Neuroplasticity: refers to the ability of the nervous system to alter its structure and function. Neuroplasticity (also deals with brain plasticity, cortical plasticity and cortical re-mapping) refers to changes that occur in the organization of the brain and entire nervous system as a result of experiences. "Plasticity" relates to the learning by adding or removing connections, or cells.
Neuroplastic changes related to pain can occur at multiple levels of the nervous system. More pain receptors may be in an area, the area of the brain that feels pain increases, the pain sensory system becomes more efficient, and the brain can learn pain.
Studies suggest that pain may play a major role in determining cortical rearrangements in the adult human somatosensory system. Most studies, however, have been performed under conditions whereby pain coexists with massive deafferentation (e.g., amputations). Moreover, no information is available on whether spinal and brainstem changes contribute to pain-related reorganizational processes in humans. The absence of correlation between the amplitude of spinal, brainstem, and cortical components of SEPs suggests that enhancement of cortical activity is not a simple amplification of subcortical enhancement.
The neuroplastic phenomenon: a physiologic link between chronic pain and learning
Neuroplasticity refers to the ability of neurons to alter their structure and function. Structural changes occur at every level of the nervous system, from enlargement and reshaping of the entire neuron (with newly developed dendritic connections), to changing synaptic quanta in presynaptic fibers and alterations in the number, type and sensitivity of postsynaptic ion channels. Thus, neuroplasticity should be viewed as a dynamic process, not a particular outcome.[28]These presynaptic and postsynaptic membrane changes occur in response to mediators which are initiated by the postsynaptic membrane. Different types of neuroplastic changes are detailed by Ganong, including: posttetanic potentiation, habituation, sensitization, long-term potentiation and long-term depression.[16] Changes in intracellular calcium ion concentration, related to the effect of the excitatory amino acid (EAA), N-methyl-D-aspartate (NMDA), seems to be the least common denominator underlying all types of neuroplastic changes.[16] The related change of intracellular calcium ion concentration produces a hyperexcitable state within the nerve.[16] The inhibitory amino acid, gamma-aminobutyric acid (GABA), normally counters the effects of NMDA and other excitatory amino acids, by exerting an effect on calcium and chloride ion channels in a way that dampens noxious stimuli.[26]
Each nerve cell employs multiple chemical signals to communicate with other cells and itself. Nerves may use entirely different combinations of chemical messengers at different times in response to changing internal and external environmental conditions. In the presence of excessive excitatory or inhibitory neurotransmitter activation, the number of excitatory receptors or inhibitory receptors decrease in density respectively.[16] The EAAs are believed responsible for the regulation of changes in synaptic plasticity, dendritic and axonal structure.
There are 3 subtypes of EAAs: NMDA, glutamate and aspartate, balanced primarily by GABA. In response to excessive excitatory activation, GABA receptors change in number and function through a phosphorylation process which allows negatively charged chloride ions to dampen the effect of synaptic hyperexcitability.[26] Excessive increases in the concentration of EAAs which are not countered by inhibitory amino acids result in neuron cellular damage and a cascade of events that increases spontaneous nerve firing, escalating EAA concentration and further adding to neuronal destruction.
The type of neuroplastic process which predominates varies with different stages of growth and development. Neuroplastic changes related to the growth of cells and the establishment of new dendritic connections occur more readily in youth because of the relative instability and rapid growth of neurons in children. This type of plasticity is associated with intelligence and creativity. With age, there is a decrease in the number of receptors and established neuroanatomical pathways (including chemical circuits), which dissolve and reform in response to environmental cues. Competing influences must be strong and repetitive for adults to change interneuronal connections and add new synapses.[20] Still, dramatic changes in the intricate circuitry and chemistry of the adult brain occur as a result of sensory, motor, behavioral, environmental or drug-related stimuli.[33] This plasticity appears to be related to changing thoughts and behaviors, and serves the purpose of promoting adaptation by allowing the person some flexibly when responding to changing environmental demands.
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