Abstract
Objectives: Infraclinical sensory alterations have been reported at early stages of amyotrophic lateral sclerosis (ALS). While previous studies mainly focused on early somatosensory evoked potentials (SEPs), late SEPs, which reflect on cortical pathways involved in cognitive-motor functions, are relatively underinvestigated. Early and late SEPs were compared to assess their alterations in ALS. Methods: Median and ulnar nerves were electrically stimulated at the wrist, at 9 times the perceptual threshold, in 21 ALS patients without clinical evidence of sensory deficits, and 21 age- and gender-matched controls. SEPs were recorded at the Erb point using surface electrodes and using a needle inserted in the scalp, in front of the primary somatosensory area (with reference electrode on the ear lobe). Results: Compared to controls, ALS patients showed comparable peripheral (N9) and early cortical component (N20, P25, N30) reductions, while the late cortical components (N60, P100) were more depressed than the early ones. Conclusions: The peripheral sensory alteration likely contributed to late SEP depression to a lesser extent than that of early SEPs. Significance: Late SEPs may provide new insights on abnormal cortical excitability affecting brain areas involved in cognitive-motor functions.
| Original language | English |
|---|---|
| Pages (from-to) | 874-884 |
| Number of pages | 11 |
| Journal | Clinical Neurophysiology |
| Volume | 129 |
| Issue number | 4 |
| DOIs | |
| Publication status | Published (in print/issue) - 1 Apr 2018 |
Funding
The authors gratefully acknowledge Dr N. Leforestier, Dr T. Lenglet, Dr F. Salachas, Dr G. Bruneteau and Dr V. Meininger for their help in patient recruitment, and Dr R. Morizot-Koutlidis for her contribution for the experimental design of SEP recordings. Our gratitude is also extended to S. Blancho for her assistance in obtaining the approval of the local ethics committee and for monitoring the project. We also thank Caroline Iglesias for her invaluable help in data acquisition. Finally, we thank Dr Peter Bede for his valuable comments. This work was supported by IRME ( ID RCB 2012-A00016-37 ) and ANR ( ANR-12-JSV4-0007-01 ). S. Sangari was supported by grants from UPMC and AFM-Téléthon.
Keywords
- Amyotrophic lateral sclerosis
- Cortical excitability
- Human
- Sensory impairment
- Somatosensory evoked potentials