REFLEX ARC

A reflex arc is the neural pathway that mediates a reflex action. In higher animals, most sensory neurons do not pass directly into the brain, but synapse in the spinal cord. This characteristic allows reflex actions to occur relatively quickly by activating spinal motor neurons without the delay of routing signals through the brain, although the brain will receive sensory input while the reflex action occurs.

There are two types of reflex arc - autonomic reflex arc (affecting inner organs) and somatic reflex arc (affecting muscles).

A reflex arc refers to the neural pathway that a nerve impulse follows. The reflex arc typically consists of five components-

1. The receptor at the end of a sensory neuron reacts to a stimulus.

2. The sensory (afferent) neuron conducts nerve impulses along an afferent pathway towards the central nervous system (CNS).

3. The integration center consists of one or more synapses in the CNS.

4. A motor (efferent) neuron conducts a nerve impulse along an efferent pathway from the integration center to an effecter.

5. An effecter responds to the efferent impulses by contracting (if the effecter is a muscle fiber) or secreting a product (if the effecter is a gland).

MONOSYNAPTIC VS POLYSYNAPTIC

When a reflex arc consists of only two neurons in an animal (one sensory neuron, and one motor neuron), it is defined as monosynaptic. Monosynaptic refers to the presence of a single chemical synapse. In the case of peripheral muscle reflexes (patellar reflex, Achilles reflex), brief stimulation to the muscle spindle results in contraction of the agonist or effectors muscle.

By contrast, in polysynaptic reflex pathways, one or more interneuron’s connect afferent (sensory) and efferent (motor) signals. All but the simplest reflexes are polysynaptic, allowing processing or inhibition of polysynaptic reflexes within the spinal cord.

THE PATELLAR REFLEX (KNEE JERK)

Patellar reflex: when the patellar tendon is tapped just below the knee, the patellar reflex is initiated and the lower leg kicks forward (via contraction of the quadriceps). The tap initiates an action potential in a specialized structure known as a muscle spindle located within the quadriceps. This action potential travels to the spinal cord, via a sensory axon which chemically communicates by releasing glutamate (see synapse) onto a motor nerve. The result of this motor nerve activity is contraction of the quadriceps muscle, leading to extension of the lower leg at the knee. The sensory input from the quadriceps also activates local interneuron that releases the inhibitory neurotransmitter glycine onto motor neurons, blocking the innervations of the antagonistic (hamstring) muscle. The relaxation of the opposing muscle facilitates extension of the lower leg.

It should be noted that 'simple' monosynaptic reflexes do also have additional components. As the sensory axon enters into the spinal cord, it sends out a collateral axon which synapses onto an inhibitory interneuron. When activated, this IA inhibitory interneuron releases GABA which inhibits the motor activity of the antagonist muscle. The result is reinforced activity of the agonist muscle by removing tonic activity.

In lower animals reflex interneurons do not necessarily reside in the spinal cord, for example as in the lateral giant neuron of crayfish.

REFLEX ACTION

The fundamental and primary purpose of the neurons is to furnish a line of communication between the sense organs or receptors and the effectors or reacting structures. The central nervous system acts as a mediator and director of such communications. In man and the higher animals, this is accomplished in each instance by no less than two neurons to the voluntary organs and three neurons to the involuntary structures. Part of these are afferent and the rest efferent. At the distal end of the afferent neuron is to be found the receptor; in the spinal cord is the center or communication between the two neurons (synapse); and at the distal end of the efferent neuron are the effectors, for instance, the muscle. The simplest structural basis for the communication between the environmental changes and stimuli which set up a disturbance in the receptor and the response of the organism in its adjustment to that change, as muscle contraction, is known as a reflex arc. The resulting response from such a mechanism is known as reflex action. A third neuron, situated wholly within the central nervous system, is usually intercalated between the afferent and efferent neurons. This then becomes a connector neuron. In normal coordinated reflex response, these reflex-arc elements most probably act in groups.

The receptors are more or less specialized receiving organs situated peripherally. They are specialized to the extent that their stimulation threshold is greatly lowered for one particular type of stimulus, as the eye is most sensitive to light, the ear to air waves, while similar thresholds for other stimuli have been greatly increased.

Reflex action may be defined as an action which takes place independently of volition but in response to peripheral stimulation. The reactions of the involuntary organs naturally, at all times, come under this caption. Examples of reflex action in the voluntary system, however, are familiar to us all. The time-worn example is the jerking of the hand away when it accidentally touches something hot. Such responses as sneezing, coughing, winking of the eye, and the knee jerk although, with the possible exception of the winking reflex, they involve more than one muscle and efferent nerve fiber, are typical of purposeful reflexes. Such reflexes are exact and well-timed and are, therefore, called coordinated reflexes. When the reflex involves the response of single effectors it is termed a simple reflex. Again, reflexes may become convulsive (convulsive reflexes). In this case the response spreads to many, if not all, parts of the body. Under these conditions, the normal resistance (probably synaptic) which retains the nerve impulse within certain definite bounds or in certain nervous channels is diminished or overcome. The result is that the excitation spreads from neuron to neuron throughout the nervous system, simultaneously bringing into action very remote and usually unrelated parts of the body.

Certain reflex acts are said to be inborn since the structural mechanism upon which they depend is present and functional at birth. Since these are not dependent for their existence on the circumstances in which the individual happens to be placed, they have been termed by Pavlov unconditioned reflexes. Biologically they are of great importance since they contribute directly to the well-bring and survival of the individual. They are common to all members of a given species. In the higher animals, while the major part of behavior has as its basis the unconditioned reflexes, other well-established responses, of a perfectly definite character, fall quite logically into another and somewhat different category. These have been acquired. The salient feature of these is that, although their motor response is typical of some one of the unconditioned reflexes, the sensory or afferent stimulation is evoked by some other than that usually associated with the observed response. These reflexes are thus built upon the structural and functional integrity of the unconditioned reflexes or some other acquired reflex. They have, therefore, been called conditioned reflexes by Pavlov. It is probably upon this type of reflex that the process of learning depends.

Without the cerebrum, the individual would be reduced to an automaton, a slave to environmental changes (stimuli) through the medium of his unconditioned-reflex mechanisms.

The simplest reflex arc and reflex act is confined to a single segment of the spinal cord with its pair of nerve roots and to the same side only. By means of connector neurons which cross to the opposite side of the cord, the reflex may be extended to the efferent neurons of the other side of the body. Through other connector fibers the reflex may extend to other levels or segments of the cord or brain stem, either on the same or opposite side. In this way parts quite remote from the point of the stimulus may be brought into action reflex. Connector fibers in the central nervous system run in the white columns or tracts, the corresponding nerve cells lie in the gray matter while their terminal end brushes come into synaptic relation with nerve cells situated at other levels of the cord and stem.

In man and the higher animals which possess a cerebrum and are capable of volitional responses, other mechanisms are brought into action. Volitional responses can be instigated or stopped at will. In these, the impulse which initiated the activity originated, not in a peripheral receptor as in the unconditioned responses, but in the uppermost part of the central nervous system-the cerebrum. Connections exist between these segmental reflex arcs and the higher brain centers. The afferent connections are completed by at least two neurons in addition to the peripheral afferent neuron. The second neuron takes origin from the gray matter of the cord at the point of termination of the first, the third terminates in the sensory cortex of the opposite side. Complete crossing or decussating occurs in the medulla oblongata. Through association neurons, connections between the sensory and motor areas of the cortex are formed. The circuit is completed through the motor efferent fibers leading from the motor cortex to the medulla, where most of these fibers cross or decussate to the opposite side of the cord, where they pass to make synaptic connections with the common efferent path (neuron) of the reflex are to the muscle. In addition there is a two-neuron pathway from the cerebrum to the cerebellum and thence to the muscles. The response may even be initiated volitionally (within the cortex) without an immediate sensation from the periphery. Thus, it is obvious that volitional and conditioned responses are built upon the structural foundation of the inherited unconditioned-reflex mechanisms.

THE TENDON JERK REFLEX

The simplest reflex is the monosynaptic reflex or the two-neuron reflex, an example of which is the tendon jerk reflex or tendon tap reflex, sometimes called the myotatic reflex. This is the reflex that is elicited by tapping the tendon just below the patella. The tap, applied to the tendons of the quadriceps muscles, stretches the muscles and their muscle spindles. A brisk tap excites the group Ia afferent fibers, because of their velocity sensitivity, ultimately causing the muscle to contract. The neural circuit for this reflex is shown in Figure. The group Ia afferent neuron enters the spinal cord through the dorsal root, penetrates into the ventral horn, and then synapses on an alpha-moto neuron. (This is the only synapse in the pathway within the spinal cord, thus the reflex is monosynaptic.) The axon of the alpha-moto neuron then exits the spinal cord through the ventral root and innervates the extrafusal fibers of the muscle from which the group Ia afferent fiber originated, i.e., the homonymous muscle. Note that the drawing shows only one neuron of each type, afferent and efferent, but that one represents many. For example, the cat soleus muscle contains about 50 group Ia afferent fibers and each soleus alpha-motoneuron appears to have a synaptic connection with each one of those 50 group Ia afferent fibers. A brief tap on the tendon will therefore activate many of the group Ia afferent fibers, producing contraction of many of the soleus muscle fibers.

Fig.- The tendon jerk reflex. A circuit diagram of the elements of the tendon jerk reflex: the muscle spinlde, group Ia afferent fiber, alpha-motoneuron, and extrafusal muscle fiber.

Tapping the tendon of the rectus femoris muscle of the quadriceps group produces a brief stretch of that muscle that acts as a powerful stimulus for the group Ia afferent fibers of the muscle, causing them to give a brief, synchronous discharge. Each discharge, after propagating down the group Ia axon to its termination, produces an EPSP in the rectus alpha-moto neurons. Because there are many EPSPs from many group Ia afferent fibers occurring nearly simultaneously in some alpha-moto neurons, the membrane potentials reach critical firing level (by spatial summation) with hypo polarization to spare, and the moto neurons discharge action potentials. The action potentials travel out by way of the ventral root to the muscle and, because the neuromuscular junction is an obligatory synapse, the muscle contracts. The contraction in turn causes the spindle to be unloaded or shortened passively, its equatorial region to relax, the group Ia afferent fiber to turn off, and the muscle to relax. This is the tendon jerk reflex.

Many of the homonymous alpha-moto neurons are not discharged by the Ia afferent fiber input, but have EPSPs evoked in them that do not achieve the critical firing level. The excitability of the moto neuron is therefore increased. This group of excited neurons is called the subliminal fringe. The presence of the subliminal fringe accounts for enhancement of the reflex response under certain circumstances, for example with the Jendrassik maneuver. In the Jendrassik maneuver, the fingers of the two hands are locked together and one hand pulls against the other while the tendon tap reflex is evoked. The reflex evoked is stronger than in the absence of the maneuver. (Interestingly, mental arithmetic and a number of other activities will do the same thing!) During the Jendrassik maneuver activity, originating perhaps in the cervical enlargement of the spinal cord or some other rostral center descends the spinal cord to excite alpha-moto neurons. This activity by itself does not cause the alpha-moto neurons to discharge or the muscle to contract, but when added to the sub threshold excitation of the subliminal fringe caused by the tap-induced muscle stretch, it causes the neurons in the subliminal fringe to discharge. The reflex contraction will therefore be larger than normal. There may also be some influence of increased gamma-moto neuron activity, increasing the sensitivity of the primary spindle endings, but this influence should be small because the stimulus for the reflex is very brief.

The value of the stretch reflex mechanism may not be clear at first, but some reflection may clarify its role in motor control. It is unlikely that muscles undergo such rapid stretches very often, with the possible exception of when a person jumps off a wall or jumps up and down on a pogo stick. However, in these instances, the rapid stretch of the rectus femoris that occurs when the feet or the pogo stick contract the ground causes a reflex contraction that helps prevent the gluteus from being overly bruised.

Usually, the postural muscles experience relatively slow, sustained stretches and the anti-gravity muscles, of which the quadriceps is an example, are pulled upon by gravitational forces. This steady force sets up a sustained discharge in each group Ia afferent fiber, but the discharges in different fibers are not synchronized as they are when the tendon is tapped. In addition, longer, larger stretches are able to excite secondary muscle spindle receptors which also have connections with homonymous alpha-moto neurons, di- and trisynaptic ones. These longer, larger stretches therefore activate the alpha-moto neurons by both monosynaptic and polysynaptic reflex pathways. The resulting reflex contraction of the muscle is called the stretch reflex. The polysynaptic effects are not seen in the tendon tap reflex for two reasons: (1) the brief stretch does not excite secondary spindle receptors and (2) the brief input over the polysynaptic pathways arrives after the monosynaptic input and finds the alpha-moto neurons in their refractory periods and therefore cannot cause them to discharge again.

In controlling posture, the asynchronous discharge in mono- and polysynaptic pathways induced by gravitational forces on muscles sums in the alpha-moto neuron with other activity from within the CNS to produce a contraction that just balances the gravitational force. If an additional force is applied, stretching the muscle, additional tension is developed by the stretch reflex to counteract that force. In this way, the stretch reflex serves as a mechanism for maintaining an upright body orientation under a variety of load conditions; the mechanism is automatic ("unconscious") and fast (19-24 msec for the quadriceps in man).

In addition to the monosynaptic connections of the group Ia afferent fibers with the homonymous alpha-moto neurons (e.g., rectus femoris Ia with rectus alpha-moto neuron), there are also monosynaptic connections with synergistic alpha-moto neurons, those innervating muscles that act in the same way at the same joint, but the effects are not as strong in the synergists as they are in the homonymous alpha-moto neurons. Thus, the rectus group Ia afferent fibers also excite the vastus alpha-moto neurons, though not as strongly as they do the rectus alpha-moto neurons. Fewer of the synergistic alpha-motoneurons actually discharge, and the subliminal fringe is larger than for homonymous alpha-moto neurons.

Most skeletal muscles exhibit a tendon tap reflex, but the reflex is strongest in the antigravity or physiological extensor muscles. This makes some sense in light of the discussion of the last paragraph. Note that physiological extensors are not necessarily anatomical extensors. The biceps brachii is a case in point; they are anatomical flexors of the elbow but they are physiological extensors, moving the forearm against gravity.

It is clinically important to note that these reflexes involve only one or two segments of the spinal cord. In fact, the spinal cord can be cut above and below these segments, and the reflexes will still occur. For this reason, testing such reflexes cannot be used as an indicator of the condition of the brain or even other segments of the spinal cord.

RECIPROCAL INNERVATION

When the extensor muscle contracts during such a reflex, there is usually a relaxation of its antagonists, the flexor muscles crossing the same joint. If this did not occur, the reflex movement could be resisted and diminished by the force of the antagonist muscle. The neural mechanism underlying this relaxation of the antagonist muscles is shown in Figure. The group Ia afferent fiber, after entering the spinal cord, gives off a collateral branch that synapses on an interneuron. This interneuron, in turn, synapses on the antagonist alpha-moto neuron, in the case of our previous example, a hamstring moto neuron. Its effect on the hamstring alpha-moto neuron is inhibitory, i.e., it causes an IPSP in the alpha-moto neuron that is ultimately manifested as a relaxation of the muscle. This is reciprocal inhibition. Notice that this is a polysynaptic reflex pathway.

It is a general principle that anything that has an excitatory (or inhibitory) influence on an alpha-moto neuron also inhibits (or excites) the alpha-moto neurons of its antagonist muscle. This is the principle of reciprocal innervations. Thus, for example, excitation of the hamstring alpha-moto neurons by group Ia afferent fibers is accompanied by inhibition of quadriceps alpha-moto neurons. Reciprocal inhibition is a specific example of the more general principle of reciprocal innervations.

Fig.- Reciprocal innervation. A circuit diagram showing the collateral of the group Ia afferent fiber synapsing on an inhibitory interneuron that synapses on the alpha-motoneruon of the antagonist muscle. F and E indicate flexor and extensor muscles.

DALE’S PRINCIPLE

Dale's principle (formulated by Sir Henry Dale) states that a single neuron synthesizes only one transmitter substance. Therefore according to the principle, if a neuron secretes acetylcholine at one of its terminals, it secretes acetylcholine at all of its terminals. Sir John Eccles has extended this notion to say that the effect of the transmitter released by a single fiber is the same at all its terminals. This would imply that the net result of activity in all group Ia afferent fibers is excitation and only excitation. Thus, if it is necessary to have inhibition in a pathway involving group Ia afferent fibers, then an inhibitory interneuron must be interposed.

Some neurons make, or at least contain, more than one of the putative transmitter substances discussed in Chapter 13. However, it is not known whether all of the substances made by a neuron are actually used as transmitter substances by that neuron. For example, some neurons contain both GABA and somatostatin or GABA and some neuropeptide. Many peptides are thought to be neuromodulators rather than traditional transmitter substances. Therefore, it is not clear that this is a violation of Dale's principle. On the other hand, the idea that the effect of a transmitter substance is everywhere the same is not tenable. It is now known that certain neurons in Aplysia californica, the sea slug, secrete acetylcholine at synapses with two different postsynaptic cells, and, in one cell, the transmitter substance evokes an EPSP and, in the other, an IPSP. Thus, the action of the transmitter substance on a neuron depends upon that neuron and the receptors or channels it possesses not on the transmitter substance or the neuron that released it. Whether this behavior is also a characteristic of mammalian neurons is not yet certain. Nevertheless, the usual approach in neurophysiology has been to interpose an interneuron whenever the sign of the effect changes, whether there is direct evidence of an interneuron or not.

Fig. Flexion reflex. A circuit diagram of the flexion reflex showing afferent fibers from skin, interneurons, and flexor alpha-motoneurons in two spinal cord segments.

THE FLEXION REFLEX

If we have ever touched a hot object or stepped on a sharp object and withdrawn our hand or foot, we have experienced a flexion reflex, a nocifensive reflex, or a withdrawal reflex, all terms describing the same event. The protective result of this reflex is obvious; it quickly removes the part of the body from the vicinity of the offending object by contracting the appropriate muscles, usually flexors, and relaxing extensor muscles (again, reciprocal innervations). The vigor of the reflex depends upon the strength of the stimulus. A weak pinch produces flexion of the foot; a slightly stronger one, flexion of both the foot and the leg; and a very strong one, flexion of foot, leg, and even hip. This spread of the reflex with stronger stimulation is called irradiation. The exact nature of the limb movement and the final position of the limb vary depending upon the site of stimulation. This phenomenon is often called local sign. Because of local sign, the withdrawal of the limb from damaging stimuli is usually appropriate in both magnitude and direction.

The pathways for the flexion reflex are illustrated in Figure. The afferent limb (the part going to the spinal cord) of this reflex consists of nociceptors with A or C fibers and fibers of groups II, III, and IV of muscle. These are sometimes referred to collectively as the flexor reflex afferent fibers. They enter the spinal cord and synapse on interneuron, whose axons distribute to other interneuron that affect alpha-moto neurons within the same and in different segments of the spinal cord. Notice that this is a polysynaptic reflex. Activity in the nociceptive afferent fibers in the common peroneal nerve serving the first and second toe leads to discharge of the peroneus alpha-moto neurons, which, in turn, leads to dorsiflexion of the foot. If the nociceptive activity is strong enough, it is able to activate other peroneus alpha-moto neurons, further increasing the flexion of the foot, and also to bring in alpha-motoneurons of synergistic muscles of the foot, as well as other related muscle groups, for example the hamstrings, to lift the leg. This may involve transmission to spinal segments other than the segment of entry.

THE CROSSED-EXTENSION REFLEX

If protection of the limb requires it to be elevated, then the rest of the body is imperiled by removal of the support the limb normally provided, unless some compensation is made. The reflex contraction of flexor muscles on one side of the body is always accompanied by contraction of the extensor muscles of the contra lateral limb. This gives increased antigravity support on the contra lateral side to hold the body upright and is called the crossed-extension reflex. The circuit for this reflex is illustrated in Figure. The flexor reflex afferent fibers also synapse on interneuron that decussate (cross the midline) and terminate on contra lateral extensor alpha-moto neurons. This pathway is polysynaptic and purely excitatory. In addition, there is the usual reciprocal inhibitory effect on the contra lateral flexor alpha-moto neurons.

Fig. Crossed-extension reflex. Circuit diagram showing branching of the flexor reflex afferent fibers and their termination on an interneuron that decussates and terminates on contralateral extensor alpha-motoneurons.

AUTO GENIC INHIBITION

Activity in the group Ib afferent fibers, associated with Golgi tendon organs, inhibits the homonymous alpha-moto neurons. The inhibition is disynaptic involving one interneuron and two synapses between the afferent fiber and the moto neuron. The effect is called autogenic inhibition (sometimes written autogenetic inhibition). Like the group Ia excitation, group Ib inhibition is exerted not only on the homonymous alpha-moto neurons, but also on the alpha-moto neurons of synergistic muscles. Reciprocal innervations is also present here, with group Ib activity exciting the alpha-moto neurons of the antagonist muscles.

It was originally thought that this inhibition served only to protect the muscle from being injured when contracting against too heavy a load. This concept came from two sources: (1) the supposed high threshold of group Ib fibers to tension (not true for developed tension) and (2) the existence of a clasp-knife reflex. The clasp-knife reflex exists only in certain pathological conditions, e.g., "upper moto neuron" disease. Under these conditions, there is an extensor spasticity that resists any attempt to flex the limbs, especially the arms. If the arm is gradually, forcibly flexed by someone other than the patient, a point will be reached when the resistance to flexion suddenly melts away, and the limb collapses easily into full flexion, reminiscent of the action of a pocket or clasp-knife. This is the clasp-knife reflex or the lengthening reaction. It was thought formerly to be mediated by autogenic inhibition and to occur near the threshold for group Ib activation by increased muscle tension. Now it is thought that it occurs at the point where autogenic inhibition is great enough to overcome the stretch reflex excitation, that is, when the membrane potential of the extensor moto neuron falls below the critical firing level and the muscle relaxes. Actually, Golgi tendon organ activity cannot entirely account for the clasp-knife reflex. As the spastic muscle is lengthened, the group Ia discharge continually increases and, because the tension is increasing, the group Ib discharge also increases. The result, at the alpha-moto neuron, is excitation from the group Ia fiber input and inhibition from the group Ib fiber input, the inhibition finally taking dominance and silencing the alpha-moto neuron. The muscle relaxes. This accounts for the relaxation of the spastic muscle, but it does not account for the failure of its immediate return. When the muscle relaxes, the tension falls, and the group Ib fiber discharge ceases. This should decrease the autogenic inhibition and allow group Ia fiber input to reestablish the spasticity, but the muscle stays relaxed until the joint is extended again, whereupon the spasticity reappears. Recent evidence suggests that group Ia fibers from muscle spindles also contribute to autogenic inhibition. Because the muscle does not shorten, but lengthens when the spasticity disappears, the group Ia fibers will discharge even more briskly, increasing both excitation and autogenic inhibition of the alpha-moto neurons. Apparently, the inhibition predominates.

In the normal person, it is certain that the Golgi tendon organ contributes to control of muscle activity over the whole range of movement, not just at its extremes. There is no reflex movement associated with stimulation of Golgi tendon organs in isolation, so that nothing can be said with certainty about their reflex function. Perhaps they do serve a protective function, but they may also be supplying tension information for complicated tension-maintaining reflexes or supplying inhibition at the appropriate moment to switch from flexion to extension movements in walking or running.

They may also play a role in increasing muscle force during fatigue. Thus, during fatigue the muscle produces less force, which reduces Golgi tendon organ activity. This leads to decreased inhibition and, therefore, increased activity of the homonymous –moto neurons. The increased moto neuron activity will lead to greater force of contraction. The problem with this scenario is that the resulting increased force should lead to increased Golgi tendon organ activity and, so, decreased force. How this complicated system is working is yet to be determined.

OTHER REFLEXS

There are a number of other reflexes commonly tested in the clinic, whose mechanism we do not understand thoroughly. The extensor thrust reflex involves extension of the lower limb when a tactile stimulus is applied to the plantar surface of the foot. This may play some role in walking or standing by maintaining contact with the surface. The Babinski sign is a reflex that is pathological in adults but normal in infants. Scraping the sole of the foot of a normal adult with a tongue depressor results in plantar flexion of the toes. In the infant and the spinal adult (with a spinal cord transection), the same stimulus leads to dorsiflexion of the toes. This pathological change (in adults) is called Babinski's sign, and, as we shall see, it is usually taken as a sign of pyramidal tract damage.

There are a great many other reflexes that could be mentioned here. We have already discussed reflex control of pupil diameter and lens shape in the eye and auditory sensitivity by the middle ear muscles and olivocochlear bundle. In addition, there are stretch receptors in the lungs, probably in the bronchi and bronchioles, that are activated by lung inflation. The activity of these receptors enters the medulla by way of the vagus nerve (Xth cranial nerve) to produce inhibition of aspiratory neurons. This effect, called the Hering-Breuer reflex, has the effect of terminating inspiration when a certain level of inflation has been attained. It is mediated through the nucleus solitaries and the reticular formation.

There are other respiratory reflexes as well. For example, the stretch reflex and autogenic inhibition play a major role in control of the intercostals muscles during inspiration. The gamma loop appears to provide an important facilitation of discharges in –moto neurons to the external intercostals in particular. A most important reflex pathway regulates the concentrations of oxygen and carbon dioxide in arterial blood by adjusting respiratory parameters. Chemoreceptor in the carotid and aortic bodies increase their discharge rates in response to a decrease in arterial oxygen concentration or an increase in arterial carbon dioxide concentration (or, alternatively, a decrease in pH). Sensory fibers from these receptors enter the brain stem through the gloss pharyngeal nerve (IX th cranial nerve), where they make connections with cells whose activity results in an increase in respiratory volume and rate, with certain changes in peripheral vasculature, to elevate blood oxygen or decrease blood carbon dioxide levels. In addition, there are chemoreceptor in the CNS that are excited by elevation of the carbon dioxide of the cerebrospinal fluid or a decrease in its pH. Their activity results in the same changes in respiration, apparently without much change in the cardiovascular system.

There are also reflexes involving the heart. Bar receptors (pressure receptors) in the carotid sinus, in the aortic arch, and perhaps elsewhere, increase their discharge rates in response to elevated blood pressure. This increase in activity leads reflex to a decrease in sympathetic discharge, resulting in peripheral vasodilatation and in an increase in parasympathetic discharge primarily through the vagus nerve, resulting in decreased heart rate. The net result is a decrease in blood pressure. Stimulation of high threshold (small diameter) primary afferent fibers in coetaneous and muscle nerves also leads to a reflex increase in blood pressure.

Vomiting is the result of a reflex arc involving receptors in the region of the pharynx, supplied by the IXth and Xth cranial nerves and also receptors in the medulla. The modularly receptors, located in a region with high permeability of the blood brain barrier, are sensitive to chemical agents in the blood. The efferent limb of the reflex involves somatic innervations of the abdominal muscles and autonomic innervations of the stomach (smooth) muscles and the cardiac sphincter. During vomiting, the cardiac sphincter relaxes, while the abdominal and stomach muscles contract, expelling the stomach contents through the esophagus.

Swallowing is also a reflex activity. The reflex is triggered by tactile stimulation of the mucosa of the palate, pharynx, and epiglottis. Receptors in these regions, perhaps free nerve endings, send their activity through the IX th cranial nerve, the superior laryngeal branch of the X th cranial nerve, and perhaps also the V th cranial nerve. The reflex pathway involves synapses in the nucleus solitaries and efferent fibers to the tongue in the hypoglossal nerve (XII th cranial nerve) and to the palate, pharyngeal, and esophageal musculature through the IX, X and XI th cranial nerves from the nucleus ambiguous.

Temperature regulation is a complicated reflex activity, involving both peripheral thermo receptors and central thermo receptors located in the anterior hypothalamus and perhaps elsewhere. The reflex pathways are not well understood, but they involve hypothalamic activation of the autonomic system, resulting in peripheral vasoconstriction, piloerection, and shivering, if heat needs to be generated or conserved, and in sweating, increased respiration, and peripheral vasodilatation, if heat needs to be lost in maintaining body core temperature at around 37C.

Micturition is a reflex activity that depends upon stretch receptors located in series with smooth muscle cells of the bladder wall. This mode of attachment allows the receptors to discharge both when the muscles are stretched and when they contract. Fibers from these receptors are carried in the pelvic nerves to the S2-S4 spinal cord segments. Somatic afferent fibers to these same segments play a role in the reflex as well. Bladder emptying is produced by contraction of the detrusor muscle of the bladder and also muscles of the abdominal wall, with relaxation of the internal (smooth muscle) and external (striated muscle) sphincters. Reflex emptying can be accomplished with an isolated sacral spinal cord, provided that the sacral roots, especially ventral root S3, are intact, but usually the reflex is under strong control from supraspinal centers.

The reflex emptying of the colon, i.e., defecation, is accomplished in a way similar to micturition. Here, the receptors are located in series with smooth muscle of the rectal wall. Tactile receptors in the skin and anus also facilitate defecation, as does the simultaneous occurrence of a micturition reflex. Emptying is under parasympathetic control from the S2-S4 spinal cord segments, producing contraction of the smooth muscle lining the rectum and relaxation of the sphincters. Evacuation is also assisted by contraction of the diaphragm and abdominal muscles with the glottis closed (Valsalva's maneuver), increasing the pressure in the abdominal cavity.

There are also sexual reflexes whose organization is partially understood. The afferent fibers for penile erection and ejaculation reflexes arise from the genitalia and course through branches of the pudenda nerve, again, to spinal cord segments S2-S4, although many other stimuli can elicit sexual responses under appropriate circumstances. Many of these other stimuli must act through higher centers. Both somatic and autonomic efferent fibers are involved in producing erection, with parasympathetic fibers producing vascular engorgement and somatic moto neurons to the bulbocavernosus and ischiocavernosus muscles producing contraction that compresses the venous outflow from erectile tissues. Sympathetic fibers also play a poorly understood role; bilateral sympathectomy reduces or eliminates both erections and ejaculations. Sympathetic, parasympathetic and somatic motor activities are all involved in producing ejaculation.

These are a few of the many reflexes mediated by the nervous system. Some are mediated by the spinal cord and can occur when the spinal cord is disconnected from the brain, but some require intact connections with the brain stem or diencephalon for their operation. All, however, are under the influence of cortical and subcortical structures in their normal operation.

THE FUNCTION AND UTILITY OF REFLEXS

Many of the reflexes are artifacts of the way we stimulate the body (although many, like the eye blink reflex, are essential to protect body parts from injury and many play specific regulatory roles). However, they tell us two useful things: (1) how the nerve circuits of the spinal cord or brain stem are put together and (2) the condition of various parts of these circuits. The first piece of information is useful to the neurophysiologist, who ultimately wants to know how the nervous system works. However, we will see in the next chapter that many reflexes are suppressed or modified during phases of the stepping cycle in order to prevent muscles from contracting at the wrong times. The state of a reflex circuit may be highly variable depending upon the condition of a person, e.g., awake, asleep, comatose; upon what he is doing, e.g., walking, running, thinking; upon his position in space or posture; and upon other factors. Therefore, the reflex pattern at any one time may not be a good indicator of the neural circuits available in the nervous system or of how they behave under a variety of conditions.

The second piece of information is useful to the clinician, who wants to know what is wrong with a patient. An example may help to show how the reflexes are used clinically. A patient complains of paresis or weakness of the right leg. There are three possible causes for this paresis: (1) he is suffering from disease of descending tracts having to do with leg function; (2) he is suffering from disease of the –moto neurons themselves; or (3) something is wrong with the muscle. A normal tendon tap reflex rules out the last two alternatives, because the –moto neurons and muscle must be functional to give a normal reflex.

REFLEXS PATHWAYS AS CONTROL SYSTEMS

One way to think of the function of reflexes is as control systems , systems that regulate the various parameters of muscle contraction. The essential feature of this type of system is the more-or-less continuous flow of information from the element controlled back to the device that controls it. This is called feedback. An everyday example of feedback is the continuous information your eyes give you about the course your automobile is taking. Without visual information, you are likely to run off the road before you can detect errors in your steering. With visual feedback, small corrections can be made in your steering before you leave the road.

Fig. - Block diagram of a generalized feedback control system. The operation performed by each component is indicated by its name. Arrows indicate the unidirectional flow of information. Any feedback control system can be drawn in this form.

A convenient way of illustrating a control system is to use a block diagram such as that shown in Figure. In a block diagram, boxes indicate the components of the system, the name of the box indicates the operation performed by the box, and arrows indicate the direction of flow of signals in the system. The terms indicated in parentheses refer to the car example. The controlled system has an input that can be varied by a controller. This input interacts with influences from outside the system, called disturbances, in producing the output of the system, which is the parameter to be controlled. In the automobile example, the input is the position of the steering wheel, the output is the position of the car on the road, and a disturbance might be a sudden gust of wind that forces the car off its intended course. The sensor is a device that measures the output of the system and its measurement is the feedback signal to the error detector. The feedback signal is compared with the control signal (the signal that specifies the intended output) by the error detector, which, when it finds a difference between the two signals, sends an error signal to the controller to increase its output and reduce the amount of error. The actual output is brought closer to the intended output, the new output is again sensed by the sensor, and a new correction is made, bringing the system even closer to the intended output, and so on. In our car example, the error detector, sensor, and controller are all within the human operator. He senses the position of the car with his eyes (sensor), compares that with the course of the road (control signal), and, if they are not the same (an error exists), uses his muscles (controller) to turn the steering wheel to bring the car (controlled system) back to the appropriate position on the road (output). When the wind gusts, the car deviates from the course that would ordinarily be determined by the

Fig.-Block diagram of the control system involving the stretch reflex. This system controls muscle length.

Position of the wheel; the driver senses this and corrects for the disturbance.

It is possible to view the control of the driver's muscles in the same way. The muscle spindle receptors and their reflex connections form a feedback system to control muscle length. In this case, the control signal is a command from some supraspinal center to maintain the biceps muscle at some fixed length in order to hold a chair at a fixed distance off the floor. This signal is fed to spinal neurons, which are the error detectors, with the alpha-moto neurons as the controller that signals the muscle (controlled system) to contract, producing enough force to decrease its length (output) and lift the chair off the floor. The muscle spindle endings (length and velocity sensors) sense the length of the muscle and transmit its length (feedback signal) back to the alpha-moto neuron, where it is compared with the control signal. If the length of the muscle (or the height of the chair) is not as intended, a new error signal is generated, commanding more or less force and so on, around the system loop until the actual and intended muscle lengths are the same. Small deviations from the length specified by the control signal, for example due to fatigue, are sensed and quickly corrected in the same way.

Suddenly, someone drops a heavy book onto the chair and a disturbance of the system is produced by the sudden downward movement of the chair and the lengthening of the muscle. The spindle receptors sense the increased length and signal this increase to the alpha-moto neurons, which detect the error and command more force to be generated by the muscle and the load to be lifted back to the intended height. In this manner, the system helps to maintain the length of the muscle in the face of changes in the load being lifted. Other disturbances are, of course, possible. The lifter's other hand could touch a hot object, evoking a flexion reflex and a crossed-extension reflex, or the ground could suddenly tilt due to an earthquake, yet the length of the muscle will be maintained constant until a new control signal comes to the alpha-moto neuron. Suppose a new control signal orders the chair to be held higher. This new control signal will produce a large error signal, because it is quite different from the feedback signal. As a consequence, the controller will increase its output, resulting in more force that decreases the error. There will be a continuous cycling around the loop until the error is reduced to zero, and the new intended length is achieved. Notice that the gamma-moto neurons affect the sensitivity of the sensors, so that any input that excites the gamma-moto neurons will result in an increase in the feedback signal because of the increase in spindle activity. The gamma-moto neurons also receive their own control signals, perhaps independent of those to alpha-moto neurons, especially from cutaneous receptors and many supraspinal pathways, including the corticospinal, reticulospinal, and rubrospinal tracts. However, in general, pathways that influence alpha-moto neurons also influence gamma-moto neurons (alpha-gamma co activation), with the striking exception that group Ia afferent fibers do not influence gamma-moto neurons.

It has been suggested that some movements are initiated, not by control signals to alpha-moto neurons, but by control signals to gamma-moto neurons. An increase in gamma-moto neuron activity would result in a shortening of the intrafusal muscle fibers and an increase in the discharge of group Ia afferent fibers. This, in turn, would lead to an increase in alpha-moto neuron activity, causing contraction of the extrafusal muscle fibers and shortening of the whole muscle. This mechanism is called the follow-up length servo mechanism of contraction; because the length of the spindle (at least the receptor region of the spindle) controls the length of the muscle, and the changes in the length of the muscle follow the changes in the length of the spindle. It is not likely that this is the only mechanism by which contractions are initiated because of the alpha-gamma co activation from most sources. Contractions are probably initiated mainly by direct action on the alpha-moto neuron, but perhaps in some situations they are initiated by the follow-up length servo mechanism.

When a movement is initiated by alpha-gamma co activation, the co activation can act as a servo-assistor. If the estimated load, as determined by the command signal, is correct, i.e., if the actual load equals the estimated load, the spindle discharge will remain constant and no further reflex alpha-moto neuron excitation will occur. If the actual load exceeds the estimated load, there will be a misalignment of the intra- and extrafusal fibers, a large spindle discharge, and an increased alpha-moto neuron discharge with increased tension. On the other hand, if the actual load is less than the estimated load, there will be a different misalignment of the intra- and extramural fibers and a reduced spindle discharge leading to reduced alpha-moto neuron activation. In any case, alpha-gamma co activation insures that the spindles will continue to act as length detectors even when the muscle shortens.