Fusimotor Function

Abstract

Spinal shock was defined by Franz 1 as the "state of depression of spinal reflexes (hyporeflexia), generally transient in character, which occurs after transection in the bodily segments caudal to the lesion." Of several hypotheses,2,3 the most widely accepted is that of Sherrington: "Reflex depression is due to the sudden withdrawal of a continuous excitation (facilitation) which normally occurs from suprasegmental levels."4 Sherrington and Fulton observed that in monkeys spinal shock and the subsequent permanent disability are more severe and much longer lasting than in cats and dogs.5,6In man it is well known that shock is even more severe and lasts longer than in monkey.Yet neither the intrinsic mechanism of the phenomenon nor its species variations are well understood.Out of recent knowledge of the fusimotor (gamma efferent) system which functions to regulate the sensitivity of muscle stretch receptors, the idea has developed that the system is specifically disturbed in pathological states. C. C. Hunt T demonstrated that the proprioceptive (monosynaptic) stretch re¬ flex can be enhanced by stimulation of effer-ent fusimotor axons going to the spindles of the same muscle. Conversely Matthews and Rushworth 8 showed that the stretch reflex is abolished during selective block of fusi¬ motor fibers by a local anesthetic.The proposal has been made that volun¬ tary reinforcement of tendon jerks in man (Jendrassik maneuver) results from in¬ creased fusimotor activity.9·10 Others have speculated that disorders of movement, such as those of cerebellar disease, spasticity and parkinsonian rigidity and tremor, may arise out of disturbances in fusimotor tone.11"19It is a paradox of human spinal shock that the polysynaptic flexion reflex recovers ear¬ lier than the monosynaptic stretch reflex.20 This finding suggests that central synaptic transmission is not wholly depressed and that the stretch receptor path may be blocked peripherally rather than centrally. Thus the rise in stretch receptor threshold could be due to decreased tonic fusimotor activation.This series of papers seeks answers to these questions. It includes the results of examinations of the state of fusimotor tone associated with spinal shock in the cat, mon¬ key, and man, and that associated with chronic spasticity in the monkey. In the ani¬ mal studies the afferent volley in a muscle nerve activated by a constant brief stretch stimulus is used as an integrated measure of the muscle stretch receptor excitability. Since receptor sensitivity under constant load is a function of the level of activity in the spindle efferents, fusimotor tone can be measured indirectly.

Recovery of neuronal and network excitability after spinal cord injury and implications for spasticity

“…For example, there is a slight hyperpolarization (2–6 mV) of the resting membrane potential in cat (Cope et al, 1980; Schadt and Barnes, 1980) and rat motoneurons (Li et al, 2007), which may explain why antidromic activation of human motoneurons, as measured by F-waves, is difficult acutely after SCI (Ashby et al, 1974). In contrast, H-reflexes, but not tendon tap reflexes, recover during spinal shock, as shown in both the cat (Hunt et al, 1963; Zapata, 1966) and human (Weaver et al, 1963; Hiersemenzel et al, 2000). This suggests that fusimotor drive is also reduced acutely after SCI given that tendon taps rely on muscle spindle excitability whereas H-reflexes do not.…”

“…The duration and severity of spinal shock differs between species, lasting only minutes to hours in the frog (Hall, 1850), cat (Sherrington, 1899; Hunt et al, 1963; Chambers et al, 1966) and dog (Sherrington, 1899; Fulton and Sherrington, 1932) but up to 2 weeks in the monkey (Sherrington, 1899; Fulton and Sherrington, 1932; Hunt et al, 1963; McCouch et al, 1966), rat (Bennett et al, 1999) and several weeks in humans (Ko et al, 1999). In humans, all reflexes are absent only for the first 24 h after SCI (Phase 1) (Ditunno et al, 2004), which coincides with the first 2 weeks of areflexia in the rat tail model of SCI (Bennett et al, 1999).…”