Opsoclonus–myoclonus–ataxia syndrome and HIV seroconversion

Abstract

Sirs, Neurological disorders are a well-known complication of human immunodeficiency virus (HIV) infection [7]. An incidence of 2–3% of clinically relevant movement disorders has been identified in patients with HIV infection seen at tertiary referral centers, and in several cases it may represent the initial manifestation of HIV infection [8]. Nevertheless, the incidence of movement disorders increases significantly, ranging between 5 and 44% in AIDS patients, with a large prevalence of tremor and Parkinsonism [2, 8]. Opsoclonus–myoclonus–ataxia syndrome (OMAS) is a rare neurological disorder associated with many clinical settings [11]. Although the pathophysiology of opsoclonus is still undefined, a dysfunction at the pontine paramedian reticular formation (PPRF) and the cerebellum secondary to a dysregulation of the humoral and cell mediated immune mechanisms is postulated [11]. To our knowledge, OMAS has been previously reported in only two HIV patients [5, 9] but not at the time of seroconversion. We report a 44-year-old white man who was admitted 24 h after the onset of acute opsoclonus, truncal ataxia and orthostatic myoclonus that led to postural instability. His personal and family medical history was unremarkable, with the exception of a mild congenital right brachial paresis. Physical examination revealed involuntary, multidirectional, high-amplitude, conjugate saccadic eye movements. Gait was moderately unsteady, due to involuntary jerking of lower extremities and wide-base standing. The remainder of the neurological and systemic examinations were normal. The routine blood chemistry tests, including thyroid function, were normal but the liver chemistry tests showed elevated s-GOT (74 units/l) and s-GPT (185 units/ l). Serology for Epstein Barr virus, CMV, hepatitis A, B and C virus and VDRL were negative. An HIV antibody test performed 2 months before the onset of symptoms was negative, but two new HIV ELISA and a Western blot (IgG) tests performed 24 h and 48 h after admission showed positive, with a CD4 count of 511 cells/ml (17%) and a viral load of 1.5 9 10 (6.17 log) (NASBA methods). The CSF constituents, a brain MRI and EEG were normal. The patient’s symptoms improved with lorazepam 1 mg/ day and resolved completely after 1 week, but he refused antiretroviral therapy. Two additional viral load assessments and CD4 counts were obtained 1 month and 1 year later, respectively (Fig. 1). This case fulfills the clinical diagnostic criteria of OMAS. Its temporal occurrence and evolution suggest that this syndrome might be not only a random association but the clinical expression of the HIV seroconversion. The HIV seroconversion in this patient was supported by a negative HIV antibody test performed 2 months before the onset of OMAS, followed by a new HIV positive test at time of admission. In accordance with A. Ayarza V. Parisi D. Visconti G. Persi C. A. Rugilo E. M. Gatto Department of Neurology, Sanatorio de la Trinidad Mitre, Bartolome Mitre 2553, CP 1039, Buenos Aires, Argentina