A 19-YEAR-OLD Lebanese man was admitted to a hospital because of status epilepticus. Following seizure control, he was noted to be quadriparetic, and a magnetic resonance image of the brain revealed a pontine lesion that was hyperintense on T2-weighted images (Figure 1) and hypointense on T1-weighted images, suggestive of an infarct. He was referred to our hospital for further evaluation and management. His medical history revealed 2 prior episodes of "aseptic" meningitis associated with generalized tonic-clonic seizures within a period of 1 year. He was empirically treated with acyclovir and valproic acid. On initial examination at our medical center, the patient was afebrile and had normal heart sounds, normal results of chest and abdominal examinations, and no evidence of lymphadenopathy or meningeal signs. Neurologically, he was awake and oriented, with quadriparesis, anarthria, and dysphagia. The deep tendon reflexes were hyperactive all over, including the jaw jerk, a bilateral positive Babinski sign, and ankle clonus. The patient also had bowel and bladder dysfunction. A review of the magnetic resonance image of the brain revealed an abnormal configuration of the basilar trunk on a T2-weighted coronal section (Figure 2). He underwent 4-vessel cerebral angiography, which showed a lobulated, fusiform aneurysmal formation at the mid portion of the basilar trunk, measuring 3 × 4 mm, with evidence of dissection (Figure 3). Complete blood cell count, results of blood chemical analysis, levels of antinuclear antibodies, anticardiolipin antibodies, lupus anticoagulant, and angiotensin-converting enzyme, and a coagulopathy profile were normal. Cerebrospinal fluid (CSF) studies showed lymphocytosis (white blood cell count, 5/mm; 82% lymphocytes, 16% segmented, and 2% eosinophils), a high protein level (2 g/L), and a low glucose level (46 mg/dL [2.5 mmol/L]). The corresponding serum glucose level was 150 mg/dL (8.3 mmol/L). Cerebrospinal fluid cultures for bacteria and mycobacteria were negative, and the polymerase chain reaction for tuberculosis in the CSF was negative. Treponema pallidum hemagglutination antibody and VDRL tests were negative. Brucella titers, using a serum agglutinin test, were positive in the blood (direct, <1/20; indirect, 1/320) and the CSF (direct, <1/20; indirect, 1/160). The patient received a course of rifampin, doxycycline, and streptomycin. Soon after the initiation of treatment, he started showing signs of neurologic recovery. Six months later, the patient improved markedly. He recovered his speech and his sphincter control, regained motor function in the upper extremities, and started to walk with assistance. Repeated 4-vessel cerebral angiography revealed regression of the basilar aneurysm (Figure 4). Nine months later, the Brucella (direct and indirect) titers in the blood were both less than 1/20.