Severe vasospasm due to tuberculous meningitis

Clinical History

43-year-old woman, treated with corticotherapy for lupus, found at home unconscious by her husband. She had complained of headache and fever two weeks before.

Imaging Findings

Emergency non enhancement head CT showed development of hydrocephalus (Fig. 1a) and angio-CT narrowing distal cerebral artery branches compatible with vasospasm (Fig. 1b).
MRI with gadolinium-contrast showed arachnoid and cranial nerves enhancement (Fig. 2a, b). Also MRI-diffusion/perfusion showed restricted diffusion in the left temporal lobe, basal ganglia, and pontomesencephalon compatible with widespread infarction (Fig. 3a, b).
Magnetic resonance angiography using 3-dimensional time-of-flight imaging showed narrowing of the distal internal carotid arteries and proximal left middle cerebral artery, as well as distal anterior and middle cerebral artery branches compatible with vasculitis (Fig. 4a, b).

CSF analysis showing high numbers of lymphocytes, neutrophils, elevated protein, and a low CSF/serum glucose ratio.

The tuberculosis tests come back positive: BAAR and GenXpert positive in CSF and broncho-alveolar washing for M.tuberculosis complex.

The diagnosis was severe vasospasm due to tuberculous meningitis complicated by widespread infarction and hydrocephalus.

Adequate treatment was initiated with antituberculosis therapy and corticosteroid therapy. Despite the treatment, the patient died thereafter.

Discussion

Meningoencephalitis produced by Koch bacillus is a disease including various symptoms, with often atypical onset and evolution, and with an aetiological diagnosis being rarely established. It therefore remains a disease with severe prognosis, despite adequate treatment. [3]

Acute tuberculous meningitis develops when old focal lesions in communication with the meninges (Rich foci) rupture, releasing massive numbers of mycobacteria, triggering a robust T-cell response and catastrophic immune reaction in and around the meninges and associated vasculature. [3]
Hydrocephalus occurs with the development of an adhesive inflammatory exudate that affects the sylvian fissures, basal cisterns, brainstem, and cerebellum, resulting in CSF obstruction. Vasculitis with ensuing infarction is likely caused by several mechanisms: strangulation of the vessels in the thick exudate at the base of the brain, T-cell–mediated inflammation of the adventitia leading to vessel wall necrosis and thrombosis, stretching of vessels by rapidly enlarging ventricles in the setting of acute hydrocephalus, and midbrain and frontal lobe infarction as the brain herniates. [2]

Diagnosis of tuberculous meningitis is not always straightforward. However, there are a few distinguishing features that should trigger suspicion. Patients with tuberculous meningitis typically present a subacute course. They are more likely to have cranial nerve palsies. They will not usually have a blood leukocytosis.
CSF is typically clear with moderate numbers of lymphocytes and neutrophils, elevated protein, and a low CSF/serum glucose ratio. CSF cultures cannot be relied on because they take weeks to grow and success depends on acquisition of a large volume. [1]
Chest radiographs are actually very useful for diagnosing active tuberculosis.
The PPD test is sensitive in most cases of active tuberculosis; however, several factors can lead to a false-negative result. These include recent vaccination with a live virus vaccine, recent corticosteroid use, concurrent HIV infection, cancer. [4]

On MRI, basal meningeal enhancement, tuberculomas, and infarction (particularly of the basal ganglia) all support a diagnosis of tuberculous meningitis, but cannot exclude cryptococcal meningitis, sarcoidosis or lymphoma.
The mortality rate for untreated tuberculous meningitis is 100%. Even if adequately treated, the mortality rate is still very high when treatment is initiated after patients have progressed to coma. [3]
Initiation of antituberculosis therapy must be instated at the first suspicion of tuberculous meningitis. [4]
The patient should also be rapidly tested for HIV and started on high-dose corticosteroids, which are strongly associated with a reduced risk of death. In addition to antituberculosis and corticosteroid therapy, development of obstructive hydrocephalus should be anticipated and immediately managed by ventricular drainage. [2]

Differential Diagnosis List

Final Diagnosis

Vasospasm due to tuberculous meningitis

URL:	https://www.eurorad.org/case/10778
DOI:	10.1594/EURORAD/CASE.10778
ISSN:	1563-4086