Neuroplasticity Neuroplasticity is another theory based off of the Gate Control Theory that focuses on how neurons can change and reorganize in the brain in response to a change in the body. These neural changes can last days all the way up to be irreversible (Peterson-Felix & Curatolo, 2002). The changes vary so much because of the different receptors, mechanism and response times of each pathway. Neuroplasticity can modulate neural activity at different steps of the neural pathway: peripheral, spinal and supraspinal. Peripheral modulation occurs when an inflammatory response is activated at the site of injury(Peterson-Felix & Curatolo, 2002). The inflammatory response releases several substances which can activate the afferent fibers. The increase of the amount of stimuli sent to the spinal cord can change the neural pathway resulting in more effective signals with each afferent stimulus. Spinal modulation occurs when an afferent input causes a fast postsynaptic response. The fast response leads to modulations and excites the sensory neurons in the peripheral and central nervous system. Specifically the dorsal horn is excited above threshold and sends signals to the pain pathway. Supraspinal modulation has the most effect on efferent and inhibitory pathways which can lead to hyperactivity of the neuron the spinal cord resulting in more pain stimulation. Neuroplasticity also can explain how ‘pain memory’ is established (Sator-Katzenschlager, 2014). When an influx of signals are sent to the brain, consecutive neural changes occur which can cause the
Lim 7 requirement of nearby regions to also be activated. This activation of neighboring neurons contributes to phantom limb sensations. In-Context Neruoplastity’s effect cannot be directly measured in patients (Peterson-Felix & Curatolo, 2002) . Although hypersensitivity can be quantified to establish where there is elevated nerve activity compared to normal subjects. Specifically in phantom limb pain, hypersensitivity can be measured and compared to individuals still with an intact limb in response to an external stimulus. The different nervous activity reactions reveal how the neural pathways have changed conveying neuroplasticity. An example of this is stimulation of the forearm after a hand amputation (Melzack et. al., 2001). The puncture stimulus produces sensations in the forearm but also causes specific phantom hand sensations. This revealed the neuroplastic changes in the central nervous system that suggest the hand amputation also removed inhibitory neurons. A later puncture stimulus was applied to the forearm of the same individual and different sensations were felt, reflecting the neural changes over time in response to limb amputation. Driving deeper into changes in neurons, it has been shown that cortical reorganization is the most referred to cause for phantom limb pain (Weeks et. al., 2010). The evidence collected has shown somatosensory and motor changes following amputation, seen through function magnetic resonance imaging (fMRI). The fMRI shows the hyperactivity and cortical rearrangement of the brain after amputation compared to an individual without an amputation. Additionally, cortical rearrangement is dependent on the location and degree of amputation. Furthermore, fMRI are used in therapeutic interventions of phantom limb pain to monitor the neuronal changes. Neurons as they change activate different pathways and the progress of alleviating phantom sensations can be checked with fMRI’s (Sator-Katzenschlager, 2014). An example of an intervention that can show improvements on an fMRI is behavior-related sensory discrimination training. This intervention allows the neurons in the brain to adapt and reduce phantom limb pain by learning how to discriminate between signals.