Page 331 - Color_Atlas_of_Physiology_5th_Ed._-_A._Despopoulos_2003

Nociception and Pain nocisensors are stimulated, they start to release neu-
ropeptides such as substance P or CGRP (calcitonin
Pain is an unpleasant sensory experience as- gene-related peptide) that cause inflammation of the
sociated with discomfort. It is protective inso- surrounding vessels (neurogenic inflammation).
Projected pain. Damage to nociceptive fibers
far as it signals that the body is being causes pain (neurogenic or neuropathic) that is often
threatened by an injury (noxa). Nociception is projected to and perceived as arising from the pe-
the perception of noxae via nocisensors, neural riphery. A prolapsed disk compressing a spinal nerve
conduction and central processing. The pain
Central Nervous System and Senses sors does not always evoke pain. nociceptive somatic neurons and nociceptive
can, for example, cause leg pain. Nociceptive fibers
can be blocked by cold or local anesthesia.
that is ultimately felt is a subjective ex-
perience. Pain can also occur without stimula-
Nociceptive tracts (! C1). The central axons of
tion of nocisensors, and excitation of nocisen-
afferents of internal organs end on neurons of
All body tissues except the brain and liver
the dorsal horn of the spinal cord. In many
contain sensors for pain, i.e., nocisensors or
cases, they terminate on the same neurons as
nociceptors (! A). Nocisensors are bead-like
the skin afferents.
endings of peripheral axons, the somata of
Referred pain (! B). Convergence of somatic and
which are located in dorsal root ganglia and in
visceral nociceptive afferents is probably the main
nuclei of the trigeminal nerve. Most of these
visceral stimuli cause a perception of pain in certain
the rest are myelinated Aδ fibers (5–30 m/s;
skin areas called Head’s zones. That for the heart, for
fiber types described on p. 49 C).
example, is located mainly in the chest region. Myo-
cardial ischemia is therefore perceived as pain on the
12 fibers are slowly conducting C fibers (! 1 m/s); cause of referred pain. In this type of pain, noxious
When an injury occurs, one first senses sharp “fast
pain” (Aδ fibers) before feeling the dull “slow pain” surface of the chest wall (angina pectoris) and often
(C fibers), which is felt longer and over a broader also in the lower arm and upper abdominal region.
area. Since nocisensors do not adapt, the pain can In the spinal cord, the neuroceptive afferents
last for days. Sensitization can even lower the cross to the opposite side (decussation) and
stimulus threshold.
Most nocisensors are polymodal sensors (C are conducted in the tracts of the anterolateral
fibers) activated by mechanical stimuli, chemical funiculus—mainly in the spinothalamic tract—
mediators of inflammation, and high-intensity heat and continue centrally via the brain stem
or cold stimuli. Unimodal nociceptors, the less where they join nociceptive afferents from the
common type, consist of thermal nocisensors (Aδ head (mainly trigeminal nerve) to the
fibers), mechanical nocisensors (Aδ fibers), and ”dor- thalamus (! C1). From the ventrolateral
mant nocisensors.” Thermal nocisensors are activated
by extremely hot (" 45 #C) or cold (! 5 #C) stimuli thalamus, sensory aspects of pain are pro-
(! p. 314). Dormant nocisensors are chiefly located jected to S1 and S2 areas of the cortex. Tracts
in internal organs and are “awakened” after pro- from the medial thalamic nuclei project to the
longed exposure (sensitization) to a stimulus, e.g., limbic system and other centers.
inflammation.
Components of pain. Pain has a sensory component
Nocisensors can be inhibited by opioids including the conscious perception of site, duration
(desensitization) and stimulated by prosta- and intensity of pain; a motor component (e.g., defen-
glandin E 2 or bradykinin, which is released in sive posture and withdrawal reflex; ! p. 320), an au-
response to inflammation (sensitization; ! A). tonomic component (e.g., tachycardia), and an affec-
tive component (e.g., aversion). In addition, pain
Endogenous opioids (e.g., dynorphin, enke- assessments based on the memory of a previous
phalin, endorphin) and exogenous opioids pain experience can lead to pain-related behavior
(e.g., morphium) as well as inhibitors of pros- (e.g., moaning).
taglandin synthesis (! p. 269) are therefore In the thalamus and spinal cord, nociception
able to alleviate pain (analgesic action).
can be inhibited via descending tracts with the
Inflammatory sensitization (e.g., sunburn) lowers aid of various transmitters (mainly opioids).
the threshold for noxious stimuli, leading to excessive The nuclei of these tracts (! C2, blue) are lo-
318 sensitivity (hyperalgesia) and additional pain cated in the brain stem and are mainly acti-
resultingfromnon-noxious stimulitotheskin(allody- vated via the nociceptive spinoreticular tract
nia), e.g., touch or warm water (37 #C). Once the
(negative feedback loop).
Despopoulos, Color Atlas of Physiology © 2003 Thieme
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