Anal sphincter EMG in the diagnosis of parkinsonian syndromes
Version of Record online: 24 SEP 2009
Copyright © 2009 The Authors. Journal compilation © 2009 Blackwell Munksgaard
Acta Neurologica Scandinavica
Volume 121, Issue 3, pages 198–203, March 2010
How to Cite
Winge, K., Jennum, P., Lokkegaard, A. and Werdelin, L. (2010), Anal sphincter EMG in the diagnosis of parkinsonian syndromes. Acta Neurologica Scandinavica, 121: 198–203. doi: 10.1111/j.1600-0404.2009.01169.x
- Issue online: 27 JAN 2010
- Version of Record online: 24 SEP 2009
- Accepted for publication December 30, 2008
- Parkinson’s disease;
- multiple system atrophy;
- progressive supranuclear palsy;
Winge K, Jennum P, Lokkegaard A, Werdelin L. Anal sphincter EMG in the diagnosis of parkinsonian syndromes. Acta Neurol Scand: 2010: 121: 198–203. © 2009 The Authors Journal compilation © 2009 Blackwell Munksgaard.
Background – The role of electromyography (EMG) recorded from the external anal sphincter (EAS) in the diagnosis of atypical parkinsonian syndromes is a matter for continuous debate. Most studies addressing this issue are retrospective.
Methods – In this study, we prospectively investigated six patients with Parkinson’s Disease (IPD), 14 patients with multiple system atrophy (MSA) and eight with progressive supranuclear palsy (PSP) using EMG of the EAS, motor-evoked potential (MEP) to the EAS and EMG of m. gastrocnemius and nerve conduction velocity measured at the sural nerve. Patients were followed up for 2 years to secure correct diagnosis.
Results – The mean duration of motor unit potentials (MUPs) recorded from the EAS was significantly longer in patients with MSA and PSP compared with MUPs recorded from patients with PD (P < 0.005 for both). There were no signs of diffuse loss of motor neurons or peripheral neuropathy. MEP revealed signs of supranuclear affection in patients with MSA, whereas in patients with PSP the mechanism is a focal loss of motor neurons in Onuf’s nucleus.
Conclusion – Abnormal EMG of the EAS is strongly suggestive of atypical parkinsonism and the pathophysiology may be different in patients with MSA and PSP.