Application with high spatial resolution fMRI rat data subjected to electric forepaw sensory stimulation (156 · 156 · 1000 μ1) shows a significant localized increase of the vector field amplitude in cortical layers 4 and 2/3 of the primary sensory cortex and in layer 2/3 of the primary motor cortex, suggesting a strong correlation with local neuronal communication.
Importantly, this increase in activity, which occurred throughout the duration of baseline trials, was not present in the primary motor cortex, suggesting that it does not reflect a late form of motor preparation.
Visual attentional load also influences plasticity in the human motor cortex, suggesting that the top-down influence of attention on plasticity is a general feature of the adult human brain [ 42].
These differences in the architecture of motor cortex clearly suggest an emphasis on the elaboration of backward rather than forward connections but the relative absence of layer 4 implies that the laminar rules developed for sensory cortex cannot be applied without some modification.
Importantly, these effects were not observed in either sensory (MT+) or primary motor cortex, further suggesting that the SAT in decision-making is a property of a central, prefrontal network rather than arising from modulations at early sensory or late motor stages of processing [16], [17], [20], [26], [30], [52].
Mecp2 null mice also display abnormalities in the cerebellum and motor cortex [12] and suggest this to be a mechanism for behaviourally recorded reductions in locomotor activity in the open-field [13 16].
Consistent with the previous study, our study found a negative correlation between UPDRS motor scores and VMHC in the primary sensorimotor and supramarginal cortex, suggesting deficient inter-hemispheric interaction as a potential mechanism for motor impairment in PD.
HF rTMS of the motor cortex has been suggested for the treatment of other pain-related diseases since the initial report by Lefaucheur in 2001 [22].
These ictal observations in reading epilepsy not only support our finding of motor cortex hyperconnectivity, but also suggest a functional link for the often noticed association of reading epilepsy and JME in the same individual, and the recently reported observation of orofacial reflex myocloni triggered by reading and talking in JME (Mayer et al., 2006).
A lack of astrocytosis in other cortical regions (eg. motor cortex and forelimb regions) suggests these changes are specific for the trigeminal circuit; however, it is unclear whether the astrocyte reactivity is due to the afferent drive from potentially hyper-excited neurons, or the mechanical forces of injury.
