Pain is a designation for a spectrum sensations of highly divergent charact and intensity ranging from unpleasa to intolerable. Pain stimuli are detecte by physiological receptors (sensor nociceptors) least differentiated mo phologically, viz., free nerve ending. The body of the bipolar afferent first-order neuron lies in a dorsal root ganglio
Nociceptive impulses are conducted vunmyelinated (C-fibers, conduction vlocity 0.2–2.0 m/s) and myelinated aons (Aδ-fibers, 5–30 m/s). The free enings of Aδ fibers respond to inten pressure or heat, those of C-fibers rspond to chemical stimuli (H+, K+, histmine, bradykinin, etc.) arising from tisue trauma. Irrespective of wheth chemical, mechanical, or thermal stimuli are involved, they become signifcantly more effective in the presence prostaglandins.
Chemical stimuli also underlie pain secondary to inflammation or ischemia (angina pectoris, myocardial infarction), or the intense pain that occurs during overdistention or spasmodic contraction of smooth muscle abdominal organs, and that may be maintained by local anoxemia developing in the area of spasm (visceral pain).
Aδ and C-fibers enter the spinal cord via the dorsal root, ascend in the dorsolateral funiculus, and then synapse on second-order neurons in the dorsal horn. The axons of the second-order neurons cross the midline and ascend to the brain as the anterolateral pathway or spinothalamic tract. Based on phylogenetic age, neo- and paleospinothalamic tracts are distinguished.
Thalamic nuclei receiving neospinothalamic input project to circumscribed areas of the postcentral gyrus. Stimuli conveyed via this path are experienced as sharp, clearly localizable pain. The nuclear regions receiving paleospinothalamic input project to the postcentral gyrus as well as the frontal, limbic cortex and most likely represent the
pathway subserving pain of a dull, aching, or burning character, i.e., pain that can be localized only poorly.
Impulse traffic in the neo- and paleospinothalamic pathways is subject to modulation by descending projections that originate from the reticular formation and terminate at second-order neurons, at their synapses with first-order neurons, or at spinal segmental interneurons (descending antinociceptive system). This system can inhibit impulse transmission from first- to second-order neurons via release of opiopeptides (enkephalins) or monoamines(norepinephrine, serotonin).
Pain sensation can be influenced or modified as follows:

elimination of the cause of pain

lowering of the sensitivity of noci-
ceptors (antipyretic analgesics, local
anesthetics)

interrupting nociceptive conduction
in sensory nerves (local anesthetics)

suppression of transmission of noci-
ceptive impulses in the spinal me-
dulla (opioids)

inhibition of pain perception (opi-
oids, general anesthetics)

altering emotional responses to
pain, i.e., pain behavior.