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Ganong's Review of Medical Physiology, 23rd Edition

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170 SECTION III Central & Peripheral Neurophysiology<br />

CLINICAL BOX 10–3<br />

Muscle Pain<br />

If a muscle contracts rhythmically in the presence <strong>of</strong> an adequate<br />

blood supply, pain does not usually result. However, if<br />

the blood supply to a muscle is occluded, contraction soon<br />

causes pain. The pain persists after the contraction until<br />

blood flow is reestablished. These observations are difficult<br />

to interpret except in terms <strong>of</strong> the release during contraction<br />

<strong>of</strong> a chemical agent (Lewis’s “P factor”) that causes pain<br />

when its local concentration is high enough. When the blood<br />

supply is restored, the material is washed out or metabolized.<br />

The identity <strong>of</strong> the P factor is not settled, but it could be<br />

K + . Clinically, the substernal pain that develops when the<br />

myocardium becomes ischemic during exertion (angina<br />

pectoris) is a classic example <strong>of</strong> the accumulation <strong>of</strong> P factor<br />

in a muscle. Angina is relieved by rest because this decreases<br />

the myocardial O 2 requirement and permits the blood supply<br />

to remove the factor. Intermittent claudication, the<br />

pain produced in the leg muscles <strong>of</strong> persons with occlusive<br />

vascular disease, is another example. It characteristically<br />

comes on while the patient is walking and disappears on<br />

stopping. Visceral pain, like deep somatic pain, initiates reflex<br />

contraction <strong>of</strong> nearby skeletal muscle. This reflex spasm<br />

is usually in the abdominal wall and makes the abdominal<br />

wall rigid. It is most marked when visceral inflammatory processes<br />

involve the peritoneum. However, it can occur without<br />

such involvement. The spasm protects the underlying inflamed<br />

structures from inadvertent trauma. Indeed, this<br />

reflex spasm is sometimes called “guarding.”<br />

The autonomic nervous system, like the somatic, has afferent<br />

components, central integrating stations, and effector pathways.<br />

The receptors for pain and the other sensory modalities<br />

present in the viscera are similar to those in skin, but there are<br />

marked differences in their distribution. There are no proprioceptors<br />

in the viscera, and few temperature and touch receptors.<br />

Nociceptors are present, although they are more sparsely<br />

distributed than in somatic structures.<br />

Afferent fibers from visceral structures reach the CNS via<br />

sympathetic and parasympathetic nerves. Their cell bodies are<br />

located in the dorsal roots and the homologous cranial nerve<br />

ganglia. Specifically, there are visceral afferents in the facial,<br />

glossopharyngeal, and vagus nerves; in the thoracic and upper<br />

lumbar dorsal roots; and in the sacral roots (Figure 10–2).<br />

There may also be visceral afferent fibers from the eye in the<br />

trigeminal nerve.<br />

As almost everyone knows from personal experience, visceral<br />

pain can be very severe. The receptors in the walls <strong>of</strong> the hollow<br />

viscera are especially sensitive to distention <strong>of</strong> these organs. Such<br />

distention can be produced experimentally in the gastrointestinal<br />

tract by inflation <strong>of</strong> a swallowed balloon attached to a tube.<br />

This produces pain that waxes and wanes (intestinal colic) as the<br />

intestine contracts and relaxes on the balloon. Similar colic is<br />

produced in intestinal obstruction by the contractions <strong>of</strong> the<br />

dilated intestine above the obstruction. When a visceral organ is<br />

inflamed or hyperemic, relatively minor stimuli cause severe<br />

pain. This is probably a form <strong>of</strong> hyperalgesia.<br />

REFERRED PAIN<br />

Irritation <strong>of</strong> a visceral organ frequently produces pain that is<br />

felt not at that site but in some somatic structure that may be a<br />

considerable distance away. Such pain is said to be referred to<br />

the somatic structure. Obviously, knowledge <strong>of</strong> referred pain<br />

and the common sites <strong>of</strong> pain referral from each <strong>of</strong> the viscera<br />

is <strong>of</strong> great importance to the physician. Perhaps the bestknown<br />

example is referral <strong>of</strong> cardiac pain to the inner aspect <strong>of</strong><br />

the left arm. Other examples include pain in the tip <strong>of</strong> the<br />

shoulder caused by irritation <strong>of</strong> the central portion <strong>of</strong> the diaphragm<br />

and pain in the testicle due to distention <strong>of</strong> the ureter.<br />

Additional instances abound in the practices <strong>of</strong> medicine, surgery,<br />

and dentistry. However, sites <strong>of</strong> reference are not stereotyped,<br />

and unusual reference sites occur with considerable<br />

frequency. Cardiac pain, for instance, may be referred to the<br />

right arm, the abdominal region, or even the back and neck.<br />

When pain is referred, it is usually to a structure that developed<br />

from the same embryonic segment or dermatome as the<br />

structure in which the pain originates. This principle is called<br />

the dermatomal rule. For example, the heart and the arm<br />

have the same segmental origin, and the testicle has migrated<br />

with its nerve supply from the primitive urogenital ridge from<br />

which the kidney and ureter have developed.<br />

The basis for referred pain may be convergence <strong>of</strong> somatic<br />

and visceral pain fibers on the same second-order neurons in<br />

the dorsal horn that project to the thalamus and then to the<br />

somatosensory cortex (Figure 10–3). This is called the convergence–projection<br />

theory. Somatic and visceral neurons converge<br />

in lamina I–VI <strong>of</strong> the ipsilateral dorsal horn, but neurons<br />

in lamina VII receive afferents from both sides <strong>of</strong> the body—a<br />

requirement if convergence is to explain referral to the side<br />

opposite that <strong>of</strong> the source <strong>of</strong> pain. The somatic nociceptive<br />

fibers normally do not activate the second-order neurons, but<br />

when the visceral stimulus is prolonged, facilitation <strong>of</strong> the<br />

somatic fiber endings occurs. They now stimulate the secondorder<br />

neurons, and <strong>of</strong> course the brain cannot determine<br />

whether the stimulus came from the viscera or from the area <strong>of</strong><br />

referral.

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