Tuberculosis (intracranial manifestations)
Updates to Article Attributes
Tuberculosis of the central nervous system can result from either haematogenous spread from distant systemic infection (e.g. pulmonary tuberculosis) or from direct extension from local infection (e.g. tuberculous otomastoiditis).
Intracranial manifestations of tuberculosis are protean and can affect all compartments and are discussed individually in separate articles. Manifestations include:
- extra-axial
- tuberculous meningitis (leptomeningitis): most common
- tuberculous pachymeningitis: rare
- intra-axial
The remainder of this article is a general discussion of CNS tuberculosis. For a general discussion please refer to the article on tuberculosis.
Epidemiology
Tuberculosis remains a leading cause of morbidity and mortality in the developing world. It may account for ≈1/6th of the 3 million of global mortality due to Mycobacterium tuberculosis infection. CNS involvement is thought to occur in 2-5% 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-specificnonspecific including fever, seizures, meningism and focal neurological deficits, e.g. altered sensorium, hemiparesis.
Pathology
HaematogeneousHaematogenous 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 postprimarypost primary infection.
Radiological spectrumRadiographic features
There is a wide radiological and pathological spectrum with CNS disease. Tuberculous meningitis and intracranial tuberculous granuloma (tuberculoma) are the most common manifestations and these are discussed in detail in separate articles. Below is brief discussion of the main imaging features of each presentation.
Tuberculous meningitis
Tuberculous meningitis may manifest in two forms:
- leptomeningitis: common
- pachymeningitis: rare
Leptomeningitis
Involvement of the leptomeningitis by TB is common and presents with thick tuberculous exudate within the subarachnoid space, particularly pronounced at the base of brain (especially in the interpeduncular fossa, anterior to the pons and around the cerebellum) and may also extend into the Sylvian fissures. In contrast to bacterial meningitis, extension over the surfaces of the cerebral hemispheres is relatively uncommon 8. Eventually mass-like regions of caesouscaseous necrosis can form within this exudate, representing extra-axial tuberculomas.
Not surprisingly CSF flow is disrupted and obstructive hydrocephalus is common.
An additional complications is an arteritis which may result in ischaemic infarcts, which are seen in approximately a third of cases, especially in children 7.
Pachymeningitis
In contrast TB pachymeningitis is rare and is characterised by thick plaque like-like regions of pachymeningeal enhancement. 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.
For further discussion please refer to separate articles on tuberculous leptomeningitis and tuberculous pachymeningitis.
Tuberculoma
Intracranial tuberculomas may occur either in isolation or combined with extra-axial TB infection. They typically appear as ring-enhancing lesions with surrounding vasogenic oedema. Centrally they tend to have only intermediate or even low signal on T2 weighted images (helpful in distinguishing them from the less common tuberculous abscess) 9. They may be associated with extensive adjacent leptomeningeal and/or pachymeningeal enhancement.
For further discussion please refer to separate articles on intracranial tuberculoma.
Treatment and prognosis
Treatment of CNS tuberculosis is based on an anti-tubercular treatment regimen. However, multi-drugmultidrug resistant tuberculosis remains a major hurdle in treatment.
-</ul><p>The remainder of this article is a general discussion of CNS tuberculosis. For a general discussion please refer to the article on <a href="/articles/tuberculosis">t</a><a href="/articles/tuberculosis-of-the-central-nervous-system-1">uberculosis</a>.</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/hivaids">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><h4>Radiological spectrum</h4><p>There is a wide radiological and pathological spectrum with CNS disease. <a href="/articles/tuberculous-meningitis">Tuberculous meningitis</a> and <a href="/articles/intracranial-tuberculous-granuloma">intracranial tuberculous granuloma</a> (tuberculoma) are the most common manifestations and these are discussed in detail in separate articles. Below is brief discussion of the main imaging features of each presentation. </p><h5>Tuberculous meningitis</h5><p>Tuberculous meningitis may manifest in two forms:</p><ol>- +</ul><p>The remainder of this article is a general discussion of CNS tuberculosis. For a general discussion please refer to the article on <a href="/articles/tuberculosis">t</a><a href="/articles/tuberculosis-of-the-central-nervous-system-1">uberculosis</a>.</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/hivaids">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 nonspecific including fever, seizures, meningism and focal neurological deficits, e.g. altered sensorium, hemiparesis.</p><h4>Pathology</h4><p>Haematogenous 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 post primary infection.</p><h4>Radiographic features</h4><p>There is a wide radiological and pathological spectrum with CNS disease. <a href="/articles/tuberculous-meningitis">Tuberculous meningitis</a> and <a href="/articles/intracranial-tuberculous-granuloma">intracranial tuberculous granuloma</a> (tuberculoma) are the most common manifestations and these are discussed in detail in separate articles. Below is brief discussion of the main imaging features of each presentation. </p><h5>Tuberculous meningitis</h5><p>Tuberculous meningitis may manifest in two forms:</p><ol>
-</ol><h6>Leptomeningitis</h6><p>Involvement of the leptomeningitis by TB is common and presents with thick tuberculous exudate within the subarachnoid space, particularly pronounced at the base of brain (especially in the <a href="/articles/interpeduncular-fossa">interpeduncular fossa</a>, anterior to the pons and around the cerebellum) and may also extend into the Sylvian fissures. In contrast to <a href="/articles/pyogenic-meningitis">bacterial meningitis</a>, extension over the surfaces of the cerebral hemispheres is relatively uncommon <sup>8</sup>. Eventually mass-like regions of caesous necrosis can form within this exudate, representing extra-axial tuberculomas.</p><p>Not surprisingly CSF flow is disrupted and <a href="/articles/obstructive-hydrocephalus">obstructive hydrocephalus</a> is common.</p><p>An additional complications is an arteritis which may result in ischaemic infarcts, which are seen in approximately a third of cases, especially in children <sup>7</sup>. </p><h6>Pachymeningitis</h6><p>In contrast TB pachymeningitis is rare and is characterised by thick plaque like regions of pachymeningeal enhancement. 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 <a href="/articles/tuberculoma">tuberculoma</a> <sup>8</sup>.</p><p>For further discussion please refer to separate articles on <a href="/articles/tuberculous-meningitis">tuberculous leptomeningitis</a> and <a href="/articles/tuberculous-pachymeningitis">tuberculous pachymeningitis</a>.</p><h6> </h6><h5>Tuberculoma</h5><p>Intracranial tuberculomas may occur either in isolation or combined with extra-axial TB infection. They typically appear as ring-enhancing lesions with surrounding <a href="/articles/vasogenic-cerebral-oedema">vasogenic oedema</a>. Centrally they tend to have only intermediate or even low signal on T2 weighted images (helpful in distinguishing them from the less common tuberculous abscess) <sup>9</sup>. They may be associated with extensive adjacent leptomeningeal and/or pachymeningeal enhancement. </p><p>For further discussion please refer to separate articles on <a href="/articles/intracranial-tuberculous-granuloma">intracranial tuberculoma</a>.</p><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>- +</ol><h6>Leptomeningitis</h6><p>Involvement of the leptomeningitis by TB is common and presents with thick tuberculous exudate within the subarachnoid space, particularly pronounced at the base of brain (especially in the <a href="/articles/interpeduncular-fossa">interpeduncular fossa</a>, anterior to the pons and around the cerebellum) and may also extend into the Sylvian fissures. In contrast to <a href="/articles/pyogenic-meningitis">bacterial meningitis</a>, extension over the surfaces of the cerebral hemispheres is relatively uncommon <sup>8</sup>. Eventually mass-like regions of caseous necrosis can form within this exudate, representing extra-axial tuberculomas.</p><p>Not surprisingly CSF flow is disrupted and <a href="/articles/obstructive-hydrocephalus">obstructive hydrocephalus</a> is common.</p><p>An additional complications is an arteritis which may result in ischaemic infarcts, which are seen in approximately a third of cases, especially in children <sup>7</sup>. </p><h6>Pachymeningitis</h6><p>In contrast TB pachymeningitis is rare and is characterised by thick plaque-like regions of pachymeningeal enhancement. 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 <a href="/articles/tuberculoma">tuberculoma</a> <sup>8</sup>.</p><p>For further discussion please refer to separate articles on <a href="/articles/tuberculous-meningitis">tuberculous leptomeningitis</a> and <a href="/articles/tuberculous-pachymeningitis">tuberculous pachymeningitis</a>.</p><h5>Tuberculoma</h5><p>Intracranial tuberculomas may occur either in isolation or combined with extra-axial TB infection. They typically appear as ring-enhancing lesions with surrounding <a href="/articles/vasogenic-cerebral-oedema">vasogenic oedema</a>. Centrally they tend to have only intermediate or even low signal on T2 weighted images (helpful in distinguishing them from the less common tuberculous abscess) <sup>9</sup>. They may be associated with extensive adjacent leptomeningeal and/or pachymeningeal enhancement. </p><p>For further discussion please refer to separate articles on <a href="/articles/intracranial-tuberculous-granuloma">intracranial tuberculoma</a>.</p><h4>Treatment and prognosis</h4><p>Treatment of CNS tuberculosis is based on an anti-tubercular treatment regimen. However, multidrug resistant tuberculosis remains a major hurdle in treatment.</p>
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