Movement-related cortical potentials in primary lateral sclerosis
Article first published online: 24 MAR 2006
Copyright © 2006 American Neurological Association
Annals of Neurology
Volume 59, Issue 4, pages 682–690, April 2006
How to Cite
Bai, O., Vorbach, S., Hallett, M. and Floeter, M. K. (2006), Movement-related cortical potentials in primary lateral sclerosis. Ann Neurol., 59: 682–690. doi: 10.1002/ana.20803
- Issue published online: 24 MAR 2006
- Article first published online: 24 MAR 2006
- Manuscript Accepted: 16 DEC 2005
- Manuscript Revised: 8 DEC 2005
- Manuscript Received: 4 NOV 2005
- Intramural Research Program of the NIH (National Institute of Neurological Disorders and Stroke). Grant Number: Z01-NS002976
Some patients with primary lateral sclerosis (PLS) have a clinical course suggestive of a length-dependent dying-back of corticospinal axons. We measured movement-related cortical potentials (MRCPs) in these patients to determine whether cortical functions that are generated through short, intracortical connections were preserved when functions conducted by longer corticospinal projections were impaired.
An electroencephalogram was recorded from scalp electrodes of 10 PLS patients and 7 age-matched healthy control subjects as they made individual finger-tap movements on a keypad. MRCPs were derived from back-averaging the electroencephalogram to the movement.
MRCPs produced by finger taps were markedly reduced in PLS patients, including components generated by premotor areas of the cortex as well as the primary motor cortex. In contrast, the β-band event-related desynchronization from the motor cortex was preserved.
These findings suggest that impairment in PLS is not limited to the distal axons of corticospinal neurons, but also affects neurons within the primary motor cortex and premotor cortical areas. The loss of the MRCP may serve as a useful marker of upper motor neuron dysfunction. Preservation of event-related desynchronization suggests that the cells of origin differ from the large pyramidal cells that generate the MRCP. Ann Neurol 2006;59:682–690