CHAPTER 48 Somatic Sensations
II. Pain, Headache, and Thermal Sensations
Pain is mainly a protective mechanism for the body because it is not a pure sensation but, rather, a response to tissue injury that is created, as it were, within the nervous system.
Fast pain is felt within about 0.1 second after the stimulation, whereas slow pain begins 1 second or more following the painful stimulus. Slow pain is usually associated with tissue damage and can be referred to as burning pain, aching pain, or chronic pain.
All pain receptors are free nerve endings. They are found in largest number and density in the skin, periosteum, arterial walls, joint surfaces, the dura, and its reflections inside the cranial vault.
Fast pain signals elicited by mechanical or thermal stimuli are transmitted over Aδ fibers in peripheral nerves at velocities between 6 and 30 m/sec. In contrast, the slow, chronic type of pain signals are transmitted over type C fibers at velocities ranging from 0.5 to 2.0 m/sec. As these two types of fiber enter the spinal cord through dorsal roots, they are segregated such that Aδ fibers primarily excite neurons in lamina I of the dorsal horn, whereas C fibers synapse with neurons in the substantia gelatinosa. The latter cells then project deeper into the gray matter and activate neurons mainly in lamina V but also in laminae VI and VII. The neurons that receive Aδ fiber input (fast pain) give rise to the neospinothalamic tract, whereas those that receive C fiber input form the paleospinothalamic tract.
Axons from neurons in lamina I that form the neospinothalamic tract cross the midline close to their origin and ascend the white matter of the spinal cord as part of the anterolateral system. Some of these fibers terminate in the brain stem reticular formation, but most project all the way to the ventral posterolateral nucleus (VPL) of the thalamus (ventrobasal thalamus). From here, thalamic neurons project to the primary somatosensory (SI) cortex. This system is primarily used during the localization of pain stimuli.
The paleospinothalamic pathway is the phylogenetically older of the two pain pathways. The axons of cells in lamina V, like those from lamina I, cross the midline near their level of origin and ascend in the anterolateral system. The axons of lamina V cells terminate almost exclusively in the brain stem, rather than in the thalamus. In the brain stem, these fibers reach the reticular formation, the superior colliculus, and the periaqueductal gray. A system of ascending fibers, mainly from the reticular formation, proceed rostrally to the intralaminar nuclei and posterior nuclei of the thalamus, as well as to portions of the hypothalamus. Pain signals transmitted over this pathway are typically localized only to a major part of the body. For example, if the stimulus originates in the hand, it may be localized to “somewhere” in the upper extremity.
There is marked variability in the degree to which individuals react to painful stimuli; this is in large part because of the existence of a mechanism for pain suppression (analgesia) that resides in the central nervous system. This pain suppression system consists of three major components.
Neurons in the periaqueductal gray and nucleus raphe magnus (but not the noradrenergic medullary reticular neurons) have opiate receptors on their surface membranes. When stimulated by exogenously administered opioid compounds (analgesics) or by endogenous opioid neurotransmitter agents (endorphins and enkephalins) found in the brain, the pain suppression circuitry is activated, which leads to reduced pain perception.
Activation of the large, rapidly conducting tactile sensory fibers of the dorsal roots appears to suppress the transmission of pain signals in the dorsal horn, probably through lateral inhibitory circuits. Although poorly understood, such circuitry probably explains the relief of pain achieved by the simple maneuver of rubbing the skin in the vicinity of a painful stimulus.
Stimulating electrodes implanted over the spinal cord dorsal columns or stereotactically positioned in the thalamus or periaqueductal gray has been used to reduce chronic pain. The level of stimulation can be regulated upward or downward by the patient to manage pain suppression more effectively.
Most often, referred pain involves signals originating in an internal (visceral) organ or tissue. The mechanism is not well understood but is thought to be due to the fact that visceral pain fibers may synapse with neurons in the spinal cord that also receive pain input from cutaneous areas seemingly unrelated to the visceral stimulation site. A common example is pain from the heart wall being referred to the surface of the left side of the jaw and neck or the left arm. Rather than associating the pain with the heart, the patient perceives the pain sensation as coming from the face or arm. This implies that visceral afferent signals from the heart converge on the same spinal cord neurons that receive cutaneous input from the periphery (or the convergence may occur in the thalamus).
In other instances, leakage of gastric secretions from a perforated or ulcerated gastrointestinal tract may directly stimulate pain endings in the peritoneum and lead to severe painful sensations in the body wall. The pain may localize to the dermatomal surface related to the embryonic location of the visceral structure. Spasms in the muscular wall of the gut or distention of a muscular wall of an organ such as the urinary bladder may also lead to painful sensations.
Pain from an internal organ such as an inflamed appendix may be experienced in two locations. If the involved appendix touches the parietal peritoneum, pain may be felt in the wall of the right lower abdominal quadrant or it can be referred to the region around the umbilicus, or both, because of the termination of visceral pain fibers in the T-10 or T-11 segments of the spinal cord, which receive cutaneous input from those dermatomes.
The source of the pain stimuli may be intra- or extracranial; in this chapter we focus on intracranial sources. The brain itself is insensitive to pain, but the dura mater and cranial nerve sheaths contain pain receptors that transmit signals traveling with cranial nerves X and XII that enter spinal cord levels C-2 and C-3. When somatosensory structures are damaged, the patient experiences the sensation of tingling, or pins and needles. The exceptions, as described previously, are tic douloureux and the thalamic pain syndrome.
Pressure on the venous sinuses and stretching of the dura or blood vessels and cranial nerves passing through the dura lead to the sensation of headache. When structures above the tentorium cerebelli are affected, pain is referred to the frontal portion of the head, whereas involvement of structures below the tentorium results in occipital headaches.
Meningeal inflammation typically produces pain involving the entire head. Likewise, if a small volume of cerebrospinal fluid is removed (as little as 20 mL) and the patient is not recumbent, gravity causes the brain to “sink”; this leads to stretching of meninges, vessels, and cranial nerves, resulting in a diffuse headache. The headache that follows an alcoholic binge is thought to be due to the direct toxic irritation of alcohol on the meninges. Constipation may also cause headache as a result of direct toxic effects of circulating metabolic substances or from circulatory changes related to the loss of fluid into the gut.
Although the mechanism is still not completely understood, migraine headaches are thought to be the result of vascular phenomena. Prolonged unpleasant emotions or anxiety produces spasm in brain arteries and leads to local ischemia in the brain. This may result in prodromal visual or olfactory symptoms. As a result of the prolonged spasm and ischemia, the muscular wall of the vessel loses its ability to maintain normal tone. The pulsation of circulating blood alternately stretches (dilates) and relaxes the vessel wall, which stimulates pain receptors in the vascular wall or in the meninges surrounding the entry points of vessels into the brain or cranium. The result is an intense headache. Other causative theories are being investigated, and a number of new and effective treatments for this condition should soon be available.
Emotional tension can cause the muscles of the head especially those attached to the scalp and neck to become spastic and irritate the attachment areas. Irritation of the nasal and accessory nasal structures that are highly sensitive can lead to the phenomenon of sinus headache. Difficulty in focusing the eyes can lead to excessive contraction of the ciliary muscle as well as the muscles of the face in an effort to squint to sharpen the focus on the object at hand. This can lead to eye and facial pain commonly known as an eyestrain type of headache.
Temperatures below 7°C and above 50°C activate pain receptors, and both of these extremes are perceived similarly as very painful, not as cold or warm. The peak temperature for activation of cold receptors is about 24°C, and the warmth receptors are maximally active at about 45°C. Both cold and warm receptors can be stimulated with temperatures in the range of 31°C to 43°C.
When the cold receptor is subjected to an abrupt temperature decrease, it is strongly stimulated initially; but then, after the first few seconds, the generation of action potentials falls off dramatically. However, the decrease in firing progresses more slowly over the next 30 minutes or so. This means that the cold and warm receptors respond to steady state temperature as well as changes in temperature. This explains why a cold outdoor temperature “feels” so much colder at first as one emerges from a warm environment.
The stimulatory mechanism in thermal receptors is believed to be related to the change in metabolic rate in the nerve fiber induced by the temperature change. It has been shown that for every 10°C temperature change there is a twofold change in the rate of intracellular chemical reactions.
The density of thermal receptors on the skin surface is relatively small. Therefore, temperature changes that affect only a small surface area are not as effectively detected as temperature changes that affect a large skin surface area. If the entire body is stimulated, a temperature change as small as 0.01°C can be detected. Thermal signals are transmitted through the central nervous system in parallel with pain signals.