The earliest challenge to the student who is investigating this material lies in the concept of the "lesion." I shall provide a definition which facilitates an understanding of the subject matter of this course only and is not meant to be so broad and conclusive as to encompass all other academic areas. However, I have found this particular concept of the lesion to be more than helpful in the study and comprehension of pathologies in general.

When we examine the cellular, tissue, organ, or systemic level of disease, it requires that the student have a fundamental realization of the unique and particular function of the area in question. For example, what does muscle tissue do? It contracts. What does a ligament do? It supports. What does an islet cell do? It secretes insulin. What does a mucus gland do? It secretes mucus. What does a nerve do? It conducts.

We can become more specific as we learn more about the cell, tissue, organ or system. For example, what does a proprioceptor do? It conducts information of a mechanical nature from muscle, tendon, ligaments, joints and skin. What does an alpha motor neuron do? It conducts commands to a skeletal muscle cell. What does a spindle do? In response to muscle stretch, it fires a signal to an alpha motor neuron which will command the muscle cells to contract.

Additional functions of the same cell, tissue, organ or system can be learned. For example, what does an annulospiral neuron do? It conducts commands to an alpha motor neuron from the spindle --- this is true. But is this all it does? Essentially, yes. However, should we also understand what those commands are and what muscle cells are involved? Of course. Therefore, a more complete understanding of the function of the annulospiral neuron would be: it conducts an excitatory command to the alpha motor neuron of its homonymous muscle and to the alpha motor neurons of the agonist muscle groups through the interneuronal pool while conducting an inhibitory command to the alpha motor neurons of the antagonistic muscle groups through the interneuronal pool. As we begin to understand more of the function of the particular cell, tissue, organ or system, we will certainly gain essential insight into the pathologies associated with it.

As to the definition of "lesion," how does the above relate? What I propose to you is that "lesion" is best defined by function. That is, "a lesion is the state of hypofunction or absence of function of a particular cell, tissue, organ, or system." When any particular area of investigation demonstrates a loss of function or a diminished capacity to perform its function, that area is defined as a "lesion site."

Please recognize that this proposed definition is very limited. The difficulty comes for the student who confuses hyperfunction with hypofunction. For example, the most common finding associated with neuromusculoskeletal problems is muscle spasm. Where is the lesion site? Is it the muscle which is in spasm? To answer that question, ask yourself "what is the function of a muscle?" Obviously, its purpose is to contract. Is the muscle which is in spasm doing what it is supposed to do? I propose that the answer is "yes!" Spasm could be defined as hyperfunction. Therefore, the muscle is not the lesion site. This is difficult for the patient (and the clinician) to accept. The temptation is to treat the muscle and to consider the therapy as appropriate. However, since the muscle (by my definition) is not the lesion site, the treatment of the muscle would constitute treating the symptom and not the cause. What about the nerve which innervates the muscle? Obviously, the nerve is sending a command to the muscle to which the muscle is responding. Why not figure a method to make the nerve conduct less? This would work, but the nerve is not the lesion site. Since the function of the muscle is to contract and the function of the nerve is to conduct, neither tissue should be defined as "in a lesioned state." So, where is the lesion? If we were to define "hyperfunction" as a "lesion," treatment of the nerve or muscle would be appropriate. This is contrary to the chiropractic paradigm of always seeking and treating the cause.

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Again, where is the lesion? The clinician must be responsible to seek out the tissue which is in a state of "hypofunction." Suppose, for example, that our patient with the muscle spasm had sprained a ligament in his spine. A sprain would logically result in a muscle spasm. The clinician would perform a routine orthopedic examination and quickly assess the function of various tissue sites including the ligaments. When the

ligament is examined, the clinician will discover that, when stressed, the ligament will not perform its function without pain and evidence of instability. Therefore, the ligament is the lesion site and was discovered by its loss of function. The sprained ligament would be the source of the stimulation to the healthy nerves in the ligament which would conduct a message to the cord. The message being conducted would be to the anterior horn cells (alpha motor neurons) which would then stimulate the muscles to become spastic. In conclusion, the nerves and muscle fibers are healthy and merely responding to the lesion site which, on examination, was revealed to be a ligament.

Pain is generally the chief complaint of patients in a chiropractic office. The tendency is to consider the nerve to be "in lesion" and to utilize a treatment modality to reduce its conduction. This could be in the form of physical modalities (ice, ultrasound, high voltage) or even chemicals (analgesic balms, medications). However, this approach would name the nerve as the lesion site and the area in need of therapy. Attention to the pain fiber which is conducting the signals is a perfect example of treating the symptoms. Clearly, the pain fiber is merely perfoming its normal and expected function. The problem (lesion site) has not been found if therapy is applied only to reduce the pain sensations. For further discussion on the topic of pain, I would expect that a needle piercing the skin would produce pain if the pain fibers are performing their function. I would be concerned if a needle piercing the skin did not produce pain. In that case, I would be suspicious of the nerve itself or some neuronal pathway in the peripheral or central nervous system.

Pain is a modality carried to the brain just as any other modality such as cold or pressure. Loss of the sensation of pain, light touch, pressure, etc…. is evidence of a deficit in conduction defined as a loss of function. Neurological tests always examine for the presence of specific modalities such as pain, point discrimination, position awareness, light touch, hot, cold, two-point, and so on. A neurological test is positive when there is a loss of one or more of these functions. Therefore, a positive neurological finding is always in the form of a deficit which provides evidence of a neurological lesion.

The essence of the term "lesion" is "a functional deficit."

The initial portion of this course will review the essential elements of neuroanatomy. Following this, our attention will be turned to recognizing dysfunction (decreased or loss of function) within the nervous system. I first wish to point out that our ability to recognize evidence of neurological dysfunction is all dedicated to locating areas of functional deficits. Regardless of the cause of the problem, we recognize the existence of pathology by uncovering loss of certain functions. For example, the inability to recognize the size or shape of an object placed in our hand (astereognosia); the inability to discriminate one or two points being touched on our hand or arm simultaneously (two point discrimination); the inability to recognize the position of a finger or toe in space (akinesthesia); the loss of vibratory sense; loss of "normal" or appropriate behavior or dress; loss of memory; loss of the sense of smell (anosmia); loss of the ability to contract a muscle against resistance; loss of the direct light reflex; loss of a superficial reflex; loss of muscle tone; loss of muscle mass; loss of a deep tendon reflex; loss of the sensation of pain; loss of muscle coordination; inability to touch the tip of our nose with our eyes, etc., etc., etc…. We begin to recognize that the discovery of the "lesion site" depends upon our uncovering the tissue site which is not performing its expected function.

If we look closely at the inability of a patient to recognize where his finger is in space (akinesthesia), the obvious first interpretation is that the patient is suffering from a neurological dysfunction. If we look up "akinesthesia" in a reference text, we will soon learn that it is, indeed, classified as a neurological disorder. However, where is the actual lesion site which is resulting in the manifestation of akinesthesia??? Could it be a loss of neurotransmitter at the finger? Could it be a loss of neurotransmitter binding sites at the finger??? Could it be a peripheral neuropathy in which the particular nerve responsible for transmission of signals from

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the finger is damaged??? Could it be a pressure complex on the peripheral nerves at the level of the thoracic outlet??? Could it be pressure applied to the nerve root at the level of the intervertebral foramen? Could it

be a loss of cell bodies in the dorsal root ganglion??? Could it be damage to the particular cord tract which transmits the signal to the brain (dorsal column lesion)??? Could it be a loss of neurons at the level of the nucleus cuneatus or gracilis???? Could it be a loss of the neurons passing through the medial lemniscus on their way to the thalamus???? Could it be a lesion within the thalamus itself???? Could it be a lesion of the thalamocortical fibers which carry the signal to the post-central gyrus??? Could it be a lesion of the post-central gyrus itself??? Or could the patient be malingering (pretending)???

Any one of these suggested lesion sites is a possibility! So what is a clinician to do???

Remember, first of all, our task is to seek evidence of neurological dysfunction. We will arm ourselves with the knowledge of what certain nerves and tracts do, we will test these nerves and tracts individually, and we will begin to narrow down our evidence to a smaller number of possible lesion sites. In order words, if something is working, it can’t be the lesion site. So, we have to first determine what is working properly. With this in mind, let’s begin.

The nervous system is easily divided into three major areas: Sensory, Motor, Autonomic

The sensory system can be subdivided into two major pathways: Pain and Proprioception

Sensory

Pain is transmitted from free nerve endings which may be stimulated both chemically and mechanically. These free nerve endings are called nociceptors. Therefore, pain perception is often termed "nociception." Certain chemicals such as Prostaglandins, bradykinin, histamine, etc… are known to result in the stimulation of these free nerve endings and to produce subsequent pain. That is why injury and the resultant inflammation which releases some of these chemicals is generally associated with pain and tenderness.

Proprioception is transmitted from receptors located in muscles, tendons, ligaments, joint capsules, skin, and specific visceral areas. If a receptor is not a free nerve ending (Nociceptor), it is likely classified as a proprioceptor or mechanoceptor. Proprioception and mechanoreception are synonymous terms. These nerve endings are stimulated generally by pulling, twisting, pushing, turning, or by some form of mechanical excitation. However, some proprioceptors are stimulated chemically as well. Examples of proprioceptors (mechanoreceptors) include: GTO, spindle, Ruffini End Organs, Pacinian corpuscles, Meissner’s corpuscles, type I and type II receptors in the joint capsules, etc….. Electrical stimulation of the skin will fire some types of mechanoreceptors found in the skin. A vibrating tuning fork will also stimulate proprioceptors in the joint capsules.

Both pain and proprioception may originate from the same location (such as the finger) and travel together along the same peripheral nerve (such as the median or radial or ulnar). Therefore, it seems logical that a peripheral neuropathy (such as pressure on the median nerve at the carpal tunnel) should cause a reduction or loss of both pain and proprioception. Therefore, with a lesion of the median nerve, the patient might likely not be able to sense pin prick (pain) or a squeezing pressure on the thumb or part of the index finger (proprioception). It is not logical that a peripheral neuropathy would isolate only the pain fibers and spare the proprioceptive fibers. The same is true as the peripheral nerves pass through the plexi on their way to the IVF. Pressure applied to the plexus should cause a deficit in both pain and proprioception. If the deficits in both pain and proprioception were, for example, limited to the little finger (pinkie) with all sensory findings being normal everywhere else, it would seem logical to limit the lesion site to the one peripheral nerve which innervates this particular area (ulnar nerve). How could pressure at the brachial plexus limit itself to only the

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ulnar nerve distribution? The same would be true for brachial plexus pressure versus carpal tunnel pressure. Brachial plexus pressure (Thoracic outlet syndrome) would not single out the median nerve distribution only. Therefore, if the deficits are located in the thumb and side of the index finger, it seems quite logical that the lesion is within the median nerve, not the plexus.

When your examination uncovers deficits in one sensory modality only (pain or proprioception), a lesion of the peripheral nerve or plexus does not seem logical. For example, suppose that the patient is unable to perceive vibration on the right upper extremity but is able to distinguish pain on pin prick of the right upper extremity. That same patient may also not perceive deep pressure applied to the upper extremity or even be unable to distinguish the location of his right index finger in space when examined. Clearly, this patient has a deficit in proprioception, but not in nociception. Again I ask you to look at the potential lesion sites. The peripheral nerves carry both proprioception and nociception. How could a peripheral neuropathy preserve pain but eliminate proprioception? It couldn’t. The same question could be asked regarding brachial plexus pressure. Pressure on any nerve in the periphery should demonstrate both pain and proprioceptive deficits. So, how does one explain the loss of one particular sensory modality? In the human anatomy, there is only one particular place where the sensations of pain and proprioception are separated. That area is in the cord. Therefore, inability to sense pressure or position sense with intact pain perception could best be explained by a dorsal column lesion. Dorsal columns transmit proprioception exclusively and are the logical choice of lesion site when only proprioception is lost. With only a few notable exceptions, loss of either pain or proprioception (exclusively) generally points to the cord. In other words, the tract lesions tend to isolate the specific sensory modalities. Please remember, once the dorsal column fibers synapse in the nuclei cuneatus/gracilis, the continuing neurons travel in the medial lemniscus to the thalamus. A lesion of the nucleus cuneatus or of the nucleus gracilis could also limit the losses to only proprioception. The same could be true of a lemniscal lesion which would eliminate proprioception but spare the nociception. However, the thalamus will once again "mix" the pain and proprioception. A lesion of the thalamus is likely to cause a loss of both pain and proprioception. The same is true of the cortex. The thalamus sends its information to the cortex (post-central gyrus of the parietal lobe) where it is finely discriminated. A lesion of this area of the cortex would also demonstrate loss of both pain and proprioception.

Let’s continue our discussion of pain. Pain is a sensation that originates from stimulation of free nerve endings which are located in various tissue sites throughout our bodies. Free nerve endings may be stimulated both chemically (histamine, prostaglandin, etc…) or mechanically. Free nerve endings are known to enter the cord and synapse on the spinothalamic neurons (tract) which then carry the signal to the thalamus. From the thalamus via the thalamocortical fibers the signals are ultimately transmitted to the somatosensory cortex (post-central gyrus of the parietal lobe) for fine discrimination. This means that the cortex is capable of placing specific qualities to the pain such as exact location and "sharpness." Those free nerve endings which are the larger, myelinated fibers are known to travel to the cord and to synapse on spinothalamic fibers which carry the signal to the thalamus and from there to the cortex. These free nerve endings and their fibers are classified as "A delta" and are capable of sending signals all the way to the cortex for fine discrimination. These fibers are also known to adapt rapidly; that is, they cease to fire soon after the initial stimulation.

A second set of free nerve endings are much smaller and poorly myelinated. Their signals travel much more slowly than the signals of the A delta fibers. These fibers are classified as "C" fibers. Their signal is received by spinothalamic neurons, but these signals only reach the level of the thalamus. They are not transmitted to the cortex. Therefore, their signals are never somatotopically discriminated by the cortex. Since their signals remain in the thalamus, their pain is merely perceived but not discriminated. Therefore, the sensations are described as deep, dull and achy. The patient is unable to discriminate the exact location of the pain and often places the entire palm of the hand over the area when describing where the pain is felt. This pain pattern is very similar to visceral pain patterns which are transmitted primarily from these "C" fibers. It is important to note that, unlike the "A delta" fibers, the "C" fibers do not adapt. That is, they continue to transmit signals so long as the stimulus is present.

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Clinically, a patient with a lesion of a structure such as a ligament will have pain being transmitted over both "A delta" and "C" fibers. The "A" fiber pain will be sharp and well localized by the patient. The patient will be able to point to the site of pain with the tip of a finger and say, "it hurts right there." If the clinician tries to examine the area and moves the particular joint, the pain will be exacerbated and will be clearly localized to the joint. After the initial injury to the ligament begins to subside, the patient will describe the pain as deep, dull and achy. He will place the palm of his hand (not the finger tip) over the area of pain. However, immediately upon re-examining the site, the pain will be sharp and well-localized again. What is happening is that the "A delta" fibers adapt and cease to fire. The remaining free nerve endings ("C" fibers) continue to fire but their signals only get as far as the thalamus. Here the pain is perceived but not discriminated. It does not reach the cortex via the thalamocortical fibers. So, the patient describes the pain as deep, dull and achy. When the clinician moves the injured ligament, the "A" fibers fire and send the signal to the cortex where the pain is readily discriminated. This clearly points out that the information which is relayed to the cortex tends to "block out" lower level information. In other words, "A" fiber information tends to obscure "C" fiber information.

This same clinical phenomenon occurs with the majority of somatic injuries such as facet, ligament, capsular, bursal, tendon, muscle, bone, etc… The dull ache which dominates after the acuteness of the injury wears off may be replaced with a very sharp, well-localized, stabbing pain when the injury site is disturbed. This is why many patients will hold the injured area in a spastic grip and resist any attempts to move the area because of the "terrible pain" which will occur. During the healing process, the acute "A" fibers reduce their firing, and the "sharpness" of the pain subsides. However, the "C" fibers continue to fire and the area is sore and achy. It will remain sore and achy until healing is complete. Remember, the "C" fibers do not adapt. As healing occurs, it will be more and more difficult to cause the "sharp" "A"fiber pains.

Clinicians often utilize this phenomenon to reduce pain. For example, since we know that signals which reach the cortex via the "A" fiber pathways can effectively block out "C" fiber pain, why not stimulate "A" fibers which would carry more pleasant sensations to the cortex and thereby block out dull achy pain coming from "C" fibers? In fact, this is one explanation for the effectiveness of deep tissue massage (stimulation of "A" fibers of proprioception) to reduce mild aches and pains. Electrical stimulation of the skin surface (TENS units) will stimulate the mechanoreceptors of the skin which will then bombard the cortex with mechanoreceptive information and block out pain coming from "C" fibers . This may be a temporary approach to management, but blocking pain without the use of drugs is a benefit to the patient. In addition, the stimulation of "A" fibers of proprioception are known to achieve a "dampening" effect on pain at the cord level. As these "A" fibers enter the cord, they are known to release an inhibiting neurotransmitter (GABA) at the cord level which actually reduces the conduction along pain fibers entering the cord as well as along the receiving tracts (spinothalamic). It is also known that "A" fiber stimulation will excite centers in the Periaqueductal Gray Area of the brain which will send out a descending fiber which also secretes (GABA) at the cord level. Clearly, the utilization of "A" fiber stimulation to reduce "C" fiber pain is well documented. From the early studies of Melzak & Wahl who developed the "gate theory," clinicians have utilized this innate method of pain modulation. Manipulation of the spine will restore great amounts of proprioception to the cord which assists in the control of pain. Thus, "proprioception blocks nociception."

We should note that sharp "A" fiber pain patterns are often difficult, if not impossible, to reduce by stimulation of proprioceptive fibers. In other words, a true sciatic neuralgia would not be expected to be relieved by massage of the back. Sensations carried over "A" fibers may block "C" fiber pain patterns, but "A" fiber proprioceptive input cannot be expected to effectively reduce "A" fiber pain patterns.

Pain patterns may take on a dermatomal pattern. The word "dermatome" actually means "a section of skin." Anatomists were able to isolate areas of skin which were innervated by pain fibers which enter the cord through specific intervertebral foramina. That would mean that compression of individual nerve roots which enter through the IVF would create pain patterns in a predictable dermatome. Therefore, when we say that the patient is experiencing C5 dermatome pain, we are saying that the patient has pain confined to a definable area of the skin which has been mapped out by anatomists as sending pain fibers through the C5 IVF. The

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likelihood of the dermatome pain being caused by a lesion of the nerve root as it enters through the particular IVF is overwhelming. Since the C5 dermatome relates to the C5 spinal segment, many clinicians refer to dermatomal pain as "segmental" pain. This makes good sense, because the dermatome does send its pain fibers into one specific segment of the spine.

When the nerve root is being compressed by a particular entity (spur, ligament, disc, narrowed IVF, etc…), it is termed a "radiculopathy." Therefore, "radicular" pain patterns are the same as "dermatomal" pain patterns which are also synonymous with "segmental" pain patterns. There are unique qualities to dermatome pain which need to be reviewed now.

Radicular (or dermatomal) pain patterns are generally described as sharp, burning and quite severe. The patient often states that "tingling" is felt in the same area either all the time or at various times. The pain is also easily reproduced by both the patient and the examiner. That is, when the patient moves the spinal area of involvement (or the examiner moves the same area), the pain radiates into the extremity with intensity. This is why most patients are reluctant to perform the range of motion examination or to have the clinician mobilize the involved area. Any stretch on the nerve root will also reproduce the same pain patterns into the dermatome. Certain orthopedic examinations such as Straight Leg Raise, Braggard, Bechterew, etc… will reproduce the radiating pain with ease. Generally speaking, the pain is expected to radiate into the digits well below the elbow or knee. Any dull, achy pain which does not radiate below the knee or elbow is suspicious of a non-radicular origin and is often associated with a somatic rather than a neurological lesion.

If the nerve root is the lesion site, the uniqueness of this particular lesion is that all symptoms and findings will be segmental. This is of paramount importance. This means that examination of the sensory, motor, and reflex functions will all point to one spinal nerve (eg., C5). If the C5 nerve root is being compressed by a lesion at the IVF, then the dermatome should be the specific site where the patient feels the pain and tingling. In addition, upon examination of the dermatome with a pinwheel, the clinician will discover losses of sensation or hypoesthesiae. This will surprise most students or new clinicians. It would seem logical that if the skin is the site of the pain, the pinwheel should create more pain or hyperesthesia. This is not the case. Remember, the lesion at the root is compressive and creates the expected loss or deficit in conduction. Therefore, when the nerve endings are stimulated by a pinwheel or other instrument, the depolarization into the cord is inhibited by the inflammation and pressure at the root level.

Then, if the pinwheel uncovers a loss of sensation, why does the patient feel so much pain and tingling in the dermatome? This question is perplexing to most clinicians, but the answer is relatively simple. The solution lies in the somatosensory area of the brain (post-central gyrus of the parietal lobe). The student will recall that a sensory nerve has the potential of being stimulated anywhere along its course, not only at the terminal ending. We all experience that when we "hit our funny bone." Striking the ulnar nerve accidentally will create a sudden burst of pain and tingling distal to the site of the injury. Why??? The ulnar nerve is actually stimulated at the site of the injury and depolarizes toward the cord. Once the signal enters the cord, it is picked up by the spinothalamic tract and carried to the thalamus and then to the cortex. Once in the cortex, the brain interprets the stimulus as pain. But, pain from where??? If you examine any neurological textbook, you will see illustrations of the human body lying over the surface of the brain. Those areas indicate the sites from which the brain assumes the stimuli arise. In other words, the cortex of the brain assumes that the received signals are coming from the terminal endings, even if the terminal ending is not the site of stimulation.

This concept was recognized in the nineteenth century and forms the basis for the clinical diagnosis of neuropathies. The radiation or peripheralization of pain upon stimulation of a lesion site is a clear indication of a neurological lesion as opposed to a somatic lesion such as a sprain/strain. For example, if an individual falls on their wrist and complains of pain in the wrist but not radiating into the fingers, the likelihood is that the lesion will be confined to the somatic tissues of the wrist. However, if the pain following the injury does radiate into the fingers with paresthesiae, then the diagnosis will include median nerve injury.

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The finding that pain and tingling radiate distally upon irritation of the lesion site is termed the "Tinel Sign." This is named for a Civil War surgeon who determined the regrowth of axons in the limbs of soldiers who had endured severe injury and whose nerves had been reattached by the surgeon. For example, if the severing of the nerve(s) had occurred in the upper arm, Dr. Tinel would document that upon tapping on this site the patient would sense tingling and pain in his fingers, even though his fingers were totally anesthetic. Then, two months later, tapping in an area below the elbow would accomplish the same sensations in the fingers. That provided evidence that axonal regrowth was occurring. Thus, the Tinel Sign has become a standard diagnostic indicator of neurological lesions in the periphery.

The Tinel sign is often elicited upon orthopedic examination. For example, if a patient experiences a disc herniation at C5 which entraps the C5 nerve root, the pain would be felt in the C5 dermatome. The examiner may perform a cervical compression test by placing downward pressure applied to the top of the patient’s head. Upon performing this particular test, the patient will likely experience an increase of the radiating pain into the C5 dermatome. This radiation of pain would not occur if the cervical lesion were a facet or sprain/strain. Asking the patient whether or not the pain radiates into the arm or leg is important. Keep in mind that neuropathies involving the peripheral nervous system are generally easily reproducible by the patient and examiner, they exhibit a Tinel sign, and will be associated with other neurological losses involving the motor and reflex functions. When the physician asks the patient how far down the arm or leg the pain is felt, the answer may provide strong clues as to whether the lesion appears to affect the nerves or simply the somatic tissues.

Pain travels to the cord via A-delta and C fibers, as you know. You also remember that C fiber pain does not generally travel to the cortex for somatotopic discrimination and remains as dull achiness. More specifically, C fibers tend to stimulate a particular pain tract in the cord called the "spinoreticulothalamic" tract. A-delta fibers tend to stimulate the lateral spinothalamic tract in the cord whose signals are then transmitted to the cortex. The spinoreticulothalamic tract travels to the reticular formation first where it may stimulate the RAS (reticular activating system). This particular system effectively keeps an individual awake. Thus, chronic pain may result in a patient’s complaint of difficult sleeping. Additionally, before reaching the thalamus, the spinoreticulothalamic tract will synapse on neurons from the Limbic system which is the seat of our emotions. Again, the patient may have difficulty sleeping and may, in your mind, be a "basket case" or emotional wreck. In general, it is believed that the signals transmitted to the thalamus via the spinoreticulothalamic tract are not transmitted on to the cortex, although some neurology texts may show them to be cortically interpreted. It remains a safe conclusion that deep, dull achy pains which are poorly localized are not cortically discriminated. Once again, the student is reminded that stimulation of proprioceptors (which are comprised of large A-beta fibers) will greatly assist in the abatement of these poorly discriminated C fiber pain patterns.

PROPRIOCEPTIVE SENSATIONS We have been discussing pain sensations exclusively to this point. It is hoped that the student understands the concept of A pain vs. C pain. Also, the spinothalamic pathway is both anatomically and clinically different from the spinoreticulothalamic pathway. When a pain nerve itself is lesioned, the patient will experience the Tinel Sign, sharp well-localized burning pain, and paresthesiae. Lack of the Tinel sign, lack of paresthesiae, and dull achy pain patterns tend to limit the lesion to somatic tissues.

Proprioception is the second member of the sensory nervous system. In fact, it is very much the larger member. I prefer to divide the proprioceptive pathways into the following outline form:

I. Conscious proprioception

1. cortically discriminated

1. Dorsal Column Pathway

1. cerebellar

1. Spinocerebellar tract

1. reflex

1. Deep tendon reflex

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Conscious proprioception travels from muscles, tendons, ligaments, joints and skin to the cord over large A-beta fibers which are fast traveling and highly myelinated. Once in the cord, the signals are transferred onto the tract fibers called the "Dorsal Column Pathway." As you recall, these fibers travel upward to the nuclei cuneatus and gracilis where they synapse, decussate, and travel onward to the thalamus over what is called the "medial lemniscus." This conscious proprioceptive pathway described above is often referred to as the "lemniscal system." Once in the thalamus, the information is transferred upward to the somatosensory cortes of the parietal lobe where it is discriminated. There are a number of examples of discriminated proprioception; I shall describe three such examples.

1. Kinesthesia: the ability to know where a digit (finger, toe) is in space. The examiner moves the finger up or down by about 1/16 of an inch and asks the patient if the finger has moved up, down, or to the side. The patient is looking away with eyes closed, so the only way this information could be getting to the cortex would be over the lemniscal pathway. Healthy patients are capable of discriminating movement of as little as 1/16^th of an inch. Inability to discriminate the position of a finger or toe in space is called "akinesthesia." What may cause akinesthesia? Loss of the peripheral nerve certainly would cause this, but this lesion would create a loss of all sensations being carried over the nerve. This would include pain, pressure, vibration, etc… and would leave the innervated area "anesthetic." A lesion of the nerve root (radiculopathy) cannot cause loss of discriminated proprioception, because this form of proprioception enters the cord through multiple IVF’s. Essentially, proprioception is a multisegmental sensation, not a segmental sensation in the dermatome such as pain. Remember, have you ever heard the expression "dermatome proprioception?" I suggest that you have not! What you have heard is "dermatome pain." While nociception from the skin is clearly segmental (dermatomal), proprioception is not segmental. The proprioceptive fibers traveling in the peripheral nerves enter the cord at many levels. Therefore, we can reasonably conclude that a single IVF lesion (radiculopathy) cannot explain a patient’s inability to discriminate where his finger is in space. That explanation must lie in the tract or sensory cortex. A lesion of the dorsal column could easily explain the loss of discriminated proprioception while preserving pain. A typical site is the cord itself or the nuclei cuneatus or gracilis. A lesion of the medial lemniscus would also cause a loss of discriminated proprioception but preserve pain. A lesion of the thalamus, thalamocortical fibers, or cortex would create losses of both discriminated proprioception and pain. Therefore, the cord is the most logical lesion site which would eliminate one sensory modality but preserve another

2.Stereognosia: This is the ability to discriminate the size and shape of a familiar object placed in the palm of the hand. The patient’s head is turned away from the hand and the eyes are closed. An object such as a key is placed in the hand. The patient is allowed to "feel" the object with the hand, and is then asked to identify it. If a patient is unable to recognize a familiar object such as a key, this would be labeled "astereognosia" and would be attributed to the lesion sites explained above. Sometimes, a three-sided object (triomino) is placed in the hand and the patient asked to identify how many points it has. This would yield the same information.

3.Graphesthesia: This is the ability to discriminate a familiar letter or number which is being written on the palm of the hand. A large letter "A" is inscribed on the open palm with the point of a reflex hammer and the patient is asked to identify the letter. Or, the number 8 is inscribed on the palm, and the same question is asked. The inability to discriminate what is being written on the palm of the hand is labeled "astereognosia." Again, the lesion sites sited in #1 above would apply in this situation as well.

The student is reminded that there are a number of other examples, such as two point discrimination, which test the integrity of this particular sensory pathway, but the ones described are most common. The major point to grasp is the loss of discriminated sensations. If the lesion is in the cortex, the patient will still be able to "perceive" the stimulus by the thalamus, but he will not be able to "discriminate" the sensation. He will definitely feel something in his hand, but he will not be able to describe (discriminate) the object. Therefore, if perception remains intact, but discrimination is lacking, the only logical site would be the cortex. In this event, there should be evidence of loss of pain discrimination as well.

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Vibration is an interesting proprioceptive sense. A vibrating tuning fork is placed on a bony prominence and the patient asked whether or not the fork is vibrating. Vibratory sense is performed by the thalamus. Therefore, if vibratory sense is intact, you know that everything from the periphery to the thalamus must be in working order. Once again, a cortical lesion should produce evidence of "discriminatory" losses but preserve "perception" of all sensations, even the ability to recognize when a tuning fork is vibrating.

The student is encouraged to go back and review the sensory losses associated with the following lesion sites:

1. peripheral nerve
2. plexus
3. root
4. tract
5. thalamus
6. cortex

Now we shall discuss the findings associated with interruption of the unconscious proprioceptive pathways. There are huge amounts of sensory information coming from the muscles, tendons, ligaments, joints and skin which never reach our cortical (conscious) awareness. In fact, the vast majority of proprioception is considered as "unconscious." The next level will include the information transmitted to the cerebellum. This information is transmitted to the cerebellum over the spinocerebellar pathway.

The cerebellum is responsible for the coordination of muscular activity. I compare it to the master computer. It takes a command from the motor cortex which informs it that a certain activity is going to occur. The cerebellum then receives input from the mechanoreceptors within the muscles, tendons, ligaments and joints of the body areas put into motion. The cerebellum is aware of the intended activity, is now aware of the position and tension within each body part accomplishing this activity, and coordinates this activity by sending commands down the cord to regulate the proper tone, speed, etc…. of the contracting muscles. This is a feedback system of incredible complexity. Loss of any part of this control system will cause the patient to experience loss of coordination of the expected activity. The inability to coordinate muscular activity is termed "ataxia." There are a number of tests for ataxia including finger to nose, touching another’s finger which is held at a distance, walking heel to toe, rapid alternating motions, standing without swaying excessively, and holding one’s arms out with eyes closed without experiencing drift of one of the arms.

Each of these above tests is designed to test for muscular coordination, and some have specific descriptive terms. For example, if the patient attempts to touch your fingertip but goes right past it, this is termed "dysmetria’ or "past pointing." Rapid, alternating movement is tested by having the patient "pat" the back of his hand and then the palm of his hand on his leg or tabletop over and over again at a rapid rate. Inability to perform this act smoothly is termed "dysdiadochokinesia." Observing the patient while standing and noting the degree of sway is known as the "Romberg" test. Holding both arms outstretched with eyes closed without either arm drifting is known as the "pronator" sign or test.

The Romberg test requires further explanation. Well over a century ago, it became apparent that a lesion of the cord or a lesion of the cerebellum could result in ataxia. The Romberg test was designed to differentiate between cord and cerebellar lesions. The patient with a cord lesion was found to be able to "compensate" for his loss of proprioception from the feet by staring at his feet. That way, even without proprioceptive input from the feet, his visual input provided sufficient input to allow him to correct his sway and prevent falling. He would still appear quite ataxic, but visual input was clearly helping him. With this understanding, the patient is asked to stand with feet approximately 6 inches apart and arms at the side. The doctor stands near the patient and remains available to help the patient should he fall. The amount of ataxia (swaying, shifting of feet, etc...) is observed first with eyes open. Then the patient is requested to close the eyes. If the patient begins to stagger and fall with eyes closed, the evidence is strongly in favor of a cord lesion. The cerebellum appears to be functional so long as information can be provided to it. In the case of cord lesions, the visual input supplies enough information to the cerebellum regarding the position of the feet, legs and surroundings to allow the patient to "right" himself each time he begins to fall. Granted, the patient will still appear quite ataxic, but the ataxia dramatically increases when the eyes are closed.

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Therefore, a positive Romberg occurs when the ataxia increases with the eyes closed. A positive Romberg indicates the greater likelihood of a cord lesion rather than a cerebellar lesion.

The same is true of the Pronator test. If the patient is able to outstretch both arms and hold them in place with eyes open but cannot hold them both outstretched with eyes closed, this also indicates a cord lesion. One arm will drift (pronate) when the patient closes his eyes. This indicates that the cerebellum is functional and will coordinate muscular activity from visual input. However, when the eyes are closed, the cerebellum no longer receives the input necessary to maintain muscular control.

Generally speaking, the patient will fall to the side of the lesion and the drifting arm will be on the side of the lesion. This is true if the lesion is in the cord or in the cerebellum. Often, one has compared the appearance of a cord or cerebellar lesion to an intoxicated state. The appearance is quite similar, without the behavioral aberrations so commonly seen in the individual who is intoxicated. The neurological texts can provide countless examples of dysfunctions observable with lesions within the spinocerebellar/cerebellar system. These all relate to the inability to coordinate muscular activity. The patient is not paralyzed, nor does the patient experience loss of discriminatory capacity when tested. Cerebellar or spinocerebellar lesions do not cause motor losses, only motor coordination losses. The investigative student will learn that nystagmus is another finding associated with cerebellar dysfunction, but is not found with cord lesions. Be aware, that nystagmus has more than one possible etiology, however! Cerebellar lesions also cause loss of muscle tone rather than the typical upper motor lesion which causes spasticity. The general finding associated with either spinocerebellar or cerebellar pathology is ataxia. This is the most important piece of information which the student should understand.

The proprioceptive pathway which is considered the most primitive is the deep tendon reflex. If the student recalls the anatomy of this pathway, it will be realized that this pathway does not enter a tract in the cord, nor does it ascend to the thalamus or cortex. Indeed, this particular proprioceptive system is initiated by a stretch stimulus placed on a skeletal which stimulates a spindle organ within the muscle. Emanating from the spindle is a large A-beta fiber called the "annulospiral" which fires a rapid signal into the cord. Once in the cord, the annulospiral nerve does not synapse onto an interneuron, but actually continues through the dorsal horn and terminates directly on the lower motor neuron (alpha motor neuron) which innervates the stretched muscle. The motor neuron then fires and the stretched muscle contracts. This ends the reflex.

The deep tendon reflex is also known as the stretch reflex. It constitutes the only "monosynaptic" reflex in the body. The purpose of this reflex is to maintain tone within each skeletal muscle. Indeed, if this reflex were to be left to its own way, each skeletal muscle would be hypertonic and the patient would be spastic and frozen in the fetal position. The CNS actually works to subdue this particular reflex. This is why those patients who have suffered CNS lesions (brain and cord) often demonstrate spastic paralysis. The spasticity results from loss of the inhibitory influences of the CNS on this reflex. This reflex qualifies as a proprioceptive pathway since it is produced by stretch on the most powerful mechanoreceptor in the body, the muscle spindle. The evaluation of this reflex (hyperreflexia, hyporeflexia, clonus, etc…) is one of the most important and time-honored methods of determining evidence of neurological dysfunction.

The deep tendon reflex requires, of course, both an afferent (SA) and an efferent (SE) branch. The afferent branch of the deep tendon reflex is the annulospiral neuron. The efferent branch is the alpha motor neuron also known as the lower motor neuron. A loss of either the afferent or efferent branch will abolish this reflex and also create a tremendous reduction in muscle tone. Loss of the efferent branch of the deep tendon reflex is known as a "lower motor neuron lesion." This entire concept will be revisited as we continue our review of the nervous system.

The motor system can be divided into two major parts:

1. Pyramidal
2. Extrapyramidal

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The Pyramidal system is synonymous with the "corticospinal" pathway. Obviously, this pathway begins in the cortex and terminates in the spine. This defines what is called an "upper motor neuron." That is, a motor neuron which remains in the brain and/or cord is classified as an upper motor neuron. This term generally refers to the pyramidal and extrapyramidal fibers. How about a cranial nerve? No! Cranial nerves which are motor send their axons into the periphery to innervate facial muscles, glands, etc…. These do not qualify as upper motor neurons because part of the nerve leaves the CNS. Again, the only nerves which qualify as upper motor neurons are members of the pyramidal and extrapyramidal systems.

Let’s begin our review of the pyramidal system. This motor system is also called the corticospinal and is the major voluntary motor system. Essentially, these fibers begin in the frontal lobe, motor cortex, as cell bodies called Betz cells. The axons then enter a descending pathway to the cord which decussates at the medullary pyramids. Approximately 80% of the fibers decussate. Those fibers which do not decussate are thought to innervate the cervical musculature. The corticospinal fibers terminate on the alpha motor neurons where they secrete an excitatory neurotransmitter on the alpha motor neuron cell body. This will result in the desired muscle contraction. A lesion of this corticospinal pathway will result in paralysis, the inability to voluntarily contract a muscle. Paralysis is one sign associated with an upper motor neuron lesion. Damage to the motor cortex itself or anywhere along the pathway of the corticospinal tract will result in paralysis.

The circulation of the brain is such that vascular lesions (occlusion or hemorrhage) will effect both the motor and sensory portions of the cortex. Therefore, cortical lesions can be expected to manifest with both motor and sensory deficits. Therefore, a patient may exhibit loss of discriminatory ability in an extremity (agnosia) as well as motor weakness or paralysis (apraxia) when the contralateral cerebral cortex is damaged. In addition, cortical lesions often involve both extremities (arm and leg) or the face as well. This helps to differentiate a cortical lesion from a cord lesion. Also important is the fact that the corticospinal pathway is not the only motor pathway potentially involved in CNS lesions. There are several other motor pathways which belong to the extrapyramidal system.

The extrapyramidal system does not begin in the cortex, but rather it derives from several nuclei scattered throughout the subcortical areas. For example, the red nucleus is the origin of the rubrospinal tract. The vestibulospinal, tectospinal, and reticulospinal tracts also originate from nuclei in areas outside the cerebral cortex. These four motor tracts collectively are known as the extrapyramidal system. This system is not under our voluntary control but is absolutely essential for normal movement to occur. If we wish to sideward elevate our shoulder, for example, the corticospinal may initiate the signal to the alpha motor neurons which innervate our supraspinatus and deltoid musculature. However, the appropriate extrapyramidal tracts will also send inhibitory signals to the appropriate adductor muscles to allow for smooth abduction of the shoulder. The extrapyramidal fibers will also maintain proper tone in the shortening and lengthening muscles. How is this accomplished? Remember, the cerebellum will play a key role by receiving the proprioceptive information from the muscles, tendons, ligaments and joints of the agonist and antagonist muscles and will determine what needs to be done. The cerebellum will then initiate proper excitation and inhibition to the muscles through the extrapyramidal fibers. All of this is undertaken through areas of the CNS which include the basal ganglion. Lesions of the basal ganglion are often classified as "extrapyramidal" lesions. In these instances, the patient is not paralyzed, but the patient may not be able to accomplish the desired motion due to spasticity, loss of coordination, etc… Think of the patient with Parkinson’s disease. This patient has a lesion of the substantia nigra which is a part of the basal ganglion. As a result, the patient is not paralyzed but is rigid. The patient is rigid because the extrapyramidal tracts cannot receive appropriate messages from the basal ganglion which would allow for proper relaxation and contraction of musculature about the joints. The basal ganglion along with the cerebellum plays a vital role in the decision-making process of inhibition/excitation and the agonist/antagonist relationship. (The student is referred to Guyton’s text on physiology or any other neuroscience text for review of the function of the basal ganglion.)

Therefore, an upper motor neuron lesion will almost certainly manifest as damage to both the pyramidal and extrapyramidal tracts. You have learned that an expected finding is spastic paralysis. The paralysis is due to loss of the pyramidal (corticospinal) pathway, whereas the spasticity is due to loss of the extrapyramidal

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inhibitory influences. Loss of this inhibition from the CNS on the alpha motor neuron would also explain the hyperreflexia so often seen with upper motor neuron lesions. Of course, the tone would alsodramatically increase without the inhibition from the extrapyramidal fibers. Both the reflex and the tone increases are due to lack of restraint on the effects of the spindle. Always keep in mind that the spindle is the most powerful excitatory influence on the alpha motor neurons.

It is helpful at this point to ask the student to picture the alpha motor neuron as a round ball (cell body) with a number of neurons synapsing upon it. Some of the synapsing neurons will excite the cell body while other synapsing neurons will inhibit the cell body. The following examples show some of the competing influences on the cell wall of the alpha motor neuron:

Inhibitory Excitatory

Extrapyramidal Pyramidal (corticospinal)

Golgi Tendon Organ Spindle

Antagonistic M. Spindle Agonist M. Spindle

Proprioception Nociception

The mechanisms behind inhibition and excitation lie in the neurotransmitter being released. The most common inhibitory neurotransmitter is GABA (gamma amino butyric acid). The excitatory neurotransmitters include glutamine, norepinephrine, serotonin, and others. So, when an alpha motor neuron has all of the competing neurotransmitters being released onto its surface, what will be the result? The result at rest is normal tone. However, if some of the inhibition is lost (extrapyramidal lesion), then the excitation dominates and the muscle is spastic. If the spindle were to lose its influence (IVF lesion), then the muscle would be hypotonic. Keep in mind that whatever the alpha motor neuron is doing at any millisecond in time is the result of the sum total of both inhibitory and excitatory influences. Balance of both (homeostasis) will result in normal tone and reflex. An imbalance (loss of homeostasis) will result in either hypo- or hyper- tonicity and reflexes.

If the above is understood well, then the following will also make sense. A muscle in spasm may result from one of two events:

1. The inhibitory influences have been lost. This is a lesion of the neurological tracts which are responsible for inhibition. The classic example is an upper motor neuron lesion which has been explained above.
2. The excitatory influences have been increased. For example, pain from a sprained ligament may enter the cord and create additional excitatory influence on the alpha motor neuron. This neuron will react by stimulating the muscle to contract into spasm. In another example, the active contraction of a muscle through the voluntary activation of the corticospinal tract will add excitatory influences to the alpha motor neurons and, therefore, increase the muscle tone.

The important thing to note from the above is that #1 is an example of a neuropathy, a neurological lesion in which some neurological function has been lost. This would be suspected when neurological tests are performed and deficits have been noted in the nervous system. The deficits would have to be in the CNS in order to explain the muscle spasm from the point of view of a neurological lesion. If the neuropathy is in the PNS, then there would be no muscle spasm. The explanation #1 above pertains to upper motor neuron lesions, never lower motor neuron lesions. This is because lower motor neuron lesions cause a loss of tone and reflexes, not an increase. The increase of tone as described in #2 above is not due to neurological lesions or deficits. On the contrary, #2 above relies upon an intact and functioning nervous system. Neurological tests conducted on this patient would reveal no neurological deficits. I believe that this patient represents the most common musculoskeletal complaint seen by physicians. This patient is in pain, has muscle spasms, but demonstrates absolutely no evidence of neurological dysfunction. Obviously, this patient does not resemble the typical upper motor neuron lesion patient with spasticity. The first part of this course will focus on the patient with the neurological lesions (#1), and the second part of the course will focus on the more common patient (#2).

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A review of reflexes would be in order at this time. There are three types of reflexes which we will discuss. These include: Deep tendon, Superficial, and Pathological (primitive) reflexes.

Deep Tendon Reflex: This particular reflex is the most well known. It involves tapping on a tendon and stretching the muscle. When a muscle is stretched, the spindles within the muscle also are stretched. The spindles interpret the stretch as lengthening and will send a signal to the cord to stop the lengthening. The signal leaves the spindle over a large, myelinated mechanoceptor known as the "annulospiral." This fiber will enter the cord and synapse directly onto the alpha motor neuron. This is known as the monosynaptic reflex and is the only one in the body to do so. Stimulation of the alpha motor neuron by the annulospiral will result in firing of the alpha motor neuron and, consequently, contraction of the muscle. The muscle contraction (shortening) actually removes the stretch from the spindle. The purpose of a spindle is to prevent over-stretch or over-lengthening of a muscle. As I have stated numerous times, the spindle stimulation of the alpha motor neuron via the annulospiral fiber is the most powerful excitatory force acting on the alpha motor neuron. Left alone, this fiber will continuously fire and result in spasm.

Superficial Reflexes: These reflexes require the stimulation of the skin or mucus membrane to create a muscle contraction. Often the muscle is directly under the skin, but not always. When the skin is stroked, receptors sense the irritation and send the message to the cord. From the cord, it enters an ascending pathway (tract) to the brain. Once in the brain, the sensation is discriminated and a response made through a descending pathway to the appropriate level of alpha motor neurons. When the alpha motor neurons are stimulated, the muscle will contract. An example of a superficial reflex is the abdominal reflex. Scratching laterally from the umbilicus will irritate the skin of one abdominal quadrant. The muscle under the skin will contract and draw the umbilicus toward that side. Superficial reflexes require functioning ascending tracts, cerebral cortex, descending tracts, and lower motor neurons. Essentially, a lesion anywhere within the PNS or CNS has the potential of eliminating this reflex. Other examples of superficial reflexes are the anal and cremasteric reflexes. Including the mucus membrane reflexes among the superficial would add the gag reflex, the corneal reflex, and other visceral reflexes such as sneezing and coughing. Again, these reflexes are quickly lost with neurological lesions. Patients in coma (cerebral cortex dysfunction) do not exhibit superficial reflexes. However, a person who is asleep will demonstrate these reflexes. Indeed, the sleeping person often awakens because of the cough reflex. The importance of the superficial reflex is often additive information to other findings. The absence of a superficial reflex rarely adds to the localization of the lesion site, although it may be useful in determining the level of a spinal lesion.

Pathological (primitive) Reflexes: Some authors include these among the superficial reflexes, but I prefer to label them separately. Most students are aware of the Babinski sign, and this is the classic example of a pathological reflex. The most important fact for the student to grasp is that the appearance of a pathological reflex means that the corticospinal tract is lesioned. The student must understand that no other neurological lesion is responsible for these pathological reflexes to appear. A lesion of the extrapyramidal tracts will not cause the appearance of a pathological reflex; nor will a lesion of the lower motor neuron pathways. The only lesion known to cause the pathological reflexes to appear is a corticospinal (pyramidal) lesion. In the newborn, these pathological (primitive) reflexes are present, but disappear with the maturation of the corticospinal pathway. When they reappear in the adult, this is evidence that the corticospinal tract is lesioned. First, let me mention several pathological reflexes. (1) The Babinski sign appears by stroking the plantar surface of the foot from medial to lateral. The + Babinski means that the toes flare out (extend) upon stimulation of the plantar surface. The usual reaction (other than an infant) would be for the toes to curl inward (flexion) or for there to be no reaction at all. Because this reflex is the result of stroking the plantar surface of the foot, a more proper labeling of this reflex is the plantar reflex. Therefore, an extensor plantar reflex is the same as a +Babinski and indicates a lesion of the corticospinal pathway. Another example of a pathological reflex is the grasp reflex. Stroking the palmar surface of the hand will result in the patient grasping the finger or object stroking the palmar surface. We expect this reaction in the infant, but not in the adult. The presence of the grasp reflex in the adult would provide evidence of a corticospinal tract lesion. The sucking reflex is a third example of a pathological reflex. In this case, stroking the side of the mouth would

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result in the patient’s mouth turning toward the side of the stimulation and the initiation of a sucking action. Again, the infant will display such behavior, but the adult should not. A final example is the glabellar reflex in which the examiner taps the patient between the eyes three to four times in a row. In the healthy individual,

the eyes may blink once or twice, but by the third tap the blinking should cease. However, in the infant, the eyes will continue to blink every time the area is tapped by the examiner. Continuous blinking provides evidence again of a corticospinal tract lesion.

The student may ask where along the corticospinal tract must the lesion be in order to create a pathological reflex. The answer is, simply, anywhere along the tract. The lesion could be in the cortex where the corticospinal Betz cells originate. Or, the lesion could be in the cord where the tract descends. It does not matter where the lesion is. Any lesion of the corticospinal tract will result in the appearance of one or more pathological reflexes. What about a cauda equinae lesion? Will this result in the appearance of a pathological reflex? The answer is NO! The cauda equinae is not the corticospinal tract. Remember, the cord ends at L2, and the cauda equinae is the lower motor neurons descending from the cord to the lower extremity. A cauda equinae lesion would manifest as a lower motor neuron lesion – flaccid weakness, hypotonia, no pathological reflex!

Let’s place our attention on the patient demonstrating evidence of a neurological dysfunction. This determination is made by doing sensory, motor, and reflex testing of the patient. When deficits in any of these areas appear, we must assume that there is a neurological lesion somewhere. I strongly advise the student to determine first whether or not the lesion appears to be within the central nervous system (brain or cord). Clearly, lesions of the CNS are much more threatening to the long-term health and welfare of the patient than lesions elsewhere in the nervous system. This is not meant to reduce the importance of a peripheral nervous system lesion, but the difference between a carpal tunnel syndrome and a space-occupying lesion in the brain is obvious. One of the simple tests to help determine whether or not the problem lies in the CNS or PNS is to ask the patient, "what can you do to bring on the symptoms you are telling me about?" If the patient is able to move a part of his body and bring on the symptoms (tingling, pain, numbness, etc….), the examiner can assume that the symptoms are reproducible by the patient. One strong clue has just been provided: When the patient’s neurological symptoms are reproducible by the patient, the lesion is very likely somewhere within the peripheral nervous system. I would not want to make this an all or nothing rule, but it is very helpful. In other words, if the patient can move his arm or shoulder and bring on the tingling or numbness, it is unlikely that the cause of the complaint would be in the brain or cord. On the other hand, if the patient were to have a space occupying lesion within the brain which was creating symptoms of weakness and numbness in the arm/leg, the patient would not be able to reproduce those symptoms. The symptoms would be rather constant and unpredictable (insidious). Again, this is only a helpful hint, not cut in stone. There are notable exceptions, especially space-occupying lesions within the spinal canal.

(Sensory) This would involve the post-central gyrus of the parietal lobe. The most important finding would be a loss of discrimination. The patient would be able to perceive pain (thalamus), but the pain would be described as deep/achy and poorly localized. The patient would also experience paresthesiae and numbness. On examination, the patient would not be able to localize accurately where the clinician was sticking a sharp needle in the skin, although the patient would likely be able to sense a dull ache. In other words, the patient would not be able to point to the exact site where the examiner stuck the needle. The patient would not be able to tell exactly which finger was being stuck. Nor would the patient be able perform a two-point discrimination test. Telling sharp from dull would be difficult, but the patient would be able to perceive that he was being touched. Tests of proproprioceptive discrimination would be very valuable. The patient would not be able to discriminate which direction (up, down, to the side) his finger would be moved by the

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examiner. This is known as "akinesthesia" or the inability to discriminate where a digit is in space. Normally, a healthy individual is able to discriminate 1/16^th inch of movement of an extremity. Several other tests include writing a common letter (A) or number (5) on the palm of the patient’s hand and asking the patient to identify it. Inability to discriminate what is being written on the palm is called "agraphesthesia." One other example is the inability of the patient to recognize a common object (key) placed in the palm of the hand. The patient will move the object around in his palm, but will be unable to tell what it is. The inability to discriminate the size and shape of an object placed in the hand is called "astereognosia." All of the examples given (loss of two-point discrimination, akinesthesia, agraphesthesia, astereognosia, sharp/dull, point localization) are placed under the large umbrella of agnosia. The term, agnosia, is defined as the inability to discriminate sensory input. Agnosia is the general finding associated with lesions of the parietal lobe of the cerebral cortex. Of utmost importance is the fact that all deficits (agnosia) occur on the side contralateral to the side of cortical lesion. In other words, a left cortical lesion will produce agnosia demonstrated upon testing the right arm and/or leg. This is because both the dorsal columns and spinothalamic tracts ultimately decussate from the right side of the cord to the left cerebral cortex. The patients are not anesthetic… they are able to feel something, but they are unable to discriminate what they are feeling.

(Motor) All motor deficits described will also appear on the side of the body which is contralateral to the side of cortical lesion. The cortical lesion will be in the frontal lobe, motor cortex. Most traumatic, vascular, or neoplastic lesions of the cortical area will encompass an area which includes both the frontal and parietal lobes. This will provide evidence of both sensory (see above) and motor deficits. The lesion will injure the corticospinal (pyramidal) and extrapyramidal motor pathways. Let’s first examine the corticospinal pathway. This pathway begins in the motor cortex of the frontal lobe and is responsible for willed, voluntary contraction of skeletal muscle. Loss of this pathway will result in weakness and paralysis. Additionally, fibers from the cortex to the basal ganglion will also be injured. Loss of cortical input to the basal ganglion will result in loss of extrapyramidal function. (The student is reminded that extrapyramidal fibers in general will have a sedating or inhibiting action on the alpha motor neuron.) Loss of this inhibitory activity of the extrapyramidal fibers will cause the alpha motor neuron to be continuously excited by the spindles. Therefore, spasticity will result. The combination of spasticity and paralysis is classic and points strongly to an upper motor neuron lesion. Loss of the corticospinal causes paralysis. Loss of the extrapyramidal fibers will cause spasticity.

A motor exam consists of evaluation of strength and tone. I have attempted to explain that strength is lost either partially (weakness) or totally (paralysis) through damage to the corticospinal pathway. Tone is spastic in effected muscles due to loss of the extrapyramidal fiber inhibition of the alpha motor neuron. Once again, remember that the spindle (annulospiral) is the most powerful excitor of the skeletal muscle. When unrestrained, the alpha motor neurons will fire under the influence of the spindle and will cause the muscles to become spastic.

(Reflexes) The deep tendon reflexes on the side contralateral to that of the cortical lesion will be hyperreactive. This, again, is due to the loss of restraint on the spindle. Tapping on the tendon will stretch the spindle, fire the annulospiral, and send a monosynaptic signal to the alpha motor neuron. Without the extrapyramidals, the alpha motor neuron will respond excessively to the annulospiral facilitation and result in spasm.

The superficial reflexes will be lost on the side contralateral to the cerebral lesion. This is due to loss of motor fibers coming from the cortical region.

The pathological reflexes will be present. The plantar response will be extensor (+Babinski) on the foot opposite to the side of cortical lesion. This is due to loss of the corticospinal pathway at the level of the motor cortex (frontal lobe). Remember, all pathological (primitive) reflexes are due to loss of the corticospinal pathway. Other pathological reflexes may also be evident. For example, the glabellar reflex (see previous notes), and the sucking and/or grasp reflexes may also be present.

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Summary

Cortical Lesion: Generally damages both the frontal and parietal lobes

Will result in both sensory and motor deficits contralateral to the cortical

lesion

Sensory lesions will be classified as "agnosia" – discriminatory deficits

Motor deficits will be spastic paralysis

Deep tendon reflexes will be "hyper".

Superficial reflexes will be absent.

Pathological reflexes will be present

All of the above will be found contralateral to the lesion site

Cranial nerve involvement is also a strong possibility. These will be

later.

It is common to begin with a discussion of what is known as "hemisection" of the cord, or the "Brown-Sequard Syndrome." This is a lesion of one side of the cord only. Examples would include cord trauma, bone fragments, disc fragments, vascular lesions and neoplasms. Obviously, nothing above the level of the lesion will be affected. The only deficits discovered will be below the level of the lesion site. All deficits will be on the same side (ipsilateral) to the lesion with one exception. That one exception is pain (nociception). So let’s begin with the sensory portion of the neurological exam.

Sensory deficits: The student is reminded that nociception enters the cord and synapses on the tracts known as the spinothalamic and spinoreticulothalamic. Both of these pathways will decussate (for the most part) in the cord and travel upward on the contralateral side. Therefore, if there is a hemisection of the cord at T5 on the right, the pain sensations entering the cord from the left side of the body below T5 will be blocked when the ascending tracts (spinothalamic, spinoreticulothalamic) reach the lesion at T5. Thus, the patient will not be able to feel pain (pin prick) on the left side of his body below the T5 lesion site. Paradoxically, the patient will be able to distinguish pain on the right side of his body. This is because the pain sensations below T5 on the right will enter the cord and terminate on the spinothalamic and spinoreticulothalamic pathways. These pathways will decussate and ascend the cord. Since the lesion is on the right side of the cord, the pain pathways are able to ascend the cord on the left side without interference.

Proprioception, on the other hand is just the opposite of nociception. The student is reminded that mechanoreception enters the cord and synapses on the dorsal columns. The dorsal columns ascend the entire cord without decussating. Thus, if there is a lesion of T5 on the right, mechanoreception on the right side will not be able to ascend the cord because the dorsal columns on the right will be involved in the lesion. As a result, proprioception will be lost on the same side (ipsilateral) as the lesion. Of course, the mechanoreceptive deficits will all be confined to areas below the level of the lesion. However, on the left side, proprioception will be intact since the dorsal columns will be able to ascend the cord on the left side without interruption. Losses will include vibratory sense, discriminatory deficts such as akinesthesia and agraphesthesia, two-point discrimination, pressure, etc…. Please understand that with a T5 hemisection on the right, the patient will not be able to sense vibration on the right ankle nor will he be able to discriminate the position of his big toe (akinesthesia), but he will be able to feel pin prick on his right leg and foot. The only lesion site capable of separating the sensory deficits in this way is a cord lesion. That is, pain intact but mechanoreception lost on one side, while pain is lost and mechanoreception preserved on the other side.

Motor deficits: All motor deficits will be on the same side as the lesion. In fact, all further lesions discussed will be on the same side as the lesion. Pain remains as the only neurological deficit on the side of the body opposite to the cord lesion site. Motor evaluation consists of strength and tone.

Strength: Ipsilateral to and below the cord hemisection, muscles will remain paralyzed. This is due to loss of the corticospinal (pyramidal) pathway which descends the cord to innervate the alpha motor neurons. No paralysis exists on the side opposite the lesion site.

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Tone: Ipsilateral to and below the cord hemisection, skeletal muscle tone will be greatly increased. This is due to loss of the descending inhibition from the extrapyramidal fibers. Loss of this inhibition will give free control of the alpha motor neuron to the muscle spindle. Therefore, the muscle will become quickly spastic. Thus, the motor exam will reveal spastic paralysis of the muscles ipsilateral to and below the site of the cord hemisection.

Reflexes: Deep tendon reflexes ipsilateral to and below the hemisection will be exaggerated. This is the result of the loss of the extrapyramidal inhibitory influence on the alpha motor neuron which "tempers" the excitatory influence of the muscle spindle. Without this inhibition, the reflex is "hyper."

Superficial reflexes are lost ipsilateral to and below the hemisection of the cord. This is primarily due to loss of the motor fibers (pyramidal and extrapyramidal) descending the cord.

Pathological reflexes are demonstrated below the lesion site on the same side. This is the result of the loss of the corticospinal (pyramidal) pathway as it descends the cord.

The hemisection of the cord does create all of the above findings. Additionally, one very unique finding associated with a hemisection lesion is the appearance of a segmental lower motor neuron lesion at the exact lesion site. Perhaps a discussion of a particular lesion will clarify the neurological findings. The lesion which I will discuss is hemisection of the cord on the right at C7.

Sensory: Pain is lost on the left side of the body below C7.

Proprioception is intact on the left side of the body.

Pain is intact on the right side of the body.

Proprioception is lost on the right side of the body below C7.

Motor: Spastic paralysis is demonstrated on the right side of the body below C7.

Reflexes: Hyperreflexia is demonstrated in the right Patellar and Achilles reflexes.

Superficial reflexes are lost on the right side below C7.

Pathological reflex (+Babinski) is demonstrated on the right foot.

C7 dermatome deficits noted on the right arm. The dermatome is insensitive to pinwheel examination. Proprioception is intact in the right arm. The C6 and C5 dermatomes are normal. The C7 myotome (triceps) is weak and hypotonic on the right. The C7 deep tendon reflex on the right is diminished. The C6 and C5 myotomes and reflexes are normal. The combination of upper and lower motor neuron presentation is unique to the cord lesions. Remember also that the cord lesion is the only place where the sensory modalities of pain and proprioception can be separated. (The student is asked to review the above findings associated with a C7 hemisection and to be able to provide mechanisms for each deficit. It is not simply a matter of memorizing signs and symptoms, but rather it is absolutely critical to be able to understand the mechanisms behind the findings. I emphasize this and encourage the student to spend sufficient time to learn the explanations behind the neurological deficits. When the mechanisms are finally understood, the associated signs and symptoms of these neurological lesions no longer need to be "memorized.")

When complete section of the cord occurs, there will obviously be loss of all sensory and motor function below the lesion site. Loss of superficial reflexes will be bilateral. Deep tendon hyperreflexia will also be bilateral. Bilateral spastic paralysis is demonstrated below the lesion site. Bilateral pathological reflexes will be evidenced below the lesion site. Lower motor presentations will occur bilaterally at the lesion site itself. All function above the lesion site is normal.

Lesions of the nerve roots are quite common in the chiropractic practice. Disc herniations, osteophytes, thickened ligaments, capsular swelling, and IVF narrowing are but a few of the possible causes of nerve root impingement. Lesions of the IVF will impact both motor and sensory functions since this area of the nerve is considered "mixed," which means that the nerve contains both sensory and motor nerves. The student is reminded that a single nerve root contains nociception specifically from one dermatome and a small amount of mechanoreception from many muscles, tendons, ligaments, joints, and skin. Therefore, loss of a single nerve root (C5 nerve root lesion, for example) will create a sensory deficit only in the related dermatome. No other sensory deficits will be evident. Therefore, on pinwheel examination, the physician will note dermatome hypoesthesia but no mechanoreceptive deficits will be found. The patient with a nerve root lesion (radiculopathy) will still have full mechanoreceptive function; that is, he will be able to sense vibration, he will have full kinesthetic, sterognostic, and graphesthetic functions. He will feel deep pressure, two-point discrimination, etc…. The only sensory deficit will be dermatome hypoesthesia on pinwheel examination. This provides strong confirmation that superficial nociception is segmental (dermatomal), but mechanoreception is not segmental. In other words, the mechanoreception which comes from muscles, tendons, ligaments, joints and skin enters the cord through multiple IVF’s. A single nerve root lesion cannot explain the presence of akinesthesia, loss of vibratory sense, anesthesia of the fingers, etc……. Note, also, that the patient will complain chiefly of pain, numbness and tingling (paresthesiae) in the dermatome. The pain is easily reproducible and results in a Tinel Sign. (The student is referred back to the earlier sections of these notes for a discussion of this topic. See p. 5, beginning with the last paragraph and continuing through page 6)

Motor deficits associated with a nerve root lesion (radiculopathy) will be of lower motor neuron presentation and will be confined to the myotome. A myotome is a group of muscles receiving innervation from one nerve root. No muscle receives all of its innervation from a single nerve root, but some muscle groups are known to receive a major portion of their nerve supply from one root. For example, C5 is commonly associated with innervation to the shoulder abductors (deltoid, supraspinatus) as well as the levator scapulae and several other muscles. A lesion of C5 should, therefore, manifest with weakness and loss of tone in the shoulder abductor muscles. C5 also supplies some innervation to the biceps, so flexion of the forearm would also be weak. A palpatory exam of the muscles should reveal loss of tone and even some evidence of atrophy. This is due to loss of the afferent branch from the muscle spindles (annulospiral nerves) as well as loss of the efferent branch to the muscles. Clearly, a radiculopathy will manifest as a lower motor neuron lesion. The student is advised that no statement of a "pinched nerve at the IVF" should be made without evidence of a segmental lower motor neuron lesion.

The deep tendon reflex will be diminished as a result of a radiculopathy. There are 5 commonly tested deep tendon reflexes, and students are asked to memorize their innervational levels: Biceps (C5), Brachioradialis (C6), Triceps (C7), Patellar (L4), Achilles (S1). Therefore, radicular entrapment of C5 should present evidence of a diminished biceps reflex. As you know, DTR response is graded as 0, 1, 1+, 2, 2+, 3, 3+, 4, 4+, and clonus. A DTR grade of 2 is considered "normal." A radiculopathy would be expected to produce a DTR grade of < 2. An upper motor neuron lesion should produce a DTR grade of >2.

Only very specific and limited superficial reflexes will be lost. For example, the most common would be loss of a portion of the abdominal reflex (perhaps the upper right quadrant) as a result of a single nerve root lesion (perhaps in the midthoracic spine).

Pathological reflexes will never result from a radiculopathy. Remember that the appearance of a pathological reflex means that the upper motor pathway (corticospinal) is lesioned. The nerve roots do not carry the corticospinal nerves. Nerve roots carry the alpha motor neuron axons known as lower motor neurons or the "final common pathway." The same can be said about the cauda equinae. The cord itself ends at L2; those alpha motor neurons in the cord send their axons downward to eventually exit from the L3-sacral foramina. These axons form a structure which resembles a "horse tail" which is the meaning of cauda equinae. The cauda equinae contains no upper motor neurons, only the axons of lower motor neurons. Therefore, pressure on the cauda equinae will never result in a pathological reflex. Cauda equinae syndromes generally present with bilateral lower motor neuron presentation, nonsegmental. In addition, certain autonomic functions will also be reduced.

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A radiculopathy not only demonstrates a uniquely segmental pattern of involvement, this lesion also affects both primary rami. Remember, when the nerve exits the IVF, it quickly divides into the anterior primary ramus and the posterior primary ramus. The posterior primary ramus contains both afferent and efferent fibers to the posterior spinal structures such as ligaments, discs, muscles, blood vessels, etc. … The anterior primary ramus enters the plexus and eventually becomes peripheral nerves which innervate the extremity. Anatomically, it makes sense to state that a lesion of the IVF (radiculopathy) should create deficits in the distribution of both the posterior and anterior primary rami. In other words, both the spinal area and the extremity will hurt and demonstrate deficits. This is an important finding when an electromyogram (EMG) and nerve conduction velocity (NCV) are performed. These tests will determine whether or not nerve function is normal. If these tests confirm that nerve deficits exist in a particular myotome and in posterior muscles as well, the only logical site of a lesion is at the nerve root. If, on the other hand, the EMG and NCV findings conclude that deficits exist only in the extremity and not in the back muscles, the diagnosis of radiculopathy is questionable at best. How could an IVF lesion affect only the anterior primary ramus and leave intact the posterior primary ramus? In conclusion, segmental deficits in the extremity with deficits also documented in the posterior musculature innervated by the same segment obviously point to the nerve root as the lesion site.

The next likely lesion site as the nerves exit the IVF is the plexus. These lesions are commonly referred to as "plexopathy" and are caused by some form of compressive lesion. The term "thoracic outlet syndrome"(TOS) is also commonly used to describe a lesion at this site. However, the TOS symptoms by definition must include a vascular component; therefore, TOS is also termed "neurovascular compression." A plexopathy will most definitely involve the nerves of the brachial plexus, but the vascular supply into the arm may be spared. Thoracic outlet syndromes will be covered in detail later in this class and others.

When considering pressure on a plexus, it is logical that the symptoms would not be confined to a single nerve or dermatome. In other words, the symptoms down the arm would not be segmental like a radiculopathy. Also, lesions of the plexus would completely leave all structures innervated by the posterior primary ramus. Again, this would mean that the spinal structures would not demonstrate any deficits and all findings would be limited to the distribution of the anterior primary rami.. Generally, shoulder movements would bring on the pain patterns, numbness, and paresthesiae. Cervical examination would be essentially normal. Any motor involvement would be of the lower motor neurons.

The major points of plexus lesions are: nonsegmental sensory deficits, pain, paresthesiae; no involvement of

back or spinal structures; cervical examination normal; motor deficits would be weakness and hypotonia.

There are a small number of common peripheral neuropathies which most clinicians quickly recognize. These include carpal tunnel syndrome (median nerve entrapment), ulnar palsy, radial palsy, tarsal tunnel syndrome,

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meralgia paresthetica, dorsal scapular nerve entrapment, and a few others. Each one of the above has a characteristic appearance. No peripheral neuropathy resembles an upper motor neuron lesion. There is no spasticity or hyperreflexia. They often are easy for the patient to reproduce. The deficits remain confined solely to structures which the clinician has learned are innervated exclusively by one peripheral nerve. Everything above the lesion site is absolutely normal.

Each of the peripheral neuropathies is unique and limited only to that one particular nerve. Generally, there will be sensory and motor symptoms since most peripheral nerves are mixed. One major exception is meralgia paresthetica which is peripheral entrapment of the lateral femoral cutaneous nerve. This nerve is purely sensory, and patients complain of pain and tingling on the anterior portion of the thigh. Stretching this area by hip extension will exacerbate the symptoms. Often there is a "bulls eye" on the anterior thigh which is anesthetic. There are no motor deficits.

Peripheral neuropathies are sometimes determined by technical means such as EMG and NCV. These two are classic means of determining with certainty the existence of a specific peripheral nerve in lesion. The use and understanding of EMG/NCV will be discussed later in the course.

Certain disease states , especially diabetes, will render peripheral nerves dysfunctional. In these cases, patients often complain of "glove and sock" symptoms. Hands and fingers tingle as well as the feet and toes. Any patient with these symptoms should be considered for diabetes. Obviously, there is more than one peripheral nerve involved with systemic diseases such as diabetes. Cranial nerves are also commonly involved with diseases like diabetes.

Ruling out upper motor neuron involvement, ruling out segmental (dermatomal/myotomal) deficits, and asking the patient to "make the symptoms happen" while you carefully observe will all assist in the diagnosis of a peripheral neuropathy.

The autonomic nervous system is divided into two major systems: sympathetic and parasympathetic.

In general, from the clinical perspective, the majority of their functions is motor to the viscera. As such, it is common to label the autonomic fibers as "VE" which means "visceral efferent." I do not want to mislead you into thinking that the autonomic system is exclusively motor, for that is not the case. There are visceral afferents which travel within the autonomic fibers from the viscera, and these fibers do carry extremely important sensory information to the cord and to the nuclei of the brain. A good example of this would be the cardiac pain (angina) felt by patients who experience ischemia of the myocardium. The pain sensations are carried to the cord over VA fibers which are considered as part of the autonomic nervous system. The vagus nerve (the largest parasympathetic nerve) carries tremendous amounts of sensory information to the CNS, and these are called "vagal afferents." Sensations such as coughing and gagging are carried to the CNS over the vagus nerve. Please do not be confused on this issue. Without these VA messages, certain life-saving reflexes would be lost.

Nevertheless, our attention will be primarily on the motor aspect of both the sympathetic and parasympathetic systems. Let’s begin with the sympathetic nervous system and examine it from both clinical and anatomical perspectives. All of this information is found in any general neuroanatomy text as well as from your own text.

The sympathetic nervous system (motor portion) begins in the cord from the lower cervical to L2. There is an area of the cord called the "lateral horn" where the cell bodies which form the beginnings of the sympathetic motor nerves are located. These beginning cells are called "preganglionic fibers" and they exit the IVF along with the alpha motor neuron axons. Immediately upon exiting the IVF, these preganglionic fibers leave the spinal nerve and synapse in a nearby sympathetic ganglion. These sympathetic ganglia are known as the

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sympathetic ganglionic chain and are quite visible lying along side the spinal column. There are three prominent cervical sympathetic ganglia which are named "inferior, middle, and superior cervical ganglia." The inferior cervical ganglion is also known as the "stellate" ganglion. The preganglionic fibers are myelinated and, therefore, white in appearance. When these fibers leave the spinal nerve to join the ganglion

they are labeled as "white ramus." Once in the ganglion, the preganglionic fiber synapses on a second fiber known as the "postganglionic sympathetic fiber." The postganglionic fiber is not myelinated and is, therefore, gray in appearance. This fiber is much longer than the preganglionic fiber. It exits the ganglion and forms what is known as the "gray ramus." This postganglionic fiber joins a spinal nerve prior to the nerve’s bifurcation into the anterior and posterior primary rami. Therefore, the primary rami both contain postganglionic sympathetic fibers. The postganglionic fiber ultimately terminates within a visceral structure where it will release its neurotransmitter on a smooth muscle, gland, or into the interstitial fluid.

The preganglionic sympathetic fiber will release within the sympathetic ganglion a neurotransmitter known as acetylcholine (Ach). For obvious reasons, the term "cholinergic" is applied to all chemicals which perform in a manner similar to acetylcholine. An "anticholinergic" substance will act to inhibit the function of acetylcholine. There are two major types of acetylcholine: nicotinic and muscarinic. Guyton’s text will explain well their unique characteristics, but it is important to know that the Ach released at the sympathetic ganglia is the nicotinic variety. The neurotransmitter released at the terminal ending of the postganglionic sympathetic fiber is norepinephrine (noradrenaline). Norepinephrine is very similar to epinephrine (adrenalin) which is secreted by the adrenal gland. Both norepinephrine and epinephrine are classified as "catecholamines." The majority of norepinephrine in the body is secreted from the postganglionic sympathetic fibers. An overproduction of norepinephrine has been described by Dr. Irwin Korr as "sympatheticotonia." The long-term effects of sympatheticotonia have been documented, and this will be covered in great detail later. Chemicals which have effects similar to the catecholamines are classified as "adrenergic." There are a number of examples of adrenergic compounds, many of which are sold over the counter. Two very well known adrenergics are ephedrine and pseudoephedrine and are found in medications to treat cold symptoms and asthma. When an adrenergic is taken into the body, the effects are identical to the effects of the natural catecholamines: pupillary dilation, increased heart rate, increased blood pressure, peripheral blood vessel constriction, cessation of digestive processes, bronchial dilation, reduction of mucus production, increased rate of breathing, nervousness, insomnia and increased metabolism. Although this will be covered later, I will indicate now that the catecholamines are also classified as "alpha" or "beta". The alpha and beta receptor sites found on tissues prefer one over the other. Norepinephrine is considered to be an "alpha adrenergic" while epinephrine is both alpha and beta. This is important for a number of reasons. For example, the SA node of the heart has beta receptors, few alpha. Therefore, epinephrine is a much greater stimulant to the heart than is norepinephrine. That is why we hear about emergency procedures in which adrenaline is injected directly into the heart muscle in order to stimulate contraction. Epinephrine is also a much stronger bronchodilator than is norepinephrine. Again, that is why producers of asthma medications such as Primateen Mist put epinephrine into the spray and not norepinephrine.

There is one major exception to the postganglionic fibers and norepinephrine. As we stated previously, norepinephrine is the neurotransmitter secreted by sympathetic postganglionic fibers at the end organ. This is true except for sweat glands. Strangely, norepinephrine is not secreted by these particular postganglionic sympathetic fibers; instead, acetylcholine is secreted by the postganglionic sympathetic fibers at the sweat gland sites. Therefore, although sweating is classified as a sympathetic function, its stimulation is considered to be "cholinergic" instead of "adrenergic."

Sympathetic atonia refers to the condition of sympathetic loss or inhibition. This can happen as a result of a neuropathy. Sympathetic atonia clearly points to a neurological lesion. Entrapment syndromes including IVF lesions, TOS, peripheral neuropathies, as well as cord lesions can create loss of function of the sympathetic nerves affected. When sympathetic loss occurs, parasympathetic function will dominate. Horner’s syndrome

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represents one of the most common examples of sympathetic loss. This syndrome is often associated with lesions of the upper thoracic spine, cervical ganglia or nearby plexus, or a space-occupying lesion somewhere along the path of the postganglionic fibers as they ascend toward the face. Essentially, Horner’s syndrome represents a loss of sympathetic innervation to facial sweat glands, the pupil, and the Muller muscle which blends in with the levator palpebrae muscle of the eyelid. As a result, three classic symptoms occur, including anhidrosis (loss of sweating), ptosis (droopy eyelid), and miosis (constricted pupil). Interestingly, the eyelid is not paralyzed which would happen with loss of the levator palpebrae muscle. Instead, the eyelid will tend to droop as the patient relaxes, and the drooping is quite visible to the observer. However, when startled or requested to look up, the eyelid will elevate almost completely. This provides evidence that loss of the sympathetic innervation to the eyelid does not paralyze the muscle. The patient still maintains voluntary control of the eyelid through the oculomotor nerve to the levator palpebrae. The sympathetic innervation to the eyelid is supplementary and focuses primarily on special fibers (the Muller muscle) which network throughout the levator palpebrae and assist in keeping the eyelid elevated on an involuntary basis.

Loss of the sympathetic innervation to the eye will obviously affect the pupillary light reflexes. Without sympathetic innervation to the dilator muscle, the pupil will always remain in a constricted state. This state, as mentioned above, is called "miosis." It is mostly visible in a darkened room when one would expect the pupils to be dilated. In a brightly lit room, the miosis is not visible since one would expect the pupils to be constricted.

Let’s review the pupillary light reflexes at this time, since this reflex best demonstrates the opposing actions of the parasympathetic and sympathetic nervous systems. We have already discussed the anatomy of the sympathetic nervous system. Please remember that the sympathetic fibers do not travel within the oculomotor nerve to the eye. The oculomotor nerve contains the parasympathetic fibers from the Edinger-Westphal nucleus. The autonomic fibers are often labeled as "VE" (visceral efferent), so the oculomotor does contain VE fibers which are parasympathetic. It does not contain the VE fibers of the sympathetic nervous system.

When a light is shone into one eye, we expect that pupil to contract. This is known as the direct light reflex. We should observe that the opposite pupil will also constrict. This is known as the consensual light reflex. Let me provide this example: When a light is shone into the right pupil and the right pupil constricts, we say that there is an intact right direct light reflex. If the left pupil also constricts, we say that there is an intact left consensual light reflex. We then move the light source to the left eye and observe whether or not there is an intact left direct light reflex. If the right pupil is also constricting, we say that there is an intact right consensual light reflex.

The student is encouraged to review all of the possible lesion sites which would interrupt these light reflexes. I will provide some examples, but it is difficult to read and visualize the findings. This will require effort to master. Here are several examples of lesion sites and the resulting deficits:

1. Patient has an oculomotor (CN III) lesion on the right.

This patient will not demonstrate a direct light reflex on the right. However, there will be an intact left consensual light reflex. This is because the right optic (CN II) is functional. The patient is not blind in the right eye, but the right pupil will never constrict on a light reflex because CN III on the right is lesioned. When the light is shone into the left pupil, the left direct is intact. However, the right consensual will be absent. Remember, the right oculomotor nerve is lesioned and the right pupil will never constrict on a light reflex. If the lesion involves all parts of the oculomotor nerve, the eyelid will also be paralysed (ptosis) and many extraocular muscles will also be paralyzed, leaving the eye in a down and out position. This patient will demonstrate anisocoria (unequal pupils) in a well-lit room, because the right eye will remain dilated (mydriasis) while the other pupil will constrict as expected. In a dimly-lit room, both pupils will appear relatively equal.

Summary: Intact left direct. Intact left consensual.

Absent right direct. Absent right consensual. (The pupil never constricts with light)

 

 

 

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2. Patient has an optic (CN II) lesion on the right.

This patient is blind in the right eye. The right pupil will not constrict on direct light. When the light is shone into the right pupil, neither will there be a left consensual light reflex. The loss of the left consensual is due to the fact that the optic nerve on the right cannot carry the light stimulation into the brain. Therefore, with the sensory portion of the reflex in lesion, the efferent portion (constriction) will not occur. When the light is shone into the left eye, the left pupil constricts directly. As the light remains on the left pupil, the right pupil also constricts consensually. Because of the intactness of the consensual light reflex in the blind right eye, the pupil on the right will always resemble the left pupil. There will be no anisocoria.

Summary: Intact left direct. Absent left consensual.

Absent right direct. Intact right consensual.

Another way of expressing the above patient findings (#2) would be to say, "the right pupil constricts consensually but not directly. The left pupil constricts directly but not consensually."

 

3. Patient suffers from Horner’s syndrome on the right.

This patient will have an abnormally small right pupil in a dimly-lit room as compared with the left. This pupil demonstrates "miosis" or persistent constriction. Since the pupil is constricted already, it is impractical to examine for direct or consensual reflexes of the right pupil. However, if a light is shone into the right pupil, the left pupil will constrict consensually. Obviously, the left pupil will also constrict directly. The reason I provide this example is to emphasize that the optic nerve is functional in the eye afflicted with Horner’s syndrome, and, therefore, the opposite eye will constrict both directly and consensually.

 

4. Try this example without explanation. The patient has an oculomotor lesion on the left.

If you find these examples difficult and do not understand the mechanisms behind them, please contact the instructor. They are also taught in the physical diagnosis labs

There are a number of other pupillary reflexes such as the Accommodation reflex. In this reflex, the pupil will constrict when it focuses on something which is very close to the eye. If the examiner brings an object to the tip of the nose of the patient and the patient follows the object with his eyes, both pupils will constrict so long as both oculomotor nerves are intact. Even a blind eye will accommodate when both eyes are focusing on something close. There is a specific case when a pupil will not react to direct light but will constrict on accommodation. (Pupil accommodates without reaction to light.) This phenomenon is known as the "Argyll-Robertson pupil" and has been associated in the past with syphilis. There are several CNS diseases which are known to cause the Argyll-Robertson pupil.

The Oculomotor nerve (CN III): This nerve performs a number of motor functions including extraocular and palpebral motion as well as pupillary constriction. The extraocular and palpebral functions are under our voluntary control. However, the pupillary function is not within our voluntary control. The student is reminded that the oculomotor nerve begins in the brainstem with the nucleus of III where the cell bodies are located. These cell bodies are actually under our voluntary control and should be labeled "SE" since they terminate on voluntary muscles (levator palpebrae, extraocular). The Edinger-Westphal nucleus is strictly a

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parasympathetic nucleus and its fibers are involuntary. These fibers are labeled as "VE" and have described previously under the autonomic nervous system. The fibers from the Edinger-Westphal nucleus join the fibers from the brainstem nucleus to form the oculomotor nerve. Ultimately, the VE fibers leave the oculomotor nerve to join the ciliary ganglion which then sends the postganglionic parasympathetic fibers to the constrictor muscle of the pupil. Therefore, a lesion of the oculomotor nerve should involve both the VE and SE fibers. Thus, the patient would lose pupillary light reflexes as well as the ability to elevate the lid or perform conjugate gaze. If a pupil maintains the SE function but loses the VE function (light reflexes), the best explanation would involve a lesion of the Edinger-Westphal nucleus or of the ciliary ganglion. Brainstem lesions could destroy the SE function but preserve the light reflexes.

This describes a loss or inhibition of the parasympathetic nervous system. Perhaps you have realized that a lesion of the VE portion of the oculomotor nerve actually could be described as parasympathetic atonia. One could say that mydriasis is the result of parasympathetic atonia, just like one could say that miosis is the result of sympathetic atonia.

Let’s quickly review the parasympathetic nervous system. This system begins in nuclei within the brain or from nuclei in the base of the sacrum. Contrary to the sympathetic nervous system, the parasympathetic preganglionic nerve fibers are long. These fibers often travel all the way to the end organ before synapsing in a parasympathetic ganglion (such as the ciliary) with the postganglionic fiber. The postganglionic fiber is very short. Acetylcholine is the neurotransmitter at both the preganglionic and postganglionic endings. Thus, this system is labeled "cholinergic." However, the acetylcholine is different at the ganglion from what is released from the postganglionic fibers. The preganglionic fibers release a form of acetylcholine at the ganglion which is labeled "nicotinic" while the postganglionic fibers release a form of acetylcholine which is labeled "muscarinic." The student is referred to Guyton’s text for further explanation of the forms of acetylcholine.

A lesion of the parasympathetic nervous system either in the pre or postganglionic structures will result in parasympathetic atonia. When this occurs, the sympathetic nervous system will dominate. This leads us into an interesting discussion. The following paragraph will challenge you to think about which direction to go when common disorders or pathologies. I will use tachycardia as an example.

Tachycardia is diagnosed when the resting heart rate is over 100 beats per minute. One might suggest two possible etiologies for tachycardia: increased sympathetic stimulation (sympatheticotonia) or loss of parasympathetic influence (parasympathetic atonia). Which is it? How do we know? To answer this question, let me remind you that parasympathetic atonia is a neuropathy, a neurological lesion with demonstrable parasympathetic deficits. Knowing this, I ask whether or not the patient with tachycardia demonstrates neurological deficits in the autonomic system? The answer is, obviously, "no." We have no evidence that the vagus nerve is dysfunctional in any way. Digestive and swallowing processes are still intact. Carotid reflexes are still intact. There does not appear to be any evidence of either an upper or lower motor neuron lesion in the vast majority of tachycardia patients. Thus, the possibility of an increase of sympathetic influence seems very logical. Indeed, measurements of catecholamine levels in the blood and/or tissue sites tend to confirm that excessive sympathetic stimulation is occurring (sympatheticotonia). The traditional treatment for tachycardia does not involve attempting to restore lost vagal function (parasympathetic), but rather to reduce the increased sympathetic function. From a medical perspective, this is often done with beta-blockers or calcium channel blockers. From a chiropractic perspective, we would look to the upper thoracic spine where subluxations may be creating an irritation phenomenon to the sympathetic nerves which provide segmental innervation to viscera.

Contrast the above with a case of miosis in which one pupil remains constricted, even in a darkened room. How should we view this finding? Is the miosis the result of too much parasympathetic influence (parasympatheticotonia) or is it the result of a loss of sympathetic influence (sympathetic atonia)? Again, do we have evidence of a neuropathy? Do we have evidence of sympathetic losses? The answer is yes. For example, the miosis is also accompanied by ptosis and anhidrosis. In addition, if the problem were too much

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parasympathetic influence, then both eyes would have to be affected. Modern science has long ago determined that miosis (and mydriasis) are indicators of a neurological lesion and should be considered as evidence of a neuropathy. If the pupillary constriction were truly the result of too much parasympathetic, then drugs like atropine which inhibit parasympathetic activity should restore the dilation to the eye. This does not happen, because the sympathetic nerves to the eye are in lesion (Horner’s syndrome).

I encourage the student to consider sympatheticotonia and parasympatheticotonia as "dis-ease," while sympathetic atonia and parasympathetic atonia should be considered as "disease." In my opinion, disease refers to loss of function, not heightened function. In dis-ease states, all tissue is essentially normal, but over reactive. Remember, only a healthy nerve can conduct. It would take a healthy nerve to over-conduct. If we think in these terms, conditions like asthma may take on another meaning. For example, what is asthma? The textbooks describe asthma as a "reversible airway disorder with bronchoconstriction and excessive mucus production." I ask, "what are bronchial smooth muscles supposed to do?" I also ask, "what are mucus glands supposed to do?" I think the answers are obvious. They are only doing what they are being commanded to do. The bronchial smooth muscles and the mucus glands are not in lesion. What about the nerves stimulating them? Again I ask, "what are nerves supposed to do?" The nerves are merely conducting, and that is their function. Of course, everything is in an excessively exaggerated state (hyper). Therefore, I prefer to view asthma as a dis-ease, not a disease. Emphysema, on the other hand, is an example of destroyed lung tissue, unrecognizable under the microscope. The condition is not reversible even for a brief period. Emphysema represents, in my opinion, a disease and not a dis-ease. The over-production of stomach acid may be considered a dis-ease, while the loss of production of sufficient stomach acid may be dis-ease. Migraine headaches are better viewed as dis-ease, while upper motor neuron lesions are considered as disease.

This concept of dis-ease and disease will be reviewed in great detail later in this course and others. The student is not obligated to accept this concept, but I ask that it be considered before being rejected.

Light reflexes, gag reflexes, coughing, sneezing, cardiac rate, carotid baroreceptor reflexes, etc…etc… all are examples of autonomic reflexes. Life itself is the result of a careful balance of these reflexes, and we call this balance, "homeostasis." Let me simply state that these reflexes require a functional nervous system. Neurological lesions will quickly destroy these reflexes and render the patient quite ill. For example, elderly patients often need assistance with feeding because they cough when swallowing food. The swallowing reflex is diminished. In other patients, the cough reflex is weak, and these patients may inhale (aspirate) food contents from the stomach into the lungs. This lack of an adequate cough reflex is especially threatening to elderly patients confined to a bed. Pneumonia is a common killer of these patients. On the other hand, people with bronchitis will cough and produce copious mucus. This is because their autonomic reflexes are intact. These people do not demonstrate any evidence of a neurological lesion.

To classify these reflexes, we use the descriptors: VA, SA, VE, SE. You have likely heard of viscerosomatic, viscerovisceral, somatosomatic and somatovisceral reflexes. The autonomic reflexes are classified as either viscerovisceral or somatovisceral. This is because the VE fibers are needed for both reflexes. An example would be the filling of the stomach which results in the production and release of bile. This is a viscerovisceral reflex (VA-VE). Pressing on the carotid body to reduce the heart rate is another example of a viscerovisceral reflex (VA-VE). On the other hand, severe pain from a fracture causing the patient to sweat and his heart to beat faster is an example of a somatovisceral reflex (SA-VE). As you can see, very few reflexes exist in isolation. The stimulation of one reflex generally is accompanied by many related events as well.

There are two major controls of the autonomic nervous system. These are the higher centers of the central nervous system (hypothalamus) and reflexes. The hypothalamus sends descending fibers to the parasympathetic and sympathetic neurons and will stimulate them into action. As stated above, reflexes may also stimulate the VE fibers into action. Reflexes do not require the brain to act. Actually, lower reflexes have

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been demonstrated to exist quite well in animals whose heads have been removed (decerebrate animals). Many people have learned how to "tap into" the higher central controls to gain some degree of management over the autono