magnetic
Resonance Imaging. 23 (3), 173-189.
11. Trivedi, R., et al. (2009). Magnetic resonance imaging in central nervous system
tuberculosis. Indian Journal of Radiology and Imaging. 19 (4), 256-263.
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