Cortical plasticity in patients with median nerve lesions studied with MEG. (1st October 2016)

• Record Type: Journal Article
• Authors: Fornander, Lotta; Brismar, Tom; Hansson, Thomas; Wikström, Heidi
• Is Part Of: Somatosensory & motor research. Volume 33:Number 3/4(2016)
• Page Start: 178
• Page End: 185
• Publication Date: 2016-10-01
• Subjects: Median nerve -- peripheral nerve injury -- regeneration -- magnetoencephalography -- plasticity; Skin -- Innervation -- Periodicals; Somesthesia -- Periodicals; Perceptual-motor processes -- Periodicals; 573.85
• DOI: 10.1080/08990220.2016.1230094
• Languages: English
• ISSNs: 0899-0220

Abstract

Abstract: We have previously shown age- and time-dependent effects on brain activity in the primary somatosensory cortex (SI), in a functional magnetic resonance imaging (fMRI) study of patients with median nerve injury. Whereas fMRI measures the hemodynamic changes in response to increased neural activity, magnetoencephalography (MEG) offers a more concise way of examining the evoked response, with superior temporal resolution. We therefore wanted to combine these imaging techniques to gain additional knowledge of the plasticity processes in response to median nerve injury. Nine patients with median nerve trauma at the wrist were examined with MEG. The N1 and P1 responses at stimulation of the injured median nerve at the wrist were lower in amplitude compared to the healthy side ( p < .04). Ulnar nerve stimulation of the injured hand resulted in larger N1 amplitude ( p < .04). The amplitude and latency of the response did not correlate with the sensory discrimination ability. There was no correlation between N1 amplitude and size of cortical activation in fMRI. There was no significant difference in N1 latency between the injured and healthy median nerve. N1 latency correlated positively with age in both the median and ulnar nerve, and in both the injured and the healthy hand ( p < .02 or p < .001). It is concluded that conduction failure in the injured segment of the median nerve decreases the amplitude of the MEG response. Disinhibition of neighboring cortical areas may explain the increased MEG response amplitude to ulnar nerve stimulation. This can be interpreted as a sign of brain plasticity.