Study of brain plasticity in upper limb amputees with non-invasive brain stimulation techniques

Background: after the amputation of the upper limb, there is an important reorganization of the primary sensory-motor cortex that can also affect the higher-order and associative sensory-motor areas and inter-hemispheric communication. The reorganization of the primary and somatosensory (S1) motor (M1) cortex is characterized by a reduction in the expansion of the representative maps of the lost muscles and skin areas and an expansion of the representation of the adjacent body areas. Despite this reorganization, the "orphan" cortical areas maintain silent connections with the periphery, that can be explored. In humans, adaptations of the motor cortex after amputation can be studied using non-invasive electrophysiological techniques such as Transcranial magnetic Stimulation (TMS). Understanding M1 intracortical excitability in upper-limb amputees provides information into brain reorganization in the sub-acute post-amputation phase and that is useful for rehabilitation and for BCI (brain-computer interfaces). Methods: in this study we evaluated the modifications of cortical excitability and the inhibitory, excitatory and interhemispheric brain circuits through Resting motor threshold (RMT) Active motor threshold (AMT) and specific TMS protocols such as Short Intracortical Inhibition (SICI), Intracortical facilitation (ICF), Short latency afferent inhibition (SAI) and Interhemispheric inhibition (IHI). We evaluated 18 patients with upper limb amputation (13 trans-radial -5 trans-humeral). Results: there were no significant differences in the value of RMT and AMT between hemispheres and between subjects with trans-radial and trans-humeral amputation. SICI show a significant inhibition of motor response in both hemispheres; the amount of inhibition was significantly greater on the AH in the trans-radial patients' group. ICF protocol SHOW that facilitation was present in both hemispheres but we cannot draw specific conclusions because we have the data for only 3 patients. IHI showed a conserved interhemispheric inhibition mechanism in both directions, and with no differences between trans-radial and trans-humeral amputees. There aren't data in the literature on interhemispheric inhibition in subjects with amputation, so we hypothesize that the cortico-cortical projections through the corpus callosum remain preserved. SAI is not present in both hemispheres. Conclusions: we found a generally higher test MEP amplitude in the AH vs UH that is coherent with the described phenomenon of increased M1 excitability after amputation. Overall, our data suggest increased GABAergic inhibition in the AH: this finding, combined with a possible hyperexcitability state following amputation, might represent a compensatory phenomenon associated with central rearrangements in the chronic amputation condition.