Background: Spasticity is defined/assessed in resting limbs, where increased stretch reflex activity and mechanical joint resistance are evident. Treatment with antispastic agents assumes that these features contribute to the movement disorder, although it is unclear whether they persist during voluntary contraction. Objectives: To compare reflex amplitude and joint resistance in spastic and normal limbs over an equivalent range of background contraction. Methods: Thirteen normal and eight hemiparetic subjects with mild/moderate spasticity and without significant contracture were studied. Reflex and passive joint resistance were compared at rest and during six small increments of biceps voluntary contraction, up to 15% of normal maximum. A novel approach was used to match contraction levels between groups. Results: Reflex amplitude and joint mechanical resistance were linearly related to contraction in both groups. The slopes of these relations were not above normal in the spastic subjects on linear regression. Thus, reflex amplitude and joint resistance were not different between groups over a comparable range of contraction levels. Spastic subjects exhibited a smaller range of reflex modulation than normals because of decreased maximal contraction levels (weakness) and significant increases of resting contraction levels. Conclusions: Spasticity was most evident at rest because subjects could not reduce background contraction to normal. When background contractions were matched to normal levels, no evidence of exaggerated reflex activity or mechanical resistance was found. Instead, reduced capacity to modulate reflex activity dynamically over the normal range may contribute to the movement disorder. This finding does not support the routine use of antispastic agents to treat the movement disorder.

Khan SI, Burne JA. Reflex inhibition of normal cramp following electrical stimulation of the muscle tendon.

No abstract

The clinical utility of electrophysiological and biomechanical methods of swallowing assessment was demonstrated. Levodopa tended to normalize the timing of the combined swallow response but not the activity of individual muscles.

Electrical stimulation over selected muscle tendons in alert human subjects produced, in each muscle, a reflex inhibition of muscle activity. This inhibition, when maximal, was seen in the surface EMG as an interval of complete electrical silence during a sustained voluntary contraction. The inhibition was clearly visible in single sweeps and in averaged records. Its onset latency and duration were respectively, 56 +/- 4.9 and 46 +/- 11.8 ms in extensor digitorum communis, 71 +/- 6.1 and 46 +/- 10.5 ms in extensor pollicis brevis, 77 +/- 11.2 and 47 +/- 10.5 ms in extensor pollicis longus, 72 +/- 7.3 and 43 +/- 8.6 ms in abductor digiti minimi, and 97 +/- 3.5 and 43 +/- 2.8 ms in tibialis anterior. The inhibitory response was produced at low stimulus intensities (< 10 mA) without electrical (M wave) or mechanical (muscle twitch) signs of direct muscle stimulation. It therefore did not arise from stimulation of la afferents (muscle spindles). The response arose from tendons since it occurred at lowest threshold when stimulation was applied directly over the tendons of the five different muscles studied. At low stimulus intensities, the response declined sharply when the stimulating electrodes were moved to the skin immediately adjacent to the tendons. The response did not arise from skin afferents since it was also presented when stimuli were delivered to the tendon by subcutaneous needle electrodes and it was not reproduced by stimulation of cutaneous nerves in the region of the tendon. In another series of experiments on extensor pollicis brevis, five skin locations were stimulated while overlying the tendon and again while the skin was stretched so that they were lying 0.6-0.8 cm dorsal to the tendon. In these experiments the response was again greatly attenuated when the stimulation was not directly over the tendon, although the same cutaneous sites were stimulated. The inhibition was followed by a pronounced excitatory component (E1) of peak latency 120-140 ms. The results of the study provide evidence for a powerful autogenic inhibitory reflex in man. The evidence is consistent with the possibility that the response arises from Golgi tendon organ afferents.