Abstract

Neurological complications are common in Behcet’s disease, with a prevalence of 5–10% in large series [1] and several patterns of involvement [2]. In the last few decades, the prevalence of primary tuberculous (TBC) meningoencephalitis in Western countries has decreased. Isolated TBC meningoencephalitis is predominantly detected in the pediatric population and human immunodeficiency virus (HIV)-infected patients [3]. In this letter, we report the development of TBC meningoencephalitis with a clinical and radiological picture mimicking acute central nervous system (CNS) involvement in a patient with known Behcet’s disease. The patient, a 21-year-old male, was brought to the emergency department (ER) with left-sided hemiparesis, vertigo, and severe headache. Clinical examination revealed a stiff neck, increased reflexes in the left arm and leg, normal sensation on both sides, and a temperature of 39 C. Laboratory studies were significant only for a white cell count of 22.4·10 l 1 (neutrophils 90%, lymphocytes 7%) and erythrocyte sedimentation rate (ESR) of 28 mm/h; serum chemistries were within normal limits. The patient’s history taken in the emergency room revealed that he had been diagnosed with Behcet’s disease and was being treated with colchicine (1 mg b.i.d.), prednisolone (5 mg/day), and cyclosporin A (CsA) (1.5 mg/kg per day). The initial diagnosis from the clinical and radiological findings (Fig. 1) was neurological involvement of Behcet’s disease and a lumbar puncture was performed. Cerebrospinal fluid (CSF) examination revealed a negative Gram staining, a total protein of 0.2 g/l, a glucose level of 1.5 mmol/l, and 70 cells/ll. The following day, the CSF polymerase chain reaction (PCR) study was positive for Mycobacterium tuberculosis, as was the CSF culture 14 days later. Treatment with four antituberculosis drugs was started, and a week later the patient had substantially improved and neurological findings recessed. He complained much less about headaches and vertigo, and there were only some episodes of mildly elevated temperature (below 38 C) that remitted during the next 2 weeks. Treatment lasted for 12 months and the patient presented no residual neurological deficits with minor findings in computed tomography and magnetic resonance imaging scans (not shown). However, he presents persistent and stable affective disturbance manifested as hypomania and his family has sought psychiatric support. CNS complications are quite common in the course of Behcet’s disease and are manifested by a broad spectrum of symptoms and signs, with fever usually accompanying the clinical picture. An acute febrile episode in immunocompromised patients always poses a diagnostic dilemma—is it disease exacerbation or a superimposed infection [4]? In our case the patient’s history, clinical picture, and imaging findings were suggestive of a neurological complication of Behcet’s disease. The diagnosis of TBC infection was therefore reached only on the basis of the PCR study of the CSF. However, the patient had a suppressed cellular immunity because of CsA treatment and long-lasting corticosteroid therapy, which are predisposing factors for A. Iliopoulos (&) AE S. Kedikoglou AE S. Kourouklis Rheumatology Department, 401 General Military Hospital of Athens, 3 Olorou str., Zografou, Athens, 15773, Greece E-mail: chryso@hol.gr Tel.: +30-210-7754824 Fax: +30-210-7754824

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