Outline the major afferent pain pathways.
Somatic pain is produced by activation of pain recep-tors in the periphery. There are two principal cutaneous nociceptors: high-threshold mechanoreceptors (HTMs) and polymodal nociceptors (PMNs). The HTMs respond to mechanical stimuli and have a receptive field of 1 cm2. PMNs respond to mechanical, thermal, and chemical irritants. HTM axons conduct via myelinated A delta fibers at a rate of 5‚Äď25 m/sec and transmit sharp pain with a rapid onset. PMN axons conduct via unmyelinated C fibers at a rate of less than 2 m/sec and convey dull aching pain with a slow onset (Figure 72.1). Pain from visceral origins is carried away from the organs by myelinated visceral B fibers.
These nerves enter the dorsal horn of the spinal cord and terminate in different laminae, which were designated histologically by Rexed. A delta and C fibers synapse with wide dynamic range neurons (activated by tactile or noxious stimuli) in lamina V and nociceptive-specific neurons in lamina I. Both types of fibers send branches into the substantia gelatinosa (laminae II and III), whose inhibitor interneurons modulate perceived nociception.
The axons of the neurons originating in laminae V and I cross over to the opposite ventrolateral funiculus of the spinal cord and ascend as the lateral spinothalamic tract. Some axons terminate in the ventropostero-lateral nucleus of the thalamus (neospinothalamic tract), where they synapse with neurons that project to the somatosensory cortex. These neurons are associated with discrimination (location, duration, and intensity) of pain. Other axons project to the medial thalamic nuclei as well as the medulla, pons, midbrain, and hypothalamus (paleo-spinothalamic tract) and are associated with emotional aspects of pain.