Afferent nerve fibers
The peripheral nervous system consists in part of Aβ, Aδ, and C fibers. These peripheral nerve fibers have a large degree of functional overlap, providing continuous sensation (Muir 2002). The Aβ fibers are large-diameter low-threshold fibers that are primarily nonnociceptive (do not transmit pain stimuli) transmitting nonpainful sensations such as touch, vibration and pressure. The Aδ and C fibers are small-diameter high-threshold free nerve endings that end in the skin. Their nociceptors are involved in the transduction of pain signals. These fibers carry nerve impulses to the dorsal horn when the nociceptor threshold (minimum stimulus required to elicit a transmittable electrical signal) is exceeded. The dorsal horn contains a gating mechanism that determines whether a pain stimulus is transmitted to the CNS. Whether the “gate” is open or closed depends in part on the balance of input from the Aβ and Aδ/C fiber groups.
Sources: Muir 2002 ; Thurmon and Tranquilli 1996
The Aβ fibers inhibit the input from Aδ and C fibers by closing the gate. This can explain why massaging and applying pressure, heat, or cold to a painful area can decrease the perception of pain.
The Aδ fibers are small-diameter, lightly myelinated, high-threshold “fast fibers.” They signal first pain in response to an acute stimulus and are responsible for the sharp pricking sensation. They enable the animal to localize pain to the site of the stimulus. They cease after sensation is discontinued. Polymodal Aδ fibers respond to mechanical, chemical, and thermal stimuli. Other Aδ fibers respond only to specific stimuli, such as cold temperature or pressure.
C fibers are small, unmyelinated, mostly high-threshold nerves with polymodal neurons that are responsible for slow pain or chronic pain. Slow pain has a burning, aching sensation, which indicates inflamed, damaged tissue. C fibers are abundant in the skin, skeletal muscle, joints, and viscera. Visceral nociception activity is primarily mediated by C fibers (Thurmon and Tranquilli 1996) (Table 32.1).
Silent nociceptors are Aδ and C fibers that are activated by tissue inflammation. Tissue damage and inflammation intensify the sensation of pain (activate silent receptors), producing hyperalgesia, allodynia, and hyperesthesia (Muir 2002).
Anatomy of the spinal cord dorsal horn
Interneurons are neurons that convey impulses from one neuron to another. They are typically inhibitory but can also be excitatory depending on which neurotransmitter is released. They serve as relays and participate in local processing. The dorsal horn is a collection of interneurons grouped into layers or laminae I to VI in the spinal cord. These laminae extend the full length of the spinal cord (Muir 2002). Nociceptive afferent fibers terminate on neurons within the dorsal horn of the spinal cord. Initial integration and modulation of nociceptive input occurs in the dorsal horn.
Most Aδ fibers terminate in the most superficial layer of lamina I, with a few projecting more deeply to lamina V. Lamina I is an important sensory relay junction for temperature and pain. Aδ and C fibers from the skin, skeletal muscle, joints, and viscera are responsible for most of the input. Nociceptive-specific neurons and projection neurons are contained within lamina I. Wide dynamic range (WDR) neurons are contained within laminae I, II, and V (Muir 2002).
It is thought that lamina II is important in the processing and modulating of nociceptive input from skin nociceptors due to its abundance of WDR neurons, which are mostly interneurons. It is also believed to be a major site of action for opioids (Morgan et al. 2002). In addition, lamina II is the end point for many C fibers (Fig. 32.2).
Laminae III and IV receive mostly nonnociceptive sensory input (Morgan et al. 2002). Lamina III combines descending information from the brain with sensory input (Muir 2002). Lamina V is where most visceral sensory fibers terminate, but lamina I may also be a termination point for these fibers. Sensory inputs received by wide dynamic range neurons (WDR) respond to both noxious and nonnoxious stimulus as well as pain sensations from visceral and somatic receptors. This unique quality can manifest clinically as referred pain (Hellyer et al. 2007 ; Morgan et al. 2002).
Second-order multireceptive neurons, WDR neurons have larger receptive fields than nociceptive-specific neurons. They respond to both noxious and nonnoxious stimuli (Hellyer et al. 2007) and receive afferent input from Aβ, Aδ, and C Fibers. WDR neurons are found throughout the dorsal horn; they are the most abundant in lamina V (Morgan et al. 2002). WDR neurons are also believed to be important in the occurrence of windup pain. C fibers are most likely the primary neuron facilitating windup pain, which occurs due to rapid and continuous firing of these fibers. It is important to recognize that general anesthesia does not prevent windup pain. Therefore preemptive analgesia becomes important and necessary for surgeries (i.e., orthopedic) likely to activate C fibers (Hellyer et al. 2007).