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

Abstract

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.

Noninvasive assessment of the injured human spinal cord by means of functional magnetic resonance imaging

“…It is already established that there is activity in the spinal cord caudal to an injury as evidenced by leg spasms that are known to involve motor reflex arcs through the spinal cord. [26][27][28] However, we have now observed the level and extent of activity in the spinal cord, and the activity related to sensory input, even when the subject has no awareness of the sensation. This information provides a more complete clinical picture of the condition of the injured spinal cord, beyond what can be obtained from the ASIA assessment scale.…”

Neuromuscular Abnormalities Associated With Spasticity of Upper Extremity Muscles in Hemiparetic Stroke

“…6B). This could, in turn, result in increased discharge of the group III/IV muscle afferents, which have potent inhibitory effects on reflex stiffness (Schmit et al 2002). In contrast, the intrinsic stiffness of the elbow showed a relatively smaller increase as the elbow was extended over the range of motion, so that the tension in elbow flexors of spastic elbow did not reach comparable levels.…”

Reflex responses to combined hip and knee motion in human chronic spinal cord injury

“…Another potential trigger for the extensor spasms observed in the current study is a reflex chain in which imposed hip and knee extension produce stretch reflex activation of the hip and knee flexors during the movement [19][20], which, in turn, produces a flexor reflex response [21][22] that then activates the neural circuitry associated with extensor spasms. However, extensor spasms are considerably reduced when the hip or knee is flexed, suggesting stretch-related afferents from hip or knee flexors may not readily account for the observed multijoint reflexes.…”