Somatic Sensations: II. Pain, Headache, and Thermal Sensations


Many ailments of the body cause pain. Furthermore, the ability to diagnose different diseases depends to a great extent on a physician’s knowledge of the different qualities of pain. For these reasons, the first part of this chapter is devoted mainly to pain and to the physiological bases of some associated clinical phenomena.

Pain occurs whenever tissues are being damaged and causes the individual to react to remove the pain stimulus. Even such simple activities as sitting for a long time can cause tissue damage because of lack of blood flow to the skin where it is compressed by the weight of the body. When the skin becomes painful as a result of the ischemia, the person normally shifts weight subconsciously. However, a person who has lost the pain sense—for example, after a spinal cord injury—fails to feel the pain and, therefore, fails to shift. This situation soon results in total breakdown and desquamation of the skin at the areas of pressure.

Fast Pain and Slow Pain and Their Qualities

Pain has been classified into two major types, fast pain and slow pain. Fast pain is felt within about 0.1 second after a pain stimulus is applied, whereas slow pain begins only after 1 second or more and then increases slowly over many seconds and sometimes even minutes. In this chapter, we shall see that the conduction pathways for these two types of pain are different and that each of them has specific qualities.

Fast pain is also described by many alternative names, such as sharp pain, pricking pain, acute pain, and electric pain. This type of pain is felt when a needle is stuck into the skin, when the skin is cut with a knife, or when the skin is burned acutely. It is also felt when the skin is subjected to electric shock. Fast-sharp pain is not felt in most deep tissues of the body.

Slow pain also goes by many names, such as slow burning pain, aching pain, throbbing pain, nauseous pain, and chronic pain. This type of pain is usually associated with tissue destruction. It can lead to prolonged, almost unbearable suffering. Slow pain can occur both in the skin and in almost any deep tissue or organ.

Pain Receptors and Their Stimulation

Pain Receptors Are Free Nerve Endings

The pain receptors in the skin and other tissues are all free nerve endings. They are widespread in the superficial layers of the skin, as well as in certain internal tissues, such as the periosteum, the arterial walls, the joint surfaces, and the falx and tentorium in the cranial vault. Most other deep tissues are only sparsely supplied with pain endings; nevertheless, any widespread tissue damage can summate to cause the slow, chronic, aching type of pain in most of these areas.

Mechanical, Thermal, and Chemical Stimuli Excite Pain Receptors

Pain can be elicited by multiple types of stimuli, classified as mechanical, thermal, and chemical pain stimuli. In general, fast pain is elicited by the mechanical and thermal types of stimuli, whereas slow pain can be elicited by all three types.

Some of the chemicals that excite the chemical type of pain are bradykinin, serotonin, histamine, potassium ions, acids, acetylcholine, and proteolytic enzymes. In addition, prostaglandins and substance P enhance the sensitivity of pain endings but do not directly excite them. The chemical substances are especially important in stimulating the slow suffering type of pain that occurs after tissue injury.

Nonadapting Nature of Pain Receptors

In contrast to most other sensory receptors of the body, pain receptors adapt very little and sometimes not at all. In fact, under some conditions, excitation of pain fibers becomes progressively greater, especially for slow, aching, nauseous pain, as the pain stimulus continues. This increase in sensitivity of the pain receptors is called hyperalgesia. One can readily understand the importance of this failure of pain receptors to adapt because it allows the pain to keep the person apprised of a tissue-damaging stimulus as long as it persists.

Rate of Tissue Damage as a Stimulus for Pain

The average person begins to perceive pain when the skin is heated above 45°C, as shown in Figure 49-1 . This is also the temperature at which the tissues begin to be damaged by heat; indeed, the tissues are eventually destroyed if the temperature remains above this level indefinitely. Therefore, it is immediately apparent that pain resulting from heat is closely correlated with the rate at which damage to the tissues is occurring and not with the total damage that has already occurred.

Figure 49-1, Distribution curve obtained from a large number of persons showing the minimal skin temperature that will cause pain.

The intensity of pain is also closely correlated with the rate of tissue damage from causes other than heat, such as bacterial infection, tissue ischemia, tissue contusion, and so forth.

Special Importance of Chemical Pain Stimuli During Tissue Damage

Extracts from damaged tissue cause intense pain when injected beneath the normal skin. Most of the chemicals listed earlier that excite the chemical pain receptors can be found in these extracts. One chemical that seems to be more painful than others is bradykinin. Researchers have suggested that bradykinin might be the agent most responsible for causing pain after tissue damage. Also, the intensity of the pain felt correlates with the local increase in potassium ion concentration or the increase in proteolytic enzymes that directly attack the nerve endings and excite pain by making the nerve membranes more permeable to ions.

Tissue Ischemia as a Cause of Pain

When blood flow to a tissue is blocked, the tissue often becomes very painful within a few minutes. The greater the rate of metabolism of the tissue, the more rapidly the pain appears. For example, if a blood pressure cuff is placed around the upper arm and inflated until the arterial blood flow ceases, exercise of the forearm muscles sometimes can cause muscle pain within 15 to 20 seconds. In the absence of muscle exercise, the pain may not appear for 3 to 4 minutes, even though the muscle blood flow remains zero.

One of the suggested causes of pain during ischemia is accumulation of large amounts of lactic acid in the tissues, formed as a consequence of anaerobic metabolism (i.e., metabolism without oxygen). It is also probable that other chemical agents, such as bradykinin and proteolytic enzymes, are formed in the tissues because of cell damage and that these agents, in addition to lactic acid, stimulate the pain nerve endings.

Muscle Spasm as a Cause of Pain

Muscle spasm is also a common cause of pain and is the basis of many clinical pain syndromes. This pain probably results partially from the direct effect of muscle spasm in stimulating mechanosensitive pain receptors, but it might also result from the indirect effect of muscle spasm to compress the blood vessels and cause ischemia. The spasm also increases the rate of metabolism in the muscle tissue, thus making the relative ischemia even greater, creating ideal conditions for the release of chemical pain-inducing substances.

Dual Pathways for Transmission of Pain Signals Into the Central Nervous System

Even though all pain receptors are free nerve endings, these endings use two separate pathways for transmitting pain signals into the central nervous system. The two pathways mainly correspond to the two types of pain—a fast-sharp pain pathway and a slow-chronic pain pathway. .

Peripheral Pain Fibers—“Fast” and “Slow” Fibers

The fast-sharp pain signals are elicited by either mechanical or thermal pain stimuli. They are transmitted in the peripheral nerves to the spinal cord by small type Aδ fibers at velocities between 6 and 30 m/sec. Conversely, the slow-chronic type of pain is elicited mostly by chemical types of pain stimuli but sometimes by persisting mechanical or thermal stimuli. This slow-chronic pain is transmitted to the spinal cord by type C fibers at velocities between 0.5 and 2 m/sec.

Because of this double system of pain innervation, a sudden painful stimulus often gives a “double” pain sensation: a fast-sharp pain that is transmitted to the brain by the Aδ fiber pathway, followed a second or so later by a slow pain that is transmitted by the C fiber pathway. The sharp pain plays an important role in making the person react immediately to remove himself or herself from the stimulus. The slow pain tends to become greater over time, eventually producing intolerable pain and making the person keep trying to relieve the cause of the pain.

On entering the spinal cord from the dorsal spinal roots, the pain fibers terminate on relay neurons in the dorsal horns. Here again, there are two systems for processing the pain signals on their way to the brain, as shown in Figures 49-2 and 49-3 .

Figure 49-2, Transmission of both fast-sharp and slow-chronic pain signals into and through the spinal cord on their way to the brain. Aδ fibers transmit fast-sharp pain, and C fibers transmit slow-chronic pain.

Figure 49-3, Transmission of pain signals into the brain stem, thalamus, and cerebral cortex via the fast pricking pain pathway and the slow burning pain pathway.

Dual Pain Pathways in the Cord and Brain Stem—The Neospinothalamic Tract and the Paleospinothalamic Tract

On entering the spinal cord, the pain signals take two pathways to the brain, through (1) the neospinothalamic tract and (2) the paleospinothalamic tract.

Neospinothalamic Tract for Fast Pain

The fast type Aδ pain fibers transmit mainly mechanical and acute thermal pain. They terminate mainly in lamina I (lamina marginalis) of the dorsal horns, as shown in Figure 49-2 , and there they excite second-order neurons of the neospinothalamic tract. These second-order neurons give rise to long fibers that cross immediately to the opposite side of the cord through the anterior commissure and then turn upward, passing to the brain in the anterolateral columns .

Termination of the Neospinothalamic Tract in the Brain Stem and Thalamus

A few fibers of the neospinothalamic tract terminate in the reticular areas of the brain stem, but most pass all the way to the thalamus without interruption, terminating in the ventrobasal complex along with the dorsal column–medial lemniscal tract for tactile sensations, as was discussed in Chapter 48 . A few fibers also terminate in the posterior nuclear group of the thalamus. From these thalamic areas, the signals are transmitted to other basal areas of the brain, as well as to the somatosensory cortex.

The Nervous System Can Localize Fast Pain in the Body

The fast-sharp type of pain can be localized much more exactly in the different parts of the body than can slow-chronic pain. However, when only pain receptors are stimulated, without the simultaneous stimulation of tactile receptors, even fast pain may be poorly localized, often only within 10 centimeters or so of the stimulated area. Yet, when tactile receptors that excite the dorsal column–medial lemniscal system are simultaneously stimulated, the localization can be nearly exact.

Glutamate, the Probable Neurotransmitter of the Type Aδ Fast Pain Fibers

It is believed that glutamate is the neurotransmitter substance secreted in the spinal cord at the type Aδ pain nerve fiber endings. Glutamate is one of the most widely used excitatory transmitters in the central nervous system, usually having a duration of action lasting for only a few milliseconds.

Paleospinothalamic Pathway for Transmitting Slow-Chronic Pain

The paleospinothalamic pathway is a much older system and transmits pain mainly from the peripheral slow-chronic type C pain fibers, although it also transmits some signals from type Aδ fibers. In this pathway, the peripheral fibers terminate in the spinal cord almost entirely in laminae II and III of the dorsal horns, which together are called the substantia gelatinosa, as shown by the lateral-most dorsal root type C fiber in Figure 49-2 . Most of the signals then pass through one or more additional short fiber neurons within the dorsal horns before entering mainly lamina V, also in the dorsal horn. Here, the last neurons in the series give rise to long axons that mostly join the fibers from the fast pain pathway, passing first through the anterior commissure to the opposite side of the cord and then upward to the brain in the anterolateral pathway.

Substance P, the Probable Slow-Chronic Neurotransmitter of Type C Nerve Endings

Type C pain fiber terminals entering the spinal cord release both glutamate transmitter and substance P transmitter. The glutamate transmitter acts instantaneously and lasts for only a few milliseconds. Substance P is released much more slowly, building up in concentration over a period of seconds or even minutes. In fact, it has been suggested that the “double” pain sensation one feels after a pinprick might result partly from the fact that the glutamate transmitter gives a faster pain sensation, whereas the substance P transmitter gives a more lagging sensation. Regardless of the yet unknown details, it seems clear that glutamate is the neurotransmitter most involved in transmitting fast pain into the central nervous system, and substance P is concerned with slow-chronic pain.

Projection of Paleospinothalamic Pathway (Slow-Chronic Pain Signals) into the Brain Stem and Thalamus

The slow-chronic paleospinothalamic pathway terminates widely in the brain stem, in the large shaded area shown in Figure 49-3 . Only 10% to 25% of the fibers pass all the way to the thalamus. Instead, most terminate in one of three areas: (1) the reticular nuclei of the medulla, pons, and mesencephalon; (2) the tectal area of the mesencephalon deep to the superior and inferior colliculi; or (3) the periaqueductal gray region surrounding the aqueduct of Sylvius. These lower regions of the brain appear to be important for feeling the suffering types of pain. From the brain stem pain areas, multiple short-fiber neurons relay the pain signals upward into the intralaminar and ventrolateral nuclei of the thalamus and into certain portions of the hypothalamus and other basal regions of the brain.

Poor Capability of the Nervous System to Localize Precisely the Source of Pain Transmitted in the Slow-Chronic Pathway

Localization of pain transmitted via the paleospinothalamic pathway is imprecise. For example, slow-chronic pain can usually be localized only to a major part of the body, such as to one arm or leg but not to a specific point on the arm or leg. This phenomenon is in keeping with the multisynaptic, diffuse connectivity of this pathway. It explains why patients often have serious difficulty in localizing the source of some chronic types of pain.

Function of the Reticular Formation, Thalamus, and Cerebral Cortex in the Appreciation of Pain

Complete removal of the somatic sensory areas of the cerebral cortex does not prevent pain perception. Therefore, it is likely that pain impulses entering the brain stem reticular formation, the thalamus, and other lower brain centers cause conscious perception of pain. This does not mean that the cerebral cortex has nothing to do with normal pain appreciation; electrical stimulation of cortical somatosensory areas does cause a person to perceive mild pain from about 3% of the points stimulated. However, it is believed that the cortex plays an especially important role in interpreting pain quality, even though pain perception might be principally the function of lower centers.

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