A 15-year-old boy originally from Somalia underwent routine TBC screening on arrival in Norway. Half a year earlier, he had a transient episode with malaise and fever, with no identified underlying cause. On the time of the TBC examination, he had no cough, fever, weight loss, or night sweats. Both the tuberculin skin test by the Mantoux method and Quantiferon GOLD test turned out positive. He was not previously vaccinated for TBC. X-ray of the chest revealed a 10 mm lesion in the right lung (Figure 1). There were no acid-fast bacilli detected on microscopic examination of smears from induced sputum, and the culture later proved negative. Pending culture results, he was started on basic TBC treatment with rifampin, isoniazid, pyrazinamide, and ethambutol. After the initiation of treatment, he felt unwell with nausea and anorexia.
Fifteen days later, he was admitted to the hospital with acute left hemiparesis. Computed tomography (CT) of the brain showed a cerebral infarction in the right hemisphere (Figure 2). Doppler ultrasonography of the cervical vessels showed a marked, homogenous, circumferential thickening of the vessel walls in the right and left common carotid artery. There was no calcification of the vessel walls. There was a stenosis of the caudal part of the right common carotid artery and a poststenotic flow with low velocities in the medial and cranial part of the vessel, while the left common carotid artery was occluded (Figure 3). The vessel walls were normal in the internal and external carotid arteries on both sides. A retrograde flow was seen in the left external carotid artery, while a slow antegrade flow was detected within the left internal carotid artery. The vertebral arteries were open with high flow velocities, but no signs of stenosis. Spiral CT angiography demonstrated a high-grade stenosis of the origin of the common carotid artery on the right side, whereas the common carotid artery on the left side was occluded (Figure 4). The internal and external carotid arteries appeared normal on both sides. The subclavian and vertebral arteries as well as the arteries of Willis circle had normal contrast enhancement. Echocardiogram and transthoracic and transesophageal echocardiography were normal. There were no bruits over the heart or the neck. The patient had full pulses in the radial arteries, with normal and symmetrical blood pressure in the arms. He had previously suffered a bilateral below-knee traumatic amputation. Due to multiple metal fragments in his stumps, magnetic resonance imaging (MRI) was not performed. During the first week of hospitalization, he complained of pain in his legs. CT of the legs showed no abscesses, and, with the theory of phantom pain, treatment with gabapentin was initiated with good pain relief. Blood tests showed a slightly elevated ESR of 18 mm/h and a CRP of 25 mg/L. The analyses were otherwise normal with respect to hemoglobin, leucocytes and platelets, international normalized ratio (INR), activated partial thromboplastin time (APTT), anti-neutrophil cytoplasmic antibodies (ANCA), rheumatoid factor (RF), antinuclear antibodies (ANA), and anticardiolipin antibodies. Blood culture showed no growth of aerobic or anaerobic bacteria, HIV test was negative, and Treponema pallidum was not detected neither in the blood nor in the cerebrospinal fluid. Lumbar puncture showed an opening pressure of 17 cm H2O with clear and colorless cerebrospinal fluid, with normal amount of cells counts, total protein, and glucose.
Treatment with aspirin was started at admittance. The raised ESR and CRP in addition to the findings on ultrasonography and CT angiography raised suspicion of vasculitis. Therefore, treatment with prednisolone was also initiated, augmented a few weeks later with methotrexate. One year thereafter, the Doppler ultrasonography findings were unchanged. Two years after the stroke, he still had a hemiparesis but developed no new clinical signs or symptoms.