Neurons with input from joint and muscle are located in the superficial and deep dorsal horn. This distribution matches the spinal termination of joint and muscle afferents which project to the superficial dorsal horn and, in particular Aß- and A8-fibers, to the deep dorsal horn.7,12 Neurons with nociceptive information from joint12,79 80 and muscle81,82,83,84 are either exclusively driven by input from deep tissue, or they exhibit convergent inputs from skin and deep structures. Neurons exclusively driven from deep tissue are excited by pressure applied to the deep tissue, but not by mechanical stimulation of the overlying skin. Their receptive fields are not restricted to a specific structure such as only a joint or a muscle belly. Rather they include a joint and adjacent muscles. Many of these neurons are high-threshold and require noxious pressure onto joint and/or muscle to be activated. Neurons with joint input may be activated by noxious movements, such as twisting of the joint against resistance of the tissue, like the articular nociceptors. The remaining neurons are wide dynamic range neurons which respond with increasing frequency when stimulus intensity is increased from the innocuous to the noxious range. Neurons with convergent inputs from deep tissue and skin are excited by mechanical stimuli applied to deep tissue (muscle, tendons, joint structures) and by mechanical stimulation of the skin. Often receptive fields in the deep tissue are located more rostral than cutaneous receptive fields thus allowing determination of both receptive fields. Most of these neurons are wide dynamic range neurons which respond to innocuous and noxious pressure onto deep tissue in a graded fashion. They may be activated by movements in the working range, but show much stronger responses to painful movements.
Neurons with input from joint and muscle project to different supraspinal sites (cerebellum, spinocervical nucleus, thalamus, reticular formation) subserving the generation of the conscious pain response and adaptations to pain (see Figure 2.1), or they project to intraspinal (segmental) interneurons and motoneurons.7,12 Spinal and supraspinal motor reflexes regulate movements and exert protective functions including flexor reflexes upon nociceptive stimulation.1 Noxious stimulation of joint afferents12, 85 and muscle afferents7, 8 can evoke nocicep-
tive withdrawal reflexes. During acute chemical stimulation of the knee and electrical stimulation of muscle nerves86 and during inflammation in the joint,85, 87 spinal motor reflexes are enhanced. In line with this, it has been thought that noxious stimulation of the muscle causes reflex muscle spasms and that muscle spasms will enhance the pain in the muscle - thus establishing a vicious circle. However, during myositis, a decrease rather than an increase of the reflex activation of motoneurons was observed,8 and during experimental joint inflammation some g-motoneurons developed progressive inhibition rather than facilitation.87 Thus, the reflex pattern is modified during inflammation. Patients with painful muscles exhibit low rather than enhanced EMG activity8 indicating that prolonged nociceptive stimulation actually induces a reduction of motor reflexes, followed by atrophy and loss of force.8,12 However, muscle spasms may be elicited from painful trigger points in adjacent muscles, and by articular dysfunction and ligamentous strain.8
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