The part of the brain that is in charge of the amputated limb or neuronal change will be dominated by adjacent cortical regions that are still receiving input, thus creating a remapped area.
"[3] In 1968, Merzenich and two neurosurgeons, Ron Paul and Herbert Goodman, conducted an experiment to determine effects on the brain after a large bundle of peripheral nerves in adolescent monkeys' hands were cut and began to regenerate again.
This experiment helped inspire questioning of the scientific "truth" that the adult brain is fixed and cannot continue to change outside of the critical period, especially by Merzenich.
A study by Gregg Recanzone demonstrates this by seeing if a monkey could distinguish between a stimulus of high and low frequency vibrations, delivered to the tip of its finger at a fixed location.
The experiment was conducted again except, the location of the high and low vibrations were varied at different parts of the monkey's fingertip.
This means, there is a possibility that remapping in the motor cortex can come from changes in the brainstem and spinal cord, locations that are difficult to experiment on, due to challenging access.
The study found a strong connection between motor and somatosensory cortical remapping after amputation and phantom limb pain.
Phantom limb pain is considered to be caused from functional cortical reorganization, sometimes called maladaptive plasticity, of the primary sensorimotor cortex.
[10] One study taught amputees over a two-week period to identify different patterns of electrical stimuli being applied to their stump to help reduce their PLP.
The tissue that surrounds the infarct (stroke damaged area) has reduced blood flow and is called the penumbra.
Due to reperfusion in the peri-infarct cortex (found next to the infarct), the neurons can help with active structural and functional remodelling after stroke.
The recovering peri-infarct regions that have bad circuits are competing with healthy tissue for cortical map space.
An in vivo study by Murphy was done using mice to help identify the sequence and kinetics of the peri-infarct cortical remapping after stroke.
The mouse that experienced a stroke had remapped responses that lasted longer and spread farther from the motor cortex than those of the control.
This means that recovery of the sensorimotor functions after stroke and cortex remodeling suggests changes in the temporal and spatial spread of sensory information.