Afferent nerve fibers transmit impulses from the sensory receptors toward the brain while efferent fibers, such as motor neurons, transmit impulses from the brain toward the periphery. 42 First-order or primary afferents transmit the impulses from the sensory receptor to the dorsal horn of the spinal cord
focusing Narrowing attention to the appropriate stimuli in the environment.
afferent Conduction of a nerve impulse toward an organ.
efferent Conduction of a nerve impulse away from an organ.
Clinical Decision-Making Exercise 3–2 In addition to managing pain through the use of therapeutic modalities, the athletic trainer should make every effort to encourage the cognitive processes that can influence pain perception.
What techniques can be taught to the patient to take advantage of the cognitive aspects of pain modulation?
Clinical Decision-Making Exercise 3–3 A patient asks the athletic trainer to explain why electric stimulation of a trigger point can help reduce pain in her shoulder. What is the explanation?
Mechanisms of pain control
• Blocking ascending pathways (gate control)
• Blocking descending pathways
• Release of β-endorphin and dynorphin
CHAPTER 3 Managing Pain with Therapeutic Modalities 41
( Figure 3–4 ). There are four different types of first-order neurons ( Table 3–2 ). Aα and Aβ are diameter afferents that have a high (fast) conduction velocity, and Aδ and C fibers are small-diameter fibers with low (slow) conduction velocity.
Second-order afferent fibers carry sensory mes-sages up the spinal cord to the brain. Second-order afferent fibers are categorized as wide dynamic range or nociceptive specific. The wide dynamic range second-order afferents receive input from Aβ, Aδ, and C fibers. These second-order afferents serve relatively large, overlapping receptor fields.
The nociceptive specific second-order afferents respond exclusively to noxious stimulation. They receive input only from Aδ and C fibers. These afferents serve smaller receptor fields that do not
Sensory cortex
Nociceptor (free nerve ending) Second-order neuron Third-order
neuron
First-order neuron
Figure 3–4 Neural afferent transmission. Sensory (pain) information from free nerve endings is transmitted to the sensory cortex in the brain via first-, second-, and third-order neurons.
overlap. All of these neurons synapse with third-order neurons, which carry information to various brain centers where the input is integrated, interpreted, and acted upon.
Facilitators and Inhibitors of Synaptic Transmission
For information to pass between neurons, a trans-mitter substance must be released from the end of one neuron terminal (presynaptic membrane), enter the synaptic cleft, and attach to a receptor site on the next neuron (postsynaptic membrane) ( Figure 3–5 ). In the past, all the activity within the synapse was attributed to neurotransmitters , such as acetylcholine. The neurotransmitters, when released in sufficient quantities, are known to cause depolarization of the postsynaptic neuron.
In the absence of the neurotransmitter, no depolar-ization occurs.
It is now apparent that several compounds that are not true neurotransmitters can facilitate or inhibit synaptic activity. Serotonin , norephi-nephrine , enkephalin , a-endorphin , dynor-phine , and substance P are each important in the body’s pain control mechanism. 4
neurotransmitter Substance that passes informa-tion between neurons.
serotonin A neurotransmitter found in descending pathways. It is thought to play a significant role in pain control.
norepinephrine A neurotransmitter.
enkephalin Neurotransmitter that blocks the pas-sage of noxious stimuli from first-order to second-order afferents. It inhibits the release of substance P and is produced by enkephalinergic neurons.
a-endorphin A neurohormone similar in structure and properties to morphine.
dynorphin An endogenous opioid.
substance P The neurotransmitter of small-diameter primary afferent. It is released from both ends of the neuron.
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TABLE 3–2 Classification of Afferent Neurons
SIZE TYPE GROUP SUBGROUP
DIAMETER (MICROMETERS)
CONDUCTION
VELOCITY RECEPTOR STIMULUS
Large A α I 1a 12–20 (22) 70–120 Proprioceptive
mechanoreceptor
Muscle velocity and length change, muscle shortening of rapid speed
A α I 1b
A β II Muscle 6–12 36–72 Proprioceptive
mechanoreceptor
Muscle length information from touch and Pacinian corpuscles
A β II Skin Cutaneous
receptors
Touch, vibration, hair receptors
A δ III Muscle 1–5 (6) 6 (12)–36 (80) 75%
mechano-receptors and thermoreceptors
Temperature change
Small A δ III Skin 25% nociceptors,
mechanoreceptors and thermorecep-tors (hot and cold)
Noxious mechanical and temperature (> 45° C,
< 10° C)
C IV Muscle 0.3–1.0 0.4–1.0 50%
mechano-receptors and thermoreceptors
Touch and temperature
C IV Skin 50% nociceptors,
20% mechano-receptors, and 30%
thermoreceptors (hot and cold)
Noxious mechanical and temperature (> 45° C,
< 10° C)
Enkephalin is an endogenous (made by the body) opioid that inhibits the depolarization of second-order nociceptive nerve fibers. It is released from interneurons , enkephalin neurons with short axons. The enkephalins are stored in nerve-ending vesicles found in the substantia gelatinosa (SG)
and in several areas of the brain. When released, enkephalin may bind to presynaptic or postsynaptic membranes. 4
Norepinephrine is released by the depolarization of some neurons and binds to the postsynaptic mem-branes. Norepinephrine is found in several areas of
CHAPTER 3 Managing Pain with Therapeutic Modalities 43 located at strategic sites, called binding sites, to receive these compounds. β-endorphin and dynor-phin have potent analgesic effects. These are released within the central nervous system by mechanisms that are not fully understood at this time.
Nociception
A nociceptor is a peripheral pain receptor. Its cell body is in the dorsal root ganglion near the spinal cord. Pain is initiated when there is injury to a cell causing a release of three chemicals, substance P , prostaglandin , and leukotrienes , which sensitize the nociceptors in and around the area of injury by lowering their depolarization threshold. This is re-ferred to as primary hyperalgesia , in which the nerve’s threshold to noxious stimuli is lowered, thus enhancing the pain response. Over a period of several hours secondary hyperalgesia occurs, as chemicals spread throughout the surrounding tis-sues, increasing the size of the painful area and cre-ating hypersensitivity.
Nociceptors initiate the electrical impulses along two afferent fibers toward the spinal cord.
Aδ and C fibers transmit sensations of pain and temperature from peripheral nociceptors. The majority of the fibers are C fibers. Aδ fibers have larger diameters and faster conduction velocities.
This difference results in two qualitatively differ-ent types of pain, termed acute and chronic. 4 Acute pain is rapidly transmitted over the larger, faster-conducting Aδ afferent neurons and originates from receptors located in the skin. 4 Acute pain is localized and short, lasting only as long as there is a stimulus, such as the initial pain of an unex-pected pinprick. Chronic pain is transmitted by the C fiber afferent neurons and originates from both superficial skin tissue and deeper ligament and muscle tissue. This pain is an aching, throbbing, or burning sensation that is poorly localized and less specifically related to the stimulus. There is a delay in the perception of pain following injury, but the pain will continue long after the noxious stimulus is removed.
the nervous system, including a tract that descends from the pons, which inhibits synaptic transmission between first-order and second-order nociceptive fibers, thus decreasing pain sensation. 22
Other endogenous opioids may be active anal-gesic agents. These neuroactive peptides are released into the central nervous system and have an action similar to that of morphine, an opiate analgesic. There are specific opiate receptors
endogenous opioids Opiate-like neuroactive peptide substances made by the body.
interneurons Neurons contained entirely in the central nervous system. They have no projections out-side the spinal cord. Their function is to serve as relay stations within the central nervous system.
substantia gelatinosa (SG) The dorsal horn of the grey matter thought to be the mechanism responsible for closing the gate to painful stimuli.
m
Figure 3–5 Synaptic transmission.
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The various types of afferent fibers follow dif-ferent courses as they ascend toward the brain.
Some Aδ and most C afferent neurons enter the spinal cord through the dorsal horn of the spinal cord and synapse in the substantia gelatinosa with a second-order neuron ( Figure 3–6 ). 22 Most noci-ceptive second-order neurons ascend to higher centers along one of three tracts—(1) the lateral spinothalamic tract, (2) spinoreticular tract, or (3) spinoencephalic tract—with the remainder ascending along the spinocervical tract. 22 About 80% of nociceptive second-order neurons ascend to higher centers along the lateral spinothalamic tract. 22 Approximately 90% of the second-order
afferents terminate in the thalamus. 22 Third-order neurons project to the sensory cortex and numer-ous other centers in the central nervnumer-ous system (see Figure 3–6).
These projections allow us to perceive pain.
They also permit the integration of past experiences and emotions that form our response to the pain experience. These connections are also believed to be parts of complex circuits that the athletic trainer may stimulate to manage pain. Most analgesic physical agents are believed to slow or block the impulses ascending along the Aδ and C afferent neuron pathways through direct input into the dor-sal horn or through descending mechanisms. These pathways are discussed in more detail in the follow-ing section.