Internuncial Pool

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More complex reflexes use even more of these inhibitory interneurons, sometimes referred to as the internuncial pool. One of these inhibitory interneurons with a special action was described by Birdsie Renshaw and is known by his name. U The Renshaw cell receives a recurrent collateral, i.e., a branch of the axon of the alpha motor neuron before it leaves the ventral horn (...Fig, 15-11 ). The axons of the Renshaw cells contact the alpha motor neuron. An action potential down the axon of the alpha motor neuron also excites the Renshaw cell through the recurrent collateral. The Renshaw cell in turn inhibits the same alpha motor neuron and other alpha motor neurons that innervate agonists. The Renshaw cell also inhibits the inhibitory interneuron mediating the reciprocal inhibition. In this way, the Renshaw cell shortens the reflex contraction of

Figure 15-10 (Figure Not Available) Reciprocal inhibition. When the agonist muscle is activated by the monosynaptic phasic stretch reflex, a branch from the 1a afferent of the muscle spindle, also excites interneurons that inhibit the antagonist motor neurons causing relaxation of the opposing antagonist muscleFrom Gardner E: Fundamentals of Neurology. Philadelphia, W. B. Saunders, 1968.)

Figure 15-11 The internuncial pool of inhibitory interneurons. White cells and synapses are excitatory; the black cells are inhibitory. 1 and 2 are anterior horn cells; 3 is the Renshaw cell; 4, 5, and 6 are interneurons. Note the spinal and supraspinal inputs to the inhibitory interneurons. Note also the recurrent collateral from the alpha motor neuron contacting the Renshaw cell, which in turn makes contact with the anterior horn cell and sends a recurrent collateral to inhibit the inhibitory interneuron mediating reciprocal inhibition.(From Curtis BA, Jacobson S, Marcus EM: Introduction to the Neurosciences. Philadelphia, W. B. Saunders, 1972.)

the agonist and, at the same time, shortens the reciprocal inhibition of the antagonist. Through this mechanism, the motor neurons can inhibit their own activity. This seems to be important in preventing alpha motor neurons from sending long trains of action potentials in response to a brief stimulus. The Renshaw cell and other internuncial neurons receive input from the higher motor centers, which can modulate the activity of these neurons and fine-tune the reflex movements. This means that the spinal reflexes provide the nervous system with elementary and automatic motor patterns that can be activated either by sensory stimuli or by descending signals from higher motor centers. Supraspinal input can therefore modify or suppress the expression of the reflex through the internuncial pool of inhibitory interneurons.

Clearly, most spinal reflexes are mediated by polysynaptic circuits that allow the reflex to be modified and the movement to be more finely coordinated. The most important of the polysynaptic spinal reflexes is the flexor reflex (Fig. 15-12 (Figure Not Available) ). It is stimulated by a noxious cutaneous stimulus to the leg. The response is a withdrawal of the leg from the source of the painful stimulus. Teleologically, this reflex is important in preventing injury to the foot from stepping on a sharp or hot object. As with other reflexes, the strength of the response corresponds to the strength of the stimulus. In a normal individual only a painful stimulus elicits the reflex. When descending motor pathways that suppress and modulate the reflex are damaged, a lighter, nonpainful stimulus may elicit the reflex. This was discovered by Babinski when he scratched the sole of the foot of a patient with central nervous system lesions. With the light nonpainful stimulus, the strength of the response parallels the extent to which the upper motor

Figure 15-12 (Figure Not Available) The polysynaptic flexor reflex. The impulses from a cutaneous receptor excite the alpha motor neuron to the effector muscles through an intermediate neuron. Additional impulses also reach the cerebral hemisphere by way of an ascending tract.(From Gardner E: Fundamentals of Neurology. Philadelphia, W. B. Saunders, 1968.)

neuron lesion has allowed upregulation of the reflex. In a patient with a small hemispheral lesion, only a small fragment of the reflex may be elicited, i.e., extension of the great toe, known as the Babinski sign (Fig. 15-13 (Figure Not Available) ). With complete transection of the spinal cord, the entire withdrawal reflex with flexion at the hip, knee, and ankle may occur.

The sensory limb of this reflex arc is mediated by cutaneous receptors of fast-conducting 1a afferents that converge on the internuncial pool of inhibitory interneurons. While the motor neurons to the flexor muscles are excited, the extensor muscles are inhibited through reciprocal inhibition. At the same time, motor neurons to the extensors of the contralateral leg are activated and the flexors are relaxed to compensate for the shift of weight to the contralateral leg while the ipsilateral leg is withdrawn from the painful stimulus. This crossed extensor reflex maintains postural support during withdrawal from a painful stimulus.

One can readily appreciate that the spinal circuits responsible for flexion withdrawal and crossed extension do more than mediate protective reflexes. They also serve to coordinate limb movements and voluntary movements. The

Figure 15-13 (Figure Not Available) Babinski signTop, The normal adult response to stimulation of the lateral plantar surface of the fcBoffom, The normal infant and abnormal adult response(From Gardner E: Fundamentals of Neurology. Philadelphia, W. B.

Saunders, 1968.)

interneurons in these pathways receive conversion inputs from different types of afferent fibers, not just pain fibers, as well as from descending pathways. Therefore, this convergence combines inputs from many different sensory sources including commands for voluntary movement through the descending pathway. This integration of sensory input is necessary for the regulation of precise movements because voluntary movements also produce excitation of cutaneous and joint receptors as well as muscle receptors.

Another cutaneous reflex of clinical significance is the superficial abdominal reflex ( .Fig 15-14 ). This reflex is elicited by stroking the skin of the abdomen, which causes a reflex contraction of the abdominal muscles beneath the stimulus. Thus, stroking the upper abdomen causes contraction of the upper abdominal muscles, whereas stimulation of the lower abdomen causes contraction of the lower abdominal muscles. This relationship between the location of the stimulus and the muscles that contract is called a local sign. Other examples are contraction of the cremasteric muscles of the scrotum in response to stroking the skin of the inner thigh and the reflex contraction of the external anal sphincter when the perianal skin is stroked.

The normal function of the short-latency phasic stretch reflex is hard to define. In a fully relaxed individual who can exert total voluntary control over the excitability of the motor neurons, the stretch reflex does not appear to contribute to muscle tone. However, when these descending influences are interrupted, the excitability of the motor neurons involved in the stretch reflex is enhanced. This can be seen in the alteration of muscle tone called spasticity.

The pathophysiology of spasticity may involve several mechanisms. Hyperexcitability of the alpha motor neurons

Figure 15-14 The superficial abdominal reflex. The examiner strokes the skin with a stick as diagrammed. Stroking the upper quadrant tests thoracic segments 7 to 9 and the lower quadrants for T10-12.

from a primary intrinsic change in membrane properties may account for certain elements of spasticity, but most of the changes in lower motor neuron function are thought to be secondary to alterations in suprasegmental synaptic input. With regard to the 1a afferent pool, there are several types of suprasegmental inhibition that may be altered in spasticity. Presynaptic inhibition mediated by axo-axonic synapses on 1a terminals is reduced by suprasegmental disease, causing normal stimuli to 1a afferents to induce an exaggerated response. In addition, the 1a system on paired flexor and extensor muscles normally functions in a coordinated fashion to reduce the likelihood that antagonistic muscle groups will be co-activated during a muscle contraction. In the condition of spasticity, this type of 1a inhibition is lost, resulting in inefficient co-contractions that can compromise motor function. In addition, 1a inhibitory interneurons are also affected by descending excitatory pathways, and when these latter paths are damaged, the interneurons from flexors to extensors and from extensors to flexors are affected differently. In addition to the changes in the 1a system, nonreciprocal 1b inhibition is also reduced or even replaced by facilitation in spastic patients, suggesting that important physiological alterations occur in this system as well. In fundamental contrast to all of these mechanisms, recurrent inhibition via Renshaw cell activity is actually increased in patients with spinal cord lesions and spastic paresis. The specific descending pathways of influence are discussed subsequently.

In addition to the short-latency monosynaptic stretch reflex, a second reflex contraction of muscle occurs at a longer latency. This long-latency stretch reflex (sometimes referred to as the long-loop stretch reflex) is mediated by a polysynaptic reflex pathway and has different properties from the short-latency monosynaptic stretch reflex.y The strength of the long-latency reflex depends on whether the muscle is relaxed or active at the time of stretching and whether the subject is instructed to resist the stretch or to let go. The strength of the reflex may also change during learning of a motor task. Therefore, this reflex can adapt quite readily to voluntary descending control from the higher motor centers. This kind of control appears to be mediated through the internuncial pool of interneurons, which can regulate the excitability of the motor neurons and therefore the degree of muscle contraction.

The function of the long-latency stretch reflex is as hard to define as that of the short-latency reflex, but based on the elegant experiments of Marsden and associates,^ it appears to compensate for changes in resistance during slow precision movements. In these experiments, while the subject flexed the thumb with a constant speed against a force of constant magnitude, the force was suddenly changed at unpredictable times. The change in compensatory force by the subject occurred at a latency that was faster than that of voluntary contraction and consistent with a polysynaptic long-latency reflex. The stretch reflex appeared to function to keep the sensitivity of the muscle spindles at a high level so that the slightest perturbations could be detected and the activity of the alpha motor neurons could be adjusted appropriately.

A disturbance in the long-latency stretch reflexes may be responsible for the characteristic increased muscle tone seen in patients with Parkinson's disease and known as

rigidity. In contrast to spasticity, rigidity is felt as a constant resistance to stretch that occurs in both flexion and extension of a joint; it may be felt during passive stretching of muscles that are too slow to elicit the spastic catch.

Delwaide's studies on spinal interneuron activity provide the best explanation for the pathophysiology of rigidity. The magnitude of rigidity correlates well with a reduction in short-latency autogenic 1b inhibition and simultaneous 1a interneuron facilitation. Activation of the descending reticulospinal tract from the nucleus reticularis gigantocellularis in experimental animals elicits this same pattern of 1b inhibition and 1a facilitation, suggesting that this system os involved in rigidity. Studies in monkeys who are rigid and parkinsonian due to exposure to the toxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) in fact show excessive activation of this pathway.

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