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Pain
Sensations interpreted as pain, including burning, aching, stinging, and soreness,
are the most distinctive forms of sensory input to the central nervous system. Pain
serves an important protective function because it causes awareness of actual or
potential tissue damage. Furthermore, it stimulates an individual to react to remove or
withdraw from the source of the pain.
Nociceptors
Nociceptors are bare or free nerve endings; therefore, they do not adapt, or stop
responding, to sustained or repeated stimulation. Nociceptors are widely distributed in
the skin, dental pulp, periosteum, joints, meninges, and some internal organs. The
three major classes of nociceptors are:
• Thermal nociceptors
• Mechanical nociceptors
• Polymodal nociceptors
Thermal nociceptors
Thermal nociceptors are activated by extreme temperatures, especially heat. One
group of these receptors is stimulated by noxious heat (>45 °C) and a second group is
stimulated by noxious cold (<5 °C).
Mechanical nociceptors
Mechanical nociceptors are activated by mechanical damage, such as cutting,
pinching, or tissue distortion, as well as by intensive pressure applied to the skin.
Polymodal nociceptors
Polymodal nociceptors are activated by all types of damaging stimuli (thermal,
mechanical, chemical), including irritating exogenous substances that may penetrate
the skin.
Endogenous substances that may stimulate these receptors to elicit pain include
potassium released from damaged cells; bradykinin; histamine; substance P; acids;
and proteolytic enzymes.
The two types of pain are:
• Fast pain
• Slow pain
Fast pain may be described as sharp or prickling pain. This pain is perceived first
(within 0.1 sec) as it is carried by the more rapidly fibers.
Slow pain may be described as dull, aching, or throbbing pain. This pain is perceived
second (only after 1 sec or more) because it is carried by fibers. Slow pain persists
longer and is typically more unpleasant; in fact, it tends to become greater over time.
Hyperalgesia
An injured area is typically more sensitive to subsequent stimuli. As a result, painful
stimuli, or even normally nonpainful stimuli, may cause an excessive pain response.
An increase in the sensitivity of nociceptors is referred to as primary hyperalgesia.
A classic example of hyperalgesia is a burn. Even light touch of a burned area may be
painful. The sensitization of nociceptors following tissue damage or inflammation
results from a variety of chemicals released or activated in the injured area. These
substances decrease the threshold for activation of the nociceptors. One such
substance that seems to be more painful than the others is bradykinin. Activated by
enzymes released from damaged cells, bradykinin causes pain by several mechanisms.
First, it activates A-delta and C fibers directly. Second, along with histamine, it
contributes to the inflammatory response to tissue injury. Third, it promotes synthesis
and release of prostaglandins from nearby cells. The prostaglandins sensitize all three
types of pain receptors, thus enhancing the response to a noxious stimulus. In other
words, it hurts more when prostaglandins are present. Aspirin and nonsteroidal antiinflammatory drugs (NSAIDs) inhibit the synthesis of prostaglandins, which
accounts, in part, for their analgesic effects.
Endogenous analgesic system
The endogenous analgesic system is a built-in neuronal system that suppresses
transmission of nervous impulses in the pain pathway. It functions by way of the
following neurotransmitters produced in the CNS:
• Endorphins
• Enkephalins
• Dynorphin
Endorphins are found primarily in the limbic system, hypothalamus, and brainstem.
Enkephalins and dynorphin (in smaller quantities) are found primarily in the gray
matter of the midbrain, the limbic system, and the hypothalamus. These endogenous
substances mimic the effects of morphine and other opiate drugs at many points in the
analgesic system, including in the dorsal horns of the spinal cord. Opioid receptors are
highly concentrated in the gray area of the midbrain. Stimulation of this region
produces long-lasting analgesia with no effect on the level of consciousness. For these
reasons, this gray area is often referred to as the endogenous analgesia center, The
endogenous analgesic system is normally inactive. It remains unclear how this system
becomes activated. Potential activating factors include exercise, stress, acupuncture,
and hypnosis.
Cutaneous pain
Cutaneous pain is felt in superficial structures such as the skin and subcutaneous
tissues. A pin prick and a paper cut are examples of cutaneous pain. It is a sharp pain
with a burning quality that may be easily localized. This pain may be abrupt or slow
in onset.
Deep somatic pain
As its name implies, deep somatic pain is generated in deep body structures, such as
the periosteum, muscles, tendons, joints, and blood vessels. This type of pain is more
diffuse than cutaneous pain. It may be elicited by strong pressure, ischemia, and tissue
damage.
Tissue ischemia
When blood flow to a tissue is decreased or interrupted, the tissue becomes painful
within a few minutes. In fact, the greater the rate of metabolism in the tissue, the more
rapid is the onset of pain. The causes of pain due to tissue ischemia include:
• Accumulation of lactic acid due to the anaerobic metabolism that occurs during
ischemia
• Release and activation of noxious chemicals in the area of tissue ischemia due to
tissue damage.
The lactic acid and other noxious chemicals stimulate polymodal nociceptors.
Muscle spasm
The pain induced by muscle spasm results partially from the direct effect of tissue
distortion on mechanical nociceptors. Muscle spasm also causes tissue ischemia. The
increased muscle tension compresses blood vessels and decreases blood flow.
Furthermore, the increased rate of metabolism associated with the spasm exacerbates
the ischemia. As discussed earlier, ischemia leads to stimulation of polymodal
nociceptors.
Visceral pain
Visceral pain occurs in organs and tissues of the thoracic and abdominal cavities. It
may be caused by several factors, including:
• Inflammation
• Chemical stimuli
• Spasm of a hollow organ
• Overdistension of a hollow organ
Referred pain
Referred pain is felt in a part of the body different from the actual tissue causing the
pain. Typically, the pain is initiated in a visceral organ or tissue and referred to an
area of the body surface. Classic examples of referred pain include headache and
angina. Interestingly, the brain does not contain nociceptors; therefore, pain perceived
as a headache originates in other tissues, such as the eyes; sinuses; muscles of the
head and neck; and meninges.
Angina, or chest pain, is caused by coronary ischemia. It may be accompanied
by pain referred to the neck, left shoulder, and left arm. Referred pain most likely
results from the convergence of visceral and somatic afferent fibers on the same
second-order neurons in the dorsal horn of the spinal cord (see Figure 8.3). Therefore,
the brain has no way of identifying the original source of the pain. Because superficial
inputs normally predominate over visceral inputs, higher centers may incorrectly
attribute the pain to the skin instead of the deeper tissue.
Phantom pain
Phantom pain is pain that appears to arise from an amputated limb or body part; as
many as 70% of amputees experience phantom pain. This pain may begin with
sensations of tingling, heat and cold, or heaviness, followed by burning, cramping, or
shooting pain. Phantom pain may disappear spontaneously or persist for many years.
The exact cause of phantom pain is not clearly understood.
One proposed mechanism involves stimulation of the sensory pathway that had once
originated in the amputated body part. An important point is that the sensory pathway
originating in a given body part transmits impulses to the region of the somatosensory
cortex devoted to that body part regardless of amputation. Stimulation at any point
along this pathway results in the same sensation that would be produced by
stimulation of the nociceptor in the body part itself. Following amputation of a body
part, the ends of the afferent nerves arising from that body part become trapped in the
scar tissue of thestump. These afferent nerve endings exhibit increased sensitivity and
are easily stimulated. Therefore, action potentials are generated at these nerve endings
and transmitted to the area of the somatosensory cortex devoted to the amputated
body part. This results in the perception of pain arising from the amputated portion of
the body.
A second theory of phantom pain suggests that second-order neurons in the dorsal
horn of the spinal cord become hyperactive. Spontaneous firing of these neurons
causes transmission of nerve impulses to the brain and the perception of pain.