Spinal Reflexes

Many theories of physical therapy focus on the use of brain stem and spinal reflexes as a way to retrain voluntary movement and affect hy-potonicity and hypertonicity. Tonic and phasic stimuli can modify the excitability of spinal motor pools, postural reflexes, and muscle cocontractions.

The response to muscle stretch during passive movement, postural adjustment, and voluntary movement is not inflexible. Moment to moment adjustments in reflexes have been partly accounted for by a variety of mecha-nisms.149,150 They include:

1. The mechanical, viscoelastic properties of muscle that vary in part with changes in actinomysin cross-bridges and alterations in connective tissues

2. Peripheral sensory receptors that respond to a perturbation from primary and secondary muscle spindles and Golgi tendon organs, but are regulated over a wide range of responsiveness by central commands

3. The convergence of segmental and descending inputs on Renshaw cells and motoneurons and interneurons that can summate in many ways, so that excitation of one peripheral receptor will not always produce the same stereotyped reflex response

4. Joint and cutaneous flexor reflex afferents that are activated during limb movements and vary in the degree to which they set the excitability of interneurons

5. Presynaptic inhibition of afferent propri-oceptive inputs to the cord that are constantly affected by the types of afferents stimulated, as well as by descending influences

6. Long-latency responses to muscle contraction that supplement the short-latency, segmental monosynaptic component of the stretch reflex to compensate especially for a large change in mechanical load

7. The variety of sources of synaptic contacts on alpha-motoneurons, along with the intrinsic membrane properties that affect their excitability and pattern of recruitment of muscle fibers

Wolpaw and colleagues demonstrated activity-driven plasticity within the spinal stretch reflex, revealing that even the neurons of a seemingly simple reflex can learn when trained. The investigators operantly conditioned the H-reflex in monkeys to increase or decrease in amplitude.151 An 8% change began within 6 hours of conditioning and then gradually changed by 1% to 2% per day. This modulation of the amplitude of the H-reflex required 3000 trials daily. The alteration persisted for several days after a low thoracic spinal transection, which suggests that the spinal circuitry for the H-reflex below the transection had learned and held a memory trace. A long-term change in presynaptic inhibition mediated by the Ia terminal presumably mediated this learning. Subsequent studies revealed that operant conditioning depends on corticospinal input, but not on other descending tracts.152 In addition, cerebellar output to the cortex contributes to the corticospinal influence.

Using electromyographic biofeedback, the stretch reflex of the human biceps brachii muscle was successfully conditioned to increase or decrease in amplitude, but also required considerable training, approximately 400 trials per session.153 Evidence for the effects of physical activity and training on the strength of spinal reflexes has also been found in active compared to sedentary people. The H-reflex and disynap-tic reciprocal inhibition responses were small in sedentary subjects, larger in moderately active subjects, and largest in very active ones.154 The reflexes were lowest, however, in professional ballerinas. The greater need for corticospinal input to the cord to stand en pointe and the sustained cocontractions involving the gastrocne-mius and soleus complex probably lead to a decrease in synaptic transmission at Ia synapses, reducing the reflex amplitude. Thus, activity-dependent plasticity in the spinal motor pools contributes to the long-term acquisition of motor skills. Short-term, task-specific modulation of the gain of the H-reflex also occurs. The stretch reflex in leg extensor muscles is high during standing, low during walking, and lower during running.155 A higher gain with standing provides greater postural stability. The gain also changes with the phases of the step cycle.

Thus, coupled spinal input and output activity can be trained, although training takes considerable and specific forms of practice. This adaptive plasticity may be of value in developing therapies to reduce spasticity and abnormal spinal reflex activity and, more importantly, to modulate the recovery of standing and walking in hemiparetic and paraparetic patients. Sensory inputs drive this plasticity.

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