Tuberculosis (intracranial manifestations)
Updates to Article Attributes
CNS tuberculosis refers to the central nervous system manifestations of tuberculosis, and can take a number of forms.
Epidemiology
Tuberculosis remains a leading cause of morbidity and mortality in the developing world. It may account for ≈ 1≈1/6th of the 3 million of global mortality due to Mycobacterium tuberculosis infection. CNS involvement is thought to occur in 2 - 5-5% of patients with tuberculosis and up to 15% of those with AIDS related tuberculosis 6,7.
Although CNS involvement by tuberculosis is seen in all age groups, there is a predilection for younger patients, with 60-70% of cases occurring in patients younger than 20 years of age 7.
In endemic regions, tuberculomas account for as many as 50% of all intracranial masses 8.
Clinical presentation
Clinical presentation depends on the specific manifestation, although in all cases symptoms and signs are non-specific including fever, seizures, meningism and focal neurological deficits (e, e.g altered. altered sensorium, hemiparesis).
Pathology
Haematogeneous spread from the lungs or gastrointestinal tract is most common, leading to small subpial or subependymal infective foci. These are termed Rich foci and form a reservoir from which intracranial manifestations may arise 5,7-8. This can occur either during the primary infection (uncommon, and more frequently seen in children) or be reactivated later and cause a postprimary infection.
Potential manifestations include:
-
tuberculous meningitis
-: most common - intracranial tuberculous granuloma (tuberculoma)
- focal tuberculous cerebritis
- intracranial tuberculous abscess
- tuberculous encephalopathy
Radiological spectrum
There is a wide radiological and pathological spectrum with CNS disease. Tuberculous meningitis and parenchymal granuloma formation (tuberculoma) are the most common manifestations. Tuberculous encephalopathy can also be seen, particularly in children 7.
Tuberculous meningitis
For further discussion please refer to separate article: tuberculous meningitis.
Tuberculous meningitis may manifest in two forms:
- leptomeningitis (menignoecephalitis): most common
- pachymeningitis
In leptomeningitis thick tuberculous exudate forms within the subarachnoid space at the base of brain, most pronounced in the interpeduncular fossa, anterior to the pons and around the cerebellum. It may also extend into the Sylvian fissures, but uncommonly over the surfaces of the cerebral hemispheres8. Eventually mass-like regions of caesous necrosis can form within this exudate.
Complications include an arteritis which may result in ischaemic infarcts. This is seen in approximately a third of cases, and is more common in children 7. Obstructive hydrocephalus is common.
CT
- non-contrast scans may be normal
- infarcts due to arteritis may be evident, especially in children
- hydrocephalus may be present
- dense basal enhancement
- an enhancing mass-like region within the basal cisterns
MRI
-
T1
- normal initially
- slight T1 shortening with disease progression 8
-
T2
- normal initially
- slight T2 shortening with disease progression 8
-
T1 C+ (Gd):
-intense heterogeneous basal enhancement
Pachymeningitis is much less common producing plaque like leptomeningeal thickening 4.
For further discussion please refer to separate article: tuberculous pachymeningitis.
This term should be reserved for cases where it is an isolated abnormality, and not confused with the sometimes dramatic thickening of dura adjacent to a tuberculoma 8.
CT
- intensely enhancing thickened meninges
MRI
-
T1:
-low signal thickened meninges -
T2:
-low signal thickened meninges -
T1 C+ (Gd):
-intense enhancement of thickened meninges
Tuberculoma
Intracranial tuberculomas may occur either in isolation or combined with tuberculous meningitis.
MRI
-
T1
- isointense to grey-matter 9
- may have central region of hyperintensity representing caseation
-
T2
- isointense to grey-matter
- may have central region of hypointensity representing gliosis and abundant monocyte infiltration 9
- lesions are surrounded by vasogenic oedema
-
T1 C+ (Gd)
- usually appears as ring-enhancement
- may appear as a conglomerate enhancing mass
-
MR spectroscopy
- decrease in NAA/Cr
- slight decrease in NAA/Cho
- lipid-lactate peaks are usually elevated (86%) 10
Focal tuberculous cerebritis
- CT scan will show intense focal gyral enhancement
- On MRI, these areas show T1 hypo intense and T2 hyper intense signal with patchy enhancement on post-gadolinium images.
Tuberculous encephalopathy
- severe unilateral or bilateral cerebral oedema is seen on neuroimaging.
- demyelination related T2
hyper intensitieshyperintensities on MR imaging. - diffuse alteration in magnetization transfer ratio in white matter
AIDS related tuberculosis
- Infarction, meningeal enhancement and parenchymal disease are more florid in HIV related tuberculosis.
- differential diagnoses are cerebral toxoplasmosis and CNS lymphoma
Complications
- secondary cerebral infarction from obliterative end artetitis
- arachnoid fibrosis with resultant hydrocephalus
Treatment and prognosis
Treatment of CNS tuberculosis is based on an anti-tubercular treatment regimen. However, multi-drug resistant tuberculosis remains a major hurdle in treatment.
Differential diagnosis
The differential diagnosis will also depend on the particular manifestation.
For tuberculous leptomenigitis consider:
For tuberculous pachymeningitis consider:
- neurosarcoidosis
- en plaque meningioma
-
lymphoma
/ leukaemic/leukaemic infiltration - Erdheim-Chester disease
For a tuberculous granuloma (intraparenchymal) consider:
The differential of tuberculomas is essentially is the differential of ring-enhancing lesions, and includes:
- other infection
- neurosarcoidosis
- cerebral metastases
- CNS lymphoma
Central isointensity or hypointensity compared to grey matter seen centrally on T2 is helpful, as it is not seen in most other causes 9.
-<p><strong>CNS tuberculosis </strong>refers to the central nervous system manifestations of <a href="/articles/tuberculosis">tuberculosis</a>, and can take a number of forms.</p><h4>Epidemiology</h4><p>Tuberculosis remains a leading cause of morbidity and mortality in the developing world. It may account for ≈ 1/6<sup>th</sup> of the 3 million of global mortality due to <em>Mycobacterium tuberculosis</em> infection. CNS involvement is thought to occur in 2 - 5% of patients with tuberculosis and up to 15% of those with <a href="/articles/hiv-aids-1">AIDS</a> related tuberculosis <sup>6,7</sup>.</p><p>Although CNS involvement by tuberculosis is seen in all age groups, there is a predilection for younger patients, with 60-70% of cases occurring in patients younger than 20 years of age <sup>7</sup>.</p><p>In endemic regions, <a href="/articles/intracranial-tuberculoma">tuberculomas</a> account for as many as 50% of all intracranial masses <sup>8</sup>.</p><h4>Clinical presentation</h4><p>Clinical presentation depends on the specific manifestation, although in all cases symptoms and signs are non-specific including fever, seizures, meningism and focal neurological deficits (e.g altered sensorium, hemiparesis).</p><h4>Pathology</h4><p>Haematogeneous spread from the lungs or gastrointestinal tract is most common, leading to small subpial or subependymal infective foci. These are termed <a href="/articles/rich-foci">Rich foci</a> and form a reservoir from which intracranial manifestations may arise <sup>5,7-8</sup>. This can occur either during the primary infection (uncommon, and more frequently seen in children) or be reactivated later and cause a postprimary infection.</p><p>Potential manifestations include:</p><ul>- +<p><strong>CNS tuberculosis </strong>refers to the central nervous system manifestations of <a href="/articles/tuberculosis">tuberculosis</a>, and can take a number of forms.</p><h4>Epidemiology</h4><p>Tuberculosis remains a leading cause of morbidity and mortality in the developing world. It may account for ≈1/6<sup>th</sup> of the 3 million of global mortality due to <em>Mycobacterium tuberculosis</em> infection. CNS involvement is thought to occur in 2-5% of patients with tuberculosis and up to 15% of those with <a href="/articles/hiv-aids-1">AIDS</a> related tuberculosis <sup>6,7</sup>.</p><p>Although CNS involvement by tuberculosis is seen in all age groups, there is a predilection for younger patients, with 60-70% of cases occurring in patients younger than 20 years of age <sup>7</sup>.</p><p>In endemic regions, <a href="/articles/intracranial-tuberculoma">tuberculomas</a> account for as many as 50% of all intracranial masses <sup>8</sup>.</p><h4>Clinical presentation</h4><p>Clinical presentation depends on the specific manifestation, although in all cases symptoms and signs are non-specific including fever, seizures, meningism and focal neurological deficits, e.g. altered sensorium, hemiparesis.</p><h4>Pathology</h4><p>Haematogeneous spread from the lungs or gastrointestinal tract is most common, leading to small subpial or subependymal infective foci. These are termed <a href="/articles/rich-foci">Rich foci</a> and form a reservoir from which intracranial manifestations may arise <sup>5,7-8</sup>. This can occur either during the primary infection (uncommon, and more frequently seen in children) or be reactivated later and cause a postprimary infection.</p><p>Potential manifestations include:</p><ul>
-<a href="/articles/tuberculous-meningitis">tuberculous meningitis</a> - most common</li>- +<a href="/articles/tuberculous-meningitis">tuberculous meningitis</a>: most common</li>
-<a href="/articles/leptomeningitis">leptomeningitis</a> (menignoecephalitis) : most common</li>- +<a href="/articles/leptomeningitis">leptomeningitis</a> (menignoecephalitis): most common</li>
-</ol><p>In <strong>leptomeningitis</strong> thick tuberculous exudate forms within the subarachnoid space at the base of brain, most pronounced in the <a href="/articles/interpeduncular-fossa">interpeduncular fossa</a>, anterior to the <a href="/articles/pons">pons</a> and around the <a href="/articles/cerebellum">cerebellum</a>. It may also extend into the <a href="/articles/sylvian-fissure">Sylvian fissures</a>, but uncommonly over the surfaces of the cerebral hemispheres<sup>8</sup>. Eventually mass-like regions of caesous necrosis can form within this exudate.</p><p>Complications include an arteritis which may result in ischaemic infarcts. This is seen in approximately a third of cases, and is more common in children <sup>7</sup>. <a href="/articles/obstructive_hydrocephalus">Obstructive hydrocephalus</a> is common.</p><h6>CT</h6><ul>- +</ol><p>In <strong>leptomeningitis</strong> thick tuberculous exudate forms within the subarachnoid space at the base of brain, most pronounced in the <a href="/articles/interpeduncular-fossa">interpeduncular fossa</a>, anterior to the <a href="/articles/pons">pons</a> and around the <a href="/articles/cerebellum">cerebellum</a>. It may also extend into the <a href="/articles/sylvian-fissure">Sylvian fissures</a>, but uncommonly over the surfaces of the cerebral hemispheres<sup>8</sup>. Eventually mass-like regions of caesous necrosis can form within this exudate.</p><p>Complications include an arteritis which may result in ischaemic infarcts. This is seen in approximately a third of cases, and is more common in children <sup>7</sup>. <a href="/articles/obstructive-hydrocephalus">Obstructive hydrocephalus</a> is common.</p><h6>CT</h6><ul>
-<strong>T1 C+ (Gd) </strong>- intense heterogeneous basal enhancement</li>- +<strong>T1 C+ (Gd):</strong> intense heterogeneous basal enhancement</li>
-<strong>T1 </strong>- low signal thickened meninges</li>- +<strong>T1:</strong> low signal thickened meninges</li>
-<strong>T2 </strong>- low signal thickened meninges</li>- +<strong>T2:</strong> low signal thickened meninges</li>
-<strong>T1 C+ (Gd) </strong>- intense enhancement of thickened meninges</li>- +<strong>T1 C+ (Gd):</strong> intense enhancement of thickened meninges</li>
-<li>demyelination related T2 hyper intensities on MR imaging.</li>- +<li>demyelination related T2 hyperintensities on MR imaging.</li>
-</ul><h4>Treatment and prognosis</h4><p>Treatment of CNS tuberculosis is based on an anti-tubercular treatment regimen. However, multi-drug resistant tuberculosis remains a major hurdle in treatment.</p><h4>Differential diagnosis</h4><p>The differential diagnosis will also depend on the particular manifestation.</p><p>For<strong> tuberculous leptomenigitis </strong>consider</p><ul>- +</ul><h4>Treatment and prognosis</h4><p>Treatment of CNS tuberculosis is based on an anti-tubercular treatment regimen. However, multi-drug resistant tuberculosis remains a major hurdle in treatment.</p><h4>Differential diagnosis</h4><p>The differential diagnosis will also depend on the particular manifestation.</p><p>For<strong> tuberculous leptomenigitis </strong>consider:</p><ul>
-</ul><p>For <strong>tuberculous pachymeningitis</strong> consider</p><ul>- +</ul><p>For <strong>tuberculous pachymeningitis</strong> consider:</p><ul>
-<a href="/articles/primary-cns-lymphoma">lymphoma</a> / leukaemic infiltration</li>- +<a href="/articles/primary-cns-lymphoma">lymphoma</a>/leukaemic infiltration</li>
-</ul><p>For a <strong>tuberculous granuloma (intraparenchymal) </strong>consider</p><p>The differential of tuberculomas is essentially is the differential of <a href="/articles/cerebral-ring-enhancing-lesions">ring-enhancing lesions</a>, and includes:</p><ul>- +</ul><p>For a <strong>tuberculous granuloma (intraparenchymal) </strong>consider:</p><p>The differential of tuberculomas is essentially is the differential of <a href="/articles/cerebral-ring-enhancing-lesions">ring-enhancing lesions</a>, and includes:</p><ul>
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