References in periodicals archive ?
GM loss in motor cortices might be a more sensitive measure of disease progression than damage in the corticospinal tract.
Ephrin-B3 is the midline barrier that prevents corticospinal tract axons from recrossing, allowing for unilateral motor control.
The deltoid, neck flexors, trapezius and respiratory muscles have combined nerve innervations via the corticospinal pathway.
Animal studies have revealed that a hierarchy of spinal and supraspinal plasticity (from the cerebellum to sensorimotor cortex to corticospinal tract to spinal cord) is involved in inducing and maintaining the operant conditioning-induced change in the evoked response [31,32].
Transcranial magnetic stimulation studies have confirmed that beta-PMBR corresponds to a period of decreased corticospinal excitability [76], suggesting that it may represent a state of cortical inhibition.
In turn, this could lead to decreased activity of the striatum, which inhibits the inhibitory output from the BG network to the thalamus modulating the activity of the corticospinal tract [2].
In consequence, the (i) MT would promote activation in the cortical visual area and in the areas involved in motor behavior [32] and (ii) the VT would promote normal motor activity patterns by modulating the excitability of motor neurons and corticospinal tract [33].
The mechanisms for FES treatment led to the speculation that the effect is achieved through the reintegration of sensorimotor pathways and corticospinal plasticity [20-22].
The changes in sensory feedback assigned to an elastic tape are probably insufficient to modulate corticospinal excitability in the functional sense [33].
Hemiplegia is associated with a reduced number of functional corticospinal and corticobulbar fibers to the spinal and brainstem because of lesions in the cerebral cortex.
Both motor learning processes and the effect of proprioceptive and cutaneous afferent signals on corticospinal excitability can be studied using electrophysiological methods.
[6] Typical patterns of brain involvement in NMOSD, although not pathognomonic, include lesions of the dorsal medulla/area postrema, periependymal regions in the brainstem, diencephalic structures, or cerebral hemispheres or long lesions spanning much of the corpus callosum or corticospinal tracts, corresponding to regions of high AQP4 expression.