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NMDA-mediated mechanisms in cortical excitability changes after limb amputation.
P Schwenkreis1, C Maier, B Pleger
1Department of Neurology, Ruhr-University Bochum, BG-Kliniken Bergmannsheil, Buerkle-de-la-Camp-Platz 1, D-44789 Bochum, Germany. Peter.Schwenkries@ruhr-uni-bochum.de
Acta Neurologica Scandinavica
|August 13, 2003
Summary
N-methyl-d-aspartate (NMDA) mechanisms influence cortical excitability after limb amputation. However, these changes in cortical excitability and phantom limb pain appear to be independent phenomena.
Area of Science:
- Neuroscience
- Pain Research
- Neurophysiology
Background:
- Limb amputation can lead to significant changes in cortical excitability.
- The role of N-methyl-d-aspartate (NMDA) receptors in these alterations and their connection to phantom pain is not fully understood.
Purpose of the Study:
- To investigate the involvement of NMDA-mediated mechanisms in cortical excitability changes post-amputation.
- To explore the relationship between these cortical changes and the intensity of phantom limb pain.
Main Methods:
- A randomized, placebo-controlled study involving 16 upper limb amputees with chronic phantom pain.
- Administration of the NMDA-antagonist memantine or placebo for 3 weeks.
- Assessment of intracortical inhibition (ICI) and intracortical facilitation (ICF) using transcranial magnetic stimulation, alongside phantom pain intensity measurements.
Main Results:
- Memantine treatment led to a reduction in intracortical facilitation (ICF) and an enhancement in intracortical inhibition (ICI).
- The observed changes in cortical excitability mirrored those found in healthy subjects in prior research.
- Crucially, these neurophysiological modifications did not correlate with any reduction in phantom pain intensity.
Conclusions:
- NMDA-mediated mechanisms play a role in modulating cortical excitability changes following limb amputation.
- The study suggests that alterations in cortical excitability and the experience of phantom limb pain are distinct and independent processes.