WFPI TB Corner July 2016

TUBERCULOUS MENINGITIS
Basal Cistern Enhancement Pattern on CT imaging
Mariaem M. Andres MD, Jacqueline Austine U. Uy MD, and Maricar P. Reyes-Paguia MD
St. Luke’s Medical Center, Philippines

Abstract Introduction
TBM is the most severe and life-threatening form of
Tuberculous meningitis (TBM) is tuberculosis in children [3,4] in which one out of every 300
the most severe form of untreated primary TB infections is complicated by TBM [5]. Its
mycobacterial infection [1] and the
peak incidence is in young children under 4-5 years of age [6]
most frequent form of central
nervous system tuberculosis [2]. although it may occur at any age. Children are most
The diagnosis of TBM relies on vulnerable and frequently affected by TBM due to their poor
both clinical assessment and immune response to contain the Mycobacterium tuberculosis
radiologic imaging features. Early bacteria within the lungs [7]. The risk of progression of primary
and prompt diagnosis is pulmonary TB to TBM is greater in children than in adults.
imperative for better outcome.
Involvement of the central nervous system in tuberculosis
Clinical presentations may overlap
with other disease entities and are occurs during hematogenous spread of the disease. Despite
very non-specific. CT plays vital advances in its management and control around the world, the
role in the early diagnosis and effort to eradicate this disease continues to be difficult and it
monitoring of the course of the still poses high risk of death which estimated to vary from 15
disease. The CT triad of basal to 32% [5,6,8]. Neurologic sequelae are noted in more than
enhancement, hydrocephalus and
half of the affected patients [6,7]. Radiologic imaging plays an
infarct strongly suggest TBM [3].
This review is an effort to examine important role in the diagnosis and management of TBM. CT
and discuss the current literature scan is an established modality for evaluating TBM, its features,
in our understanding of TBM and progression, and complications. It is also important in
to demonstrate the myriad of CT providing differential diagnoses for disease entities that may
imaging features with focus on
present similarly.
basal cistern involvement pattern,
a n d t o p ro v i d e d i ff e r e n t i a l
diagnoses. Clinical Scenario
The patient is an 18 year old male admitted at a
Key Facts
pediatric hospital for persistent severe biparietal headache,
TB Meningitis dizziness, vomiting and changes in sensorium.  He was being
treated as a case of bacterial meningitis.   It was disclosed that
Clinical Presentation: Non- the patient was diagnosed with left ankle septic arthritis one
specific month prior to admission.   He had no known history of
o Adults: typical meningeal
primary tuberculosis, but had contact with infected family
signs
o Children: prodrome members.   Chest X-Ray was done and showed clear lungs
lasting 2-8 weeks without mediastinal lymphadenopathy.   A Mantoux tuberculin
o Headache: Adults > skin test done demonstrated an induration of 20 mm. Physical
children examination and ultrasound of the neck also revealed cervical
o Seizures: Children > Adults lymphadenopathies.  The patient was referred to our institution
o Cranial nerve palsies:
for CT scan of the brain.
VI>III>IV>VII

Andres MM et al. TB Corner 2016; 2(5):1-9 1

WFPI TB Corner July 2016

Key Facts
A B

Triad of CT Imaging Findings

1. Basal meningeal enhancement:
sensitivity of 35-73% and
specificity of 69-88%
2. Hydrocephalus: sensitivity of
57-93% and specificity of
69-83%
3. Infarct: sensitivity is valued at
18-75% and its specificity is at
82-100%

Objective Criteria for Basal Figure 1. Initial CT of the brain plain (A) and (B) with contrast. Plain
Cistern Enhancement: scan reveals hyperdensity at the basal cisterns (arrow). Multiple
1. Contrast filling the cisterns variable sized rim-enhancing nodular foci along both cerebral
2. ‘Double and triple line’ signs hemispheres and cerebellum predominantly in the basal and
3. ‘Linear enhancement’ at MCA perimesencephalic cisterns and both Sylvian fissures, Obstructive
cistern hydrocephalus is present. Contrast enhancement of the basal cisterns
4. ‘ϒ’ sign at suprasellar junction
and MCA cistern
5. Enhancement at posterior
infundibular recess of the 3rd
ventricle The patient received anti-TB medications. The symptoms
6. Ill-defined enhancement
improved and there were no neurologic deficits on follow-up.
7. ‘Join the dots’ sign
Before the end of therapy, a repeat CT scan was requested.
8. Nodular enhancement
9. Asymmetry of any of the
above

Differential Diagnoses
A. Granulomatous processes
• Sarcoidosis
• Wegener granulomatosis
• Luetic gummas
• Rheumatoid nodules
• Fungal disease
B. Infection
• Non-tuberculous
bacteria
• Viruses
• Parasites
C. Malignancies (less likely in
children)
Figure 2. Follow-up contrast-enhanced CT scan in axial views during
• Secondary CNS lymphoma
near the end-term of the patient’s anti-TB medications. The rim-
• Seeding from primary
enhancing lesions show decrease in size and number. The
brain tumour
hydrocephalus has resolved and minimal residual basal cistern
• Metastases (less likely in
enhancement was noted.
children)

Andres MM et al. TB Corner 2016; 2(5):1-9 2

WFPI TB Corner July 2016

Discussion


Pathogenesis

The pathogenesis of TBM is a two-step process. 1) It begins with the Mycobacterium

tuberculosis bacilli entering the host by droplet inhalation, which intensifies within the lungs, spreads to
the regional lymph nodes, and then continues towards the hematogenous route [5,9]. 2)
Hematogenous seeding of TB bacilli into the central nervous system with predilection into the
interpeduncular and suprasellar cisterns creates a granulomatous hypersensitivity reaction that incites
production of exudates [9]. These exudates surround and penetrate the cortical and meningeal blood
vessels thereby producing inflammation and vasculitis, CSF pathway obstruction, and obliterative
endarteritis leading to infarction [9,10].

Clinical Presentation
A family history of TB is elicited in 50 to 60%, along with a personal history of previous infection
in 10% of adults and 50% of children [11]. Adults usually develop the classical meningeal signs of
fever, headache and stiff neck in cases of TBM. Children on the other hand, can present with a
prodrome of malaise and myalgia that lasts for 2-8 weeks before signs of meningeal irritation arise.
Early diagnosis of TBM in the pediatric population is especially difficult [11] as onset may be insidious,
and its variety of symptoms is non-specific. Clinical epidemiological data show that TBM develops most
often within 3 months of primary infection in children [9,11]. Headache less commonly occurs in
children compared to adults, although the former more often present with seizures [12].

Thwaites and colleagues stated differences in the clinical signs and symptoms of TBM between
adults and children [13] as enumerated in the table below.

SYMPTOMS CLINICAL SIGNS

CHILDREN Early symptoms are non-specific Initial apathy or irritability that progresses to
and include cough, fever, vomiting meningism, decreased level of consciousness,
(without diarrhea), malaise, and signs of increased intracranial pressure (often
weight faltering bulging anterior fontanelle and palsy of
abducens nerve) and focal neurological signs
(most often hemiplegia)

ADULTS Non-specific prodrome of malaise, Variable degrees of neck stiffness; cranial

weight loss, low-grade fever, and nerve palsies (VI>III>IV>VII) develop as
gradual onset of headache over disease progresses and confusion and coma
1–2 weeks; followed by worsening deepen; monoplegia, hemiplegia, or paraplegia
headache, vomiting, and confusion, in about 20% of cases
leading to coma and death if
untreated

Table 1. Common Clinical Features of Tuberculous Meningitis in Children and Adults 


(Source: Thwaites GE, Van Toorn R, and Schoeman J. Tuberculous Meningitis: more questions, still few answers.
Lancet Neurol, 2013; 12:999-1010). DOI: 10.101016/S1474-4422(13)70168-6).

Andres MM et al. TB Corner 2016; 2(5):1-9 3

WFPI TB Corner July 2016

Radiologic Features
CT scanning is an established diagnostic modality in the detection of TBM. It is widely used and
aids in distinguishing TBM from other similar TBM-like entities [14,15]. Although not regarded as a
substitute for microbiological evaluation, CT scan has the advantage of image acquisition speed, easy
accessibility, and non-invasiveness, which aids in rapid assessment and diagnosis. Due to these
reasons, CT plays a major role in the early and prompt detection of TBM. This in turn ensures a better
patient prognosis.

The triad of hydrocephalus, infarct, and basal meningeal enhancement make up the CT imaging
features of TBM [2,3,4,5,17,18]. Combination of these features increases the specificity for the disease.

Hydrocephalus is the most frequent abnormality noted in TBM [16]. It is demonstrated on CT as

either symmetric or asymmetric dilatation of the ventricles. Exudates in the cisterns are responsible for
CSF pathway obstruction and subsequent development of this finding. This imaging predictor has
sensitivity of 57-93% and specificity of 69-83% [4,15].

Inflammatory exudates are predominantly distributed in the basal subarachnoid cisterns around
the circle of Willis. The most commonly affected vessels in children are the perforating vessels at the
base of the brain and lenticulostriate branches of the middle cerebral artery. These explain why the
ischemic infarctions are usually located in the basal ganglia, anterior limbs of the internal capsules, and
thalami [16]. These exudates surround and infiltrate the vessels at the base of the brain causing
inflammation and intimal damage leading to panarteritis, thrombosis, obstruction, and then eventually
ischemic infarction. Infarction is demonstrated on CT as areas of hypoattenuation with loss of gray-white
matter delineation. Its sensitivity is valued at 18-75% and its specificity is at 82-100% [4,15]. Infarction is
related to poor outcome in patients with TBM and is associated with increased risk of neurologic
complications.

On non-contrast CT images, meningeal involvement is isodense or hyperdense relative to the

basal cisterns due to the accumulation of inflammatory exudates. Contrast-enhanced CT images
provide better detection of the presence of meningeal involvement, infarction, and hydrocephalus.
Basal meningeal enhancement as a predictor of TBM, and has a sensitivity of 35-73% and specificity of
69-88% [4,15].

Basal cistern enhancement is non-specific, and is not pathognomonic for TBM when it presents
in isolation. Other predictors such as hydrocephalus, infarcts and TB elsewhere in the body should aid
in pointing towards TB as the etiology. Several granulomatous processes aside from TB may also affect
the basilar meninges, which include sarcoidosis, Wegener granulomatosis, luetic gummas, rheumatoid
nodules and fungal disease that produce similar nodular basal cistern enhancement [19]. Other
infectious agents such as non-tuberculous bacteria, viruses, and parasites may also give rise to
abnormal enhancement [20]. Secondary CNS lymphoma, seeding from a primary brain tumor, or
metastatic disease usually from breast and prostate cancers can cause similar appearances [19],
however these are less considered in the pediatric population.

Andres MM et al. TB Corner 2016; 2(5):1-9 4

WFPI TB Corner July 2016

Table 2. Objective Criteria in demonstrating abnormal basal enhancement in TBM 


(Source: Przybojewski S, Andronikou S, and Wilmshurst J, Objective Criteria to Determine the Presence of Abnormal
Basal Enhancement in Children with Suspected Tuberculous Meningitis. Pediatr Radiol, 2006; 36: 687-696).

Patterns of Basal Description Image

Meningeal
Enhancement

Contrast filling CSF spaces that surround normal

the cisterns vascular enhancement are obliterated by
contrast medium

Double and triple Two or three lines of enhancement are

lines identified in the middle cerebral artery
cisterns. They represent enhancement of
the meninges lining the adjacent frontal
and temporal lobes with or without visible
enhancement of the middle cerebral artery
itself. This sign should not be looked for at
the distal middle cerebral artery where it
divides into its Sylvian branches

!
Linear Linear enhancement is seen in the middle
enhancement cerebral artery cistern. Linear
enhancement seen over two or more
contiguous slices is abnormal. The middle
cerebral artery itself is too small to be
seen in its full horizontal length over more
than one slice. It is usually tortuous and,
therefore, is seen in an interrupted fashion
on one slice and not as an intact line

Andres MM et al. TB Corner 2016; 2(5):1-9 5

WFPI TB Corner July 2016

Y-sign The Y-sign is seen at the junction of the

suprasellar and middle cerebral artery
cistern. Pure vessel enhancement in this
region lacks an arm of the ‘Y’ because the
posterior communicating artery is not
often seen on CT due to its small size

Infundibular The posterior aspect of the infundibular

recess of the third recess of the third ventricle in the
suprasellar cistern is enhanced. There is
no known vessel that lies here that can be
confused with meningeal enhancement

Ill-defined edge There is an ill-defined edge to the

enhancement, as opposed to the sharply
marginated enhancement of normal
vessels

Andres MM et al. TB Corner 2016; 2(5):1-9 6

WFPI TB Corner July 2016

Join the dots Normal enhancement of the Sylvian

vessels is seen as separate dots because
the branches are seen in cross section.
Abnormal enhancement is present when
the dots are joined by linear enhancement

Nodular Nodular enhancement is always

enhancement pathological as normal meninges and
vessels are smooth and sharply
marginated

Asymmetry Asymmetry of any of the above features

aids recognition of abnormal basal
enhancement as comparison can be
made with the normal side

Conclusion
Tuberculous meningitis is the most common presentation of CNS Tuberculosis. CT scanning is
an established diagnostic modality in detection of TBM due to its accessibility, non-invasiveness, and
rapid acquisition of images for evaluation.

There is a common triad of findings for TBM that includes abnormal basal cistern enhancement
(sensitivity of 35-73% and specificity of 69-88%), hydrocephalus (sensitivity of 57-93% and specificity of
69-83%), and infarction (sensitivity is valued at 18-75% and its specificity is at 82-100%). Several
patterns of basal meningeal enhancement are stated in the literature although these are non-specific,

Andres MM et al. TB Corner 2016; 2(5):1-9 7

WFPI TB Corner July 2016

and are not pathognomonic for TBM especially when presenting in isolation. Hence, findings of basal
cistern enhancement should be correlated with other associated imaging and clinical presentations.

References
1. Duque-Silva A, Robsky K, Fllod J, and Barry P. Risk Factors for Central Nervous System
Tuberculosis. Pediatrics, 2015; 136(5). DOI: 10.1542/peds.2014-3958.
2. Theron S, Andronikou S, Grobbelaar, Steyn F, Mapukata A, Du Plessis J. Localized Basal
Meningeal Enhancement in Tuberculous Meningitis. Pediatr Radiol, 2006; 36:11182-1185.
DOI: 10.1007/s00247-006-312-1
3. Andronikou, Wieselthaler N, Smith B, Douis H, Fieggen G, Van Toorn R, and Wilmshurst J. Value
of Early Follow-up CT in Pediatric Tuberculous Meningitis. Pediatr Radiol, 2005; 35:1092-1099.
DOI:10.1007/s00247-005-1549-9.
4. Andronikou, Savvas and Wieselthaler, Nicky. Modern Imaging of Tuberculosis in Children:
Thoracic, Central Nervous System and Abdominal Tuberculosis. Pediatr Radiol, 2004; 34:
861-875. DOI: 10.1007/s00247-004-1236-2.
5. Reyes-Paguia MP, Laya BF, De Jesus JM, and Piedad RO. Accuracy of Established Cranial CT Scan
Findings in the Diagnosis of Cranial Tuberculosis. St. Luke’s Journal of Medicine, 2011; 7(1):
33-42.
6. Torok ME. Tuberculous Meningitis: Advances in Diagnosis and Treatment. British Medical
Bulletin, 2015;113:117-131. DOI: 10.1093/bmb/ldv003.
7. Principi N and Esposito S. Diagnosis and Therapy of Tuberculous Meningitis in Children.
Tuberculosis, 2012;92:377-383. http://dx.doi.org/10.1016/j.tube.2012.05.011.
8. Chiang SS, Khan FA, Milstein MB et al. Treatment Outcomes of Childhood Tuberculous
Meningitis: A Systematic Review and Meta-Analysis. Lancet Infect Dis, 2014; 14(10):947-957.
9. Van Rensburg PJ, Andronikou S, Van Toorn R, and Pienaar M. Magnetic Resonance Imaging of
Tuberculosis of the Central Nervous System in Children with Tuberculous Meningitis. Pediatr
Radiol, 2008; 38:1306-1313.
10.Donald Pr and Schoeman JF. Tuberculous Meningitis. N Engl J Med, 2004; 351:1719-1720.
11.Chatterjee S. Brain tuberculomas, tubercular meningitis, and post-tubercular hydrocephalus in
children. J Pediatr Neurosci. 2011;6 (3):96.
12.Changal KH, Raina AH. Central Nervous System Manifestations of Tuberculosis: A Review Article.
Mycobacterial Diseases. 2014; 4(2).
13.Thwaites GE, Van Toorn R, and Schoeman J. Tuberculous Meningitis: more questions, still few
answers. Lancet Neurol, 2013; 12:999-1010). DOI: 10.101016/S1474-4422(13)70168-6).
14.Nabukeera-Barungi N, Wilmshurst J, Rudzani M, Nuttall J. Presentation and outcome of
tuberculous meningitis among children: experiences from a tertiary children’s hospital.
African Health Sciences.2014;14(1):143-9.
15.Botha H, Ackerman C, Candy S, Carr JA, Griffith-Richards S, and Bateman KJ. Reliability and
Diagnostic Performance of CT Imaging Criteria in the Diagnosis of Tuberculous Meningitis.
PLoS ONE, 2012; 7(6):1-8 e38982 DOI: 10.1371/journal.pone..0038982
16.Wallace RC, Burton EM, Barrett FF, Leggiadro RJ, Gerald BE, and Lasater OE. Intracranial
Tuberculosis in Children: CT Appearance and Clinical Outcome. Pediatr Radiol, 1991;
21:241-246.
17.Andronikou, S, Wilmshurst J, Hatherill M, and Van Toorn R. Distribution of Brain Infarction in
Children with Tuberculous Meningitis and Correlation with Outcome Score at 6 months.
Pediatr Radiol, 2006;36:1289-1294. DOI: 10.1007/s00247-006-0319-7.

Andres MM et al. TB Corner 2016; 2(5):1-9 8

WFPI TB Corner July 2016

18.Przybojewski S, Andronikou S, and Wilmshurst J. Objective Criteria to Determine the Presence of

Abnormal Basal Enhancement in Children with Suspected Tuberculous Meningitis. Pediatr
Radiol, 2006; 36:687-696.
19.Smirniotopoullos J, Murphy F, Rushing E, Rees J, Schroeder J. Patterns of Contrast Enhancement
in the Brain and Meninges1. Radiographics, 2007;27(2):523-551.
20.Harisinghani M, McLoud T, Shepard J, Ko J, Shroff M, Mueller P. Tuberculosis from Head to Toe.
Radiographics, 2000;20:449-470.

Corresponding author:
Mariaem Andres
St. Luke’s Medical Center
Philippines
mariaem139@yahoo.com

Andres MM et al. TB Corner 2016; 2(5):1-9 9