The movement-related cortical potential (MRCP) is an electroencephalography (EEG) component related to voluntary movement, which is a slow negative shift starting 1-1.5 sec before volitional movement. MRCPs consist of at least 3 subcomponents, the Bereitschaftspontial (BP), the negative slope (NS’), and the motor potential (MP). It is generally agreed that the generator for the BP is from the mesial prefrontal cortex and that for the NS’ can be sufficiently explained by the activation of generators in the sensorimotor cortex bilaterally. The MP can be accounted for by the activation of a source in the contralateral central region. The generating sources of these subcomponents of MRCP were deduced from the scalp or subdural recordings and the hypothesis should be further verified by determining whether functional perturbation of the candidate regions could actually modulate the behavior of MRCP. At least 2 methods may be adopted for this purpose. The first is lesion study of MRCP over the target sites. The second way is to modulate the candidate regions by external electrophysiological functional perturbation (e.g. repetitive transcranial magnetic stimulation, rTMS) to observe how the interference would affect the MRCP conformation. The present research is designed to elucidate the MRCP issue relying on lesion study in stroke patients with anterior cerebral artery (ACA) territory infarct. ACA territory is an uncommon site for occlusive vascular strokes. We hypothesized a deficit in the neuronal motor network after ACA infarct would lead to alterations in the movement related cortical network in the ACA infarct patients. We conduct the study in 7 patients and 7 age matched control. Three main results can be summarized as following: (1) some of the MRCP subcomponents showed a more pronounced negativity in the patient group than could be observed in the control group; (2) the amplitudes of NS’ were especially noted to be increased over the bilateral hemispheres in the patient group on the right hand movement as compared with the controls; (3) loss of lateralization of NS’ was noted in the patient group on the right hand movement, similar trend can also be observed on the left hand movement.
The results could be due to diminution of pre-SMA (Area F6) inhibitory inputs to the subsequent motor regions or due to the recruitment of the nearby excitatory cortical regions for the compensation of motor impairment of the medial frontal lobe infarct. These results are in line with the idea of prefrontally mediated early preparatory processes prior to the execution of motion and illustrate that medial frontal region are crucial for the modulation or generation of MRCP.
