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Why is the Patellar reflex not triggered when the tendon is extended slowly?

Why is the Patellar reflex not triggered when the tendon is extended slowly?


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I have been previously told that the Patellar reflex (knee-jerk-reaction) exists to prevent the hyper-extension of the patellar tendon. Yet if the impact to the tendon is delivered slowly - i.e. by pressing down on it rather than striking it - there is no reflex response. Why is this, as surely the tendon is being extended by the same amount?


This effect you are observing has to do with the nature of the afferent neurons (Ia fibers), which carry a signal into the spinal cord and synapse onto motor neurons directly. See this text (scroll down to section 1.10) for a diagram. At their other end, these Ia fibers penetrate into the muscle and wrap themselves around the body of the muscle spindles,"[which] are specialized receptors that signal (a) the length and (b) the rate of change of length (velocity) of the muscle."

Because the main role of these spindles is to monitor the muscles for very rapid changes in length, the neurons have a static range which is optimized for these quick jerks (rather than firing over a wide range of velocities). When you are stretching the muscle slowly, the Ia fiber is not building up a sufficient depolarization to fire off an action potential.


This article presents a case study of a patient diagnosed with dysfunction of the sternocleidomastoid (SCM) muscle, a condition which can result in head and face pain, nausea, dizziness, coryza, and lacrimation. In this particular case, the SCM muscle had developed tightness and weakness with presence of multiple trigger points within both heads. A combination of passive and active treatments were utilized to successfully treat this condition.

Cet article présente une étude menພ auprès d’un patient souffrant d’une lésion du muscle sterno-cléido-masto໽ien (SCM), un état pouvant causer de l𠆚lgie craniofaciale, des nausພs, des étourdissements, de la rhinite et du larmoiement. Dans ce cas particulier, le muscle SCM était devenu tendu et faible et présentait des zones gฬhettes multiples aux deux chefs. On a utilisé une combinaison de traitements passifs et actifs pour traiter ce syndrome avec succès.


How to Loosen a Tight Ligament

Ligaments are bands of fibrous connective tissue that connect bones to other bones. When a ligament is tight, it may be difficult to move a joint through its entire range of motion and the muscles surrounding the ligaments may hurt. If you experience pain in a ligament after stretching or after an injury, avoid doing anything to loosen the ligament before you see the doctor. You might have a tear or other injury requiring medical treatment. If, however, your ligaments merely feel tight, you may be able to loosen them up.

Step 1

Roll the affected area on a foam roller. Foam rollers are long cylindrical pieces of foam that can safely stretch, exercise and loosen tense muscles. When muscles loosen up, ligaments may also loosen. Place the roller on the floor and then position the affected area on top of the roller. Slowly roll back and forth across the foam roller five to 10 times. You can repeat this exercise several times each day. If you experience pain, tingling or strange sensations while rolling, stop immediately and consult a physician.

Step 2

Exercise the affected area using low-intensity exercises such as walking or stretching. This increases blood flow and speeds healing time, according to "The Sports Physiotherapist." Additionally, tightness in the ligaments can be caused by a sedentary lifestyle or insufficient exercise, and by keeping your body moving you can reduce ligament tightness.

Step 3

Massage the muscles surrounding the ligament using myofascial trigger point techniques. Muscles frequently develop small knots or nodules from which tension and pain radiate. Apply pressure using your fingers or a massage cane directly to the area and massage in one direction only. This technique should be painful, but not unbearable. By massaging muscle knots, you can gradually loosen them. This, in turn, can help alleviate ligament tightness and reduce pain.


How is tennis elbow diagnosed?

Your healthcare provider can usually diagnosis your tennis elbow by a physical exam. In some cases, you may certain tests, such as:

An X-ray to look at the bones of your elbow to see if you have arthritis in your elbow.

Magnetic resonance imaging (MRI) can show your tendons and how severe the damage is. An MRI of your neck can show if arthritis in your neck, or disk problems in your spine are causing your arm pain.

Electromyography (EMG) of your elbow may show if you have any nerve problems that may be causing your pain.


Diseases of the Neurologic System

Spinal Reflexes

Five spinal reflexes should be evaluated in sheep and goats with suspected neurologic disease: the extensor reflex of the front limb, the panniculus reflex, the patellar reflex, the perineal reflex, and the withdrawal reflexes of the forelimbs and hindlimbs. The spinal reflexes are best examined with the animal in lateral recumbency, with the side to be evaluated in the upper position. Spinal reflexes involve a local reflex arc that includes a stretch or touch receptor, an afferent peripheral nerve that relays information to the spinal cord gray matter, spinal cord interneurons that can stimulate or inhibit other neurons, an efferent motor neuron that exits the spinal cord, and a muscle. Spinal reflexes do not require conscious or voluntary input for normal function.

Assessment of spinal reflexes tests the integrity of the lower motor neuron (LMN) but also can provide some information on influences of the upper motor neurons (UMNs) on the LMN ( Table 13-1 ). The UMNs are a group of neurons that do not physically exit the nervous system and provide stimulatory or inhibitory influences to the LMN. The LMNs are composed of the peripheral nerves and the effector organs (primarily skeletal muscles). Several responses can be observed when spinal reflexes are tested. A normal response can be observed, which indicates normal sensory and motor components of the reflex arc. An exaggerated response often is observed with UMN pathway abnormalities. A diminished or absent response indicates LMN disease in either its sensory or motor components. In addition to diminished responses, animals with LMN disease exhibit muscle atrophy, hyporeflexia or areflexia, hypotonia or atonia, and paresis.

Testing the extensor reflex of the front limb assesses the radial nerve. The radial nerve is responsible for weight-bearing of the front limb and innervates the triceps muscle group. With the animal in lateral recumbency, the extensor reflex is assessed by placing a hand under the foot of the animal and pushing the limb gently toward the animal until extensor tone is noted. The normal reflex is for the animal to “push back” with its leg. Animals with LMN disease display decreased or absent resistance, and those with UMN disease may exhibit increased tone of the triceps muscle.

Testing the patellar reflex evaluates motor and sensory components of the femoral nerve. The femoral nerve innervates the quadriceps muscles, which are responsible for extension of the stifle and weight-bearing in the hindlimb. The patellar reflex is a tendinous reflex and is elicited by lightly tapping the patellar tendon with a reflex hammer while observing an extension of the stifle. Patellar reflex testing is a subjective assessment, and clinicians should be as consistent as possible in technique. To begin, the limb should be in relaxed flexion with the patellar tendon just barely tightened. The tendon is palpated, and then, while the examiner’s fingers are kept on the tendon, the limb is flexed until the tendon feels tight. To raise tension in the tendon, the clinician can place a hand under the foot while extending the digits. The tapping on the tendon is done with a pendulum motion. The reflex cannot be elicited if the limb is tense, but by tapping the tendon rhythmically, the animal relaxes over time. The strength of the patellar reflex is proportional to the force applied to the tendon. The plexor (hammer) used for examination of large dogs is adequate for testing the reflex of small ruminants. The patellar reflex combined with the proprioceptive reaction is used to determine the integrity of the LMN. With LMN lesions, deficits exist in conscious proprioception and patellar reflexes, whereas deficits of conscious proprioception in animals with intact patellar reflexes indicate lesions in the UMN.

Withdrawal reflexes also are referred to as flexion reflexes, and testing is performed by applying a noxious stimulus to the medial or lateral digits of the front limbs and hindlimbs. A hemostat often is used to apply the stimulus. In the front limb, the withdrawal reflex evaluates the axillary, median, and ulnar nerves. In the hindlimb, the reflex evaluates the sciatic nerve on the lateral part of the limb and the femoral nerve on the medial part of the limb. A normal response is the flexion of the limb fully away from the stimulus.

Testing the perineal reflex is performed by pinching the skin around the anus. The perineal reflex tests the afferent pudendal nerve, whereas the efferent nerve fibers are part of the caudal nerves. The normal response is anal sphincter contraction and downward contraction of the tail. During the reflex test, the tail should not be manipulated, because this may cause contraction of the anus.

The panniculus reflex or cutaneous trunci reflex also relies on a reflex arc. This test is performed by applying stimuli to both sides of the body starting caudally at the wing of the ileum to the cranial thoracic area (at the T2 level). The stimulus usually is applied with the tip of a ballpoint pen or a hemostat. The sensory fibers from the skin enter the dorsal root of the spinal cord and then ascend to the C8 and T1 segments, where the efferent limb of the reflex is the motor neurons of the lateral thoracic nerve. A normal reflex is flinching of the skin. If twitching of the skin occurs at the level of the wing of the ileum, then the afferent limb is intact in its entirety. However, a transection of the spinal cord caudal to T1 may result in a decreased or absent cutaneous response in the area caudal to the transection.


Integrative Functions of the Enteric Nervous System

22.3.3 Propulsive Motility

The peristaltic reflex is a polysynaptic reflex circuit in the ENS that underlies all of the propulsive motility patterns found in the small and large intestine and esophagus. It is the intestinal analog of spinal motor reflexes (e.g., monosynaptic patellar and Achilles tendon reflexes and polysynaptic withdrawal reflexes). Spinal reflexes are investigator-evoked artifacts arising from connections of stretch receptors in the muscle or nociceptors in the skin that activate alpha spinal motor neurons to evoke contractions/twitches in particular somatic muscles (e.g., the quadriceps muscle in a patellar tendon reflex). Monosynaptic spinal reflexes reflect the effects of abrupt activation of stretch receptors (i.e., muscle spindles) in the muscle and have little relevance for full understanding of the complexity of neural control of posture and movement. The peristaltic reflex is similar in that it is a fixed response evoked by investigational stretching of the intestinal wall or stroking of the mucosa. It is like a polysynaptic spinal reflex because it is a motor response to sensory stimulation that is repeated the same way each time the “hardwired” reflex circuit is activated. The peristaltic reflex circuit is “wired” such that it evokes relaxation of the circumferentially oriented muscle layer and contraction of the longitudinal muscle below the point of stimulation and contraction of the circumferentially oriented muscle layer above the point of stimulation. This is the reflex underlying propulsive motility in the aboral direction from the esophagus to the large intestine. The connections in the reflex are reversed for propulsive motility moving luminal contents in the oral direction during emesis in the small intestine and in normal states and responses to an obstruction in the large intestine. 51,52 In the latter cases, the reflex circuit is wired such that it evokes relaxation of the circumferentially oriented muscle layer and contraction of the longitudinal muscle in the oral direction and contraction of the circumferentially oriented muscle layer as the trailing event.

Like spinal reflexes, the peristaltic reflex is positioned at the lowest level of the hierarchical organization of neural control of intestinal motility and underlies each of the various patterns of propulsive motility that impart functionality to the intestine during daily life. As with a spinal motor reflex, the sequencing of the pattern of behavior of the intestinal longitudinal and circular muscles is hardwired into the circuitry, whereas the strength of each motor component of the pattern and the repetition rate of the pattern are adjusted by sensory feedback or other commands to automatically compensate for local loads and higher functional demands on the intestine as a whole. The distance over which propulsion occurs and the direction in which it occurs in the specific patterns of motility, which characterize the various digestive states, are additional factors requiring a higher order of neural control. Short distance propulsion in the postprandial digestive state, propulsion over intermediate distances during interdigestive motility (i.e., migrating motor complex), and long distance power propulsion, all in the orthograde direction, and long-distance retropulsion during emesis are neural control requirements that are met by the integrative microcircuitry of the ENS. Further improvement in understanding of the neural integration of intestinal motility will require moving forward from the “over-used” concept of the peristaltic reflex and on to investigation of microcircuits in positions at levels of organization above the reflex “hardwiring” that faithfully reproduces the muscle behavior each time the investigator stretches the intestinal wall or strokes the mucosa.

The muscle layers of the intestine contract and relax in a stereotyped pattern during peristaltic propulsion ( Figure 22.3 ). This pattern is determined by the sequence in which the peristaltic polysynaptic reflex circuit activates excitatory and inhibitory musculomotor neurons to the longitudinal and circular muscle layers. During propulsion, the longitudinal muscle layer in the segment ahead of the advancing intraluminal contents contracts in response to activation of its excitatory motor innervation, while at the same time, the circular muscle layer relaxes in response to activation of its inhibitory motor innervation. The intestinal tube behaves geometrically like a cylinder with constant surface area. 48 Shortening of the longitudinal axis of the cylinder during contraction of the longitudinal muscle is accompanied by a widening of the cross-sectional diameter. The simultaneous shortening of the longitudinal axis and relaxation of the circular muscle results in expansion of the lumen, which prepares a receiving segment ( Figure 22.3 ) for the forward-moving intraluminal contents during peristaltic propulsion.

Figure 22.3 . Integrated control of contractile behavior of the longitudinal and circular muscle coats forms propulsive and receiving segments in stereotypic fashion during peristaltic propulsion in the intestine.

(A) The circumferential and longitudinal muscle layers of the intestine behave in a stereotypical pattern during peristaltic propulsion. A “hardwired” reflex circuit in the enteric nervous system determines the pattern of behavior of the two muscle layers. During peristaltic propulsion, the longitudinal muscle layer in the segment ahead of the advancing intraluminal contents contracts, while the circumferential muscle layer relaxes. Simultaneous shortening of the longitudinal intestinal axis and relaxation of the circumferential muscle in the same segment results in expansion of the lumen, which becomes a receiving segment for the forward-moving contents. The second component of the reflex is contraction of the circular muscle in the segment behind the advancing intraluminal contents. The longitudinal muscle layer in the same segment relaxes simultaneously with contraction of the circular muscle, which results in conversion of this region to a propulsive segment that propels the luminal contents ahead into the receiving segment. (B) Motor behavior of the intestinal wall during the peristaltic reflex in a segment of guinea pig ileum in response to distension by infusion of saline at time = xs. Shortening of the longitudinal axis and expansion of the lumen is seen in the receiving segment, and contraction of the circular muscle and reduction in the diameter of the receiving segment is apparent at time = 3xs as propulsion proceeds to empty the lumen through the outlet.

(Wall behavior was redrawn from photographic images provided to the author by Professor M. Takaki, Dept. of Physiology, Nara Medical University, Nara University, Japan.)

Organization of a receiving segment constitutes the leading component and one-half of propulsive peristaltic reflex behavior. The second half is contraction of the circular muscle in the segment behind the advancing intraluminal contents. This is a propulsive segment that propels the luminal contents ahead into the receiving segment ( Figure 22.3 ). Behavior of the longitudinal muscle in the propulsive segment is unclear. In view of the fact that shortening of the much stronger circular muscle and reduction of the intestinal radius in this segment generates forces that oppose shortening in the longitudinal axis, it would appear that the two muscle coats are antagonistic in the same sense that the quadriceps femoris and gastrocnemius are antagonistic muscles that oppose one another in the movement of the lower leg. In this arrangement contraction of the longitudinal muscle coat in the propulsive segment would be energy inefficient and most likely does not occur. On the other hand, one laboratory has interpreted observations during imaging of changes in intramuscular Ca 2+ concentrations as support for a conclusion that the longitudinal muscle coat contracts simultaneously with the circular muscle coat in the propulsive segment during peristaltic propulsion. 49–52

The propulsive segment is formed when neural connections in the reflex circuit “turn off” the inhibitory musculomotor innervation to the circular muscle. Silencing of the inhibitory innervation permits the omnipresent electrical slow waves that spread electrotonically into the circular muscle to depolarize the muscle fibers to action potential threshold and evoke contraction of the circular muscle in the propulsive segment. Contractions recorded by sensing devices implanted on the bowel during digestive and interdigestive small intestinal motor behavior reflect the formation of propulsive segments. They occur at the frequency of the electrical slow waves because removal of inhibition from the circular muscle allows it to respond to the electrical current flowing from the ICC network during each slow wave cycle. On the other hand, formation of the propulsive segment during power propulsion (see Section 22.3.6 ) occurs unrelated to the frequency of the electrical slow waves and involves much stronger contraction of the circular muscle in the propulsive segment than occurs during peristaltic propulsion in the digestive and interdigestive motor patterns.

The heuristic model for peristaltic propulsion has blocks of the basic polysynaptic reflex circuit connected “in series” along the length of small intestine and large intestine ( Figure 22.4 ). A block of the basic polysynaptic circuit is formed by synaptic connections between interneurons and motor neurons ( Figure 22.5 ). Propulsion occurs over extended lengths of intestine as blocks of the basic circuit are recruited to activity in consecutive segments. In this respect, the intestine is like the spinal cord where connections for polysynaptic reflexes remain irrespective of the destruction of adjacent regions of the spinal cord. Resection of an intestinal segment does not alter the reflex circuitry in the two segments remaining on either side of the resection. Consequently, organized propulsion is not impaired after resection of various lengths of bowel.

Figure 22.4 . Synaptic gates determine distance of propagation of peristaltic propulsive motility.

Presynaptic mechanisms gate the transfer of signals between sequentially positioned blocks of polysynaptic peristaltic reflex circuitry. Synapses between the neurons, which carry activating signals to each successive block of circuitry, function as gating points for control of the distance over which peristaltic propulsion travels. Messenger substances that act presynaptically to inhibit the release of transmitter at the excitatory synapses close the gates for transfer of information, thereby determining the distance of propagation. Drugs that facilitate the release of neurotransmitters at the excitatory synapses (e.g., cisapride and 5-HT4 partial agonists) have therapeutic efficacy by increasing the probability of information transfer at the synaptic gates, thereby enhancing propulsive motility.

Figure 22.5 . A “hardwired” polysynaptic peristaltic reflex circuit in the ENS underlies intestinal propulsive motility.

Two kinds of input activate the circuit: distension of the intestinal wall and activation of mechanoreceptors and stimulation of release of 5-HTfrom enterochromaffin cells by mechanical stimulation of the mucosa. When the reflex circuit is active, excitatory motor neurons to the longitudinal muscle coat and inhibitory motor neurons to the circular muscle coat are activated to form the receiving segment below the point of stimulation (see Figure 22.3 ). At the same time activation of excitatory motor neurons to the circular muscle coat and inactivation of inhibitory motor neurons to the circular muscle coat occurs in the propulsive segment above the point of stimulation.

Synaptic gates connect the blocks of basic circuitry in the heuristic model and contribute to a mechanism for controlling the distance over which the complex of propulsive and receiving segments travel ( Figure 22.4 ). When the gates are opened, neural signals pass between successive blocks of the basic circuit resulting in propagation of the peristaltic event over extended distances. Long-distance propulsion is prevented when all gates are closed.

Well-understood presynaptic facilitatory and inhibitory mechanisms in the microcircuitry of the ENS are presumed to be involved in gating the transfer of signals between sequentially positioned blocks of reflex circuitry in the heuristic model (see Chapter 21 ). Synapses formed by the interneurons that transmit excitatory signals to the next downstream block of circuitry are gating points for controlling the distance over which peristaltic propulsion travels ( Figure 22.4 ). Messenger substances that act presynaptically to inhibit the release of transmitter at the excitatory synapses stop transmission and close the entrance gates to the next downstream block of circuitry, thereby determining the distance of propagation. Drugs that facilitate the release of neurotransmitters at the excitatory synapses (e.g., cisapride and tegaserod) 53–55 have therapeutic application by increasing the probability of information transfer at the synaptic gates, thereby enhancing propulsive motility.


Improve Movements to Eliminate Knee Pain

The lower extremity works as a comprehensive unit performing many of the repetitive tasks at home, work, and during recreational sports. Injuries to one area of the musculature often indicate that additional damage has been incurred by other muscles.

Many therapeutic exercises can help restore proper strength and endurance to the leg muscles. Isometric exercises are often the initial treatment exercises, followed by single plane rubber band exercises for the hip, knee, and ankle: flexion, extension, adduction, abduction, circumduction, inversion, and eversion. Dynamic exercises involving stability foam, rubber discs, an exercise ball, and BOSU balls can be performed on the floor. The more unstable of the surface, the more effort and stabilization is required of all the lower extremity muscles.

Vibration plates enhance neuromuscular learning throughout the ankle, knee, foot, hip, and back muscles. Additional strength exercises can be found on the hip, knee, and foot strengthening pages. More information for injuries and treatments for knee pain and foot pain.

Our Chandler Chiropractic & Physical Therapy clinic treats patients with a variety of muscle, tendon, joint, and ligament injuries. The clinic provides treatment for runners, tri-athletes, and weekend warriors in addition to common headache, neck, and back patients traditionally seen in Chiropractic, Physical Therapy, Massage Therapy clinics. We work with all ages and abilities of the residents in Phoenix, Tempe, Gilbert, Mesa, and Chandler AZ.


Why is the Patellar reflex not triggered when the tendon is extended slowly? - Biology

A special thanks to The Washington University School of Medicine

Although we usually study the spinal cord as a series of cross sections, it is important to remember that it is in fact a column, with continuous tracts and cell columns. However, the cord can be divided into segments by the nerve roots that come off of it although the rootlets branch off nearly continuously, they coalesce into about 31 discrete nerves along the cord (8 cervical, 12 thoracic, 5 lumbar, 5 sacral, and 1 coccygeal nerves). At each segment, rootlets appear to come out of both the dorsal and ventral halves of the spinal cord, as you see here:

In fact, only the ventral roots are coming out of the cord - the dorsal roots are actually going in. Throughout the cord, the dorsal grey matter (dorsal horns) deals with sensory perception, and receives information from the periphery through the dorsal root. The ventral horns contain the a -motor neurons , whose axons exit the cord via the ventral roots and travel directly to the muscles.

Along the dorsal root is a collection of cell bodies called the dorsal root ganglion. Inside the ganglion are the cell bodies of all the receptor neurons that send processes out to the periphery. The free nerve ending in the tip of your finger that feels the paper cut actually has its cell body back in the dorsal root ganglion. As you can see from the picture, the dorsal root ganglion is actually located ventrally, but you can tell that it is part of the dorsal root.

B. Levels of the spinal cord:

By this time in the course you have probably noticed that different levels of the cord are different in shape. Could you identify the source of a section if you had nothing to compare it to? In general, you should be able to differentiate cervical from thoracic from lumbar from sacral. Here is a series of cross sections:

The first thing to notice is overall shape. Cervical sections tend to be wide and squashed looking, like an oval. Compare the cervical section to the round lumbar section.

The second thing to check for is a ventral horn enlargement. At segments that control a limb, the motor neurons are large and numerous. This causes enlarged ventral horns in two places: the lower cervical sections (C5-C8) and the lumbar/sacral sections. If you see an enlargement, you just need to differentiate cervical from lumbar. This can be done by shape (see above) or by proportion of white matter.

C. Muscle spindles and the myotatic reflex:

One of the most familiar reflexes is the stretch reflex, also known as the knee-jerk reflex and the myotatic reflex. In its simplest form it is a 2-neuron loop, one afferent neuron and one efferent neuron. The afferent neuron is connected to a muscle spindle, which detects stretch in the muscle. The efferent neuron is the motor neuron, which causes the muscle to twitch.

But there are actually several types of afferents reporting on the status of the muscle. Let's look more closely at the muscle spindle:

The muscle spindle is a small group of muscle fibers walled off from the rest of the muscle by a collagen sheath. The sheath has a spindle or "fusiform" shape, so these fibers are called intrafusal fibers, and are contrasted with the extrafusal fibers, which are the power-generating muscle fibers. There are two types of nerve endings wrapped around this intrafusal fiber, both of which monitor its degree of stretch - as the muscle stretches, so does this capsule within it. These two stretch receptors are sensitive to different time scales, however. The first is called a Ia (that's one-A) fiber the classification scheme is based on diameter and conduction velocity, so the Ia's are the largest and fastest. The Ia fiber fires like crazy when the muscle is stretching, but it is rapidly adapting. As soon as the muscle stops changing length, and holds a new position, the Ia adapts to the new length and stops firing. But you also need to know the position of your muscle when it is still. The second type of stretch receptor is called a II fiber, and it is slowly adapting. It also responds when the muscle is stretching, but it maintains a firing rate after the muscle has stopped moving (essentially, it is non-adapting). This information is part of what allows you to tell the position of your arm when your eyes are closed.

Rule of nomenclature - if there is a Ia, where is Ib? The Ib fibers are not connected to muscle spindles at all. Instead they are embedded in the tendon, and monitor overall muscle tension from there. They are also called Golgi tendon organs (the word "Golgi" is littered throughout neuroanatomy - he was a famous early anatomist).

Now, there is a potential problem with the muscle spindle system which may have occurred to you. What happens when the muscle gets shorter? Does the spindle go limp and slack? How can it remain sensitive to stretch at short lengths? This is where the intrafusal fiber comes into play. Like any muscle fiber, it can contract. When it contracts, the entire spindle shortens, remaining taut, and the sensitivity is intact. There are small motor neurons in the ventral horn that innervate the intrafusal muscle fibers and cause them to contract - they are the g -motor neurons . These neurons are excited every time the a -motor neurons fire, so that as the muscle contracts, the intrafusals contract with it.

How are they all hooked together? There are two simple rules: 1) When the stretch receptors fire, the a -motor neuron is excited, and the muscle contracts.

2) When the Golgi tendon organ fires, the a -motor neuron is inhibited (via an inhibitory interneuron), and the muscle relaxes. The purpose here is that the stretch receptors tell the muscle when it needs a little more force - that despite intending to contract the muscle is lengthening. This helps you to maintain the correct muscle tone. The Golgi tendon organs, on the other hand, begin to fire when the tension on the tendon is so great that you are in danger of injury. They have a protective function, and therefore they tell the muscle to ease off before it tears.

Occasionally, especially in cases of pyramidal tract damage, these two systems can get stuck in a loop, where they alternately trigger each other, causing the muscle to contract-relax-contract-relax, several times a second. This rapid trembling is called clonus, and can be a sign of pathology or extreme muscle fatigue.

D. Multiple motor pathways in the cord:

There are several pathways which innervate the a -motor neurons. They can be roughly grouped into the voluntary motion pathways and the postural pathways. The voluntary pathways include the lateral and anterior corticospinal systems, as covered in the "Basic motor" section. The postural pathways do not originate in cortex instead their function is to maintain an upright posture against gravity, a task which requires hundreds of little muscular adjustments that we are not aware of. There are three principal pathways in humans: the vestibulospinal, tectospinal, and reticulospinal pathways. Pathways are always named beginning-to-end, so these originate in the vestibular nuclei, tectum (superior colliculi), and reticular formation, respectively. The rubrospinal system (from the red nucleus) is also sometimes included, but in humans it may be insignificant.

Although these pathways do not originate in cortex, they are controlled to some degree by cortical structures. You must be able to turn off selective postural systems to accomplish other movements. This becomes apparent when the cortex is damaged or cut off from the postural pathways, and can no longer control them. If the cortical input is damaged close to its source, (i.e., in the internal capsule), the result is what is called a decorticate posture. Here the postural pathways flex the upper limbs and extend the lower limbs by default, since they are getting no input from cortex.

If the damage cuts off not just cortical input but all input from the entire cerebrum, such as with a massive brainstem injury, the result is a decerebrate posture. In the decerebrate position all four limbs are extended and somewhat turned in (pronated). This sort of injury is much more serious than an injury of the internal capsule the prognosis is usually very poor.

E. Injury to the corticospinal tract:

Just as the postural pathways have a "mind of their own" when cortical control is cut off, the spine can also produce some weird behaviors when the corticospinal tract is damaged. All of the spinal reflexes are local - all of the cells involved are contained within one or two segments, and cortex is not necessary. Therefore reflexes would still be present in a transected spinal cord. However, the cortex normally keeps a tight rein on reflexive behavior, so that it doesn't interfere with normal movements. When the cortex is cut off, the spinal cord becomes hyperreflexic. All of the normal reflexes become exaggerated, and some new ones appear. For example, stroking the lateral sole of your foot with a sharp object would normally make your toes curl downward. In a patient with corticospinal damage (also called upper motor neuron damage), the big toe would lift up and the toes would fan out. This is called the Babinski sign, and it is always pathological (with the exception of very young infants).


Special Tests

Spurling’s Test

Testing For:
Compression of a cervical nerve root or facet joint irritation in the Lower Cervical Spine

  • Patient is seated. Therapist stands behind patient.
  • Patient slowly extends, sidebends, and rotates the head to the affected side.
  • Therapist carefully apply compression downward on the head of patient.

Positive Sign:
Radiating pain or other neurological signs in the same side arm (nerve root) and/ or pain local to the neck or shoulder (facet joint irritation).


Why Doctors Test Reflexes

Neurologists use different reflexes to see how different parts of the nervous system are functioning. For example, for the knee-jerk reflex to work, the nerves to and from the muscle must be intact, and the spinal cord needs to be working at that level. Similarly, a brainstem reflex, such as the pupils constricting to light, can help a neurologist know that the brainstem is working properly.  

Furthermore, reflexes are moderated by many other things in the body. For example, the brain usually sends impulses down the spinal cord that keeps reflexes like the knee-jerk relatively calm. After a stroke or other injury to the brain, the calming influence on the reflex is slowly lost, and this results in reflexes being hyperactive.   One of the reasons neurologists check reflexes is to see if there is an imbalance between the left and right sides, which can be a clue to damage to the brain or spinal cord.

Sometimes a reflex can look a lot like conscious behavior. For example, in the “triple flexion” reflex, the knee, hip, and foot flex in such a way that the leg withdraws when a painful stimulus is applied. This can happen even if an electrical signal never reaches the brain—it can be completely orchestrated by the spinal cord.   It’s important to distinguish between a reflex and intentional movement in cases of ​coma or altered consciousness.

Not knowing everything that reflexes do for us saves us a lot of trouble in day-to-day life. However, knowing about reflexes and how to test them can shed a lot of light on how the nervous system works and where a problem may lie in a nervous system disorder.


Watch the video: 2-Minute Neuroscience: Knee-jerk Reflex (October 2022).