Lumbar Vertebral Compression, End Plate Fracture, and Disc Degradation

By Mark A. King, DC

Clinical Anatomy of the Lumbar Spine is one of the great books in print regarding the lumbar spine. It is written by Drs. Bogduk and Twomey, and published by Churchill Livingstone. The book gives information about the structure and function of the lumbar spine as it relates to the most common source of low back pain, mechanical low back pain. 
In the chapter on the pathology of mechanical lumbar back pain, the various body movements are discussed. I would like to visit the topic of lumbar compression.

When excessive lumbar compression occurs, the lumbar discs do not typically herniate, but rather the vertebral end plate may fracture. This can occur with heavy axial loads, such as falling into a standing or seated position, or during heavy lifting when the back muscles exert a large compressive load on the discs and vertebrae. Just as muscles become conditioned with use to loading stress, so do bones, such as the lumbar vertebrae.

While the end plate fracture can occur with a fall into a standing or seated position, it also occurs in poorly conditioned individuals who undertake heavy lifting that their bodies are not accustomed to handle.

Take for example the person who works at a desk all week, then decides on the weekend to move furniture or lift some other heavy object with a maximum pull. Proper lifting techniques would help in this situation, but the risk of an end plate fracture still remains. Obviously, persons with osteoporosis or osteomalacia would be significantly more susceptible to this.

Because the end plate is not innervated, this end plate fracture is not typically painful. A person could heal and not even know that they had such an injury.

Another possibility, however, is disc degradation via an inflammatory repair process, or from an autoimmune response. Autolytic enzymes can become activated by changes in the pH, secondary to the disturbance caused by this end plate fracture. Another theory following end plate fracture is that the nucleus pulposus elicits an autoimmune response. The nucleus pulposus does not have a blood supply and, in the presence of an end plate fracture, the nucleus is exposed to circulation within the vertebral spongiosa. This elicits an immune response.

Whether the mechanism is autoimmune or an inflammatory process, the nucleus pulposus begins the process of progressive degradation. This process is a consequence of trauma, not age-related degeneration. There is a progressive loss of the water binding capacity and a deterioration of nuclear function. Since the nucleus is less able to sustain pressure because it is not able to bind water, greater loads are placed on the annulus fibrosus. Eventually the annulus is unable to sustain the load; the disc loses height; and this changes the function of all the joints in the affected area. This can lead to osteophyte formation around the zygapophyseal joints and vertebral bodies.

This nuclear degradation eventually extends peripherally to affect annular fibers, typically along radial fissures that have formed. This condition is known as an internal disc derangement or internal disc disruption. At this point, there is no disc bulge or disc herniation. It is possible for the internal disc derangement to progress to a disc herniation because the nucleus pulposus is no longer normal, coupled with the radial tears that occur in the annulus, setting up a situation that allows for herniation of the nucleus, typically during flexion or flexion and rotation movements.

Before a disc herniation occurs, and before any osteophyte formation and subsequent inflammatory response causing radicular type pain can occur, the internal disc derangement can become painful as a result of mechanical or chemical irritation of the nerve endings in the annulus fibrosis. More stress is imparted on the annular fibers and, since these annular fibers are innervated, pain can result. If there are radial fissures in the annular fibers extending into the outer third, inflammatory chemicals can be brought into the area and pain can occur.

This chemical stimulation of nociceptive fibers can explain the constant pain that is unrelated to activities. Certainly, they can have both chemical and mechanical pain, so that the pain is increased with activity on top of their ongoing constant pain. With this internal disc derangement, there would be no neurologic deficit, as the problem is centrally located within the disc, so CT scans, MRI, and myelography would be normal, as would an electrodiagnostic evaluation.

Discography, an expensive and invasive procedure, would help identify this problem. Over time, other imaging that is less invasive can be used to help explain some of these patients with ongoing low back pain, despite the absence of neurologic deficit.

While not always visible on plain film radiography, Schmorl's nodes often form secondary to these end plate fractures. Excellent pictures and radiographs are given in the textbook Essentials of Skeletal Radiology, second edition, by Yochum and Rowe.

One of the problems with this model for low back mechanical and/or chemical pain secondary to stimulation of nociceptive fibers is the annulus fibrosis in the clinical setting, with the current health care environment, is the need for documentation. As discussed, outside of discography, there is not a great deal that we can do that I know of to document these lesions. I do not believe, as some physicians do, that everyone with long-term low back pain is simply malingering. The theories discussed above offer some possible explanations. I feel we owe it to our patients to learn more about these possibilities to explain their pain syndromes. Chiropractic care can help many of these people via chiropractic adjustments and the resultant firing of mechanoreceptors and inhibition of nociceptors.

Spinal Instability and Pain: Is There a Connection?

By Craig Liebenson, DC

A new study examined the theory that antagonistic trunk muscle coactivation is necessary to provide mechanical stability to the lumbar spine around a neutral posture. The authors found that antagonistic muscle coactivation increased in response to increased axial load on the spine.
EMG measurements were gathered from three flexors -- external oblique; internal oblique; and rectus abdominous; and three extensors -- multifidus; lumbar erector spinae; and thoracic erector spinae.

The subjects were asked to perform slow trunk flexion and extension movements in a semi-seated position with hip motion restricted, but trunk motion free. Weights were then added to the torso. One conclusion was that "increased levels of muscle coactivation may constitute an objective indicator of the dysfunction in the passive stabilizing system of the lumbar spine."

Cholewicki J, Panjabi MM, Khachatryan A. Stabilizing function of the trunk flexor-extensor muscles around a neutral spine posture. Spine 1997;19:2207-2212.

Other recent studies have looked at various aspects of motor control and evaluated their correlation with pain and injury.

Reaction Time

When comparing back pain patients to asymptomatic subjects, the back pain patients had a slower reaction time, decreased peak output, increased after discharges when irregular load is handled. This study had particularly strong methodology because treatment was given and the reactions improved. Then sitting was shown to disturb these variables and a brief walking break to improve them again.

Wilder DG, Aleksiev AR, Magnusson ML, Poper MH et al. Muscular response to sudden load. Spine 1996;21(22):2628-2639.

Delayed activation of transverse abdominous during arm movements distinguishes lower back pain patients from normals.

Hodges PW, Richardson CA. Inefficient muscular stabilization of the lumbar spine associated with low back pain. Spine 1996;21:2640-2650.

Coordination

Loss of control of center of rotation during isoinertial resisted trunk movements in the sagittal plane occurred in low back pain patients, but not in normals. Increase in rotation and side bending and decrease in sagittal motion occurred.

Paarnianpour M, Nordin M, Kahanovitz N, Frank V. The triaxial coupling of torque generation of trunk muscles during isometric exertions and the effect of fatiguing isoinertial movements on the motor output and movement patterns. Spine 1988;13:982-992.

Spinal loading forces were increased during a fatiguing isometric trunk extension effort without a loss of torque output. Torque output remained constant because as the erector spinae fatigued, substitution by secondary extensors such as the internal oblique and latissimus dorsi muscles occurred.

Sparto PJ, Paarnianpour M, Massa WS, Granata KP, Reinsel TE, Simon S. Neuromuscular trunk performance and spinal loading during a fatiguing isometric trunk extension with varying torque requirements. Spine 1997;10:145-156.

Overactivity of antagonist back muscles during the ipsilateral swing phase of gait and decreased agonist peak muscle activity during double stance phase differentiated back pain patients from asymptomatics.

Arendt-Nielson L, Graven-Nielson T, Svarrer H, Svensson P. The influence of low back pain on muscle activity and coordination during gait. Pain 1995;64:231-240.

Increased ratio of rectus abdominous to transverse abdominous/oblique abdominals is correlated with lower back pain. 

• Control subjects were able to preferentially activate internal oblique and transverse abdominous muscles without significant rectus abdominous activation.


• Low back pain patients could not do this.


• Performance of trunk curl fast instead of slow correlated with greater ratio of rectus abdominous to transverse abdominous/oblique abdominals.

O'Sullivan P, Twomey L, Allison G, et al. Altered patterns of abdominal muscle activation in patients with chronic low back pain. Aust J Physio 1997;43:91-98.

Altered muscle activation ratios of synergist spinal muscles during a variety of motor tasks differentiated from injured and uninjured individuals. Underactivity of agonists and overactivity of synergists was able to discriminate pain patients with 88% accuracy.

Edgerton VR, Wolf SL, Levendowski DJ, Roy RR. Theoretical basis for patterning EMG amplitudes to assess muscle dysfunction. Med Sci Sp Exer 1996;28:744-751.

Endurance

Decreased endurance of the trunk extensors has not only been shown to correlate with pain, but to predict recurrences and first time onset in healthy individuals. This evidence is extremely strong because it is prospective and thus the findings are not merely correlated by association, but by etiology.

Biering-Sorensen F. Physical measurements as risk indicators for low-back trouble over a one-year period. Spine 1984;9:106-119.
Luuto S, Heliovaara M, Hurri H, Alaranta H. Static back endurance and the risk of low-back pain. Clin Biomech 1995;10:323-324.
Vink P, van de Velde EA, Verbout AJ. A functional subdivision of the lumbar extensor musculature. Electromyogr Clin Neurophysiol 1988;28:517-25.

Atrophy

The multifidus in the low back has been shown to be atrophied in patients with acute low back pain, those recovered from acute low back pain, and those having surgery for nerve root compression. The acute patients' atrophy was unilateral to the pain and at the same segmental level as palpable joint dysfunction. Recovery from acute pain did not automatically result in restoration of the normal girth of the muscle. However, spinal stabilization exercises successfully did rebuild the muscle's size.

Hides JA, Richardson CA, Jull GA. Multifidus muscle recovery is not automatic after resolution of acute, first-episode of low back pain. Spine 1996;21(23):2763-2769.
Hides JA, Stokes MJ, Saide M, Jull GA, Cooper DH. Evidence of lumbar multifidus muscle wasting ipsilateral to symptoms in patients with acute/subacute low back pain. Spine 1993;19(2):165-172.

According to Edgerton et al., "The nervous system apparently can detect a reduced capacity to generate force from a specific muscle or group of muscles and compensate by recruiting more motoneurons. This compensation can be made by recruiting motor units from an uninjured area of the muscle or from other muscles capable of performing the same tasks ..."

According to Korr, "The brain thinks in terms of whole motions, not individual muscles."

Korr I. The spinal cord as organizer of disease processes. J Am Osteopath Assoc 1976:76;35.

For Your Practice: 

• Inspect posture for poor stability (i.e., forward drawn posture);
• Inspect gait for poor stability (i.e., hyperpronation);
• Palpate joints for dysfunction (i.e., restricted mobility);
• Inspect movement patterns for incoordination (i.e., poor scapulo-humeral rhythm);
• Palpate muscles for hyperactivity (i.e., trigger points);
• Advise patients about good posture (i.e., sit and lift with neutral spine);
• Mobilize joints and soft tissues to improve mobility;
• Exercise patients' balance and reaction time with propriosensory training;
• Exercise patients with emphasis on co-activation of agonists and antagonists and maintenance of neutral spine posture (i.e., neutral lumbar spine during trunk curls, neutral head/neck posture during pull downs).

Motion Palpation

By Keith Innes

Motion palpation is not a technique. Motion palpation is a method of examining the various components of the subluxation complex. Motion palpation is based upon the work of many authors and clinicians from a diverse background and from locations throughout the world. 
The history of motion palpation includes the contributions of Illi; Gillet; Kaltenborn; Grieve; Mennel; Cyriax; Dvorak; Faye; Grice; Gittleman; Fligg; Palmer; Wyke; Korr; Carrick; Seaman; Edwards; Gonstead; Lantz, etc.

Motion palpation has many components, each of which is a major study of its own. Many of the authors mentioned above have contributed to the various components of the subluxation complex, none of which can be separated from the complex itself. In other words, each and every component is a component of the other, and it is their relative interaction that motion palpation is all about.

Motion palpation and the subluxation complex in chiropractic are inseparable, as the two coexist, with the final complex being greater than the sum of its parts. The subluxation complex as it exists today includes eight component parts: 

• kinesiopathology
• neuropathology
• myopathology
• connective tissue pathology
• vascular abnormalities
• inflammatory response
• histopathology
• biochemical abnormalities

As research continues, new parts will be added as they apply to the science of today's chiropractic.

Motion palpation itself allows the doctor or student of chiropractic to evaluate the kinesiological component of the subluxation more than any other component and will be dealt with in this paper more so than the obviously associated muscular component. A common language is necessary; therefore, prior to beginning this discussion, a number of terms will be defined for use in this paper.

Joint Play

According to Magee, in his textbook Orthopedic Physical Assessment: "All synovial and secondary cartilaginous joints, to some extent, are capable of an active range-of-motion, termed voluntary movement. In addition, there is a small range of movement that can be obtained only passively by the examiner; this movement is called joint play, or accessory, movement. These accessory movements are not under voluntary control; they are necessary, however, for full painless function of the joint and full range-of-motion of the joint. Joint dysfunction signifies a loss of joint play movement. The existence of joint play movement is necessary for pain free voluntary movement to occur. An essential part of the detailed assessment of any joint includes an examination of its joint movements. If any joint play movement is found to be absent, this movement must be freed before functional voluntary movement can be fully restored. In most joints, this movement is less than 4 mm in any one direction."

Kaltenborn defines joint play as "short, straight-lined (rectilinear), passive bone movements. When this movement is performed parallel to the treatment plane, it is called translatoric gliding. When passive, rectilinear bone movement is at a right angle and away from the treatment plane, it is called traction. The third joint play movement, compression, is performed by moving a bone perpendicular and towards the treatment plane. All three joint play movements are utilized to test passive joint movements."

Dvorak and Dvorak describe joint play in their text Manual Medicine: "Decreased angular range-of-motion or diminished joint play, either with hard or soft end feel. A hard end feel is most likely due to articular (structural) degenerative changes, while soft end feel is usually associated with shortened muscles. Pain in conjunction with introduced motion indicates a segmental somatic dysfunction."

Dr. Bruce Fligg, in chapter six of the text entitled Upper Cervical Syndrome, states "that the greatest advantage of motion palpation, however, lies within the specific objectives. These objectives center around the actual application of the manipulation. Motion palpation procedures help us to select the specific manipulation and to identify the specific motion segments that require manipulating. They also establish the angle of thrust, the depth of thrust (amplitude), and most importantly, a tool for outcome assessment, the effectiveness of our manipulation. Ultimately, we must ensure that (1) the coupled motion manipulation, (adjustment/reduction -- mine, not a part of the quote) produced increased mobility at the motion segment specifically desired, and (2) the dysfunction motion pattern has been corrected." It should also be noted that the specific mechanoreceptor pathways will have been activated and the doctor should be aware of the appropriate pathways activated.

Rotation

Rotation is a curved motion around an axis which lies within or outside the boundaries of the moving bone. All points in the bone move in a curved manner and form an arc of motion. Rotation, however, produces an associated roll-gliding in the joint as it forms the arc. Rotation, therefore, causes the joint to participate in the physiological motion of roll-gliding in whichever plane it is moving in.

Roll-gliding is a combined motion that is only possible between incongruent, curved surfaces. Since all of our joints are, for the most part, incongruent, it follows that physiologic motions will result in roll-gliding. Generally speaking, the more congruent the surfaces the greater the proportion of gliding motion to rolling motion. This fact is paramount to joint play, as a decrease in glide will effect movement in other planes of joints that are near congruent in nature.

The rolling motion is always in the same direction as the bone movement and rarely occurs without gliding, as this could result in joint injury. Joint damage could occur if only rolling took place as the joint surfaces could be compressed on the same side towards which the bone is moving. This could pinch intra-articular structures such as meniscoids or cartilage; therefore, pure rolling movements are never used when making an adjustment.

The direction of glide in the joint depends on whether a concave or convex articular surface is moving. If a concave surface is the moving segment, then joint gliding and bone motion are in the same direction. In other words, the moving segment and its concave articular surface are on the same side of the axis of motion. If a convex joint surface is the motion segment, then the articular gliding and segmental motion are in the opposite directions, as the moving segment and its convex articular surface are on the opposite sides of the axis of motion. These are important concepts to remember. As joint hypomobility is treated by manipulative techniques through translatoric gliding motions, it follows that one should know the direction of the fixated joint gliding motion or one will be thrusting for nothing but noise.

Translatoric Gliding (translation of a bone)

As previously stated, translatoric gliding is a motion in a straight line or rectilinear movement and the corresponding joint play motions are traction, compression and gliding. These motions are not pure motions, as we are not symmetrical or congruent beings; therefore it is crucial to the comprehension of motion palpation joint play analysis that these motions be performed in a combined movement way. We will call this coupled joint motion palpation.

Joint play is what takes place in a joint when translatoric bone motions are initiated; joint play is not possible without translatoric motion. The significance of translatoric gliding motion to motion palpation is that all synovial joints can be examined in all planes of motion thus allowing the doctor to be very accurate relative to the adjustive procedures' direction of thrust as well as enabling the usage of coupled motion adjusting, the body's own naturally occurring movements.

Coupled or Combined Movements

Coupled or combined movements are motions that naturally occur simultaneously around more than one axis and in more than one plane. For example, flexion of the cervical spine occurs in a transverse axis; a roll-glide movement, through the formation of the segmental arches of the cervical spine. In a sagittal plane, the translatoric motion that will allow us to perform joint play analysis; right and left lateral flexion occur in a sagittal axis, a roll-glide and spin (ipsi- or contralateral in nature) motion; in a frontal plane, the translatoric portion; and rotation (remember that there is no such thing as pure rotation as it is always coupled with another motion) occurs in around a vertical axis, the roll-glide portion, and a transverse plane about which the angles of inclination predetermine the translatoric component.

From the above descriptions, it should be obvious that functional movements around combined axes and in multiple planes are necessary to reproduce the patient's chief complaint, and to understand the exact mechanism of injury. Your diagnosis and subsequent treatment plan depend on it as well.

End Feel

End feel of a joint motion is the relationship between the pain experienced and the axis and plane in which the resistance is encountered. The doctor's ability to palpate and glean meaningful information from this coupled joint motion palpation end feel is directly proportional to his or her understanding of the myology, osteology and arthrokinematics beneath the fingers. The single biggest reason for failure is a lack of practice and the taking of short cuts.

The range-of-motion is not a good indicator of the source of the dysfunction. Take, for example, a patient that has pain on rotation of the cervical spine during the first 12-15 degrees, but can continue to full rotation without any significant change in the pain. A second patient also has pain during the initial 12-15 degrees of rotation; however, when attempting to reach full range-of-motion the pain now radiates down the arm and posterior thoracic region. Note that both patients have the exact same range-of-motion, however they produce totally different symptoms. These patients must be treated differently as fixations of coupled motions in multiple planes and axes dictate the presenting complaint and pain patterns.

Motion Characteristics

Motion characteristics that impact upon one another are important to the examination. The following list details, these according to Grieve.

"(1). Flexion reduces lateral flexion and rotation ranges; it eradicates the cervical curve, usually most noticeably at segments C-4-5-6, and sometimes slightly reverses the lumbar curve from the L-3 segment upwards.

"(2). Extension also reduces the range of lateral flexion and rotation.

"(3). Lateral flexion restricts flexion and extension, and while the vertebral region concerned is held in the position of lateral flexion, the following tendencies will be noted:

a. In the cervical spine, lateral flexion makes rotation easier to the concavity than to the convexity, whether the neck be in neutral, flexion or extension.

b. In the thoracic spine below T-3 and in the lumbar spine, lateral flexion makes rotation easier to the convexity than the concavity, when lateral flexion occurs in neutral or extended position. If the thoracic and lumbar spine be flexed, and then bent to one side, rotation will be easier to the concavity.

"(4). Rotation restricts flexion and extension, and is invariably accompanied by a degree of lateral flexion.

"The physiological tendencies are thus: Typical cervical region (C2-C6) lateral flexion is invariably accompanied by rotation to the same side, and vice versa, from all positions of sagittal movement, i.e. whether the neck be flexed, neutral or extended.

"Cervicothoracic region (C6-T3). Although movement rapidly diminishes from above, downwards lateral flexion is accompanied by rotation to the same side, and vice versa.

"Thoracic and lumbar regions. Lateral flexion is accompanied by rotation to the same side (and vice versa) only in flexion. In the neutral or extended position, side bending is naturally accompanied by rotation to the opposite side, and vice versa.

"Summarised, in all sagittal starting positions of the cervical spine, and in the flexed thoracic (below T-3) and lumbar spines, lateral flexion is per force accompanied by rotation to the same side, and vice versa; in the neutral or extended thoracic (below T-3) and lumbar spines, lateral flexion is perforce accompanied by rotation to the opposite side."
Motion palpation is a vital link between the patient's subjective symptoms and the why, where, and how you are going to adjust the patient. The major indication for joint manipulation is reversible hypomobility; however, it must always be paramount in the doctor's mind that the maintenance of mobility and the slowing or prevention of progressive joint dysfunction, maintenance of the mechanoreceptor-nociceptor relationship, and the prevention of the formation of the subluxation complex is always omnipresent.

Three major differential diagnostic criteria are emphasized in coupled joint motion palpation analysis: 

1. The determination of joint hypomobility vs. muscular fixation vs. compensatory joint dysfunction elsewhere as the primary cause;


2. The existence of the arthrokinetic reflex as a major contributor to reflex sympathetic dysfunction via the dorsal horn, and to a lesser extent, the ventral horn. These two locations are the origins of second order neurons involved with pain. The dorsal horn is also a focal point for mediating autonomic and somatomotor reflexes initiated by nociceptive stimulation. Quite simply, it is uncontrolled nociceptive activity that causes pain, muscle spasm and vasoconstriction; the very things we see and feel in and on our patients every day;


3. In the acute stage, joint pain and inflammation occur together and often will limit the doctor's ability to perform a thorough examination. In this situation, treatment is predetermined by the patient's symptoms and only procedures intended to decrease pain and/or inflammation are performed during this session.

Anterior Cruciate Ligament Deficiency in Women

By Thomas Souza, DC, DACBSP

Since the passage of the Title IX Educational Assistance Act of 1972 (requiring institutions receiving federal funds to provide equal access to men and women in both curricular and extra-curricular activities), the numbers of female participants has exponentially increased.¹ Some of the advantages of this increase are: 

• the "legitimizing" of female athletes (taking female athletes seriously);
• the reminder that most sport's research had been focused on male athletes, and the need for female-specific research; and
• the need to evaluate any valid differences between male and female athletes physiologically to determine gender-specific strategies for sport-specific training.

A disadvantage of this dramatic increase in female participation in sport is the lack of preparedness by coaches and trainers for what training requirements would be needed to prevent injury and to properly prepare someone for sport-specific participation. 
As a result, many females are often allowed to "learn as they go" without specific instruction in focusing on specific strength deficiencies and proprioceptive demands.

A pattern has surfaced over the last decade of an increased incidence of anterior cruciate injuries in female athletes. One stark example was in the 1988 Olympic basketball tryouts, where both male and female injury rates were documented.² Eighty-one per cent of the ACL injuries were sustained by the female athletes! These injury rates were similar to those found with other sports, such as volleyball, rugby, and soccer.^1,3 These and other studies have struggled to determine why females are more prone to injury than males given the same sport activity. A fine review was published by Traina and Bromberg detailing some of the current thinking in this area.⁴ The following is a synopsis of their work.

The theories regarding a female predisposition to ACL injury generally fall into two general categories: (1) extrinsic factors, and (2) intrinsic factors. The extrinsic factors focus on conditioning and training. Some questions are: 

• Is there a relationship between lower levels of conditioning and injury rates, and are women generally entering sports activities at a lower level of conditioning?
• Is there a relationship between how women are coached in jumping, landing, and decelerating/cutting and ACL injury rates?
• Are there inherent strength differences and reaction-time differences between men and women?

A study conducted by the U.S. Naval Academy illustrated the generally lower level of conditioning seen in females as compared with males.⁵ This same study indicated that females responded more dramatically to training then their male counterparts. Several studies indicate that at the high-school level, many girls enter at a "novice" level, having never before participated seriously in sports.⁶ Statistically, it appears that this trend is changing with an enormous increase in girls at younger ages participating in traditionally male-dominated sports, such as soccer, basketball, softball, and hockey.

It is clear that the vast majority (78% in one study) of ACL injuries are noncontact, often occurring when landing from a jump.⁷ This is even more true in sports such as basketball and volleyball. One study divided these noncontact injuries into three types and documented the percentage of incidence.⁸ Together they account for most ACL injuries in the study, and individually are essentially equal in occurrence (26%-29%): 

1. planting and cutting;
2. straight leg landing; and
3. one-step landing with the knee hyperextended.

ACL injury rates were reduced among a group of women by almost 90 percent by simply modifying the plant-and-cut maneuver to a three-step stop, with an emphasis on avoiding knee extension.⁸

It is clear that women have less hamstring and quadriceps strength when compared to males; however, this holds true even when body weight is factored in.⁹ This is a clear signal that a focus on general knee strength training should be part of all women's pre-event training schedule. It appears that another factor is the recruitment of muscles. In one study, females were more inclined to use quadriceps contraction when an anterior tibial force was applied, as compared to males, who used hamstring contraction.⁹ It is clear that the hamstring contraction is the more protective response and suggests a possible gender or lack-of-training effect that must be corrected prior to event performance.

The time to torque production for hamstring contraction differs between male and female athletes. It appears that males have a quicker response time when compared to females.⁹There may be a training effect at play, yet what should be incorporated into women's training programs is proprioceptive training with the goal of decreasing response time to imposed demands. One study indicated that this could be accomplished through a progressive stability challenge program using balance and rocker boards.¹⁰ Training begins first with the patient seated while the trainer attempts to move the unbalanced platform out from under the patient's foot. This progresses to more challenging positioning with less support available.

Intrinsic factors that may predispose females to ACL injury include instability at the knee, a wide pelvis (affecting limb alignment), and size of the intercondylar notch. It has long been noted that women appear to have "looser" joints than males. Does this static laxity play a part, or is the determining factor more the combination of capsular/ligament laxity and muscle strength?

There has been an assumption that hormonal influences allow for more flexibility and therefore laxity of female's ligaments. Yet, two studies using an objective measurement of ACL laxity with the KT-1000 did not demonstrate a gender specific laxity of the ACL.^11,12 Disagreement regarding the role of ACL laxity as a cause of ACL injury still exists. Although joint laxity may predispose an athlete to injury, it appears that other factors are important, such as muscle strength and reaction time (discussed above).

Although the female predisposition for patellar tracking problems seems to be related to a wider pelvis, femoral anteversion, and increased genu valgum as compared to men, these factors have not been shown to influence predisposition to ACL injury.¹³

An interesting finding has been an apparent relationship between the intercondylar notch size and ACL injury. It appears that many athletes with ACL injury have a smaller notch size, and women in general have smaller notch sizes.¹⁴ Radiographically, this is measured with the notch width index (ratio of intercondylar notch width to distal femur width) measured at the level of the popliteal groove on a tunnel view.¹⁴ This smaller notch (stenotic notch) may indicate a smaller ACL or an increased tendency for impingement and stress to the ACL.

Even if the factors of notch width, pelvis width, and inherent joint laxity are factors, they generally can't be modified. The focus, therefore, should remain on proper training to ensure proper hamstring and quadriceps strength, decrease in reaction time, and proper recruitment sequence of muscle firing.

References 

1. Arendt E, Dick R. Knee injury patterns among men and women in collegiate basketball and soccer. Am J Sports Med 1995;23:694-701.
2. Ferretti A, Papandrea P, Conteduca F, et al. Knee ligament injuries in volleyball players. Am J Sports Med 1992;20:203-207.
3. Levy AS, Wetzler MJ, Lewars M, Laughlin W. Knee injuries in women collegiate rugby players. Am J Sports Med 1997;25:360.
4. Traina SM, Bromberg DC. ACL injury patterns in women. Orthopedics 1997;20:545-549.
5. Cox J, Heinz WL. Women midshipmen in sport. Am J Sports Med 1984;12:241-243.
6. Garrick J, Requa R. Girls' sports injuries in high school athletics. JAMA 1978;239:2245-2248.
7. Noyes FR, Mooar PA, Mathews DS, et al. The symptomatic ACL-deficient knee. J Bone Joint Surg (Am) 1983;65:154-174.
8. Griffis ND, Vequist SW, Yearout KM, et al. Injury prevention of the anterior cruciate ligament. In: American Orthopaedic Society for Sports Medicine: Meeting Abstracts, Symposia, and Instructional Courses, 15th annual meeting, June 19-22, 1989, Traverse City, Michigan.
9. Huston L, Wojtys E. Neuromuscular performance characteristic in elite female athletes. Am J Sports Med 1996;24:427-436.
10. Ihara H, Yakahama A. Dynamic joint control training for knee ligament injuries. Am J Sports Med 1988;14:309-315.
11. Daniel D, Malcom L, Losse G, et al. Instrumented measurement of ACL disruption. Orthopaedic Transactions 1983;7:585.
12. Weesner CL, Albohm MJ, Riter MA. A comparison of anterior and posterior cruciate ligament laxity between female and male basketball players. Phys Sports Med 1986;14:149-154.
13. Gray J, Taunton JE, McKenzie DC, et al. A survey of injuries to the anterior cruciate ligament of the knee in female basketball players. Int. J Sports Med 1985;6:314-316.
14. Souryal T, Moore HA, Evans P. Bilaterality in anterior cruciate ligament injuries: associated intercondylar notch stenosis. Am J Sports Med 1988;16:449-454.

Lower Leg Pain: Part II

By Thomas Souza, DC, DACBSP

Last month, we discussed some of the causes of lower leg pain. Specifically, we addressed shin splints. This month the focus will be on two conditions that are fairly exclusive to the athletic population: tibial stress fractures and compartment syndrome. 
The difficulty with differentiating shin splints and stress fracture is that they often represent a continuum of bone reaction to stress. Initially, pull of muscle on the periosteal attachment leads to shin splints (or sometimes referred to as either periostitis or tibial stress syndrome). Progression to a stress fracture is then possible. The difficulty with differentiating compartment syndrome from the other tibial pain entities is that initially the patient's complaint of pain related to exertion is quite similar.

Tibial Stress Fractures

Tibial stress fractures occur more often than other stress fractures, accounting for half of all stress fractures in athletes.¹ Normally there is a balance between bone resorption and remodeling. When there is inadequate time for healing, resorption dominates. Tibial stress fractures are due to repetitive loading or stress from muscle pull. Factors that increase an individual's predisposition include performance of repetitive activity on hard surfaces, weak supportive musculature, sudden change in training routine, hyperpronation, and poor bone status. The training factors are easily determined through a qualification of how much the person performs an activity, on what surface, what type of shoe is worn, whether orthotics are used, and whether any pre-training exercise is performed.

Other clues are the type of activity. Middle and distal third tibial stress fractures are more common in runners; proximal tibial fractures with military recruits, and middle tibial fractures with dancers.¹ Bone status is less clear from the history, however, in females; delayed menarche or amenorrhea are suggestive of poor bone quality. Certainly, questions regarding dietary intake of calcium through food or supplementation may add important information when providing preventive recommendations.

Classically, the athlete will report pain with activity that is relieved with rest. Soon, though, the pain is persistent occurring anytime the athlete bears weight. Although the pain is sometimes diffuse over several inches, palpation often reveals a discrete site of tenderness on the tibia. Attempts at increasing pain with a tuning fork or percussion at a site proximal or distal to the suspected site on occasion may work, however, results are variable. Radiographs may demonstrate a thin radiolucent line early in the process, or reveal calcific healing after a few weeks. It is recommended to include standard anterior to posterior, lateral, and oblique films of the area to better catch the "angle" of the fracture. One study indicated that radiographs were sensitive to only 10% of stress fractures (confirmed with bone scan).¹ If radiographs are negative, however, and the stress fracture is suspected, it is recommended to order a bone scan. For those females with stress fractures, a dual photon absorptiometry scan may be helpful in determining bone status and help in recommendations regarding diet or exercise.

A triple phase bone scan may help differentiate among shin splints, stress fracture, and compartment syndrome.² The initial phase represents intravascular perfusion. The second phase demonstrates the extravascular "blood pool" phase of radionuclide uptake. The third phase demonstrates the amount of radionuclide found in the hydra shell of bone, referred to as the "delayed" or "bone scan" phase. It is important to remember that the radiation exposure with these studies is low, representing between 0.1 to 0.5 rads (gonadal dose 0.2 to 0.5 rads), which is comparable to a standard lumbar spine x-ray. The three phases also differentiate acute from chronic stress fracture with all three phases positive in the acute phase (2-4 weeks). The second and third phases become progressively normal as healing occurs.

Generally stated, the uptake pattern differs with each condition as follows: 

• shin splints -- linear, mild uptake of radionuclide
• stress fractures -- "hot spot" of increased uptake (round or fusiform)
• compartment syndrome -- "hourglass" appearance (increased uptake above and below the involved compartment)

Management of stress fractures is determined by the compliance of the athlete to recommendations, the need for maintenance of cardiovascular fitness, the bone status, and the athlete's ability to bear weight without pain. Generally, bed rest or casting is unnecessary. Recommendations to avoid impact loading for several weeks, yet allow everyday walking, is usually sufficient. However, if the athlete is noncompliant it may be necessary to jail them in a short leg fiberglass cast for several weeks. For those who cannot bear weight without pain, crutches for a week or two may be needed, allowing mild toe contact progressing to heel contact for proprioceptive maintenance.

One exception to the above is when a large radiolucent line is discovered radiographically in a dancer. This is referred to as the "dreaded black line."³ This type of fracture has a reputation for poor healing and often progresses to full fracture. These individuals must have immobilization imposed to better guarantee healing. Obviously, calcium supplementation should be emphasized with a minimum of 1.5 grams per day for several weeks during healing and one gram daily as a preventive measure. Cardiovascular fitness can be maintained with non-weightbearing activities, such as bicycle riding or pool running using a water vest. Although there has been some discussion of electromagnetic healing of fractures, there is little evidence to support this approach. Yet, many feel it is worth an attempt to incorporate microamperange stimulation in hopes to affect cell metabolism in the area.

Compartment Syndrome

To understand compartment syndrome, it is necessary to visualize the fascial compartments of the lower leg and their contents. Generally, four compartments are recognized (although there is some disagreement about the posterior division). Within each compartment are muscles, nerves, and vasculature: 

1. anterior -- tibialis anterior, toe extensors, tibial artery and vein, and the deep peroneal nerve;
2. lateral -- peroneal muscles and superficial peroneal nerve;
3. superficial posterior -- soleus, gastrocnemius, and plantaris; and
4. deep posterior -- posterior tibialis, toe flexors, and posterior tibial artery and vein.F

When pressure inside the compartment rises, it usually is not sufficient enough to cause compression of the contents; however, in an acute injury such as fracture, swelling within the compartment may be dramatic enough to compress and eventually destroy its contents if persistent. In a more insidious manner, overuse may lead to transient increases in pressure that produce activity related complaints, namely pain, swelling, and possibly numbness/tingling, or weakness.

With runners, symptoms seem to occur at a consistent time often between 10-30 minutes after starting to run. For a given individual, the onset is often consistent enough to be anticipated at every run. Pain usually subsides, however, varying from minutes to hours. In between occurrences, the athlete is often asymptomatic. The examination is also unrevealing unless the athlete provokes the symptoms with a run prior to the appointment. Interestingly, pulses are often normal. There are some sensory changes evident in many athletes. Tenderness and swelling in the compartment are more evident when compared with the opposite "well-leg." Fascial defects may allow muscle herniation that is palpable in 40% of patients following provocation of symptoms. The definitive tool is slit-catheter measurement. Without detailing out the variations, generally it can be said that normal pressure at rest is 4+/-4mm Hg and will rise to between 30 to 50mm Hg following exercise. With compartment syndrome, resting pressure is greater than 15mm Hg that may rise to 80mm Hg or higher during exercise. Levels that remain elevated for 15 to 30 minutes after activity indicate compartment syndrome, especially when elevated above 40mm Hg.

If misdiagnosed, management may include taping or an ace bandage. This will obviously increase pressure and therefore pain. It is also true that myofascial work may aggravate symptoms in the acute phase. No studies have been performed to determine the effect of myofascial work on increasing the compliance of the fascial compartment, yet it theoretically may be of benefit with exertional compartment syndrome (a good research project for one of the readers). Management for chronic compartment syndrome is simply a period of rest from the inciting activity for 4-8 weeks. If recurrent, surgical release using a fasciotomy has a relatively good success rate.

References 

1. Matheson GO, Clement DB, McKenzie DC et al. Stress fractures in athletes: a study of 320 cases. Am J Sports Med 1987;15:46-58.
2. BenEliyahu DJ. Radionuclide bone scan imaging of periostitis and stress fractures commonly seen in athletic injuries. Top Clin Chiro 1997:4(1):50-57.
3. Green NE, Rogers RA, Lipscomb AB. Nonunion of stress fractures of the tibia. Am J Sports Med 1985;13:171-176.

Lower Leg Pain: Part I

By Thomas Souza, DC, DACBSP

Lower leg pain is more common in patients who participate in running or walking activities. The waste-basket diagnosis for many patients is often "shin-splints," however, this ill-defined entity may mimic or overlap with other causes.
Certainly less common, yet significant differentials are stress fracture and compartment syndrome. In the elderly, calf pain may appear insidiously or arise secondary to minor trauma (e.g., bumping the leg against a coffee table). If the older patient is also active, a distinction between muscle sprain, shin-splints, or deep vein thrombosis is not as clear as one might first assume.

Shin Splints

While shin splints is a common diagnosis, the actual entity is not well understood. Depending on who you ask, shin splints are defined as a form of tendinitis, periostitis, muscle strain, or interosseous muscle strain. Various authors have attempted to classify shin-splints based on the source of pathology, but this too has led to much confusion. You may see classifications that include stress fracture and compartment syndrome under the main heading of shin splints. The rationale for this classification is that the underlying cause of these different entities is the same and that they may represent different degrees or sites of "stress" reaction. The underlying causes appear to fit two general categories: (1) muscles that serve the function of shock absorbers allow forces to be transmitted to bone if they are weak; and (2) repetitive overstrain of muscles or tendons causes strain or sprain, or excessively stress the bony origin of the muscle involved.

Generally, shin splints are geographically classified as anterior/lateral and posterior/medial. The anterior type is generally due to walking or running on hard surfaces or poor shock absorbing ability of the involved muscles or shoes. The tibialis anterior, extensor hallucis longus and extensor digitorum longus all act to dissipate the forces imposed by heel strike. If they are weak or asked to perform overtime, shin splints may result. It has been demonstrated electromyographically that the tibialis anterior fires at greater than 20% maximum contraction for 85% of the gait cycle in runners.¹ This will lead to fatigue if the muscle is not properly trained or an extra burden of performing on a hard surface is added.

Posterior/medial type is common in athletes who are hyperpronated or who perform on a surface that imposes excessive or prolonged pronation. Therefore, the muscles that help support the arch are the most commonly affected. These muscles include the tibialis posterior, flexor hallucis longus, and the flexor digitorum longus muscles. You may read of the medial tibial stress syndrome.² This is a broad classification system that includes tendinitis (tibialis posterior), stress fracture, compartment syndrome, vascular, and muscle pathology. Therefore, medial tibial stress syndrome identifies conditions that share common etiology; excessive stress to the middle/distal tibia and its attachments.

Historically, it is important to determine any inciting activity. Sports with the highest frequency of shin splints include long distance running, jogging, race walking, aerobic dance, sprinting, cross country skiing, soccer, and volleyball. In addition, the surface that these activities are performed on must be determined. Hard surfaces require more shock absorption. Shoes that are worn or provide poor support or shock absorption may also be contributing factors. Tightness of the gastrocnemius may provide more resistance for anterior or medial muscles to overcome. Factors often missed include hydration and the amount of daily dietary calcium consumed.

Pain and/or tenderness for the anterior/lateral type is usually just lateral to the middle tibia. For the posterior/medial type, the pain and/or tenderness is posteromedial to the middle or lower tibia. Pain may be increased with contraction into dorsiflexion and inversion with the anterior type; resisted plantarflexion and inversion may increase pain with the posterior type. It is interesting that for some athletes, stretching to the involved muscles may increase pain, while for others, the pain is temporarily relieved. Also, performing a mild contraction from the stretch position for a few seconds followed by stretching seems to temporarily relieve the pain for many. Many patients report that squeezing the area with their hand provides some relief.

Radiographs are rarely needed unless stress fracture is being considered. With stress fracture, it is more likely that the patient has significant increase in pain with weightbearing that prevents further performance. Other clues are the bone status of young females, which may be related to the degree of activity and menstrual status.

Acute care for shin splints fits into four broad categories: 

1. ice and compression
2. myofascial release
3. functional taping
4. modification of activity

Each of these approaches seems specifically effective in a subgroup of patients while ineffective with others. This may depend to some degree on the site of irritation or inflammation. If the site of irritation is at the tibia, taping may be the most effective approach while myofascial stripping or release may be more effective for muscle involvement. It will be interesting to see if further research can separate out these groups.

There are two general taping approaches. The first involves "compressing" or shortening the involved muscle/tendon through the use of elastic tape. The tape spirals from distal to proximal starting on the opposite side of the leg spiraling to the site of tenderness. For example, with the anterior/lateral type, the tape would first begin at the medial leg above the malleolus and spiral posterior ending at the site of tenderness at the anterior/lateral tibia.

The second type employs "strapping" tape. This is the same tape used by McConnell for patellofemoral tracking disorders.³ A thin protective tape is applied first (Fixomill Stretch, BDF Deiersdorf, AG Hamburg) followed by the strapping tape (Leukosport). The tape is applied as a functional support for the involved muscle. For example, if the tibialis posterior was involved, the tape would be applied to substitute or support the function of this muscle tendon on the medial side of the leg.

Preventative strategies include: 

1. replacing worn-out shoes
2. evaluating the need for orthotics
3. stretching prior to activity with emphasis on the gastrocnemius
4. eccentric training of the involved muscles
5. increase calcium to 1 gm/day

Next month, we will discuss compartment syndromes and stress fractures.

References 

1. Reber L, Perry J, Pink M. Muscular control of the ankle in running. Am J Sports Med 1993;21:805-810.


2. Reid D. Sports Injury and Rehabilitation. New York, NY. Churchill Livingstone. 1992, p. 271.


3. McConnell J. The management of chondromalacia patellae: a long term solution. Aust J Phys Ther 1986;32:215.

Hip and Groin Pain/Discomfort: Its Diagnosis and Treatment

By Joseph D. Kurnik, DC

This article is written based upon the personal experiences in my practices. I have found that the diagnosis and treatment of hip and groin discomfort requires spinal and extra-spinal inspection and treatment.

It requires the examination and treatment of muscles, tendons, ligaments and joint dysfunction.

Part I

It is my observation that most hip and groin discomfort observed is initiated by dysfunction of the lower lumbar spine and consequent sacroiliac dysfunction. In general, what is usually observed is the following: 

1. The lower lumbar spine (usually L-5) fixates. The fixation is almost always an LP (left post) listing. L-5 also may develop general inflammation with or without a listing dysfunction. L-5 predominates and usually rotates with spinous right. Other lumbars may be involved.


2. The left and/or right sacroiliac joint will fixate in the AS position (anterior superior, with the PSIS as the point of reference). If there is lumbar disorder, the left ilium always fixes in the AS mode.


3. The hip joint proper will develop strain because the SI joint no longer assists in hip flexion. Hip popping or clicking may result. Strain in the gluteal muscles due to over-stretching will develop. Reactive stress on the hip flexor muscles will develop lumbar extension and can contract and strain. The end result will be hip and groin strain/discomfort.

Proper analysis depends upon proper static and motion palpation procedures. One must be proficient in the analysis of AS (anterior superior) and PI (posterior inferior) motion and fixation patterns. There is a sidedness observed. The fifth lumbar is the usual primary difficulty. It will misalign and fixate in the LP position mainly, or it may develop degenerative inflammatory disorders. Other lumbars may be involved also. The sequela which develops is as follows: 

1. The left and/or right ilium will fixate in the anterior superior position, usually secondary to a lumbar disorder.


2. As described, the hip and groin will develop stress and possible symptoms. A most classical example is right hip clicking during hip flexion.


3. As described, the hip flexors develop strain in opposition to the gluteal antagonists, which have become hypertonic. The groin develops strained symptoms. The adductors may also antagonize the flexors. Spinal muscles attaching to the ilium may become hypertonic as well.

The key, most of the time, is to correct the lumbar disorder. Correcting a fifth lumbar fixation LP listing or compression disorder, usually starts the ball rolling. The appropriate lumbar correction will surely free the left AS fixation and usually the right AS fixation. After correcting the lumbar problem, re-palpate to see what the status of the SI fixations are. The left side usually is free. The right side will often become free, but not always. If right hip and groin discomfort are present, then an AS correction is in order on the right. Correction of the lumbar will be done by adjusting or flexion traction, as discerned.

The right ilium may fixate in the AS position independent of the lumbar status, but usually never the left. It is due to trauma or micro-trauma of some sort. It can be corrected with an AS adjustment on the right side. Motion and static palpation are the determining analytic procedures of choice in determining status and procedure.

This is a condensation of procedure to follow: 

1. Static and motion palpate the SI joints seated and standing. Static and motion palpate the lumbars seated and prone.


2. If the left ilium is fixated in the AS position, there is an L-5 or L-4 problem. The L-4 or L-5 problem is the usual problem; with rotation usually present.


3. Re-palpate the SI joints. The left SI will be free if the lumbar was properly treated. The right SI may or may not be free. If there is no groin or hip discomfort, do not rush to adjust the right side. If there is significant right L/S pain with AS fixation right, then adjust the right AS.

The above presentation was a general condensation of observations and procedures. The concepts revolve around processes called nutation and counter-nutation. According to Kapandji (Physiology of the Joints, Volume III), movement of the sacral base anteriorly and inferiorly is called nutation. Motion posteriorly and superiorly is called counter-nutation. As the sacral base moves, the ilium moves in the opposite direction. If the sacral base moves posteriorly and superiorly, the ilia ideally move anteriorly and superiorly, with the PSIS as the point of reference. If there is a lower lumbar problem, one or both ilia will fixate in the AS positions. This is a self-protective mechanism, not to be lightly messed with. The problem is usually the lower lumbar spine with the ilia assuming the AS position, the sacral base will move posteriorly and superiorly to stabilize the spine. When the process goes too far, groin and hip discomfort will result.

Reckless adjusting of the AS fixations can weaken the spine due to nutation. Decisions based on knowledge have to be made. If there is a left sided AS fixation, there is a lumbar problem predominant. Correct it first and then repalpate. Correct the right AS only if it is still fixated, and with significant right L/S pain, hip and/or groin discomfort.

If an AS fixation exists long enough, gluteal and hip flexors will become strained. Correction of the lumbar and AS fixations may correct the groin discomfort/hip discomfort automatically. If left uncorrected, secondary problems such as gluteal and hip flexor strain may become independent problems, requiring specific nonadjustive therapy. The lower lumbar extensors may also become strained. It may require soft tissue therapy. I have found that in diagnosing and treating soft tissue injuries, the procedures of Lyn Paul Taylor are the most exacting and efficient. They primarily involve diagnosis and treatment of gluteal and lumbar extensor muscles and anterior/medial thigh muscles. An instrument for locating areas of inflammation is utilized. The general procedure for diagnosis will be outlined in Part II.

Part II

Evaluation and Treatment of Inflammatory Disorders

The inflammatory process which occurs following too much soft tissue stress is basically a chemical process designed to promote healing. Basically, the stressed tissues are provoked into producing three classes of chemicals including; 1) bradykinins, 2) histamine and, 3) prostaglandins. These chemicals produce the symptoms of sensitivity, swelling, and pain; also promoting the ongoing production of each other. Together, this all constitutes the initial stage of the healing process. It only becomes a problem if the aggregate of these chemicals is allowed to build up and remain in the affected region. This is usually prevented by the release of enzymes, carried by the blood, which are supposed to break these chemicals down soon after their production.

If capillary activity in the involved region is less than optimal (such as with aging or inactivity), these chemicals may build up and become a source of chronic inflammatory conditions, due to their mutually cross-fostering nature. This is especially true if sustained levels of prostaglandins (an organic acid) have caused the body to react to the constant "burning" by inundating the region with collagen (in the form of collagen fibrils), which further restricts capillary activity, augmenting the effects of histamine. These collagen fibrils may further complicate matters by forming adhesions between tissues (fascial) layers, preventing them from sliding past one another and causing them to "catch." This produces a source of ongoing irritation and inflammation and further fosters the chronic evolution of such injuries. This was a general condensation or overview of the inflammatory process and its beginnings.

A peculiar physiological mechanism causes blood to be "shunted" from the surface (skin) to be concentrated around the deeper inflamed tissues. This, in effect, increases the resistance of the skin to the passage of an electrical current. A monitor can be utilized to measure such resistance, if in the proper range. It can thus show the practitioner which areas are inflamed, which often differ from the site of pain. For example, look at groin and hip pain. The groin may hurt, but it is not necessarily inflamed. Areas of inflammation show in the gluteals, hip flexor muscles, and other regions; but not the tendinous regions of the groin.

In my practice, I utilize a specially designed and modified OHM meter which may be used for a differential skin resistance survey.
Such instruments must be able to measure resistance levels in the micro-OHM range, though the resistance may be measured in forms of how much current gets from one electrode to the other, as microampuees or mamps. In other words, you simply measure the amount of current passing from one probe to another. The more the resistance, the less current passes, and the more inflammation present.

The treatment of inflammation should be based on, 1) increasing circulation in the involved tissues; 2) stopping the production of inflammatory chemicals; and 3) decreasing the potential of ongoing soft tissue stress.

Increasing circulation in the involved tissues may be accomplished through the use of electrical stimulation (wide-pulsed, low frequency) to provoke intermittent muscle contractions, massage and vibration. This can drive out noxious chemicals and soften the underlying tissues. Aerobic exercise may also be helpful if no tendinitis or nerve impingement is present.

The interception of inflammatory chemical production may be accomplished through the use of ultra high frequency sound to drive effective anti-inflammatory chemicals into inflamed areas (phonophoresis). These chemicals include preparations containing various types of substances having an anti-inflammatory action (e.g., Ibuprophen). Some doctors use more natural herbal or other preparations, but the molecular size of the constituents must be able to pass through the skin to be effective.

Decreasing the potential for on-going stress may be accomplished by: 

1. Reduction of any adhesion formations which may be present through a combination of medium frequency electrical stimulation and soft tissue manipulation.


2. Lengthening any tight musculature through the use of intermittent low frequency electrical stimulation, followed by brief mechanical vibration of the tight muscles' antagonists, with a five minute rest with the tight musculature continually on stretch.


3. Vertebral or joint manipulation.


4. The toning or strengthening of involved musculature through isometric or isotonic exercise (the latter performed only if there is no tendinitis or nerve impingement present).

In conclusion, efficient resolution of any soft tissue injury will depend on an accurate evaluation, coupled with appropriate treatment. This approach has given me a path and direction to follow when presented with soft tissue inflammatory lesions which have not responded to spinal or extra-spinal adjusting. As I practice, I become more efficient and effective. Masters of this type of treatment often clear out difficult cases within a week or less.