C h a p t e r 3 5
Somatosensory Function, Pain, and Headache
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occur at several levels of the CNS rostral to the input seg-
ment. Perhaps the most puzzling aspect of locally applied
stimuli, such as brushing, that can block the experience
of pain is the relatively long-lasting effect (minutes to
hours) of such treatments. This prolonged effect has been
difficult to explain on the basis of specificity theories,
including the gate control theory. Other important fac-
tors include the effect of endogenous opioids and their
receptors at the segmental and brain stem level, descend-
ing feedback modulation, altered sensitivity, learning,
and culture.
More recently, Melzack has developed the
neuroma-
trix theory
to further address the brain’s role in pain
as well as the psychological and emotional dimensions
of pain.
7
This theory proposes that the brain contains a
widely distributed neural network, called the
body–self
neuromatrix,
that has multiple somatosensory, limbic,
and thalamocortical components. Genetic and sensory
influences determine the architecture of each individ-
ual’s neuromatrix, which integrates multiple sources
of inputs. These include somatosensory inputs; other
sensory inputs affecting interpretation of the situation;
inputs from the brain addressing such things as atten-
tion, expectation, culture, and personality; various com-
ponents of stress regulation systems; and other sources.
The neuromatrix theory of pain, which places genetic
and neuroendocrine mechanisms on a level equal to that
of neural transmission, has important implications for
research and therapy.
7
Pain Mechanisms and Pathways
Pain can be either nociceptive or neuropathic in origin.
The term
nociception,
which means “pain sense,” comes
from the Latin word
nocere,
“to injure.”
Nociceptive
pain
is initiated by nociceptors that are activated by
injury to peripheral tissues.
Neuropathic pain,
on the
other hand, arises from direct injury or dysfunction of
the sensory axons of peripheral or central nerves.
Two aspects of pain affect an individual’s response
to a painful stimulus—pain threshold and tolerance.
Although the terms often are used interchangeably, they
have distinct meanings.
Pain threshold
is closely asso-
ciated with the point at which a nociceptive stimulus
is perceived as painful.
Pain tolerance
relates more to
the total pain experience; it is defined as the maximum
intensity or duration of pain that a person is willing to
endure before the person wants something done about
the pain. Psychological, familial, cultural, and environ-
mental factors significantly influence the amount of pain
a person is willing to tolerate. The threshold for pain is
fairly uniform from one person to another, whereas pain
tolerance is extremely variable.
The mechanisms of pain are many and complex. As
with other forms of somatosensation, the pathways are
composed of first-, second-, and third-order neurons
1,2
(Fig. 35-7). The first-order neurons and their recep-
tive endings detect stimuli that threaten the integrity of
innervated tissues. Second-order neurons are located in
the spinal cord and process nociceptive information.
Third-order neurons project pain information to the
brain. The thalamus and somatosensory cortex integrate
and modulate pain as well as the person’s subjective
reaction to the pain experience.
Pain Receptors and Primary Afferent
Pathways
Nociceptors, or pain receptors, are activated by noxious
insults to peripheral tissues. Structurally, they are free
nerve endings of the peripheral pain fibers. These recep-
tive endings translate noxious stimuli into signals that
are transmitted by a dorsal root ganglion to the dorsal
horn of the spinal cord.
Nociceptive Simulation.
Unlike other sensory recep-
tors, nociceptors respond to several forms of stimula-
tion, including mechanical, thermal, and chemical. Some
receptors respond to a single type of stimuli (mechani-
cal or thermal) and others, called
polymodal receptors,
Spinothalamic
pathway
Substance P
Prostaglandins
Serotonin
Acetylcholine
Nociceptor
Dorsal root
ganglion
Mediator release
Inflammation
Tissue injury
RAS
Thalamus
Somatosensory
cortex
Pain
1
2
3
FIGURE 35-7.
Mechanism of acute pain.Tissue injury leads to
release of inflammatory mediators with subsequent nociceptor
stimulation. Pain impulses are then transmitted to the dorsal
horn of the spinal cord, where they make contact with second-
order neurons that cross to the opposite side of the cord and
ascend by the spinothalamic tract to the reticular activating
system (RAS) and thalamus.The localization and meaning of
pain occur at the level of the somatosensory cortex. 1, first-
order sensory neurons; 2, second-order sensory neurons;
3, third-order sensory neurons.
