The Root of Pain

The latest theories on nerve damage redefine the causes of pain—and stress the importance of an active rehab program.

By Adriaan Louw

Adriaan Louw, PT, is a Physical Therapist at Platte County Physical Therapy, in Platte City, Mo., an Associate Instructor at Rockhurst University and the University of Kansas Medical Center, and an Instructor at the Neuro Orthopaedic Institute, based in Unley, Australia.

Training & Conditioning, 10.6, September 2000,

It is unfortunate that most clinicians are familiar with the term “pinched nerve.” Visions of a “slipped disc” or a “bulging disc, with a gel-like substance pushing against a nerve” come to mind, as these are the ideas taught in mainstream medicine. This model, however, has severe shortcomings in the diagnosis and treatment of such disorders.
In the last five years there has been an explosion in the research exploring the pathobiology of the intervertebral disc (IVD) and neurodynamics (the mobility of the nervous system), which plays a very important role in any athlete’s physical fitness and performance. The purpose of this article is twofold:
(i) to introduce the clinical relevance of new and updated material regarding the pathology of the IVD, especially in relation to the nerve root, and
(ii) to discuss the mobility of the nervous system and its relation to sports injuries and their treatment.
Physical therapists and athletic trainers are skilled in the diagnosis and treatment of musculoskeletal injuries seen in sports. The challenge for each clinician is to add neural tissue to his or her differential diagnosis paradigm. The nervous system will be affected in every injury. It is the responsibility of the ATC and PT to prevent the development of a chronic disorder that may plague an athlete for a long time.

The traditional concept of a “pinched nerve” refers to direct mechanical pressure of the IVD on the nerve root, or in extreme degenerative conditions, the pressure applied to the nerve by osteophytes. To take this concept even further, the pressure can be applied to any peripheral nerve, especially in vulnerable areas, such as tunnels (for example, carpal tunnel syndrome) or bony areas. Recent studies have shown, however, that direct pressure to the nerve will result in paresthesia, but not pain. Pain responses result from chemical rather than physical irritation to the nerve. Therefore, the term “abnormal sensitivity of the nervous system” is becoming the preferred term, rather than pinched nerve.
Pressure can be applied to the nerve in various forms. Direct mechanical pressure can be applied by any tissue infringing the space occupied by the nerve. These could be anything from a “bulging disc” to a poorly fitted athletic knee brace. A second, more powerful, interference may be caused by immediate swelling in surrounding tissues that have been damaged. Not only will this inflammatory exudate cause swelling (mechanical pressure) around the nerve, but the chemical substances (histamines and enzymes) will cause a chemical irritation, which is not only more painful, but more dangerous, with the potential to lay down scar tissue in and around the nerve with lasting effects.
The three pathobiological processes that occur when a nerve is injured relate to altered blood flow to the nerve, altered axoplasm flow in the nerve, and the development of abnormal impulse-generating sites. All three of these can be effectively treated with active rehabilitation.
Clinicians are taught to handle the nervous system carefully—that nerves are very delicate structures that do not handle any pressure or injury well. Although the nerves themselves do have limited recovery ability, the nervous system as a whole is actually very well designed to handle extraordinary stresses, including those involved in high-speed, repetitive sporting events.
Altered blood flow. The nervous system comprises only seven percent of total body weight, yet it demands 25 percent of the body’s cardiac output, because nerves require adequate blood supply to function. Only 30 mm Hg of pressure is needed to stop venous blood flow. Injury to the nerve is dependent on the duration, severity, and number of sites of compression. When pressure is increased in the space surrounding the nerve, venous stases occur, which in turn cause a hypoxic state of the nerve as well as the buildup of edema, thus causing the nerve to become swollen. With the continued edema, fibroblasts infiltrate the area, eventually leading to scarring in and around the nerve or its fascicle. Often, patients with nerve pain caused by altered blood flow will complain of waking up at night with pain. This is because the decreased venous flow at night exacerbates the problem.
Altered axoplasm flow. Axoplasm is the transport mechanism in the nerve that allows the cell components to be transported to their functional site where they maintain tissue health. Any pressure directly applied to the nerve, or in the surrounding tissue following injury, will cause the axoplasmic flow to slow down, causing the nerve to “become sick.” If pressure is applied to two (double crush) or multiple areas (multiple crush), the nerve will be considerably more prone to injury.
Abnormal Impulse-Generating Site (AIGS). Axons are primarily designed for impulse conduction, not generation. When the nerve becomes injured as a result of vascular or axoplasmic changes, the axon has the potential to develop an AIGS, whereby ion channels into the axolemma become plugged where the nerve is injured. A key treatment component is that the ion channels are replaced in the body every 48 hours, so the sensitivity of the nerve to these stimuli can be changed. Depending on the type of ion channels laid down, the nerve can become sensitive to metabolic changes, such as adrenaline, temperature, mechanical pressure, or a lack of stimuli. Physical activity or movement is needed to help with the replacement of these ion channels. If, for example, an injured athlete is active or receives massage following his or her injury, the new channels will not be sensitive to movement or pressure.

As the body ages, natural changes take effect in the IVD that cause it to lose its ability to store and take up water. From the time of birth to the mid-20s, there is a rapid fluid loss in the nucleus pulposus. After the mid-20s, the fluid loss continues, but at a slower rate. The nucleus pulposus gradually stops being a fluid or a gel in the early adult years. Chemical changes in the substance of the nucleus pulposus cause it to become stiffer, harder, and almost solid.
Based on this information, the theory of a “bulging nucleus” needs to be inspected more thoroughly. A nucleus prolapse or bulge can only occur if the nucleus is a fluid and can thus “flow,” and a nucleus herniation can only occur in two situations, both of which require the nucleus pulposus to have a fluid content. The first is in the young child or in adolescence, where the nucleus is still liquefied; the other process is where the adult nucleus liquefies.

Likewise, the concept of a “slipped disc” also needs re-examination. The inner layers of the annulus fibrosis are strongly embedded in the cartilaginous end plate, while the outer half of the annulus fibrosis is steadily anchored into the VB. Thus, the IVD cannot physically move or slip out of place.
On the other hand, the nucleus pulposus is contained by the annulus fibrosis. If the annulus is injured, there is the real possibility of an “annular bulge.” In the event of decreased nucleus fluid (such as occurs at the end of the day), it is accepted that with loading, the annular fibers will bulge outward. Thus, with sudden loading, as frequently required in sports such as football or basketball, not only an outward, but also an inward bulge of the annulus fibers can be found. This process is known as metaplastic proliferation. With the inward bulge, matrix and collagen is laid down in response to the annular stress in the form of bundles, rather than sheets, along the line of the existing annular lamellae. As the spaces between the lamellae fill, tension on the annulus fibrosis increases, causing a painful stretch of the outer third, innervated, annulus fibers. The increased tension will also cause the annulus fibers to bulge toward the intervertebral foramen.
However, even in the case of a severe annulus bulge, there is sufficient space between the annulus and the nerve root. Furthermore, if mechanical pressure occurs, a patient will feel paresthesia only, no pain. Several studies have found that following discectomies, extruded material is annulus fibers, not nucleus material. The extruded material has the same appearance as a nucleus, but is new annulus fibrosis material.

Nerves can and do present in varied forms, from the classic dermatomal patterns to some fairly weird, unpredictable symptoms. In the acute stages, nerves tend to follow classic dermatomal patterns, but as the injury prevails, the more unpredictable symptoms, such as “spot pain/stripe pain,” will appear. Commonly, nerves will present with deep burning pain, with or without paresthesia. Apart from these apparent pain patterns, pain associated with the peripheral nerves commonly presents with symptoms closely related to common soft tissue injuries. Again, however, it is important to note that injury to a nerve does not necessarily cause pain.
It is highly recommended that each clinician add neuroanatomy and neurodynamics to his or her clinical reasoning process when evaluating and treating an athlete, especially when time has passed and the tissue “should have healed.” The clinician should be aware of the ability of the nervous system to increase in sensitivity and check the relevance of neurodynamics. Table One lists common sports injuries and the nerves closely related to maintained pain states.

It is extremely difficult to diagnose injury to or increased sensitivity in the nervous system with the use of current medical tests. Most scans (CT, MRI, bone) will be able to pick up damage to surrounding tissue, but not to the nerve itself. To add to athletes’ and clinicians’ frustrations, EMG tests have also been shown to be inconclusive. A key factor is the nerve conduction during needle placement of the EMG—the needle may be placed in healthy fascicle rather than the adjacent injured fascicle, or vice versa. Furthermore, the EMG is designed to determine if there is abnormal conduction, and not the state of the surrounding connective tissues.
As a result, the importance of physical evaluation cannot be stressed enough. This should include (1) neurological evaluation (reflexes, sensation, muscle power); (2) palpation of the nerves; and (3) neurodynamic tests.
The neurodynamic tests are designed to selectively test the mobility of the nervous system as it relates to function. For a long time, clinicians were taught to determine if the test was “positive” or “negative.” Given the nature of nerves in their clinical presentation, they may not be “positive” but rather should be considered “relevant.” For example, does the fact that an athlete’s straight-leg raise is 10 degrees less on the left leg become relevant when he or she keeps tearing his or her hamstring? There are numerous tests to challenge all neural structures; some of the most important are listed in Table Two, at the end of this article.

Physical therapists and athletic trainers are ideal clinicians to treat these neural injuries since the best treatment focuses on movement and education. Movement not only restores and maintains blood and axoplasm flow, but reduces the chances of the nerve developing an AIGS that may become sensitive to movement or pressure. Gentle passive or active movement also helps increase circulation in and around the nerve, thus diminishing its ability to become ischemic.
As part of his or her treatment plan, the clinician should focus on the following during the acute phase of any injury (see also Sidebar - “Solving the Case of the Pinched Nerve,” at the end of this article):
• Explain the injury to the athlete, including the healing process, as well as what he or she can expect and what he or she can do to assist the recovery. This reduces the potential development of AIGSs that can become sensitive to adrenaline.
• Treat the surrounding tissue with the rest, ice, compression, and elevation (RICE) regimen, and add movement as a critical element in this protocol. The analgesic effect of ice, along with the elevation, will reduce the nociception and help reduce swelling. Compression should be alternated with periods of no pressure to avoid clamping the nerve.
Movement may be the most important factor. The nerve needs to have gentle movement applied to it, without producing pain or paresthesia. The rule here is fewer, but more frequent, repetitions of the chosen exercise. Move extremities distal, or opposite, to the injured joint, thus causing the nerve to gently move. For example, in a knee injury, when the joint is hot and swollen, the same leg’s ankle can be dorsi- and plantarflexed, or straight-leg-raise “pumps/sliders” can be performed on the other leg. An important concept when dealing with any type of nerve damage is that of tissue borrowing: when we move one part of the body, corresponding nerves in other parts of the body move as well. For example, when we breath in, the median nerve moves approximately two inches; and, when we move our left hand, wrist, or elbow, nerves in the right arm will also move. Thus, in order to affect a nerve in an injured area, it is not necessary to move that area, but to move the corresponding area that will also affect that nerve.
Tensioners and sliders can be used to gently move any nerve. In a tensioner, the neural tissue and its connective tissue are stretched at the same time in opposite directions, such as neck flexion while dorsiflexing the ankle. Sliders move the nerve towards one end (dorsiflexion) while putting the other side on slack (neck extension). Tensioners may be performed in a neurally loaded position, where the position already challenges the neurodynamics (that is, before the athlete moves or stretches the area, the position itself provides some stretch to the nerve). In a slider, the patient should be in a comfortable, neurally unloaded position to avoid unwanted stress on the nervous system. During tensioners, the end-position may be kept for one to two seconds, but during the slider, an end-ROM stretch should be avoided by using gentle, easy movements. Sliders will be more advantageous in the acute phase. As the injury heals, more and more tensioners should be added.
A critical component of neural tissue mobilization requires that the nerves be “primed” before any tensioners or strong stretches are applied. This way, the nerve will not become ischemic, which could cause increased pain or spasm. A very good example is the traditional hamstring stretch. Very often, after a thorough static-stretching process, the athlete will come back with increased pain and no change in ROM or function. If the sciatic nerve is part of the dysfunction, the prolonged stretches only cause an ischemic reaction, which results in increased pain. The dynamic warmup will prevent this. First, have the athlete bike or walk backwards on a treadmill to mobilize the nerve and surrounding tissue. Then, he or she should perform 15 to 20 gentle sliders and a series of hamstring stretches. After these stretches, another set of sliders should be done to once again flush the nervous system with blood.
The important thing to remember for all athletes—not just injured ones—is that nerves need movement. As a preventative measure, neurodynamics should be incorporated into the warmup of each and every athlete. This will allow the nerve to get used to the movement of any given sport in all planes of motion, prime it for competition, and prepare it in order to be able to avoid injury.

Recognition: Special thanks to David Butler and The Neuro Orthopaedic Institute for selected sections.

Table ONE -- Some common sports injuries and the corresponding nerves that may be involved
Injury and Possible nerve involved
Plantaris fasciitis - Medial plantar nerve
Chronic lateral ankle sprain - Peroneal nerve
Posterior meniscus knee pain - Tibial nerve
Achilles tendinitis - Sural nerve
Medial knee pain-s/p arthroscopic surgery- Saphenous nerve
Chronic hamstring tear - Sciatic nerve
Lateral and/or medial epicondylitis - Radial and median nerve

Table TWO -- Common tests to challenge neural structures
Test and Structures being tested
Passive neck flexion - Medulla/pons/spinal tracts
Straight-leg raise - Sciatic/tibial/peroneal nerves
Prone knee bend - Femoral nerve
Slump - Sciatic/tibial/peroneal nerves
Upper-limb neurodynamic tests - Median nerve, Radial nerve, Ulnar nerve

Sidebar - Solving the Case of the Pinched Nerve
An 18-year-old soccer player is kicked on his right lateral ankle during a game. The athletic trainer assesses the athlete on the field and discovers severe swelling, bruising, and pain around the lateral malleolus. After thorough evaluation, apart from managing the apparent soft tissue injury, the athletic trainer should consider the following interventions to maintain the health of the nervous system.
• institute R.I.C.E. (rest, ice, compression, and elevation): reduces swelling, bleeding, and provides an analgesic effect
• inform the athlete about his injury and prognosis: reduces adrenosensitivity
• move extremities and joints adjacent to the injured ankle. For example, flexing and extending the left knee while maintaining dorsiflexion mobilizes the neural and connective tissue in the legs as well as in the lumbar plexus and spinal cord. With the ankle iced and bandaged, heel slides should be initiated, without reproducing pain and/or pins and needles.
• provide him with a thorough home exercise program of the above interventions.
Neurological symptoms can persist for several weeks following the injury, and must therefore be addressed through the sub-acute (roughly two to eight weeks) and chronic phases. As the ankle gets better, the nervous system in and around the joint can tolerate more stress and requires some mobility and stretching to maintain and eventually increase the functional length of the tissue needed in soccer.
Possible symptoms in the sub-acute phase for the ankle injury described above include pain, swelling, cramping in the calf, and numbness or sensations of pins and needles. The goal of treatment at this point is to increase single-leg-raise and ankle ROM without increased numbness or pain. Interventions during this phase include:
• ice
• gentle self-massage around the lateral malleolus
• mobilization of the ankle jojnt by hand or on a ball in all planes (circles)
• sliders
• gentle tensioners (straight-leg-raise pumps with the injured leg with and without dorsiflexion and plantarflexion).
Note that minimal pins and needles may be present with these techniques.
In the chronic phase, the athlete may still be experiencing symptoms such as spot pain or tenderness, the joint may be sensitive to cold or pressure, and he may have limited ROM, mobility, or function in the ankle. In this phase, the goal of treatment should focus on restoring full function and preparing the athlete for soccer while minimizing pain and increasing ROM. The athlete should be advised about neurosensitivity and told that the spot pain is normal and not, in itself, harmful. Interventions include:
• ankle joint mobility and function exercises
• single-leg raises and slumps with added tension on the nerve with dorsiflexion and plantarflexion
• long sitting slump
• dynamic warmups, including ball kicks with a neurodynamic bias and single-leg raises
• balance/agility/and coordination exercises and drills that prepare the athlete for game situations.