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Brian D Schmit

Publications and source records attributed to Brian D Schmit.

20 records · Page 2Linked to original sources

Afferent mechanisms for the reflex response to imposed ankle movement in chronic spinal cord injury.

We have reported earlier that externally imposed ankle movements trigger ankle and hip flexion reflexes in individuals with spinal cord injury (SCI). In order to examine the afferent mechanisms underlying these movement-triggered reflexes, controlled ankle movements were imposed in 17 SCI subjects. In 13 of these subjects, reflex torques were recorded at the hip, knee and ankle in response to 5 ankle movement ranges, and 4 movement speeds. Subjects were tested using both ankle plantarflexion and dorsiflexion movements. The principal outcome measure, peak hip flexion torque of the induced reflexes, was used for comparing the effects of movement range and speed on the reflex response. We found that movement-triggered reflexes were sensitive to the angular range of ankle deflection, but insensitive to the velocity of the movement. Movement amplitudes sufficient to trigger hip and ankle flexion were routinely associated with increases in ankle passive force, suggesting that force-sensitive receptors participated in the reflex response. However, increases in angular range also corresponded to increases in muscle length, making it difficult to distinguish whether the response was triggered by a load-sensitive receptor (e.g., Golgi tendon organ or muscle free nerve ending) or a position-sensitive receptor responsive to absolute ankle angle (e.g., muscle spindle secondary afferent). The absence of velocity dependence of the reflex suggested that spindle Ia afferents were not major contributors. These results suggest movement-triggered reflexes originate in muscle receptors that are sensitive to either absolute muscle length, to muscle force or to both. Although receptors that are sensitive to absolute muscle length cannot be excluded with certainty, the finding that reflex responses require that ankle movements elicit an increase in passive force argues for a prominent role of nonspindle mechanoreceptors, such as group III/IV muscle afferents. These afferents are activated preferentially as muscles are stretched to near maximum length, and they appear to have potent reflex effects in spinal cord injury.

Adolescent↗

Reflex mechanisms for motor impairment in spinal cord injury.

Spasticity is common feature of human spinal cord injury. It contributes to motor impairment and it also promotes joint deformity in patients who have sustained such injury. The classical definition of spasticity highlights the increased resistance of a joint to externally imposed motion. This resistance is attributable largely to changes in stretch reflex excitability, and it is manifested primarily in those muscles being stretched by the motion. Under this definition, there would be little activity in muscles crossing other joints. In spinal cord injury, however, muscles innervated from distal spinal segments often exhibit little hypertonia, yet patients report the occurrence of disabling spasms. These spasms appear as coordinated patterns of muscle activation throughout the limb, involving either limb flexors or extensors. These patterns are therefore quite different from those of classical spasticity. The receptor origins and neural pathways responsible for the spasms in spinal cord injury will be addressed.

Electric Stimulation↗