Fusimotor Function

Abstract

The depression of neural activity which takes place in the distal spinal cord abruptly separated from rostral control is the classical model for interpreting the transient disturbances of neural function that follow acute lesions of the nervous system. The behavior of isolated spinal cord has been relatively easy to analyze because its afferent and efferent pathways are so accessible.Modern neurological thinking is firmly based upon the observations of spinal cord behavior made in animals by Sherrington and in man by many clinicians of his generation. The riddle of spinal shock and the even more puzzling recovery to a hyperactive state which evolves out of it are little nearer solution now than when originally described. The most widely accepted explanation of shock is that the cord's internuncial pool and final common path are depressed below normal levels of excitability by the sudden transection of descending, largely excitatory pathways.1 Some recent observations in man 2 show that the monosynaptic stretch reflex recovers earlier in the more caudal spinal segments. From this it was inferred that rostrad recovery from spinal shock may ex¬ plain the evolution from the early flexor plantar reflex seen immediately after cord section to the extensor response of the chronic state.A paradox noted in that study and docu¬ mented much earlier is that the polysynaptic plantar (flexion) reflex may be evident im¬ mediately after cord section, when the monoor oligosynaptic segmental stretch reflex of

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.…”

Revisit Spinal Shock: Pattern of Reflex Evolution during Spinal Shock

“…The loss of tone and depression of the reflexes may be the result of a disturbance of the fusiform, γ-efferent, system that regulates the sensitivity of the muscle stretch receptors. 45) Gamma-motoneurons that regulate muscle spindle tension may potentially be fired to maintain background excitability in muscle spindles. Gamma-motoneurons may lose tonic descending facilitation distal to the level of spinal cord injury, resulting in decreased muscle spindle excitability and decreased segmental input to motoneurons by stretch reflex afferents.…”

“…The disturbance of fusiform function is caused by the loss of normal spinal cord activity, which depends on continuous tonic discharges from higher centers, including the tone discharge transmitted through the vestibulospinal and reticulospinal tracts. 45) …”

Developing a predictive model for spinal shock in dogs with spinal cord injury

“…The condition is thought to be caused by acute injury‐associated interruption in descending, primary faciliatory, motor tracts and transient localized changes in the reflex centers of the spinal cord. 3 , 5 , 6 , 7 , 8 , 9 , 10 , 11 , 12 , 13 , 14 , 15 , 16 , 17 , 18 , 19 , 20 , 21 , 22 , 23 , 24 , 25 , 26 , 27 , 28 , 29 , 30 , 31 , 32 , 33 , 34 , 35 , 36 , 37 , 38 , 39 , 40 , 41 , 42 , 43 , 44 , 45 , 46 , 47 , 48 , 49 , 50 , 51 , 52 Currently, prioritization of spinal shock over other causes of reduced pelvic limb reflexes and other lower motor neuron signs is solely based on the clinician's intuition and is highly influenced by training and experience. Specifically, the clinical presentation of spinal shock can lead to clinical confusion in dogs with T3‐L3 myelopathies, and might cause the clinicia...…”

“…For dogs with a T3‐L3 myelopathy, this presents as transiently reduced segmental spinal reflexes in the pelvic limbs, giving a false appearance of a lower motor neuron lesion. The condition is thought to be caused by acute injury‐associated interruption in descending, primary faciliatory, motor tracts and transient localized changes in the reflex centers of the spinal cord 3,5‐52 . Currently, prioritization of spinal shock over other causes of reduced pelvic limb reflexes and other lower motor neuron signs is solely based on the clinician's intuition and is highly influenced by training and experience.…”