Movement Disorders (revue)

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Nerve conduction study in Sydenham's chorea

Identifieur interne : 003E56 ( Main/Exploration ); précédent : 003E55; suivant : 003E57

Nerve conduction study in Sydenham's chorea

Auteurs : Francisco Cardoso [Brésil] ; Leonardo Dornas [Brésil] ; Mauro Cunningham [Brésil] ; José Teotonio Oliveira [Brésil]

Source :

RBID : Pascal:05-0225485

Descripteurs français

English descriptors

Abstract

Sydenham's chorea (SC) is a late complication of group A β-hemolytic streptococci infection presumably caused by an abnormal autoimmune reaction. Despite rare case reports of peripheral neuropathy associated with streptococcal infection, there is no investigation of peripheral nerve in SC. We performed nerve conduction studies in a cohort of patients with SC. The neurophysiology investigation comprised measurement of amplitude and sensory conduction velocity of median, ulnar, and sural nerves; amplitude and motor conduction velocity; and F-wave latency of median, ulnar, fibular, and tibial nerves. Twenty-six patients entered the study (12 females, 14 males; mean age 12.8 ± 3.6 years). Thirteen subjects had absent or decreased deep reflexes. All investigated neurophysiological parameters fell within the normal range for our population. We failed to find neurophysiological evidence of peripheral nerve involvement in patients with a history of SC. Our findings suggest that the possible autoimmune dysfunction in SC patients is not targeted against epitopes present in peripheral nerves.


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Le document en format XML

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<div type="abstract" xml:lang="en">Sydenham's chorea (SC) is a late complication of group A β-hemolytic streptococci infection presumably caused by an abnormal autoimmune reaction. Despite rare case reports of peripheral neuropathy associated with streptococcal infection, there is no investigation of peripheral nerve in SC. We performed nerve conduction studies in a cohort of patients with SC. The neurophysiology investigation comprised measurement of amplitude and sensory conduction velocity of median, ulnar, and sural nerves; amplitude and motor conduction velocity; and F-wave latency of median, ulnar, fibular, and tibial nerves. Twenty-six patients entered the study (12 females, 14 males; mean age 12.8 ± 3.6 years). Thirteen subjects had absent or decreased deep reflexes. All investigated neurophysiological parameters fell within the normal range for our population. We failed to find neurophysiological evidence of peripheral nerve involvement in patients with a history of SC. Our findings suggest that the possible autoimmune dysfunction in SC patients is not targeted against epitopes present in peripheral nerves.</div>
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