Central Nervous System Tuberculosis: Pathophysiology and Imaging Findings

Pathogenesis

Mycobacterium TB is the most common organism causing tuberculous infection of CNS. Other species of mycobacteria may be involved in immunocompromised patients.⁶ Based on the observations of Rich and McCordock,⁶ a 2-step model has been proposed for the pathogenesis of CNS TB. During the initial pulmonary infection, tuberculous bacteria may enter the systemic circulation and subsequently reach the oxygen-rich CNS, establishing a focus called the Rich focus. This focus may be in the meninges,

Hydrocephalus

Hydrocephalus can be communicating, noncommunicating, or complex in patients with TBM. Tubercular hydrocephalus is usually communicating, accounting for 80% of cases.³³ It occurs because of obstruction to CSF flow in the basal cisterns by inflammatory exudate (Fig. 3). Noncommunicating or obstructive hydrocephalus can occur either because of obstruction of fourth ventricular outlet foramina by the basal exudates or mass effect by a focal parenchymal tuberculoma, because of brain abscess, or

Vasculitis

The basal exudates cause inflammatory changes in the vessels predominantly involving the circle of Willis. At first, the vessel wall is involved, and later the lumen of the vessel, leading to complete occlusion by reactive subendothelial cellular proliferation and thrombus formation. Middle cerebral and lenticulostriate arteries are the most common vessels involved.47, 48 The conventional angiographic features of TBM include a triad of a hydrocephalic pattern, narrowing of arteries at the base

Cranial nerve involvement

Cranial nerve involvement in TBM is seen in 17% to 70% of patients. Nerve involvement occurs because of ischemia of the nerve or entrapment of the nerve in basal exudates.22, 53 Direct mass effect of a tuberculoma on the nerve within the subarachnoid course or by direct involvement of the cranial nerve nuclei in the brain are the other mechanisms (Fig. 7).²² Fibrotic changes in the late stage can cause permanent loss of function in these nerves.¹³

The affected nerve shows thickening and

Sequelae of TBM

Focal or diffuse cerebral atrophy and areas of encephalomalacia secondary to infarcts and hydrocephalus (Fig. 8), meningeal or ependymal calcifications, and occasionally syringomyelia or syringobulbia, are the sequelae of TBM.11, 22

Spinal meningitis and spinal arachnoiditis

These are inflammatory spinal diseases caused by M tuberculosis.¹⁰¹ The pathophysiology of spinal meningitis is similar to that of TBM: a submeningeal tubercle forms during primary infection and ruptures into the subarachnoid space, eliciting mediators of delayed hypersensitivity.⁵⁵ As with intracranial lesions, there is granulomatous inflammation with areas of caseation and tubercles with eventual development of fibrous tissue in chronic or treated cases. MR imaging features include CSF

Summary

CNS TB is a common clinical concern in developing countries, with increasing incidence in developed countries because of the HIV pandemic. Imaging, particularly MR imaging, is a cornerstone in the diagnosis of CNS TB and its associated complications as well as in monitoring response to treatment. A thorough knowledge of typical and atypical imaging characteristics help in accurate diagnosis as well as in the differential diagnosis. The newer imaging modalities help in improved characterization