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The gate control theory of pain asserts that non-painful input closes the nerve "gates" to painful input, which prevents pain sensation from traveling to the central nervous system. In the top panel, the nonnociceptive, large-diameter sensory fiber (orange) is more active than the nociceptive small-diameter fiber (blue), therefore the net input ...
1.7 Gate control theory. 2 Modern theories. ... It is clear from this definition that while it is understood that pain is a physical phenomenon, ...
One type of EEG measure used for sensory gating research is the event-related potential (ERP). EEG research on sensory gating shows that gating starts almost immediately after receiving a stimulus. Positron emission tomography (PET) studies have shown that an increased need to gate information is accompanied by increased engagement of the ...
Another type of pain, known as neuropathic pain, is caused by a direct problem or disease that affects the nerves in the central nervous system. [11] The sensory pathways the WDR neurons can play a role in. A subset of this neuropathic pain, known as chronic neuropathic pain, is characterized by its long lasting and high pain intensity.
Gate control theory of pain. A major hypothesis in the theory of pain perception is the gate control theory of pain, proposed by Wall and Melzack in 1965. The theory predicts that the activation of central pain inhibitory neurons by non-pain sensing neurons prevents the transmission of non-harmful stimuli to pain centers in the brain.
Diffuse noxious inhibitory controls (DNIC) or conditioned pain modulation (CPM) refers to an endogenous pain modulatory pathway which has often been described as "pain inhibits pain". [1] It occurs when response from a painful stimulus is inhibited by another, often spatially distant, noxious stimulus.
Presynaptic inhibition is a phenomenon in which an inhibitory neuron provides synaptic input to the axon of another neuron (axo-axonal synapse) to make it less likely to fire an action potential. Presynaptic inhibition occurs when an inhibitory neurotransmitter, like GABA , acts on GABA receptors on the axon terminal .
Its function is unknown, though several potential functions related to "limbic–motor integration" have been proposed, such as controlling visceral activity and pain; gating sensory input and synchronizing cortical and subcortical brain rhythms. Its dysfunction may play a role in central pain syndrome.