170
SECTION III
Central & Peripheral Neurophysiology
The autonomic nervous system, like the somatic, has afferent
components, central integrating stations, and effector path-
ways. The receptors for pain and the other sensory modalities
present in the viscera are similar to those in skin, but there are
marked differences in their distribution. There are no proprio-
ceptors in the viscera, and few temperature and touch recep-
tors. Nociceptors are present, although they are more sparsely
distributed than in somatic structures.
Afferent fibers from visceral structures reach the CNS via
sympathetic and parasympathetic nerves. Their cell bodies are
located in the dorsal roots and the homologous cranial nerve
ganglia. Specifically, there are visceral afferents in the facial,
glossopharyngeal, and vagus nerves; in the thoracic and upper
lumbar dorsal roots; and in the sacral roots (Figure 10–2).
There may also be visceral afferent fibers from the eye in the
trigeminal nerve.
As almost everyone knows from personal experience, visceral
pain can be very severe. The receptors in the walls of the hollow
viscera are especially sensitive to distention of these organs. Such
distention can be produced experimentally in the gastrointesti-
nal tract by inflation of a swallowed balloon attached to a tube.
This produces pain that waxes and wanes (intestinal colic) as the
intestine contracts and relaxes on the balloon. Similar colic is
produced in intestinal obstruction by the contractions of the
dilated intestine above the obstruction. When a visceral organ is
inflamed or hyperemic, relatively minor stimuli cause severe
pain. This is probably a form of hyperalgesia.REFERRED PAIN
Irritation of a visceral organ frequently produces pain that is
felt not at that site but in some somatic structure that may be a
considerable distance away. Such pain is said to be referred to
the somatic structure. Obviously, knowledge of
referred pain
and the common sites of pain referral from each of the viscera
is of great importance to the physician. Perhaps the best-
known example is referral of cardiac pain to the inner aspect of
the left arm. Other examples include pain in the tip of the
shoulder caused by irritation of the central portion of the dia-
phragm and pain in the testicle due to distention of the ureter.
Additional instances abound in the practices of medicine, sur-
gery, and dentistry. However, sites of reference are not ster-
eotyped, and unusual reference sites occur with considerable
frequency. Cardiac pain, for instance, may be referred to the
right arm, the abdominal region, or even the back and neck.
When pain is referred, it is usually to a structure that devel-
oped from the same embryonic segment or dermatome as the
structure in which the pain originates. This principle is called
the
dermatomal rule.
For example, the heart and the arm
have the same segmental origin, and the testicle has migrated
with its nerve supply from the primitive urogenital ridge from
which the kidney and ureter have developed.
The basis for referred pain may be convergence of somatic
and visceral pain fibers on the same second-order neurons in
the dorsal horn that project to the thalamus and then to the
somatosensory cortex (Figure 10–3). This is called the
conver-
gence–projection theory.
Somatic and visceral neurons con-
verge in lamina I–VI of the ipsilateral dorsal horn, but neurons
in lamina VII receive afferents from both sides of the body—a
requirement if convergence is to explain referral to the side
opposite that of the source of pain. The somatic nociceptive
fibers normally do not activate the second-order neurons, but
when the visceral stimulus is prolonged, facilitation of the
somatic fiber endings occurs. They now stimulate the second-
order neurons, and of course the brain cannot determine
whether the stimulus came from the viscera or from the area of
referral.CLINICAL BOX 10–3
Muscle Pain
If a muscle contracts rhythmically in the presence of an ade-
quate blood supply, pain does not usually result. However, if
the blood supply to a muscle is occluded, contraction soon
causes pain. The pain persists after the contraction until
blood flow is reestablished. These observations are difficult
to interpret except in terms of the release during contraction
of a chemical agent (Lewis’s
“P factor”
) that causes pain
when its local concentration is high enough. When the blood
supply is restored, the material is washed out or metabo-
lized. The identity of the P factor is not settled, but it could be
K
+. Clinically, the substernal pain that develops when the
myocardium becomes ischemic during exertion
(angina
pectoris)
is a classic example of the accumulation of P factor
in a muscle. Angina is relieved by rest because this decreases
the myocardial O
2
requirement and permits the blood sup-
ply to remove the factor.
Intermittent claudication,
the
pain produced in the leg muscles of persons with occlusive
vascular disease, is another example. It characteristically
comes on while the patient is walking and disappears on
stopping. Visceral pain, like deep somatic pain, initiates re-
flex contraction of nearby skeletal muscle. This reflex spasm
is usually in the abdominal wall and makes the abdominal
wall rigid. It is most marked when visceral inflammatory pro-
cesses involve the peritoneum. However, it can occur with-
out such involvement. The spasm protects the underlying in-
flamed structures from inadvertent trauma. Indeed, this
reflex spasm is sometimes called
“guarding.”