What is the difference between tendon reflex and stretch reflex

Gamma fibers are ideally suited for this and whenever a command is sent to alpha motor fibers, gamma fibers are also excited. There occurs alpha—gamma co-activation to produce contraction of both extrafusal and intrafusal fibers according to the position and force commands from the brain to the spinal cord. Clonus occurs when the dynamic stretch reflex is highly sensitized and facilitated.

The dynamic response dies out within a fraction of a second to elicit a new cycle and in this way the muscle contraction e. Interneurons: Most integrative functions in the spinal cord are mediated by interneurons. Interneurons which are involved in every segmental and stretch reflex pathways are excited or inhibited by several peripheral and descending fiber systems Lundberg, Interneuron systems involved in the stretch reflex arc and in the pathophysiology of spasticity are discussed below.

Renshaw cells are situated in lamina VII of ventral horn medial to motoneurons. Collateral from an alpha motoneuron axon excites Renshaw cell which in turn inhibits the same and also other motoneuron innervating the synergistic muscles. This alpha motoneuron-Renshaw cell — alpha motoneuron pathway of inhibition forms a negative feedback circuit to control motoneuron excitation and is called recurrent inhibition Pompetano, In addition, Renshaw cells inhibit gamma motoneurons and la inhibitory interneurons Jankowska and Roberts, Stretch of a muscle activates la afferent fires to produce monosynaptic excitation of homonymous alpha motoneurons.

There occurs in addition disynaptic inhibition of alpha motoneurons innervating antagonist muscles reciprocal inhibition. It is now established that la interneurons receive the same diverse excitatory and inhibitory inputs from segmental afferents e. These inputs excite alpha motoneurons to contract synergistic muscles and also excite la inhibitory interneurons to inhibit in turn alpha motoneurons to antagonistic muscles during stretch reflex activity.

Clinical electrophysiological studies by H — reflex demonstrating this phenomenon had been performed early by Misra and Pandey in Neurolathyrism — a pure motor spastic tropical paraparesis caused by ingestion of grass peas containing the neurotoxin beta — ODAP.

These authors demonstrated increased motoneuron excitability, altered transmission in the premotoneuronal pathway and lack of reciprocal inhibition in the generation of spasticity in this condition. More recently, Crone et al. In addition to established role of group II fibers in stretch reflex arc, these fibers from secondary spindle endings are known to produce flexion reflex by exciting flexor alpha motoneurons and inhibiting extensor motoneurons.

Like Renshaw cell and la inhibitory interneurons, lb interneurons also receive diverse segmental and supraspinal inputs. Therefore, lb inhibition is not a simple autogenic inhibitory safety mechanism to regulate muscle tension only. It is a part of complex system regulating muscle tension to control posture and movement. The amplitude of EPSP generated in a motoneuron in response to la afferent stimulation diminishes if there occurs prior depolarization of this la afferent fiber through axo—axonic synapse with a specific interneuron.

The specific interneurons involved in this process of presynaptic inhibition are also controlled by descending pathways. This permits automatic suppression of unimportant afferent informations Schmidt, Nociceptive reflex or simply pain reflex produces contraction of flexor muscles of a limb withdrawal and crossed extensor reflex of opposite limb. This is mediated by polysynaptic connection between flexor reflex afferents FRA , interneurons and motoneurons of extensor as well as flexor muscles.

Increased fusimotor drive: Exaggerated muscle stretch reflexes in spasticity was attributed to the increased sensitivity of the muscle spindles due to increased fusimotor activity some 20—30 years ago. The posterior root section for treatment of spasticity in cerebral palsy and diluted procaine injection near intramuscular nerve for treating hyperactive stretch reflex Rushworth, were based on this theory.

The local anesthetic injection was assumed to block small diameter fusimotor fibers but not larger diameter alpha motor axons. Later experiments using microneurography studies Hagbarth, failed to demonstrate any change in the discharge of muscle spindle afferents in spastic patients making it unlikely that any significant changes in fusimotor drive exist. The hypothesis that increased fusimotor outflow is involved in the pathophysiology of spasticity has consequently been discredited.

Primary hyperexcitability of alpha motoneurons following spinal lesions — plateau potentials: Recent research has shown that several active membrane properties can shape the motoneuronal output Rekling et al. When a graded depolarizing current is introduced through an intracellular electrode into a motoneuron of a decerebrate cat, a critical threshold plateau threshold is reached.

Above this threshold, further depolarization will trigger a regenerative activation of sustained inward current. In the decerebrate cat with tonic descending serotonergic drive the plateau potentials are easily evoked.

However, following an acute spinal transaction they cannot be evoked unless the persistent inward current is specifically increased, e. In a few cases, it was possible to demonstrate that plateau potentials can again be induced in the chronic spinal state without adding any neurotransmitter precursors or agonists Feganel and Dumtrijevic, This suggested that plateau potentials, returning long after spinal injury, can play a role in the pathophysiology of spasticity.

Little is known about the possible contribution of plateau potentials to the development of spasticity in humans because of the difficulty in demonstrating the existence of such intrinsic membrane properties in the intact organism. Enhanced cutaneous reflexes: In spasticity, cutaneous reflexes flexor or withdrawal are enhanced.

Dorsal horn neurons give rise to both long axons which form ascending tracts and short propriospinal axons to innervate motor neurons of cord. Rostral lesions in CNS disrupting descending reticulospinal tract RST or spinothalamic tract alter normal gating mechanisms in dorsal horn so that pain is experienced to rather innocuous stimuli.

This mishandling of segmental inputs helped by failure of presynaptic inhibition mediated through GABA-ergic synapses on primary afferents in substantia gelatinosa results in hyperactivity in long tract neurons to be felt as pain as an associated feature in spasticity. Similarly excitation of short propriospinal interneuron system in the cord produces hyperactive nociceptive reflexes. This system acts as an arousal system for motoneurons in absence of brainstem reticular system in a cord deprived of supraspinal influences Burke and Ashby, Current hypotheses stress more on alterations in inhibitory mechanisms in spinal neuronal circuitry than an excitatory processes although both may be inter-related in a patient with spasticity.

Figure 2 illustrates the spinal reflex circuits that could be involved in the development of spasticity. The monosynaptic Ia excitation which underlies the dynamic and tonic components of the stretch reflex may be inhibited by various spinal reflexes pathways.

Figure 2. Spinal pathways which may be responsible for development of spasticity. Disynaptic reciproval Ia inhibition from muscle spindle Ia afferents from the antagonist muscles. Inhibition from muscle spindle group II afferents not shown in the Figure 3.

Figure 3. Supraspinal descending pathways in spinal cord RF, reticular formation. The changes in reflex transmission in these pathways may depend both on an altered supraspinal drive if any remains and on secondary changes at cellular level in the spinal cord below the lesion which may include:. As discussed before, the inhibition is through axo—axonic synapses which are GABA-ergic and on activation reduces the amount of transmitter released by Ia terminals on the motoneuron.

If there occurs a reduction in the normally maintained tonic level of presynaptic inhibition, there will be increased response on alpha motoneurons by Ia input and spasticity may ensure. A technique used to study presynaptic inhibition in human subjects was to vibrate the Achilles tendon and record the resulting depression of the soleus H-reflex Burke and Ashby, ; Ashby et al.

As this vibratory inhibition was subsequently found to be decreased in spastic patients, it became generally accepted that spasticity involved reduced presynaptic inhibition of Ia afferents Ashby et al. However, later studies have cast doubts on this interpretation.

Using a more optimal technique to evaluate presynaptic inhibition, Nielsen et al. A similar finding was made for patients with spinal cord injury, but not for hemiplegic stroke patients Paist et al.

Presynaptic inhibition thus seems to be reduced in some spastic patients but not in all. Reduced reciprocal inhibition is a strong candidate for playing a major role in the pathophysiology of spasticity Crone and Nielsen, ; Crone et al. In spastic patients, reflex spread is common with reflex induced co-contraction of antagonist muscle groups, a failure of reciprocal inhibition. The Ia inhibitory interneurons are activated by descending motor fibers, damage to which could reduce this type of inhibition.

Recurrent inhibition mediated by Renshaw cells have been studied by complex H-reflex techniques Pierrot-Deseilligny and Bussel, In some patients with both supraspinal as well as traumatic spinal lesions increased recurrent inhibition may be seen, which obviously plays no role in development of spasticity Katz and Pierrot-Deseilligny, ; Shefner et al. Only in patients with progressive paraparesis of ALS is a reduction found at rest and it is doubtful that this reduction contributes to the spasticity observed in these patients Mazzochio and Rossi, ; Shefner et al.

Changes in recurrent inhibition thus probably plays no major role in the pathophysiology of spasticity. This inhibition is caused by activation of Ib afferents coming from Golgi tendon organs and is mediated by segmental interneurons projecting to mononeurons of the same muscle.

Ib inhibition may be demonstrated in human subjects by specialized H reflex studies Raynor and Shefner, Whereas this inhibition is easily demonstrated in healthy subjects, there was failure to produce any inhibition on the paretic side in hemiplegic patients, along with a facilitatory effect in some subjects Pierrot-Deseilligny et al. This observation suggests that alteration of Ib inhibition excitation plays a role in the pathophysiology of spasticity.

However, reflex effects from Golgi tendon Ib afferents are unchanged after spinal cord lesions in humans. At this stage it is important to take note of the fact that the anterior horn cell AHC or spinal motoneuron is the key nucleus in the operation of all spinal reflexes. Dysfunction of AHC leads to hypotonicity — as is evident in pure AHC affecting diseases like poliomyelitis, spinal muscular atrophy and the progressive muscular atrophic form of motor neuron disease MND.

Associated dysfunction of supraspinal pathways with some surviving spinal motoneurons might cause spastic weakness as commonly seen in the amyotrophic lateral sclerosis form of MND. The importance of supraspinal and suprasegmental control of spinal reflexes was progressively understood since the role of muscle stretch reflex to generate muscle contraction was discovered by Liddell and Sherrington , Delwaide and Oliver Descending influences control spinal reflexes by converging along with primary peripheral afferents on common interneuronal pool projecting to motoneurons.

Imbalance of the descending inhibitory and facilitatory influences on muscle stretch reflexes is thought to be the cause of spasticity Lundberg, These influences are discussed below. There are five important descending tracts, of these, corticospinal tract originates from cerebral cortex. Other four come from closely neighboring parts in the brain stem and these are — Reticulospinal Vestibulospinal, Rubrospinal, and Tectospinal tracts.

In human spastic paretic syndrome, the three important pathways are — corticospinal, reticulospinal, and vestibulospinal. Corticospinal pathway — Isolated pyramidal lesions have not produced spasticity in conditions such as destruction of motor cortex area 4 , unilateral lesion in cerebral peduncle, lesions in basis pontis and medullary pyramid Bucy et al. Instead of spasticity these lesions produced weakness, hypotonia, and hyporeflexia.

Spasticity however may be caused in lesions of area 4 if the lesions include the premotor and supplementary motor areas. Fibers responsible for spasticity run with the pyramidal tract to end in the bulbar reticular formation corticoreticular pathway. James Knierim, Ph. As noted in the previous chapter, a sense of body position is necessary for adaptive motor control.

In order to move a limb toward a particular location, it is imperative to know the initial starting position of the limb, as well as any force applied to the limb. Muscle spindles and Golgi tendon organs provide this type of information. In addition, these receptors are components of certain spinal reflexes that are important for both clinical diagnosis as well as for a basic understanding of the principles of motor control. Figure 2. This is also known as the stretch reflex, the knee-jerk reflex, and the deep tendon reflex.

Note: Locations of neurons within spinal cord are not meant to be anatomically accurate. The myotatic reflex is illustrated in Figure 2. A waiter is holding an empty tray, when unexpectedly a pitcher of water is placed on the tray.

However, a spinal reflex is automatically initiated to keep the tray relatively stable. The Ia afferents have their cell bodies in the dorsal root ganglia of the spinal cord, send projections into the spinal cord, and make synapses directly on alpha motor neurons that innervate the same homonymous muscle. Thus, activation of the Ia afferent causes a monosynaptic activation of the alpha motor neuron that causes the muscle to contract.

As a result, the stretch of the muscle is quickly counteracted, and the waiter is able to maintain the tray at the same position.

A major role of the myotatic reflex is the maintenance of posture. If one is standing upright and starts to sway to the left, muscles in the legs and torso are stretched, activating the myotatic reflex to counteract the sway.

The lower levels of the hierarchy implement the command with such mechanisms as the myotatic reflex, freeing the higher levels to perform other tasks such as planning the next sequence of movements.

The myotatic reflex is an important clinical reflex. It is the same circuit that produces the knee-jerk , or stretch , reflex. When the physician taps the patellar tendon with a hammer, this action causes the knee extensor muscle to stretch abruptly. This stretch activates the myotatic reflex, causing an extension of the lower leg. Because the physician taps the tendon, this reflex is also referred to as the deep tendon reflex.

Do not be confused, however, between this terminology and the Golgi tendon organ. The myotatic reflex is initiated by the muscle spindle, not the Golgi tendon organ. As discussed below, spinal reflexes can be modulated by higher levels of the hierarchy, and thus a hyperactive or hypoactive stretch reflex is an important clinical sign to localize neurological damage. Joints are controlled by two opposing sets of muscles, extensors and flexors, which must work in synchrony.

Thus, when a muscle spindle is stretched and the stretch reflex is activated, the opposing muscle group must be inhibited to prevent it from working against the resulting contraction of the homonymous muscle Figure 2.

This inhibition is accomplished by an inhibitory interneuron in the spinal cord. The Ia afferent of the muscle spindle bifurcates in the spinal cord See Chapter 6 of Section I for review. One branch innervates the alpha motor neuron that causes the homonymous muscle to contract, producing the behavioral reflex. The other branch innervates the Ia inhibitory interneuron, which in turn innervates the alpha motor neuron that synapses onto the opposing muscle.

Because the interneuron is inhibitory, it prevents the opposing alpha motor neuron from firing, thereby reducing the contraction of the opposing muscle. Without this reciprocal inhibition, both groups of muscles might contract simultaneously and work against each other. Both extensor and flexor motor neurons are firing to maintain the arm at its location. When the pitcher is placed on the tray, the stretch reflex activates the flexor and inhibits the extensor.

The Golgi tendon organ is involved in a spinal reflex known as the autogenic inhibition reflex Figure 2. When tension is applied to a muscle, the Group Ib fibers that innervate the Golgi tendon organ are activated. These afferents have their cell bodies in the dorsal root ganglia, and they project into the spinal cord and synapse onto an interneuron called the Ib inhibitory interneuron. This interneuron makes an inhibitory synapse onto the alpha motor neuron that innervates the same muscle that caused the Ib afferent to fire.

The alpha motor neuron fires to contract the extensor muscle, until the Golgi tendon organ is activated, thereby inhibiting the alpha motor neuron and causing the leg to drop.

As a result of this reflex, activation of the Ib afferent causes the muscle to cease contraction, as the alpha motor neuron becomes inhibited. Because this reflex contains an interneuron between the sensory afferent and the motor neuron, it is an example of a disynaptic reflex. For many years, it was thought that the function of the autogenic inhibition circuit was to protect the muscle from excessive amounts of force that might damage it.

A classic example is that of the weightlifter straining to raise a heavy load, when suddenly the autogenic inhibition reflex is activated and the muscle loses power, causing the weight to fall to the ground. This function was ascribed to the reflex because early work suggested that the Golgi tendon organ was only activated when large amounts of force were applied to it. More recent evidence indicates, however, that the Golgi tendon organ is sensitive to much lower levels of force than previously believed.

Thus, the autogenic inhibition reflex may be more extensively involved in motor control under normal conditions. One possibility is that this reflex helps to spread the amount of work evenly across the entire muscle, so that all motor units are working efficiently.

An example of this is when a person steps on a nail, the leg that is stepping on the nail pulls away, while the other leg takes the weight of the whole body. The crossed extensor reflex is contralateral, meaning the reflex occurs on the opposite side of the body from the stimulus. To produce this reflex, branches of the afferent nerve fibers cross from the stimulated side of the body to the contralateral side of the spinal cord.

There, they synapse with interneurons, which in turn, excite or inhibit alpha motor neurons to the muscles of the contralateral limb. The withdrawal reflex nociceptive or flexor withdrawal reflex is a spinal reflex intended to protect the body from damaging stimuli. It is polysynaptic, and causes the stimulation of sensory, association, and motor neurons. When a person touches a hot object and withdraws his hand from it without thinking about it, the heat stimulates temperature and danger receptors in the skin, triggering a sensory impulse that travels to the central nervous system.

The sensory neuron then synapses with interneurons that connect to motor neurons. Some of these send motor impulses to the flexors to allow withdrawal. Some motor neurons send inhibitory impulses to the extensors so flexion is not inhibited—this is referred to as reciprocal innervation. Although this is a reflex, there are two interesting aspects to it:. Golgi tendon organ : The Golgi tendon organ, responsible for the Golgi tendon reflex, is diagrammed with its typical position in a muscle left , neuronal connections in spinal cord middle , and expanded schematic right.

The tendon organ is a stretch receptor that signals the amount of force on the muscle and protects the muscle from excessively heavy loads by causing the muscle to relax and drop the load. Privacy Policy. Skip to main content. Peripheral Nervous System. Search for:. Components of a Reflex Arc A reflex arc defines the pathway by which a reflex travels—from the stimulus to sensory neuron to motor neuron to reflex muscle movement.

Learning Objectives Describe the components of a reflex arc. Key Takeaways Key Points Reflexes, or reflex actions, are involuntary, almost instantaneous movements in response to a specific stimulus. Golgi tendon organ : The Golgi tendon organ, responsible for the Golgi tendon reflex, is diagrammed with its typical position in a muscle left , neuronal connections in spinal cord middle , and expanded schematic right. The tendon organ is a stretch receptor that signals the amount of force on the muscle and protects the muscle from excessively heavy loads by causing the muscle to relax and drop the load.

Stretch Reflex The stretch reflex myotatic reflex is a muscle contraction in response to stretching within the muscle. Golgi Tendon Reflex The Golgi tendon reflex is a normal component of the reflex arc of the peripheral nervous system.

Crossed Extensor Reflex Jendrassik maneuver : The Jendrassik maneuver is a medical maneuver wherein the patient flexes both sets of fingers into a hook-like form and interlocks those sets of fingers together note the hands of the patient in the chair. Withdrawal Reflex The withdrawal reflex nociceptive or flexor withdrawal reflex is a spinal reflex intended to protect the body from damaging stimuli. Although this is a reflex, there are two interesting aspects to it: The body can be trained to override that reflex.

An unconscious body or even drunk or drugged bodies will not exhibit the reflex. Key Points The stretch reflex is a monosynaptic reflex that regulates muscle length through neuronal stimulation at the muscle spindle. The alpha motor neurons resist stretching by causing contraction, and the gamma motor neurons control the sensitivity of the reflex.

The stretch and Golgi tendon reflexes work in tandem to control muscle length and tension. Both are examples of ipsilateral reflexes, meaning the reflex occurs on the same side of the body as the stimulus. The crossed extensor reflex is a contralateral reflex that allows the body to compensate on one side for a stimulus on the other. The withdrawal reflex and the more-specific pain withdrawal reflex involve withdrawal in response to a stimulus or pain.