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著者: Seika Nakamura, Reika Wate, Akiyo Shinde, Shinya Asayama, Satoshi Nakano, Hirofumi Kusaka
雑誌名: Rinsho Shinkeigaku. 2009 Oct;49(10):651-5.
Abstract/Text
A 36-year-old man was hospitalized because of subacutely progressive gait disturbance. Neurological examination disclosed severe ataxia of gait and trunk and moderate ataxia of the four limbs, without signs of cognitive impairment. There were no manifestations of systemic infections. Brain MRI showed mild atrophy of the cerebellar vermis and hemispheres. Extensive laboratory search failed to disclose the cause of subacute ataxia. Cerebellar ataxia progressed, leading to the patient becoming wheelchair-bound two months after admission, when PCR analysis of the cerebrospinal fluid was positive for Epstein-Barr, JC, and hepatitis B viruses. In addition, the quantity of serum HIV1-RNA was 2.9 x 10(4) copies, the absolute count of CD4+ lymphocyte was 28/mm3, and the CD4/CD8 ratio was 0.04, despite clear denials by both the patient and his wife regarding any apparent infectious opportunities. Accordingly thereafter, highly active antiretroviral therapy was initiated. Several weeks after the initiation of therapy, ataxia stabilized with disappearance of serum HIV and cerebrospinal fluid JCV viral load. He returned to his occupation 20 months after disease onset without progression of ataxia or development of other neurological dysfunctions including dementia. We could not establish the exact pathogenesis of ataxia in this patient It could have been primary cerebellar degeneration caused by HIV, or the other viruses detected (EBV, JCV) or autoimmune mechanisms caused by these viruses. However, HIV infection should be considered as an etiology in clinical setting of subacute ataxia, particularly in a young or immunocompromised patient.
PMID 19999147 Rinsho Shinkeigaku. 2009 Oct;49(10):651-5.
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