Tuberculosis (TB) is an infectious disease that continues to be a significant public health concern (1). Mycobacterium tuberculosis is the organism that is the causative agent for tuberculosis. In most patients, TB involving the leptomeninges is thought to spread by hematogenous dissemination from a primary source outside the CNS such as the lung or gastrointestinal tract. In the brain, a meningeal pattern of spread can occur, and the cerebrospinal fluid typically shows a high protein, low glucose and lymphocytosis. The most common finding in the image studies is communicating hydrocephalus, and it may be the only clue for diagnosis. Hydrocephalus may result from blockage of the basal subarachnoid cisterns by the dense basal exudate, or narrowing of the aqueduct and third ventricles by tuberculomas.
The base of the brain is often involved, so the proximal ends of the basal arteries are involved. The extension of the inflammatory exudate along the perforating blood vessels into the brain substance causes vascular damage, which may lead to spasm or thrombosis of the vessels, with resulting ischemia or infarction, most frequently seen at the basal ganglia and internal capsule. Although a basal ganglia infarct was found in this patient, the extensive ischemic lesions seen in the MRI were not found in the pathologic examination. Furthermore, vessels examination did not show the extensive vasculitis or thrombosis that we suspected. Despite the undisputed improvements in cerebral imaging with MRI, the consistency between the radiological and pathological findings is still poor. The pivotal event of ischemia is the decrease of cerebral blood flow (CBF), and flow thresholds may predict the tissue fate in the acute phase. CBF threshold that defines critical ischemia leading to irreversible infarction ranges from 8 to 12ml/100g per minute (5). Tissues experiencing perfusion values below this threshold have high probability to turn into irreversible infarction unless perfusion is quickly restored. The CBF values >20mL/100g per minute on the other hand, do not lead to a functional impairment of neuronal tissue and are termed as oligemia or normoperfusion. Thus, we assume that even with the dramatic brain images we showed, such low CBF was not achieved in our patient. This is relevant in the setting that many patients with infectious infarcts show great improvement and no neurological sequels after the infection is resolved, and it should be considered when doubt exists, as in this case, of pursuing more aggressive approaches as neurosurgery for treating the hydrocephalus.
Other interesting aspect of this case was the thick, yellowish, pus-like exudate in the basal surface of the brain, and the absence of epithelioid cell granulomas with caseous necrosis in the meninges or brain parenchyma. This appearing-like suppurative lesion could have been misdiagnosed pathologically as acute purulent meningitis caused by pyogenic bacteria, fortunately, numerous acid-fast bacilli were found, but they could have been obviated if special stains would have not been used. Purulent meningitis has only been reported in 1.3% of the cases of meningeal tuberculosis (2). While the typical granulomatous reaction is typical of tuberculosis, the diagnosis of tuberculosis meningitis may be established solely with the demonstration of tubercle bacilli (4). These type of "non-reactive tuberculous lesions" have been previously associated with severely immune compromised patients (4). The case demonstrates the variability that exists not only of the clinical but also of the pathological picture seen in patients with mycobacterium tuberculosis infection.
Contributed by Alejandra González-Duarte, MD, PhD, Juan Pablor Venzor-Castellanos, MD, Irene Treviño-Frenk, MD, Fernando Cano-García, MD, Ariadna Barrios-Ordoñez