The Classic Wanderer

What Is Reciprocal Inhibition In Psychology?

• Sabrina Sarro
• 05.05.2023
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Definitions of reciprocal-inhibition therapy. a method of behavior therapy based on the inhibition of one response by the occurrence of another response that is mutually incompatible with it ; a relaxation response might be conditioned to a stimulus that previously evoked anxiety.

What is an example of reciprocal inhibition in psychology?

Assessment | Biopsychology | Comparative | Cognitive | Developmental | Language | Individual differences | Personality | Philosophy | Social | Methods | Statistics | Clinical | Educational | Industrial | Professional items | World psychology | Clinical: Approaches · Group therapy · Techniques · Types of problem · Areas of specialism · Taxonomies · Therapeutic issues · Modes of delivery · Model translation project · Personal experiences · Reciprocal inhibition therapy is a form of behaviour therapy based on the principles of reciprocal inhibition and counterconditioning as developed by J.

Wolpe In Wolpe’s search for a more effective way in treating anxiety he developed different reciprocal inhibition techniques, utilizing assertiveness training. Reciprocal inhibition can defined as anxiety being inhibited by a feeling or response that is not compatible with the feeling of anxiety. Wolpe first started using eating as a response to inhibited anxiety in the laboratory cats.

He would offer them food while presenting a conditioned fear stimulus. After his experiments in the laboratory he applied reciprocal inhibition to his clients in the form of assertiveness training. The idea behind assertiveness training was that you could not be angry or aggressive while simultaneously anxious at same time.

1. Importantly, Wolpe believed that these techniques would lessen the anxiety producing association.
2. Assertiveness training proved especially useful for clients who had anxiety about social situations.
3. However, assertiveness training did have a potential flaw in the sense that it could not be applied to other kinds of phobias,

Wolpe’s use of reciprocal inhibition led to his discovery of systematic desensitization, He believed that facing your fears did not always result in overcoming them but rather lead to frustration, According to Wolpe, the key to overcoming fears was “by degrees.” Over a period he developed a comprehensive approach to a broad range of symptoms and mental disorders and this formed the basis of reciprocal inhibition therapy which he outlined in his book “Psychotherapy by Reciprocal Inhibition”.

What is meant by reciprocal inhibition in psychology?

According to Wolpe, reciprocal inhibition refers to the complete or partial suppression of anxiety responses as a consequence of the immediate evocation of other responses physiologically antagonistic to anxiety, i.e., the technique seeks to condition a new response that is considered incompatible with the response to

What is the principle of reciprocal inhibition?

6.8.2 Control of a single limb – With respect to the control of a single limb, we should mention the principle of reciprocal inhibition, which suggests that the stretch of extensor muscles inhibits the activity of flexor motor neurons, and vice versa ( Crone, 1993 ).

An upward force to the wrist deactivates the biceps during a cocontraction of the biceps and triceps muscles ( Fig.6.15, right). This principle originates in neural connections to the spinal cord that release an inhibitory transmitter substance. This can be shown in any joint of the body and is used to prevent muscles from competing with one another in the presence of an externally applied load.

The body has a variety of reflexes that involve the spinal cord without use of higher processing centers ( Crone, 1993 ). Figure 6.15, The principle of reciprocal inhibition: ( left ) cocontraction and ( right ) inhibition when a force is applied to the wrist. Source : Recreated from McMahon, T. (1984). Muscles, reflexes, and locomotion (Princeton paperbacks), Princeton, NJ: Princeton University Press. Read full chapter URL: https://www.sciencedirect.com/science/article/pii/B9780128133729000063

What is reciprocal inhibition in systematic desensitization?

a. Description of Treatment – Systematic desensitization is a form of exposure therapy developed by Joseph Wolpe in 1958. Based on reciprocal inhibition, it posits that an individual cannot be relaxed and anxious simultaneously. A hierarchy of the patient’s fears is developed.

In the first part of the therapy, the patient is taught relaxation training. Once proficiency in relaxation is attained, the patient is gradually exposed to the trauma-related items that frighten him or her, starting with the least feared situation object or memory. The patient is instructed to note the onset of anxiety symptoms, and the treatment is paused while the patient initiates relaxation techniques.

When the patient has regained a sense of comfort, the exposure resumes. This cycle continues until the patient can tolerate all the stimuli on the fear hierarchy without anxiety. Read full chapter URL: https://www.sciencedirect.com/science/article/pii/B0123430100001665

What is an example of reciprocal behavior?

Examples of Reciprocity – Examples of reciprocity in business include:

A salesperson giving a freebie to a potential customer, hoping that it will lead them to return the favor by purchasing somethingA leader offering attention and mentorship to followers in exchange for loyalty Offering customers some valuable information in exchange for signing up for future marketing offers

In relationships, reciprocity often looks like supporting one another in different situations. For example, you might comfort your partner when something doesn’t go their way. In return, they will provide comfort and support when you are having a bad day.

What is an example of reciprocal in psychology?

Positive and negative reciprocity – Positive reciprocity occurs when an action committed by one individual that has a positive effect on someone else is returned with an action that has an approximately equal positive effect. For example, if someone takes care of another person’s dog, the person who received this favor should then return this action with another favor such as with a small gift.

1. However, the reciprocated action should be approximately equal to the first action in terms of positive value, otherwise this can result in an uncomfortable social situation.
2. If someone takes care of another person’s dog and that person returns the favor by buying that individual a car, the reciprocated gift is inappropriate because it does not equal the initial gesture.

Individuals expect actions to be reciprocated by actions that are approximately equal in value. One example of positive reciprocity is that waitresses who smile broadly receive more tips than waitresses who present a minimal smile. Also, free samples are not merely opportunities to taste a product but rather invitations to engage in the rule of reciprocity.

Many people find it difficult to accept the free sample and walk away. Instead, they buy some of the product even when they did not find it that enjoyable. Negative reciprocity occurs when an action that has a negative effect on someone is returned with an action that has an approximately equal negative effect.

For example, if an individual commits a violent act against a person, it is expected that person would return with a similar act of violence. If, however, the reaction to the initial negative action is not approximately equal in negative value, this violates the norm of reciprocity and what is prescribed as allowable.

Retaliatory aspects i.e. the aspects of trying to get back and cause harm, are known as negative reciprocity. This definition of negative reciprocity is distinct from the way negative reciprocity is defined in other domains. In cultural anthropology, negative reciprocity refers to an attempt to get something for nothing.

It is often referred to as “bartering” or “haggling” (see reciprocity (cultural anthropology) for more information).

Why does reciprocal inhibition occur?

Reciprocal Inhibition – Reciprocal inhibition is the spinal process of inhibition of a motor neuron pool when the antagonist motor neuron pool is activated.1 This can be studied by assessing the influence on an H reflex of stimulation of a nerve with afferents from muscles antagonist to the muscle where the H reflex is produced.

• There are several normal periods of inhibition, depending on the interval between the stimulus to the antagonist nerve and that eliciting the H reflex.
• The period of inhibition best understood is that occurring when the two nerves are stimulated close to the same time.
• This inhibition is mediated by the Ia inhibitory interneuron.

In the arm, reciprocal inhibition has been studied by looking at the effects of radial nerve stimulation upon the H reflex of the flexor carpi radialis. Via various pathways, and therefore at various time intervals after the radial nerve stimulus, the radial afferent traffic can inhibit the motor neuron pool of this muscle.

• The first period of inhibition is caused by disynaptic Ia inhibition; the second period of inhibition is probably presynaptic inhibition; and little is known about the third period of inhibition.
• Reciprocal inhibition is reduced in patients with dystonia, including those with generalized dystonia, writer’s cramp, spasmodic torticollis, and blepharospasm.

It should be noted that reciprocal inhibition can be abnormal even in asymptomatic arms, as is the situation with blepharospasm. Reciprocal inhibition studies can be used as a sensitive method for detecting abnormality in patients with dystonia; however, the method is not specific.

What is reciprocal inhibition for trauma?

Discussion – Although studies have reported an array of clinical differences between PTSD patients with emotional undermodulation and those with emotional overmodulation, little is known about whether individual patients experience switching between the emotional under- and overmodulatory states.

• In this study, we tested our model in which reciprocal inhibition between the amygdala and vmPFC is predicted to generate alternations between these states within individual patients.
• Supporting the predictions of our model, our results indicated that two emotional modulatory states exist and that these can alternate even within the same individual patient.

The results further supported the assumption of our model that reciprocal inhibition between the amygdala and the vmPFC underlies the alternations between these two emotional modulatory states. The results of the behavioral meta-analysis and our behavioral experiment supported the prediction that two opposing emotional modulatory states—which encompass corresponding attentional biases and symptoms—exist.

Across patients, re-experiencing and avoidance symptoms were found to be respectively associated with attentional bias toward (AB TOWARD ) and away from (AB AWAY ) threat. Because attentional bias and symptoms were found to alternate together in this predicted manner, this result suggests that emotional under- and overmodulation at the levels of behavior and symptomology share a common neural mechanism.

In addition, the results of our behavioral experiment showed that these opposing emotional modulatory states can alternate within the same individual patient. Specifically, bimodal distributions of detection times during the b-CFS task, indicative of two opposing emotional modulatory states, were found not only in patients as a group but also within individual patients.

Moreover, the distances between the two clusters of detection times in the bimodal distributions were positively correlated with the strength of re-experiencing and avoidance symptoms across patients. This correlation suggests that the degree of alternations between the two modulatory states at the level of symptom is related to the degree of alternations at the level of attentional bias within patients.

The results of the imaging meta-analysis supported the predictions of our model regarding neural mechanisms. Consistent with the hypothesis that symptom alternating dynamics of PTSD are produced from reciprocal inhibition between the amygdala and vmPFC, the imbalance between re-experiencing and avoidance symptoms was found to be correlated with left amygdala activity to threat.

1. When there were relatively more re-experiencing symptoms, the left amygdala tended to be more active; when there were relatively more avoidance symptoms the left amygdala tended to be less active.
2. This fits with the model proposal that the amygdala dominates the vmPFC during the emotional undermodulatory state, while the vmPFC dominates the amygdala during the emotional overmodulatory state.

However, future experiments where the vmPFC and the amygdala are simultaneously imaged are required to more directly examine this basic proposal of the reciprocal inhibition model. Our results may help to enhance treatment response by predicting better timing of treatment based on the emotional modulatory states of individual patients.

For example, previous studies showed that patients with the dissociative PTSD subtype, which is characterized by reduced amygdala reactivity, usually show a lower treatment response, On the other hand, exaggerated amygdala reactivity, which is a typical characteristic of the nondissociative subtype, has been shown to predict a poor response to exposure-based therapy,

These results suggest that excessively under- or overmodulatory states may hamper the treatment response. Based on such findings and our model, we can hypothesize that treatment response at a given time point could be predicted by the current imbalance between amygdala and vmPFC activity within individual patients.

When predicting treatment response, it is important to consider the general characteristics of reciprocal inhibitory circuits which could induce a switch of states within the short time scale found here but also in the order of weeks, This may explain the different periods of symptom fluctuations observed in previous studies,

Future studies based on the reciprocal inhibition model may lead to development of new therapies to maximize their effectiveness by targeting the period of a given emotional modulatory state. The reciprocal inhibition model may also aid in the understanding of subtype development in PTSD.

Imbalance in the time a person spends in emotional under- and overmodulatory states, at the early phase of PTSD development, is predicted to get exaggerated in the long term by Hebbian-like synaptic plasticity, Even if amygdala activity is only temporarily dominant in the early phase of PTSD development (Fig.1a bottom), this might result in long-term potentiation of inhibitory synapses from the amygdala to the vmPFC and long-term depression of inhibitory synapses from the vmPFC to the amygdala.

For people for whom this is the case, the undermodulatory state may progressively become more dominant, contributing to them to eventually receive the diagnosis of nondissociative PTSD. Along a similar vein, dominance of the vmPFC in early phases of PTSD development may eventually lead to a prolonged overmodulatory state and thus the eventual diagnosis of dissociative PTSD.

• Based on this synaptic plasticity reasoning, the amount of time a patient spends in each state may reflect how far along their disorder has progressed.
• In this way, the reciprocal inhibition model may partly explain the development of the PTSD subtypes.
• Although our model may partially explain the development of PTSD subtypes, we note that emotional under- or overmodulatory states may not completely and directly correspond to current definitions of nondissociative and dissociative PTSD subtypes.

This is because, in our model, we used avoidance symptoms as an index of the emotional overmodulatory state, considering that these are a prerequisite for PTSD diagnosis, and thus all patients express some avoidance symptoms regardless of subtype. Nonetheless, analyses of our experimental data showed the similar results regardless of whether the avoidance symptom cluster was used by itself or together with dissociative symptoms.

1. While this suggests that common underlying neural mechanisms may underlie avoidance symptoms and dissociative symptoms, future analyses are required to fully understand relationships of the two states, symptoms, and subtypes.
2. Our results suggest that time spent in each emotional modulatory state differs between PTSD subtypes.

That is, the findings of our behavioral experiment revealed that the relative frequency of the emotional undermodulatory state, as indexed by the number of trials on which attention was biased toward threat, was numerically but not statistically greater in patients with the nondissociative subtype compared with those with the dissociative subtype ( t  (19) = 1.38, p  = 0.18).

• This result is consistent with the assumption of the inhibitory reciprocal inhibition model that the two emotional modulatory states alternate in a continuous manner.
• Future studies may further test this assumption with a larger sample size.
• This is because a medium effect size (Hedge’s d  = 0.60) was found, which indicates that a sample size of N  = 44 for each group is required to reach statistical significance.

Some limitations of this study are as follows. First, there was nonuniformity in the studies included in the behavioral meta-analysis, as well as those included in the imaging meta-analysis, regarding several factors such as the experimental conditions and preprocessing methods.

However, despite these methodology differences, we still observed symptom imbalance to strongly correlate with both TAB and amygdala activity, which indicates the robustness of our findings. Second, we only selected nine studies each for the behavioral and imaging meta-analyses. However, each study reported the results with relatively large sample sizes (total N  = 316, N  = 491, respectively).

Third, although neural evidence from previous studies, such as data from functional magnetic resonance imaging (fMRI) studies, may support individual fluctuations and a pivotal role of vmPFC, we did not obtain neuroimaging data in the current experimental study.

Therefore, there is a need for future neuroimaging studies on patients with PTSD focusing on within individual alternating dynamics. Although more extensive examination of our reciprocal inhibition model is necessary, we believe that the proposed model provides a novel useful tool for advancing the diagnosis and treatment of PTSD.

Classifying patients with PTSD with different symptoms into different subtypes has allowed more careful analysis of their differential responses to psychological trauma, which is expected to lead to a more sophisticated understanding of the neurobiology and treatment of PTSD,

• For example, understanding of the relationships between subtype classifications and related clinically important findings have been largely advanced by the “model of emotional under- and overmodulation in PTSD”,
• By extending their model to include alternating dynamics between the two different PTSD states within individual patients, our model should hopefully further such advancements.

Overall, our reciprocal inhibition model coherently explains the dynamic alternations and associations between PTSD neural states, attentional biases, and symptoms. Therefore, the reciprocal inhibition model may be useful as a unifying framework to understand the complicated alternating dynamics of the diverse characteristics of PTSD.

What is the opposite of reciprocal inhibition?

What is the Difference Between Autogenic and Reciprocal Inhibition? – Autogenic inhibition relaxation is the ability of a muscle to remain relaxed while it experiences a stretch. On the other hand, reciprocal inhibition relaxation is the relaxation of the opposite muscle when the agonist muscle experiences a stretch.

• Thus, this is the key difference between autogenic and reciprocal inhibition.
• Autogenic inhibition takes place in the same muscle while reciprocal inhibition takes place in the opposite muscle.
• Autogenic inhibition is mainly recognized by the GTO, while reciprocal inhibition is mainly recognized by the muscle spindles.

So, this is also a significant difference between autogenic and reciprocal inhibition. Moreover, another important difference between autogenic and reciprocal inhibition is that the autogenic inhibition is mainly responsible for preventing muscle and tendon undergoing extreme tension, while reciprocal inhibition mainly protects muscle from injuries.

What are the three 3 factors of reciprocal determinism?

Albert Bandura’s theory of Reciprocal Determinism posits that how humans act is influenced by three factors: environment, individual characteristics, and behavior. In addition, all three factors are influenced by each other, known as triadic reciprocal causation.

What is reciprocal influence in psychology?

Reciprocal determinism is a social-cognitive theory which argues that behavior, cognition, and environment all interact with and influence one another.

What is reciprocal relationship in psychology?

The situation in which two variables can mutually influence one another ; that is, each can be both a cause and an effect.

What is reciprocal easy examples?

Other Definitions of Reciprocal – It has many other definitions too :

• It is also called the multiplicative inverse,
• It is similar to turning the number upside down,
• It is also found by interchanging the numerator and denominator.
• All the numbers have reciprocal except 0.
• The product of a number and its reciprocal is equal to 1.
• Generally, reciprocal is written as, 1/x or x -1 for a number x.

• Example : The reciprocals of 3 and 8 are 1/3 and 1 /8.
• It is also expressed by the number raised to the power of negative one and can be found for fractions and decimal numbers too.
• In maths, when you take the reciprocal twice, you will get the same number that you started with.

Example: The reciprocal of 4 is 1/4. When you repeat this step it becomes 4/1 or 4, Thus, you get the same number where you started with.

What is reciprocal Behaviour?

A reciprocal action or arrangement involves two people or groups of people who behave in the same way or agree to help each other and give each other advantages.

What is an example of reciprocal inhibition reflex?

2.1 Spinal Reflexes 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.

Figure 2.1 Myotatic reflex. 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 2.1. A waiter is holding an empty tray, when unexpectedly a pitcher of water is placed on the tray. Because the waiter’s muscles were not prepared to support the increased weight, the tray should fall. However, a spinal reflex is automatically initiated to keep the tray relatively stable.

1. When the heavy pitcher is placed on the tray, the increased weight stretches the biceps muscle, which results in the activation of the muscle spindle ‘s Ia afferents.
2. 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. In this way, the higher levels of the motor system are able to send a simple command (“maintain current posture”) and then be uninvolved in its implementation.

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.

Reciprocal inhibition in the stretch reflex 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 2.2).

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.

Figure 2.2 Reciprocal inhibition in stretch reflex. 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. Note: Locations of neurons within spinal cord are not meant to be anatomically accurate.

Autogenic inhibition reflex The Golgi tendon organ is involved in a spinal reflex known as the autogenic inhibition reflex (Figure 2.3). 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,

Figure 2.3 Autogenic inhibition. 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. Note: Locations of neurons within spinal cord are not meant to be anatomically accurate.

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.
• That is, if some muscle fibers are bearing more of the load than others, their Golgi tendon organs will be more active, which will tend to inhibit the contraction of those fibers.

As a result, other muscle fibers that are less active will have to contract more to pick up the slack, thereby sharing the work load more efficiently. Reciprocal excitation in the autogenic inhibition reflex Just as in the stretch reflex, the autogenic inhibition reflex must coordinate the activity of the extensor and flexor muscle groups (Figure 2.4).

Figure 2.4 Reciprocal excitation in the autogenic inhibition reflex. Note: Locations of neurons within spinal cord are not meant to be anatomically accurate.

Flexor reflex Spinal reflexes can be initiated by nonproprioceptive receptors as well as by proprioceptors. An important reflex initiated by cutaneous receptors and pain receptors is the flexor reflex. We have all experienced this reflex after accidentally touching a hot stove or a sharp object, as we withdraw our hand even before we consciously experience the sensation of pain.

1. This quick reflex removes the limb from the damaging stimulus more quickly than if the pain signal had to travel up to the brain, be brought to conscious awareness, and then trigger a decision to withdraw the limb.
2. The reflex circuit is illustrated in Figure 2.5.
3. A sharp object touching the foot causes the activation of Group III afferents of pain receptors.

These afferents enter the spinal cord and then travel up the cord. A branch of the afferent innervates an excitatory interneuron in the lumbar region of the spinal cord, which then excites an alpha motor neuron that causes contraction of the thigh flexor muscle.

1. The Group III afferent also continues upward to the L2 vertebra, where another branch innervates an excitatory interneuron at this level.
2. This interneuron excites the alpha motor neurons that excite the hip flexor muscle, allowing the coordinated activity of two muscle groups to withdraw the whole leg away from the painful stimulus.

Thus, spinal reflexes work not only at a single joint; they can also coordinate the activity of multiple joints simultaneously.

Figure 2.5 Flexor reflex. (Nolte, 2002) Note: Locations of neurons within spinal cord are not meant to be anatomically accurate.

Reciprocal inhibition in the flexor reflex When the knee joints and the hip joints are flexed, the antagonist extensor muscles must be inhibited (just as in the stretch reflex). Thus, the Group III afferents innervate inhibitory interneurons that in turn innervate the alpha motor neurons controlling the antagonist muscle.

Crossed extension reflex Further circuitry is needed to make the flexor reflex adaptive. Because the weight of the body is supported by both legs, the flexor reflex must coordinate the activity not only of the leg being withdrawn but also of the opposite leg (Figure 2.6). Imagine stepping on a tack, and having the flexor reflex withdraw your right leg immediately.

The left leg must simultaneously extend in order to support the body weight that would have been supported by the right leg. Without this coordination of the two legs, the shift in body mass would cause a loss of balance. Thus, the flexor reflex incorporates a crossed extension reflex.

Figure 2.6 Crossed extension reflex. (Nolte, 2002) Note: Locations of neurons within spinal cord are not meant to be anatomically accurate.

Recurrent inhibition of motor neurons (Renshaw cells) Axons of alpha motor neurons bifurcate in the spinal cord and innervate a special inhibitory interneuron called the Renshaw cell (Figure 2.7). This interneuron innervates and inhibits the very same motor neuron that caused it to fire.

Thus, a motor neuron regulates its own activity by inhibiting itself when it fires. This negative feedback loop is thought to stabilize the firing rate of motor neurons.2.2 Descending Motor Pathways The reflex circuits demonstrate that sophisticated neural processing occurs at the lowest level of the motor hierarchy.

These automatic reflexes can be modulated, however, by higher levels of the hierarchy. For example, when touching an iron to see if it is hot, your flexor reflex may be hypersensitive. As a result, you pull your hand away repeatedly before even touching the iron, anticipating that it may be hot.

Conversely, if you remove a hot dish from the oven and the heat starts to go through the oven mitt, you will suppress the flexor response so that you do not drop your dinner as you rush to put it down on a table. These modulations (both facilitatory and inhibitory) of the spinal reflexes arise from the descending pathways from the brainstem and cortex.

Voluntary movement and some sensory-driven reflex actions are also controlled by the descending pathways. The corticospinal system controls motor neurons and interneurons in the spinal cord. The corticobulbar system controls brainstem nuclei that innervate cranial muscles.

1. Parallel and Serial Processing Although the motor system is organized hierarchically, the hierarchy is not a simple chain of processing from higher to lower areas.
2. Many pathways enable the different levels of the hierarchy to influence each other.
3. Thus, the flow of information through the motor system has both a serial organization (communication between levels) and a parallel organization (multiple pathways between each level).

This parallel organization is critically important in understanding the various dysfunctions that can result from damage to the motor system. If the motor hierarchy had a strictly serial organization, like a series of links on a chain, then damage to any part of the system would produce severe deficits or paralysis in almost all types of movements.

However, because of the parallel nature of processing, paralysis is actually a relatively rare outcome, produced by damage to the lowest level of the hierarchy. Damage to higher levels results in deficits in motor planning, initiation, coordination, and so forth, but movement is still possible. The parallel nature of organization is also important for the ability of undamaged parts of the motor system to compensate (at least partially) for injuries to other parts of the system.

Descending motor pathways arise from multiple regions of the brain and send axons down the spinal cord that innervate alpha motor neurons, gamma motor neurons, and interneurons. The motor neurons are topographically organized in the anterior horn of the spinal cord according to two rules: the flexor-extensor rule and the proximal-distal rule (Figure 2.8).

Figure 2.8 Flexor-extensor rule and proximal-distal rule.

Flexor-extensor rule : motor neurons that innervate flexor muscles are located posteriorly to motor neurons that innervate extensor muscles. Proximal-distal rule : motor neurons that innervate distal muscles (e.g., hand muscles) are located lateral to motor neurons that innervate proximal muscles (e.g., trunk muscles). Descending motor pathways are organized into two major groups:

1. Lateral pathways control both proximal and distal muscles and are responsible for most voluntary movements of arms and legs. They include the
   1. lateral corticospinal tract
   2. rubrospinal tract
2. Medial pathways control axial muscles and are responsible for posture, balance, and coarse control of axial and proximal muscles. They include the
   1. vestibulospinal tracts (both lateral and medial)
   2. reticulospinal tracts (both pontine and medullary)
   3. tectospinal tract
   4. anterior corticospinal tract

Figure 2.9 Corticospinal tracts (also called pyramidal tracts). C lick on the labels to see the highlighted area.

Corticospinal tracts, The corticospinal tract originates in the motor cortex (Figure 2.9). The axons of motor projection neurons collect in the internal capsule, and then course through the crus cerebri (cerebral peduncle) in the midbrain. At the level of the medulla, these axons form the medullary pyramids on the ventral surface of the brainstem (hence, this tract is also called the pyramidal tract ).

At the level of the caudal medulla, the corticospinal tract splits into two tracts. Approximately 90% of the axons cross over to the contralateral side at the pyramidal decussation, forming the lateral corticospinal tract, These axons continue to course through the lateral funiculus of the spinal cord, before synapsing either directly onto alpha motor neurons or onto interneurons in the ventral horn.

The remaining 10% of the axons that do not cross at the caudal medulla constitute the anterior corticospinal tract, as they continue down the spinal cord in the anterior funiculus. When they reach the spinal segment at which they terminate, they cross over to the contralateral side through the anterior white commissure and innervate alpha motor neurons or interneurons in the anterior horn.

Thus, both the lateral and anterior corticospinal tracts are crossed pathways; they cross the midline at different locations, however. Function. The corticospinal tract (along with the corticobulbar tract) is the primary pathway that carries the motor commands that underlie voluntary movement. The lateral corticospinal tract is responsible for the control of the distal musculature and the anterior corticospinal tract is responsible for the control of the proximal musculature.

A particularly important function of the lateral corticospinal tract is the fine control of the digits of the hand. The corticospinal tract is the only descending pathway in which some axons make synaptic contacts directly onto alpha motor neurons. This direct cortical innervation presumably is necessary to allow the powerful processing networks of the cortex to control the activity of the spinal circuits that direct the exquisite movements of the fingers and hands.

• The percentage of axons in the corticospinal tract that innervate alpha motor neurons directly is greater in humans and nonhuman primates than in other mammals, presumably reflecting the increased manual dexterity of primates.
• Damage to the corticospinal tract results in a permanent loss of the fine control of the extremities.

Although parallel descending pathways can often recover the function of more coarse movements, these pathways are not capable of generating fine, skilled movements. In addition to the fine control of distal muscles, the corticospinal tract also plays a role in the voluntary control of axial muscles.

Figure 2.10 Rubrospinal tract. C lick on the labels to see the highlighted area.

Rubrospinal tract, The rubrospinal tract originates in the red nucleus of the midbrain (Figure 2.10). The axons immediately cross to the contralateral side of the brain, and they course through the brainstem and the lateral funiculus of the spinal cord.

• The axons innervate spinal neurons at all levels of the spinal cord. Function.
• The rubrospinal tract is an alternative by which voluntary motor commands can be sent to the spinal cord.
• Although it is a major pathway in many animals, it is relatively minor in humans.
• Activation of this tract causes excitation of flexor muscles and inhibition of extensor muscles.

The rubrospinal tract is thought to play a role in movement velocity, as rubrospinal lesions cause a temporary slowness in movement. In addition, because the red nucleus receives most of its input from the cerebellum, the rubrospinal tract probably plays a role in transmitting learned motor commands from the cerebellum to the musculature.

1. The red nucleus also receives some input from the motor cortex, and it is therefore probably an important pathway for the recovery of some voluntary motor function after damage to the corticospinal tract.
2. Vestibulospinal tracts,
3. The two vestibulospinal tracts originate in 2 of the 4 vestibular nuclei (Figure 2.11).

The lateral vestibulospinal tract originates in the lateral vestibular nucleus, It courses through the brainstem and through the anterior funiculus of the spinal cord on the ipsilateral side, before exiting ipsilaterally at all levels of the spinal cord.

• The medial vestibulospinal tract originates in the medial vestibular nucleus, splits immediately and courses bilaterally through the brainstem via the medial longitudinal fasciculus (MLF) and through the anterior funiculus of the spinal cord, before exiting at or above the T6 vertebra. Function.
• The vestibulospinal tracts mediate postural adjustments and head movements.

They also help the body to maintain balance. Small movements of the body are detected by the vestibular sensory neurons, and motor commands to counteract these movements are sent through the vestibulospinal tracts to appropriate muscle groups throughout the body.

Figure 2.11 Vestibulospinal tracts. Click on the labels to see the highlighted area.

Reticulospinal tracts, The two reticulospinal tracts originate in the brainstem reticular formation, a large, diffusely organized collection of neurons in the pons and medulla (Figure 2.12). The pontine reticulospinal tract originates in the pontine reticular formation, courses ipsilaterally through the medial longitudinal fasciculus and through the anterior funiculus of the spinal cord, and exits ipsilaterally at all spinal levels.

1. The medullary reticulospinal tract originates in the medullary reticular formation, courses mainly ipsilaterally (although some fibers cross the midline) through the anterior funiculus of the spinal cord, and exits at all spinal levels. Function.
2. The reticulospinal tracts are a major alternative to the corticospinal tract, by which cortical neurons can control motor function by their inputs onto reticular neurons.

These tracts regulate the sensitivity of flexor responses to ensure that only noxious stimuli elicit the responses. Damage to the reticulospinal tract can thus cause harmless stimuli, such as gentle touches, to elicit a flexor reflex, The reticular formation also contains circuitry for many complex actions, such as orienting, stretching, and maintaining a complex posture.

Figure 2.12 Reticulospinal tracts. Click on the labels to see the highlighted area.

Tectospinal tract, The tectospinal tract (Figure 2.13) originates in the deep layers of the superior colliculus and crosses the midline immediately. It then courses through the pons and medulla, just anterior to the medial longitudinal fasciculus. It courses through the anterior funiculus of the spinal cord, where the majority of the fibers terminate in the upper cervical levels.

Figure 2.13 Tectospinal tract. Click on the labels to see the highlighted area.

2.3 Influences of Descending Pathways on Spinal Circuits Voluntary movement, The most distinctive function of the descending motor pathways is the control of voluntary movement. These movements are initiated in the cerebral cortex, and the motor commands are transmitted to the musculature through a variety of descending pathways, including the corticospinal tract, the rubrospinal tract, and reticulospinal tracts.

• How voluntary movements are initiated and coordinated by the motor cortex is the subject of the next chapter.
• Reflex modulation,
• Another critical function of the descending motor pathways is to modulate the reflex circuits in the spinal cord.
• The adaptiveness of spinal reflexes can change depending on the behavioral context; sometimes the gain (strength) or even the sign (extension vs.

flexion) of a reflex must be changed in order to make the resulting movement adaptive. The descending pathways are responsible for controlling these variables. For example, consider the flexor reflex under two conditions.

1. Imagine a situation in which you want to pick up a dish from the stove top, but you are uncertain whether it is hot or cold. You may attempt to lightly touch the surface, and this will often lower the threshold of the flexor reflex, making you more likely to pull your hand away even if the dish is not particularly hot. (You may even withdraw your hand numerous times before even touching the dish!) Descending pathways have lowered the threshold for producing the reflex in this case, making it easier for a weaker nociceptive input to trigger the reflex; these pathways can also change the gain of the reflex, making the withdrawal response greater than usual.
2. Imagine now picking up the dish in order to move it to the table. As you hold the dish, more of its heat begins to transfer to your hand, and it starts to get quite hot. Rather than dropping the dish and spilling your dinner all over the floor, you rush to the table to put it down, before withdrawing your hand and wishing you had used an oven mitt. In this case, the descending pathways inhibited the flexor response.

Gamma bias, Recall from the previous chapter that there are two types of spinal motor neurons. Alpha motor neurons innervate extrafusal muscle fibers, which provide the force for a muscle contraction. Gamma motor neurons innervate the ends of intrafusal fibers and help to maintain the tautness of muscle spindles, such that they are sensitive to changes of muscle length over a wide range.

In order to work adaptively, the activity of alpha and gamma motor neurons must be coordinated. Thus, whenever motor commands are sent by descending pathways to alpha motor neurons, the appropriate compensating commands are sent to gamma motor neurons. This coordination of alpha-gamma motor commands is called alpha-gamma coactivation, and the adjustment of spindle sensitivity by gamma activation is called gamma bias,

Consider the following two examples:

1. When a command is given to a muscle to contract, the muscle spindles become slack, thereby making them insensitive to further changes in muscle length. To compensate for this, the gamma motor neurons that innervate these intrafusal muscle fibers are activated in concert with the alpha motor neurons, allowing the intrafusal fibers to contract with the muscle. This preserves the sensitivity of the muscle to unexpected stretches of the muscle (see Figure 1.10 of the chapter on Motor Unit and Muscle Receptors ).
2. When a muscle contracts, the antagonist muscle is stretched during the movement. An obvious problem arises when one considers the stretch reflex of the antagonist muscle. If contraction of a muscle causes the activation of the stretch reflex of the antagonist muscle, the antagonist muscle will contract to resist the movement of the limb. How is it possible to ever flex a joint when the stretch reflex of the extensor muscle causes it to extend the joint instead? Alpha-gamma coactivation solves this problem by relaxing the contraction of the intrafusal fibers of the antagonist muscle, allowing the muscle to be stretched without triggering the stretch reflex during a voluntary movement.

Test Your Knowledge

• Question 1
• A
• B
• C
• D
• E

The lateral corticospinal tract.A. Undergoes a 50% decussation in the caudal medulla.B. Arises exclusively from the primary motor cortex.C. Is an uncrossed pathway.D. Plays a major role in the fine control of distal musculature.E. Terminates primarily in the posterior (dorsal) horn.

The lateral corticospinal tract.A. Undergoes a 50% decussation in the caudal medulla. This answer is INCORRECT. About 90% of the corticospinal tract fibers cross to form the lateral corticospinal tract.B. Arises exclusively from the primary motor cortex.C. Is an uncrossed pathway.D. Plays a major role in the fine control of distal musculature.E.

Terminates primarily in the posterior (dorsal) horn. The lateral corticospinal tract.A. Undergoes a 50% decussation in the caudal medulla.B. Arises exclusively from the primary motor cortex. This answer is INCORRECT. The corticospinal tract arises from numerous cortical areas.C.

Is an uncrossed pathway.D. Plays a major role in the fine control of distal musculature.E. Terminates primarily in the posterior (dorsal) horn. The lateral corticospinal tract.A. Undergoes a 50% decussation in the caudal medulla.B. Arises exclusively from the primary motor cortex.C. Is an uncrossed pathway.

This answer is INCORRECT. The lateral corticospinal tract crosses at the pyramidal decussation.D. Plays a major role in the fine control of distal musculature.E. Terminates primarily in the posterior (dorsal) horn. The lateral corticospinal tract.A. Undergoes a 50% decussation in the caudal medulla.B.

• Arises exclusively from the primary motor cortex.C.
• Is an uncrossed pathway.D.
• Plays a major role in the fine control of distal musculature.
• This answer is CORRECT! E.
• Terminates primarily in the posterior (dorsal) horn.
• The lateral corticospinal tract.A.
• Undergoes a 50% decussation in the caudal medulla.B.

Arises exclusively from the primary motor cortex.C. Is an uncrossed pathway.D. Plays a major role in the fine control of distal musculature.E. Terminates primarily in the posterior (dorsal) horn. This answer is INCORRECT. Most lateral corticospinal fibers terminate in the intermediate zone.

• Question 2
• A
• B
• C
• D
• E

In reciprocal excitation of the Golgi tendon reflex, stimulation of.A. Ia afferent fibers causes inhibition of synergistic muscles.B. Ib afferent fibers causes inhibition of antagonist muscles.C. Ia afferent fibers causes inhibition of antagonist muscles.D. Ib afferent fibers causes excitation of antagonist muscles.E. Ia afferent fibers causes excitation of muscles on the contralateral side. In reciprocal excitation of the Golgi tendon reflex, stimulation of.A. Ia afferent fibers causes inhibition of synergistic muscles. This answer is INCORRECT. Ia afferents innervate the muscle spindle, not the Golgi tendon organ.B. Ib afferent fibers causes inhibition of antagonist muscles.C. Ia afferent fibers causes inhibition of antagonist muscles.D. Ib afferent fibers causes excitation of antagonist muscles.E. Ia afferent fibers causes excitation of muscles on the contralateral side. In reciprocal excitation of the Golgi tendon reflex, stimulation of.A. Ia afferent fibers causes inhibition of synergistic muscles.B. Ib afferent fibers causes inhibition of antagonist muscles. This answer is INCORRECT. Ib afferents inhibit the homonymous muscle, not the antagonist muscle.C. Ia afferent fibers causes inhibition of antagonist muscles.D. Ib afferent fibers causes excitation of antagonist muscles.E. Ia afferent fibers causes excitation of muscles on the contralateral side. In reciprocal excitation of the Golgi tendon reflex, stimulation of.A. Ia afferent fibers causes inhibition of synergistic muscles.B. Ib afferent fibers causes inhibition of antagonist muscles.C. Ia afferent fibers causes inhibition of antagonist muscles. This answer is INCORRECT. Ia afferents innervate the muscle spindle, not the Golgi tendon organ.D. Ib afferent fibers causes excitation of antagonist muscles.E. Ia afferent fibers causes excitation of muscles on the contralateral side. In reciprocal excitation of the Golgi tendon reflex, stimulation of.A. Ia afferent fibers causes inhibition of synergistic muscles.B. Ib afferent fibers causes inhibition of antagonist muscles.C. Ia afferent fibers causes inhibition of antagonist muscles.D. Ib afferent fibers causes excitation of antagonist muscles. This answer is CORRECT! E. Ia afferent fibers causes excitation of muscles on the contralateral side. In reciprocal excitation of the Golgi tendon reflex, stimulation of.A. Ia afferent fibers causes inhibition of synergistic muscles.B. Ib afferent fibers causes inhibition of antagonist muscles.C. Ia afferent fibers causes inhibition of antagonist muscles.D. Ib afferent fibers causes excitation of antagonist muscles.E. Ia afferent fibers causes excitation of muscles on the contralateral side. This answer is INCORRECT. Ia afferent fibers innervate the muscle spindle, and the Golgi tendon reflex affects the ipsilateral side.

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