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Nerve conduction study in Sydenham's chorea
Francisco Cardoso1, Leonardo Dornas, Mauro Cunningham
1Movement Disorders Clinic, Department of Psychiatry and Neurology, The Federal University of Minas Gerais, Belo Horizonte, Minas Gerais, Brazil. cardosofe@terra.com.br
Movement Disorders : Official Journal of the Movement Disorder Society
|November 20, 2004
Summary
Sydenham's chorea (SC) patients show no nerve damage on neurophysiological tests. This suggests the autoimmune response in SC does not target peripheral nerves, despite links to streptococcal infections.
Area of Science:
- Neuroscience
- Immunology
- Infectious Diseases
Background:
- Sydenham's chorea (SC) is a neurological complication following group A beta-hemolytic streptococci infection.
- The underlying mechanism is presumed to be an autoimmune reaction.
- Peripheral neuropathy is rarely reported with streptococcal infections, but its role in SC is uninvestigated.
Purpose of the Study:
- To investigate peripheral nerve involvement in patients with Sydenham's chorea using neurophysiological methods.
- To determine if autoimmune responses in SC target peripheral nerves.
Main Methods:
- Nerve conduction studies were performed on 26 patients with SC.
- Measurements included sensory and motor nerve conduction velocities, amplitudes, and F-wave latencies.
- Specific nerves investigated were median, ulnar, sural, fibular, and tibial nerves.
Main Results:
- All neurophysiological parameters measured in SC patients were within normal ranges.
- No evidence of peripheral nerve dysfunction was detected.
- Thirteen patients exhibited absent or decreased deep reflexes, but nerve conduction remained normal.
Conclusions:
- Neurophysiological investigations did not reveal peripheral nerve involvement in patients with Sydenham's chorea.
- The autoimmune dysfunction in SC appears not to target peripheral nerve epitopes.
- Further research may explore other potential autoimmune targets in SC pathogenesis.