Recurrent 'migrainelike' episodes in patients with HIV disease
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Published on: June 2, 2014
R Rinaldi1, R Manfredi, G Azzimondi
1Neurology Unit, University of Bologna, Italy.
Recurrent transient neurological deficits have been described in human immunodeficiency virus (HIV)-infected subjects, but their frequency, pathogenesis, and outcome are still unsettled. We describe 10 HIV-infected patients with transient neurological deficits (0.8% of all patients followed in our department during the last decade). All patients were in the advanced stage of immunological disease. None of the clinical or special investigations performed outside of the attacks indicated an underlying structural lesion of the central nervous system. In 80% of these patients, anticardiolipin antibodies were present. The final outcome was unrelated to these transient neurological deficits which, per se, had a benign course. We discuss the possible etiopathogenetic mechanisms of such episodes and suggest that they may be "migrainelike" events, possibly related to transient functional circulatory abnormalities secondary to an immunological antiphospholipid antibody-dependent mechanism.
Recurrent transient neurological deficits have been described in human immunodeficiency virus (HIV)-infected subjects, but their frequency, pathogenesis, and outcome are still unsettled. We describe 10 HIV-infected patients with transient neurological deficits (0.8% of all patients followed in our department during the last decade). All patients were in the advanced stage of immunological disease. None of the clinical or special investigations performed outside of the attacks indicated an underlying structural lesion of the central nervous system. In 80% of these patients, anticardiolipin antibodies were present. The final outcome was unrelated to these transient neurological deficits which, per se, had a benign course. We discuss the possible etiopathogenetic mechanisms of such episodes and suggest that they may be "migrainelike" events, possibly related to transient functional circulatory abnormalities secondary to an immunological antiphospholipid antibody-dependent mechanism.
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