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Ann Saudi MedAnn Saudi MedAnnals of Saudi Medicine0256-49470975-4466King Faisal Specialist Hospital and Research Centre 1839828310.5144/0256-4947.2008.148asm-2-148ImagesNeurobrucellosis mimicking demyelinizating disorders Karaoglan Ilkay aAkcali Aylin bOzkur Ayhan cNamęduru Mustafa a
a Department of Infectious Disease, Gaziantep University, Medical Faculty, Gaziantep, Turkey
b Department of Neurology, Gaziantep University, Medical Faculty, Gaziantep, Turkey
c Department of Radiology, Gaziantep University, Medical Faculty, Gaziantep, TurkeyCorrespondence and reprints: Dr. Aylin Akcali, Universite Bul. 23 Nisan Mah. Ozkaya Apt. No:285/7 Gaziantep, Turkey, akcali@gantep.edu.trMar-Apr 2008 28 2 148 149 01 12 2007 Copyright © 2008, Annals of Saudi Medicine2008This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.
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A 25-year-old female was admitted because of fever, backache, headache, confusion, convulsion, left hemiparesis, nausea and urinary incontinance. She was diagnosed as having multiple sclerosis and received intravenous pulse corticosteroids (1000 mg/day) for 5 days. Three weeks later, she did not improve and was transfered to our hospital. She had no history of contact with unpasteurized milk or milk products. On the physical exam, her temperature was 38°C, she was alert and cooperative, her left leg and arm muscle strength was 3/5, she had features of neck stiffness, and Kernig and Brudzinski signs. Her white blood cell count was 11.95 Ś109/L, hemoglobin was 101 g/L, erythrocyte sedimentation rate was 40 mm/h, lactate dehydrogenase was 607 U/L, and C-reactive protein was 19.9 mg/L. The serum Brucella agglutination test was positive at 1:640 titers. A lumbar puncture was performed; for the opening pressure was 280 mm Hg, 136 lymphocytes per mm3, 34 polymorphs per mm3, with 129 mg/dL protein, 33 mg/dL glucose (serum glucose was 95 mg/dL). The CSF oligoclonal band was negative. Brucella agglutination in CSF was 1:80 titers (positive). Brucella species grew in the CSF culture. In several blood cultures collected from the patient, Brucella species were obtained in one. The TORCH panel On the CSF was negative. Cranial MRI revealed a heterogeneous well-demarcated lesion, a right crus cerebri lesion and multiple hyperintense lesions. After contrast material administration, the lesion (crus cerebri) showed ring-type enhancement (Figure 1), and peripherally to the central enhancing spot, a faint ill-defined parenchymal enhancement was present. The patient had a repeat MRI of the brain 1 month after treatment and these images showed a marked improvement in the suprasellar granulomatous formation (Figure 2).

The patient was treated with doxycycline, rifampicin and trimethoprim-sulfamethoxazle. After 2 weeks, urinary incontinance, and hemiparesis on the left leg and arm improved. After 8 weeks, there was 1/5 motor dysfunction on the left arm and leg. A follow-up lumbar puncture was performed and the opening pressure, protein, and glucose were within normal limits. The lymphocyte count was 60 cells/mm3. Brucella agglutination in CSF was 1:20 titer (positive). After two months a repeat cranial MRI showed a marked reduction in the size of the lesions. The patient recovered from neurobrucellosis with minimal sequelae.

Figure 1 (A) Axial FLAIR image shows the edematous changes of the right crus cerebri lesion, (B) post-contrast T1- weighted axial image showing ringlike enhancement of the lesion and pathologic enhancement within parenchyma.

Figure 2 Gadolinium-enhanced T1-weighted brain MR images obtained 1 month after treatment showing resolution of the granuloma.