The Pinched Nerve Conundrum

By Erik Dalton, PhD

For decades, manual therapists, biomedical researchers and neuroscientists have battled over the conceptual ideology of pinched nerves. One group holds the belief that spinal misalignments cause or contribute to disease by choking "nerve energy" to body tissues.

Others generally agree that the human body probably does possess some sort of universal energy system, but quickly point out that nerves do not appear as conductors of this "life-force" energy. To allow the reader to grasp both sides of this very important issue, this article will provide an overview of current theories that spur the controversy. Following an initial review of the various nerve impingement theories, let us review the two most pressing, yet basic, questions:

1. How do nerves get pinched?
2. Are pinched nerves really a contributing factor in common pain conditions observed daily in our offices and clinics?

One age-old premise supporting the pinched nerve theory follows this logic: If a spinal segment is not in its normal position, nerve pathways between the vertebrae (intravertebral foramina) will partially close resulting in nerve impingement. As the nerve root undergoes compression, soft tissues and organs supplied by the pinched nerve suffer from decreased nerve energy flow to the affected body parts. Thus, according to this theory, alterations in joint structure and function result not only in pain but an increased susceptibility to disease from spinal obstructions impinging on these nerves.

Detractors counter that nerves do not emit a flow of energy. Since nerves are gland cells, their primary function is to produce and release a hormone that causes muscle cell inhibition or contraction. Basically, that is all they do - no more, no less; therefore, these supporters believe that nerves do not actually conduct electricity or any other form of energy.

When a nerve cell undergoes its function of hormonal secretion, changes occur in its outer cell membrane allowing electrically charged ions to move in and out of the cell in a step-by-step fashion along the full extent of the nerve. This is often referred to as "conducting an impulse" or "firing." A spinal nerve as it exits the intervertebral foraminal opening is actually a thin tube of connective tissue containing extensions of millions of nerve cells. These extensions are axons or "fibers." The latter term appears misleading for it connotes a certain firmness similar to fine electrical wires. Sadly, nothing could be further from the truth.

Axons are delicate, flimsy structures. Since they consist of elongated or drawn out parts of cells, nourishment is needed along with the cells that make up their sheaths. Vital nutrients are supplied by blood vessels embedded in what is termed a "visible-level nerve." If acute nerve compression does not directly kill the axons, they may die from compressive forces blocking blood flow within the vessels of the nerve. Nerve occlusion prevents axoplasmic flow of nutrients to be properly transported up and down the length of the nerve.

Another Snapshot of Pinched Nerves

The nerve root itself has been dismissed by most researchers as a pain-sensitive structure, although most clinicians do agree that nerve compression from herniated discs, spinal stenosis and spondylolisthesis can cause radiculopathies such as sciatica. Acute compression of a normal healthy nerve may lead to paresthesias, motor loss, sensory deficits and reflex abnormalities, but pain is absent. However, if an inflamed nerve suffering intraneural edema is compressed, pain is present. This "silent nerve root compression syndrome" hypothesizes that time is required for functional alterations, such as nerve tethering, to cause mechanical nerve fiber deformation and resulting pain.

Compression of an inflamed nerve anywhere along its extent can cause it to secrete its specific hormone. Pressure on an inflamed sensory nerve cell can cause the brain to experience pain (nociception). If an obstruction compresses a motor nerve cell, the hormone secretion can cause a muscle cell to contract (protective muscle spasm). When motor nerve cells to a skeletal muscle die from complete occlusion, the muscle becomes paralyzed as observed in extreme cases of sciatica and thoracic outlet syndrome. One of the first signs of complete nerve occlusion is muscle atrophy followed by a loss of normal neurological reflexes.

Nociceptive ... or Pinched Nerve Pain?

Over the past decade, researchers working with magnetic resonance imaging (MRIs) have demonstrated that no matter how much a normally functioning spine is compressed or twisted, there is ample room in the intervertebral foramina for free movement of the nerve. It is postulated that in a healthy spine, nerve root compression shouldn't exist even with all the intervertebral discs removed. Still, another viewpoint bears consideration.

While conditions such as intraneural edema and ischemia from prolonged nerve-root abuse certainly causes pain in a certain percentage of the population, it is also possible much of the reported pain may be due to sensory receptor overload from postural imbalances. For example, recall what happens when the typical client injures their back. As the spine is subjected to sudden asymmetrical loading, the major stress focuses at the capsule of the articular facets as the joint is moved beyond its acceptable range of motion (physiologic barrier).

Sprained capsules and ligaments cause joint mechanoreceptor hyperexcitability and protective muscle guarding. Muscles aren't designed to be restraining tissues even though the deepest transversospinalis muscles are often awarded that task. As deep intrinsic muscles are subjected to abnormal sustained loading, nociceptive stimuli warn the brain of the possibility of tissue damage.

When nociceptors fire in response to actual tissue damage from macro- or microtrauma during routine daily activities, they quickly become major myofascial and spinal pain generators. Through a process called sensitization, an aberrant hard-wiring pattern is "burned" into the central nervous system (CNS). Long-term CNS agitation from angry nociceptors causes the brain to twist and torque the body in an effort to avoid pain.

Understanding and Treating the Dysfunction

As discussed earlier, the joint receptor concepts attempt to override the idea that pain is primarily a consequence of "pinched nerves" that could ultimately be freed by removing the bony or muscular obstruction. Many neurophysiologists now believe that restoration of proper postural alignment and range of motion successfully reduces pain by stimulating mechanoreceptors in fibrous joint capsules, spinal ligaments and transversospinalis muscles. To achieve a noticeable reduction of increased excitability in the neuronal pool, the pain-generating stimulus must be interrupted until the memory burned into the nerve cells has been completely "forgotten." For many chronic pain cases, a "serial-type" deep tissue therapy works best where clients are seen twice weekly until hyperexcited receptors feeding the CNS are quieted.

Conclusion

Although spinal nerves travel through small intervertebral foramen openings, rarely does a bone-on-nerve dysfunction occur. Significant facet hypertrophy, disc collapse or intraneural edema must accompany the vertebral misalignment before the client experiences pain. While commonly associated with the spine, pinched nerve compressive lesions are actually rare.

What has made the "pinched nerve theory" so popular is that therapists viewing anatomy texts or cadavers can easily visualize how spinal nerves could become entrapped as they make their way through the bony little holes between vertebrae. Regrettably, nociceptors and mechanoreceptors cannot be seen.

For most of mankind, it is far easier to believe something we can see versus something invisible to the naked eye. Despite this human tendency, massage therapists must understand that spinal joints and muscles have massive nociceptive innervation that is profoundly affected by sustained compressional loading from tension, trauma and poor posture. While not clearly apparent, sensory receptors are the primary reason for client visits.

Simplifying Sensitization

By Erik Dalton, PhD

Most of the human race suffers some form of neck and back pain during their lifetime just as common as a headache, stomach ache or knee pain. "Until it was turned into a medical condition in the early 20^th century, back pain was considered an inevitable human experience," said Canadian surgeon Hamilton Hall, MD.

"There is no simple cure because there is usually not a clear-cut precipitating trigger associated with many forms of musculoskeletal pain," notes Hall.

Despite the liberal use of the words "back injury" across modern societies, most episodes of back pain do not have an obvious cause. "Research indicates that approximately two of every three people who experience pain in the spine are unable to identify any specific event that may have caused their problems," states Hall. Back pain simply happens!

The modern perspective that neck and back pain is a variable, intermittent illness rather than a one-time condition should not be considered a threatening event for our clients. In the vast majority of cases, recurrences of these painful conditions are not signs of advancing disease, an omen of chronic disability or even a cause for significant worry.

Some researchers draw an analogy between back pain and upper respiratory infections. Many individuals get colds or respiratory infections several times each year, yet are typically not viewed as a significant threat to their health. Colds don't require high-tech diagnostic testing, heroic treatment interventions or significant absence from work. These conditions, like most cases of neck/back pain, simply are bumps in the road.

However, some have begun to question the possibility of previously unrecognized neurobiological processes that might unravel the question: Why are some people more susceptible to pain than others? One interesting new area of pain management research that is gaining a great deal of attention proposes alternative ways that nerve impulses are transmitted and learned by the central nervous system.

Sensitization

For decades, it was thought that spinal cord, brain and peripheral pain transmission pathways were hardwired circuits whose job was simply to communicate pain signals from injured or diseased parts of the body to specific message centers in the brain. But based on recent scientific research, new ideas are emerging on how pain transmission actually works and how the brain has the ability tocreate the conscious experience of pain.

A process called sensitization has become a topic of great interest to neuroscientists studying transmission mechanisms of painful stimuli. The puzzling question is: How are pain messages actually delivered? A discussion of sensitization might help somatic practitioners better understand why a client's chronic pain can be so severe, but in some cases, seem out of proportion to the degree of injury or disease in the affected body tissues. This understanding also might help explain why specific treatments directed at pain relief often provide'only limited benefit.

The neurobiology of sensitization is extremely complex, but the basic idea behind it is fairly straightforward. When pain signals are transmitted from injured or diseased tissues, these signals can then activate (sensitize) pain circuits in the peripheral nervous system, spinal cord and brain by burning a memory pathway (See Figure).

The process of sensitization can be compared to overly adjusting the volume control on a stereo system, thereby amplifying and sometimes distorting the pain message. This results in a painful condition that is severe and out of proportion to the actual dysfunction or original injury. Sensitization has the innate ability to alter all regions of the central nervous system that process pain messages. This includes the sensing, feeling and thinking centers of the brain. Here lies one explanation why chronic pain often is associated with, not only physical disorders, but also emotional and psychological suffering as well.

Phantom Limb Pain

A perfect example of the workings of sensitization can be found in the sometimes mysterious condition called phantom limb pain. In the presence of phantom limb pain, the client might feel intense pain in an area where the body part is missing. Common examples are seen in amputated arms and legs, as well as in women experiencing abdominal pain years after undergoing a hysterectomy. The difficult-to-treat problem of phantom limb pain is consciously actualized by persistent activation (sensitization) of the pain transmission pathways from the site of amputation up to the brain.

But what about the presence of sensitization in various pain conditions where amputation or surgeries to remove diseased organs don't exist? Too often, manual therapy treatments in such cases are directed to body areas that were once actual pain-generators, (i.e., where the injured or diseased tissues once existed). Regrettably, "chasing the pain" by directing therapy to where the client currently is hurting will have little effect on the sensitized pain pathways in the spinal cord and brain. As a result, little benefit is experienced.

Having said that, the author has found that application of specific deep tissue and assisted stretching techniques to torsioned and compressed joint-related soft tissues co-activates and desensitizes noxious mechanoreceptive activity leading to a reduction in pain. Successful outcomes require the therapist concentrate treatment to areas proximal to the previously injured or amputated tissues (usually beginning in the lamina groove). Proper treatment to deep intrinsic muscles, spinal ligaments, joint capsules, and visceral structures co-activates a wider range of neuro-receptors, which enhances the desensitization process.

References

1. Hall H. Consultation with a Back Doctor, McCleland & Stewart; 2003.
2. Dalton E. Advanced Myoskeletal Techniques, pg. 72, Freedom From Pain Institute, 2005.

Minutes, Myofascia and Maintenance

By Erik Dalton, PhD

Contemporary bodyworkers are blessed with freedoms rarely afforded other professional health care practitioners the three M's: Minutes, Myofascia and Maintenance.

Let's Talk Minutes

With most sessions lasting from 45 minutes to 90 minutes, today's massage and bodywork practitioners are allotted sufficient hands-on time to develop a keen awareness of the client's ability to function in physical, emotional and spiritual planes.

It's unfortunate for both client and therapist when time constraints (common in many manual medicine practices) become a primary determinant in the success or failure of the therapeutic intervention. Fear of "running late" and anxiety intensified by rushing from one client to another often disrupt a session's rhythm, preventing the development of physical and mental rapport. Clock-watching is the enemy of attunement, focus and intent as the therapist unconsciously drifts from being totally "present" with the client to suddenly worrying about getting enough "techniques" completed in the allotted time frame.

"Minutes" allows the therapist time to observe, assimilate and record such things as postural abnormalities, present state of mind, painful past experiences (both physical and mental), positive or negative attitudes about their condition, and preconceived ideas about their recovery.

In a relaxed pain management practice, therapists can practice honing such skills as visual screening evaluations, anatomical landmark comparisons, injury assessments and history intakes. This physical examination process can be performed with clients clothed, in bathing suits, sportswear, etc. Make it a habit to observe clients as they enter your therapy room. Look for clues by noting how they sit, remove a jacket, lean forward to untie a shoe, or get up from a chair. Clients often reveal more information when performing normal unconscious movement patterns than when asked to actually execute such tasks as walking, forward bending, range-of-motion maneuvers, etc. More truthful patterns often emerge if the clients are unaware that they are being observed.

Since our ultimate therapeutic goal is to establish pain-free movement during the walking cycle, gait evaluations rank high in every assessment protocol. By making mental notes during gait observations and comparing them with anatomical landmark findings, valuable information can be recorded and stored for future reference. Always check for obvious dysfunctions such as short legs, pelvic tilts, low shoulders, cocked heads, scoliotic patterns, etc. With practice, visual and physical assessments can be performed quickly and efficiently, even with the client completely dressed. The following is a laundry list of some things to look for during a typical client evaluation:

• holding patterns during gait;
• asymmetrical anatomic landmarks;
• presence of upper and lower crossed syndromes;
• abnormal front-to-back (A/P) and side-to-side (scoliotic) curvatures;
• aberrant muscle-firing order patterns;
• arthritic hands;
• pronated/supinated feet;
• excessive wear patterns on the client's shoes; and
• emotional states (extreme anxiety, "bug-eyed," withdrawn, angry, etc).

When therapists take time to focus, relax and carefully listen to a client's history during a typical intake session, a clear picture often emerges. Unfortunately, the picture frequently changes from visit to visit as the client recounts past events. So, what is the best way of arriving at a true pain portrait of this individual?

Medical history-taking often is unstable, according to psychiatrist Arthur Barsky, MD.¹ "Patients frequently fail to recall (and therefore under-report) the incidence of previous symptoms and events; tend to combine separate, similar occurrences into a single generic memory; and falsely recall medical events and symptoms that did in fact occur," Barsky explains.

In both acute and chronic neck/back pain clients, history often relates to individual personality characteristics, state of health and mind at the time of recall, and preformed beliefs about symptoms and prognosis. Most manual therapists would agree that clients also are less likely to recount distant events accurately than they are more recent occurrences. Therefore, it behooves today's manual therapist to consider the following factors when interpreting a client's history.

Practical intake tips:

1. Establish anchor points or memorable events that might help clients recall their symptoms.
2. Encourage clients to convert generic memories of symptoms into more concrete episodes.
3. Ask clients to recall their symptoms in reverse order, starting from the present.
4. Take the history in a similar way each time.

Questioning clients about events surrounding traumas or work-related injuries during the therapy session often reveals new and helpful insights. The addition of touch not only calms nervous system hyperexcitability, allowing thoughts to flow more freely, but also triggers tissue memory as the injured area is being worked. Accurate, focused assessment is crucial, particularly in chronic cases, since time might have elapsed since the event(s) leading up to the painful condition. Therapeutic outcomes improve dramatically as therapists develop creative, yet consistent methods of helping clients present an accurate portrait of their past and present musculoskeletal health problems.

As mentioned above, the art of history-taking possibly is the most underrated and least appreciated of all therapeutic interventions. A client's history is never taken but continually updated and expounded upon throughout each therapy session. Effective history-taking develops rapport, while extracting key pieces of pain puzzle information.

During a traditional relaxation massage session, silence is golden. However, in pain management settings, history-gathering via subtle ongoing conversations frequently produces sudden intuitive insights that might prove instrumental in their recovery. Caring therapeutic touch not only forms a bond of trust, but often triggers important suppressed memories. It's amazing how much key information people tend to forget or are unable to verbalize until you get your hands on them. The more they feel the therapist is emotionally committed to helping solve their ailments, the greater the chances unconsciously blocked information concerning a past injury or stressful incident might resurface.

The therapeutic use of anchors saves time by empowering the therapist with a reference point so clients can be mentally guided back to certain events, injuries, accidents or stressful situations that might have precipitated the pain. We have all experienced the frustration of searching unsuccessfully for that key event that triggers a chronic pain episode when the client suddenly belts out, "I completely forgot about that snow boarding accident my neck began hurting a couple days after that kid knocked me down," or "You don't think it had anything to do with the new mattress and pillow, do you?" or "Mom thinks I fake my migraine headaches so I don't have to go to school, but they didn't start until I got braces." Once the therapist establishes reference points, they can be used as anchors during subsequent sessions to secure new insights on the type and cause of the client's injury or illness.

The key to performing good intakes and evaluations is to listen, listen, listen. Enter each session with open eyes, an open mind, and most of all - an open heart. The goal is in refining and combining intuitive skills with a well-rounded therapeutic background. Touch therapists, especially those specializing in pain management, should begin each session with the open-minded wonderment of a child waiting excitedly to see what the body has to teach you that day. Let the energy systems do the talking and the hands do the walking.

Body-Listening

Body-listening is an art form that, when perfected, clearly guides our therapeutic intent. Entering a session with preconceived therapeutic goals often leads the therapist down a blind path. We often forget it's the client who knows what is going on in his or her own body, rather than some expert voicing opinions and making decisions on what he or she perceives to be the problem. Because therapist and client interact in many conscious and unconscious ways during a session, body-listening through skillful touch provides the anchor that promotes healthy mutual communication. Development of clear intent and keen palpation skills provide the keys for unlocking the door to the art of body-listening.

Therapists' hands palpate for many different things. Where one therapist might focus on a client's aberrant postural patterns, another might be palpating respiratory, cranial or visceral rhythms. Practitioners of myoskeletal bodywork add another dimension by imagining the shifting skeletal architecture as specific deep-tissue structural techniques are applied. Regardless of a practitioner's personal preference, to truly tune in physically and emotionally, personal communication must be in a form understandable to the cli-ent. The approaches presented in neurolinguistic programming (NLP) best explain how the client and therapist's inner world of communication might not conform, causing a breakdown of auditory and tactile communication.

For example, the therapist might be stuck in a visual or kinesthetic language exchange with a client who is basically an auditory communicator. It's helpful for the therapist to listen for clues, both in language and touch, as to the client's communication preference. For example, if the client frequently uses words like, "I see what you mean" or "It looks like my neck turns better to the right," the therapist also might try communicating with more visual terms.

The same applies to touch. Oddly, a large number of manual therapists tend to be right-brained, visually dominant communicators, whereas many clients - being hard-core bodywork advocates - lean more toward the kinesthetic side. If the client communicates best from a kinesthetic (tactile) space, the therapist must learn to elevate his or her body-listening skills to better communicate with the special needs of these touch-sensitive clients. Slowing down and working with the client's ventilatory (breathing) or craniosacral processes helps form an unconscious bond that delights the kinesthetically attuned client.

Myofascia

One reason the massage and bodywork profession continues to grow at a staggering rate is that we have been blessed with specialized training in the most pervasive of all body structures, the myofascial system. This complex neuromyofascial network is the first to exhibit change, and also the first to show dysfunction.

Beginning with superficial structures, the therapist's fingers, elbows and fists slowly engage the body's marvelous myofascial web. This neurologic, electrically charged connective tissue matrix is continuous throughout the body. Fascia is not just the gross outer covering of muscles and organs; it's also prevalent in muscles and organs covering every muscle unit and organ part ultimately impacting the contour of the human body.

Since the myofascial system is composed of dense, regular connective tissues, it falls into a histological category that includes ligaments, tendons, fasciae and aponeuroses. Its makeup consists of collagen fibrils, fibroblasts and elastic fibrils. Fascia both wraps and compartmentalizes the body, the extremities and the muscles via a living web, enveloping the entire physical structure. From this perspective, one can see that fascia possesses the ability to shape the body and its spinal curvatures into either optimal or aberrant postural patterns.

Recall that the myofascial system has virtually no parasympathetic innervation. All soft tissues are innervated by the sympathetic nervous system which, among other things, controls the rate and flow of blood. Since the cardiovascular system has a sympathetic nerve attached to it, the two systems - neuromuscular and cardiovascular - both are regulated by the sympathetic nervous system. When functioning properly, they establish homeostatic balance in the vasomotor system. Obviously, there is a dynamic symbiotic relationship between these two systems.

Because the sympathetic nervous system consumes the greatest amount of the body's energy, uses more oxygen, and produces the most waste byproducts, it should be regarded as the fundamental underlying system of the body. In healthy individuals, the sympathetic nervous system works in perfect balance with the viscera or enteric nervous system - which is primarily responsible for the digestion of food - to process and produce essential amino and fatty acids as fuel for metabolism.

When the brain's limbic system or cranial accessory nerves are stressed through tension, trauma and poor posture, an overstimulated myofascial system sympathetically tightens. Soon, protective guarding results in contractures, fibrin deposition and myospasm. Regrettably, increased stimulus to the myofascial system's neuromuscular component results in decreased visceral activity and resultant sympathetic nervous system dominance.

The myofascial advantage is that it allows therapists to work within this embryologically primitive system, with a goal of bringing balance to muscles and other connective tissues to improve posturally related pain conditions. This leads to a more efficient self-regulating, self-correcting, more adaptive human being. Establishing proper postural balance initiates more refined proprioceptive skills, smoother locomotion during gait, and energy efficiency throughout the entire neuromyofascial system.

Maintenance

When living in an overstimulated society filled with cultural pratfalls such as job-related prolonged sitting, stressful (and often competitive) workplaces, divorces, dysfunctional peer-pressured children, and other family matters, it's essential that individuals be put on a regular maintenance schedule much like we do with animals, automobiles and medical exams. What better and more evolving thing can people do for themselves and their family than preventive body maintenance?

Long-term observation and experimentation opens the door to innovation. Some of our best training is learned "in the trenches" in a full-time practice. Here we are given the opportunity to see what works and what doesn't, as each individual brings in therapeutic challenges that mold and hone our skills. Most body therapists discover their abilities improve exponentially when allowed to track and treat clients over a period of time. Being exposed to difficult cases raises the bar and inspires a passion for developing more therapeutic and efficient ways to evolve and rehabilitate those in need.

Over a period of years, a gradual evolution and paradigm shift transpired in my practice that led me to collect a diverse group of like-minded eccentric individuals I really enjoy being around. I am forever indebted to these people for allowing me to nurture, maintain and elevate their physical condition - and mine.These people have become part of my extended family, and I expect to "maintain" them and their families for the rest of our lives.

Each October, as the new appointment book arrives, history intakes are reviewed and progress evaluations conducted. A mutual decision is made as to how much maintenance might be necessary for the following year. Some have pathologies requiring regular, weekly visits; many adhere strictly to home retraining exercises, and are seen monthly or even quarterly. By the middle of December, all of my regular clients have been scheduled, and my appointment book is full for the upcoming year.

In order to accommodate newly referred clients that might just need a quick fix, I keep a waiting list. My regular clients are encouraged to cancel if they are feeling well, monetarily stressed, or have conflicting appointments. This permits new clients to be filtered in, screened and helped if possible. If my schedule does not permit, or their condition seems to fit better with another practitioner, I refer them out. Over time, I have accumulated a broad referral base of complementary medicine providers such as chiropractors, MDs, DOs, PTs, acupuncturists, Rolfers, and other myoskeletal therapists.

For this type of long-term maintenance to be successful, however, an open and honest dialogue must be established early to prevent development of a transference or counter-transference situation. The more knowledge I gather and share from observing my client's bodies, the more educated they become about their own bodies, which promotes self-reliance. Always erring on the side of modesty has proven the best recipe as far as my own personal comfort level. My work has become much more attuned, relaxed and centered knowing my clients feel safe in the caring atmosphere of my office.

Therapists specializing in pain management require adequate session time to filter the results of the client's history, palpatory findings, and all other pertinent tests through a physiologic lens formed via the scientific scope of basic science and clinical experience. Recently, there has been a noticeable upsurge of fine therapists entering the pain management field, and for obvious reasons.People feel personally rewarded when helping others in need. But, entering this discipline requires the transition be accompanied by advanced study in palpation skills, assessment, history taking, biomechanics, and pathology. Therapists must resist the temptation to mentally "box" the client's complaint into a "fix-it" formula that excludes the body as the primary healer. Fortunately, the human body is not a machine. It possesses the ability to heal with some help from friendly hands and the three M's: Minutes, Myofascia and Maintenance.

Reference

1. Barsky A. Annals of Medicine, 2002.

A Reflexogenic Relationship

A Reflexogenic Relationship: The Muscle/Joint Battle, Part 1

By Erik Dalton, PhD

Reflexogenic - Producing or increasing reflex actions between muscles and joints.

Myoskeletal - All soft tissues forming from the mesoderm including muscles, ligaments, joint capsules, discs, fascia and bones.

 One distinguishing feature of the Myoskeletal Alignment Technique® is the inclusion of deep-tissue routines for unlocking motion-restricted joints. For decades, massage therapists have searched for practical ways to identify and release fibrotic joint capsules, spinal ligaments and fixated facets while staying within their scope of practice. In the early 90s, a holistic soft-tissue approach emerged to help therapists accurately identify and correct pain-generating reflexogenic muscle/joint conditions.

Surprisingly, the "key" that unlocked the door to this muscle/joint mystery initially was revealed in a presentation to the American Back Association by the legendary osteopath Dr. Philip Greenman when he stated, "In the presence of vertebral dysfunction, palpable fourth-layer muscle hypertonicity will always be found." The fourth-layer transversospinalis muscles include the rotatores, multifidus, levator costalis and intertransversarii (Fig. 1). These phylogenetically old laminar-groove muscles are the first structures neurologically stressed by joint blockage, and often are the very same tissues that prolong the dysfunction.

Working with the understanding contained in Greenman's statement, the massage therapist can maximize therapeutic outcomes by:

• palpating and releasing fourth-layer muscle fibrosis;
• testing for underlying joint dysfunction (facets not opening or closing); and
• restoring range of motion using sustained directional pressure on spinal-groove muscles and bones as the client flexes and extends through the fixated area.

Joint Play

Figure 2Under normal conditions, the superior vertebra of each joint smoothly flexes, extends, sidebends and rotates on its inferior neighbor. Too often, however, hypertonically short spinal muscles bind one side of a joint altering its axis of rotation and center of gravity (Fig. 2). When therapists continually palpate lumpy, stringy or wiry fourth-layer intrinsic muscles session after session, underlying joint dysfunction is present and must be addressed.

According to John Mennell, MD, all of the body's synovial joints must have at least 1/8 inch of movement not controlled by voluntary muscle contraction. The term "joint play" was coined to describe this essential principle of normal, pain-free, non-restricted vertebral movement. Deep-tissue myoskeletal techniques focus on restoring joint play and stopping the reflexogenic battle between muscles and joints.

This article offers an overview of current theories and myoskeletal strategies for preventing and correcting "catch 22" pain/spasm/pain cycles perpetuated by abnormal muscle/joint reflex actions.

Fourth-Layer Spinal Muscles

Figure 3Working through the bulky paravertebral muscles and fascia, bodyworkers' sensitive fingers frequently encounter small, hard and sometimes tender knots in the deep transversospinalis muscles of the erector spinae group. These highly innervated tissues located in the medial groove adjacent to the spinous processes contribute to rotation, sidebending and extension in each spinal segment. According to Greenman, "Fourth-layer muscles are dense in spindles and function more as proprioceptors than prime movers. When dysfunctional, they alter joint mechanics locally and alter the behavior of the larger muscles of the erector spinae group." Therefore, muscles such as the multifidus and rotatores (and suboccipitals) are perceived as dynamic ligaments designed to stabilize the spine. Acting as supporting, information-gatheringligaments, they allow the brain to coordinate more gross movements of the vertebral column via longer-lever muscles that have greater leverage and mechanical advantage.

Figure 4The power generated by short fourth-layer spinal muscles is easily underestimated. These highly innervated little critters readily pack enough punch to lock spinal joints open or closed with their strong torsional forces (Fig. 3). Holding a telephone with the shoulder to one ear is a perfect example in which prolonged cervicothoracic sidebending unilaterally compresses joint surfaces, creating reflex transversospinalis and erector spinae spasm. This predictable neurological firing pattern represents the beginning of many functional scoliotic cases seen in the clinic. However, specially designed deep-tissue massage techniques can be very effective in releasing hypertonic myofascia and recovering joint play to fixated facets. Regrettably, some of the tightest transversospinalis muscles are buried deep to more superficial groove muscles such as the multifidus and spinalis, making it difficult and sometimes impossible to mobilize them with fingers and thumbs (Fig. 4). So, how can massage therapists access and release short, concealed spinal muscles that bind joints and perpetuate aberrant pain and posture problems? In part two of the "Reflexogenic Relationship" series, I will demonstrate innovative soft tissue techniques for creating joint-play in fixated facets.

Part 2

Myoskeletal Muscle Manipulation Through Joint Mobilization

A confounding situation arises as the therapist's fingers attempt to pry between joint surfaces to contact the short rotators, intertransversarii, and intertransverse muscles.

Although these tiny, one-joint rotators/side-benders typically are the tightest in the presence of joint dysfunction, application of direct localized pressure sometimes is impossible, given the limited space between articular surfaces. Here's when the myoskeletal technique comes in handy. The therapist utilizes sustained manual pressure on the superior fixated vertebra as the joint is taken through a specific range of motion. Basically, bones are used as levers to create a Golgi tendon organ (GTO) release in all fourth-layer muscles, causing the joint blockage. The question then arises as to the nature of the fixated joint: Is it locked, open or closed? And which side of the spine is stuck?

Using the myoskeletal approach, the therapist's fingers and thumbs wade through the paraspinal laminar groove tissues, scanning for lumpy, wiry and knotty transversospinalis muscles. Once the hypertonic little muscles are found, what information is revealed about the nature of the dysfunctional joint? Not much! By Greenman's definition, it's obvious that joint dysfunction exists, but what type? Is one side of the joint jammed closed and unable to open during forward bending, or is a superior facet not closing on the vertebra below during backward bending?

Stuck Closed

In Figure 5, the therapist's thumbs apply sustained pressure to the bony knot where the fibrosis was found, as the side-lying client flexes and extends the spine through the affected area using a chin-tucking enhancer. If the bony knot pushes back into the thumbs as flexion is introduced, the joint on the ipsilateral side is not opening. The joint's axis of rotation is forced to revolve around the fixated facets, causing the superior transverse process to push back against the therapist's thumbs. The thumbs hold a gentle, sustained headward pressure on the superior transverse process as the client flexes the chin toward his chest. This produces a GTO release in the deep groove muscles and stretches the fibrosed spinal ligaments and joint capsule, allowing the fixated facets to open. In the myoskeletal method, bones are only applied as levers to release adhesive spinal soft tissues that cannot be liberated directly with traditional deep-tissue techniques.

During the fourth-layer assessment, if the bony knot does not push back into the palpating thumbs or fingers as the client flexes through the area, the joint is not closing on thecontralateral side. To free the hypertonic tissues preventing closure of the superior facets on their inferior neighbor, the client assumes a prone position. The therapist's fingers, thumbs or elbow slowly glide down each side of the lamina groove as the client rhythmically raises and lowers his head. In Figure 6, the therapist uses the elbow to traverse down the groove while the client extends and lowers his neck and upper thoracic spine. If a bony knot is palpated, the joint is not closing on the contralateral side. Gentle, sustained pressure (with client-enhancing movement) releases fibrotic groove muscles, joint capsules, and spinal ligaments, allowing the superior facets joints to glide inferiorly and close on the vertebra below.

Scope of Practice

As with all treatment protocols, exceptions occur that can render the myoskeletal method ineffective. Damaged joints often create stubborn fixations that cannot be released by working muscles alone. Vertebrae that have undergone adherent cartilage degradation, apophyseal joint swelling and facet "nipping" due to prolonged microtrauma, typically will not regain lost motion simply by releasing the fibrotic muscles, joint capsules and spinal ligaments. True adhesive joint-fixation problems point to a more serious condition. However, massage therapists who regularly work in conjunction with chiropractors and manipulative osteopaths can enhance therapeutic outcomes by "prepping" the affected area, so that high-velocity thrusting maneuvers are more effective. Manual therapists must develop a good complementary health care referral base so prompt referrals can occur if soft-tissue approaches do not alleviate all the client's pain and/or posture problems.

Combining muscle and joint modalities increases therapeutic efficiency and encourages referrals as therapists resolve stubborn, long-standing pain/spasm/pain cycles. By incorporating holistic-minded reflexogenic routines, today's touch therapist can help solve America's epidemic musculoskeletal pain crisis. Therapeutic outcomes are enhanced as assessment and treatment routines are expanded to include all soft tissues forming from the mesoderm, including muscles, fascia, joint capsules, spinal ligaments, nerve dura, and intervertebral discs.

Although myoskeletal therapy delves deep into body structures, the intent is still slow and sustained soft-tissue work combined with specific client-initiated enhancers, such as chin-tucking, eye movements, deep breathing, pelvic tilting, etc. The client's experience following a myoskeletal session should be one of invigoration, pain relief, increased range of motion and postural improvement. Bones are assessed and treated as soft tissues in the myoskeletal system, with pressure often applied directly to myofascia overlying transverse processes. It's of the utmost importance to stress that bones only are used as levers to release hard-to-access, fourth-layer muscles, ligaments and fibrotic joint capsules (much like frozen shoulder work). Therapists always must remember that joints should never be taken into a nonphysiologic range of motion, which remains outside the scope of practice for most massage and bodywork practitioners.

References

1. Mennell, J MCM. Joint Pain. Little Brown & Company, Boston, 1964.
2. Greenman PE. Principles of Manual Medicine, pg. 67. Lippincott, Williams & Wilkins, 2003.

Coccyx Controversy

By Erik Dalton, PhD

Many of today's medical texts tell us the coccyx fuses into one rigid segment by adulthood in most people. However, several well-designed studies have shown that a normal coccyx should have two or three movable parts that gently curve forward and slightly flex as we sit.

Two medical papers (Postacchini and Massobrio¹ and Kim and Suk²) found that test subjects with fused coccyxes that didn't flex upon sitting were more likely to experience tailbone pain than those with a normal coccyx. Postacchini and Massobrio performed radiographic studies of 171 coccyxes, and found less than 10 percent were fused into one piece...most had two or three, and a few had four segments. The primary conditions they found to be associated with coccyx pain were: coccyx angled sharply forward; coccyx side-bending more to one side than the other; and coccyx completely rigid (all segments fused together and fused to the sacrum).

Idiopathic head and low back pain syndromes frequently manifest when a distorted coccyx tugs on the dural tube, causing reverberating tensional forces to travel all the way up to the occiput.
© www.erikdalton.comAlthough none of the abnormalities listed above always cause pain, clients seem more likely to experience coccyx problems when one or more of these conditions exist. Over the years, I have noticed clients with particularly long coccyxes also seem more likely to report local tenderness and pain. Although not reported in the literature, it seems obvious that a long coccyx would be more likely to suffer damage than a shorter one.

Why some hurt and others don't is unclear. In the case of a misaligned coccyx, it might be that the pain is caused by the coccyx pulling on muscles, ligaments or overstretching the filamen terminale (end of the dural tube). Connective tissues called the filum durae spinalis enclose the end of the spinal cord and attach it to the deep dorsal sacrococcygeal ligament. A major source of hip and back pain occurs as fibrotic sacrococcygeal ligaments anteriorly flex (hook) the coccyx and compress/overstretch the sensitive filum terminale (Fig.1). In the case of a rigid coccyx, it might be that the tissues under the inferior segments might create a pad of irritated tissue (like a bunion) that can rub the dura raw. But the most common pain-generator helped by manual therapists is neuroreceptor pain from a misaligned sacrococcygeal joint.

Coccydynia (Coccyx Pain)

When sitting, the coccyx shifts forward and acts as a shock absorber. However, falling on the tailbone or events such as childbirth can lead to coccygeal pain, known as coccydynia. In most cases, the pain is caused by an unstable coccyx, resulting in chronic inflammation of the sacrococcygeal joint. Coccydynia also can be attributed to a malformed or dislocated coccyx and the growth of bony spurs on the coccyx. Resulting pain often is resolved by performing specific soft tissue techniques to release the levator ani muscle, anococcygeal, sacrotuberal and sacrospinal ligaments, as well as the gluteus maximus muscles.

Another common etiology is childbirth. The coccyx is considered by some to be in the way during childbirth. At the end of the third trimester, certain hormonal changes enable the synchondrosis between the sacrum and the coccyx to soften and become more mobile. This increased mobility of three to five coccygeal segments allows for more flexion and extension, which might permanently change the resting tension of the surrounding ligaments and muscles. Unlike fractures, which can remodel, injuries to the sacrococcygeal junction often become inflamed as the joint is repeatedly forced out of its normal position. Physical examination should include direct palpation of the coccyx for tenderness. In true coccydynia, the coccygeal region usually is markedly tender. If the client reports coccygeal pain but is not tender upon palpation, the therapist should refer out for an orthopedic workup to rule out lumbar disk disease.

Hooked Coccyx

Coccyx Release. Therapist releases tight right pelvic ligaments by reaching across the body and contacting the left ischial tuberosity with his dominant thumb and sliding up and under attachments at the inferior border of the sacrum. The therapist's other thumb braces on top, maintaining sustained "scooping" pressure to release ligaments and gently lift the coccyx from its hooked position.
© www.erikdalton.comIda Rolf, PhD, referring to the coccyx as the "seat of the soul," insisted on correcting hooked and side-bent coccyxes during her famous session six of the Rolfing® series. When this tiny group of bones "hooks" anteriorly or bends to one side (typically the left), the dural tube tightens. In reported cases, a hooked coccyx actually has shut down the entire CNS by hindering cerebrospinal fluid flow. A hooked coccyx also can lead to loss of psychological integrity. Reported cases cite severe emotional disturbances in people whose coccyx has been removed or broken off, leaving no anchor for the dura mater. The coccyx has been implicated in clients presenting with functional scoliotic patterns. Through its connection with the sphenoid, excessive dural tension stresses the eleventh cranial accessory nerve, which, in turn, shortens the SCMs and upper trapezius muscles. A modified version of Dr. Rolf's coccyx technique is demonstrated in Fig. 2.

Coccyx pain often is caused by falling backwards or by childbirth, although in many cases, the exact etiology is unknown. There are various treatment modalities available, and the great majority of sufferers can be helped. Due to the vertebra's direct attachment to the dural membrane through the filum terminale, coccyx work can cause a client to become very emotional. Prior to treating coccyx dysfunction, always ask the client's permission to perform this technique due to possible physical and emotional hypersensitivity in the area. Before performing any type of coccyx work, take time to clearly explain your therapeutic intent and the desired outcome. All coccyx alignment techniques should be performed through underwear or draping.

References

1. Postacchini F, Massobrio M, Idiopathic coccygodynia. Analysis of fifty-one operative cases and a radiographic study of the normal coccyx. The Journal of Bone and Joint Surgery. 1983 65(8): 1116-1124.
2. Kim NH; Suk KS: Clinical and radiological differences between traumatic and idiopathic coccygodynia. Yonsei Med J, 1999 Jun, 40:3, 215-20.

Prevención y tratamiento de la osteoporosis con la actividad física y el deporte

Prevention and treatment of osteoporosis with physical activity and sports

JA Martin Urrialde ^a, N Alonso Mendaña <sup>b

a</sup> Profesor Titular Fisioterapia Universidad San Pablo CEU.
^b Fisioterapeuta Especialista Formación Actividad Física y Deporte.

Palabras Clave

Osteoporosis; Caídas; Fracturas; Ejercicio y actividad física.

Keywords

Osteoporosis; Falls; Fractures; Exercise and physical activit.

Resumen

Varias técnicas fisioterápicas y agentes físicos pueden proporcionar muchos beneficios al paciente osteoporótico pero especialmente la actividad física y el deporte. Tiene un efecto preventivo de pérdida de masa ósea y caídas. El ejercicio se ha mostrado eficaz en la reducción de caídas y fracturas que son el resultado, la mayoría de veces, de esta enfermedad. La indicación de mantener una actividad física constante, adecuada a las posibilidades de cada paciente osteoporótico debe formar parte obligatoriamente de su tratamiento.

Abstract

Several techniques of physiotherapy and physical agents may provide a lot of benefits to the osteoporotic patient but specially physical activity and sport. It has a preventive effect because it prevents loss of mineral mass and falls. Exercise has been shown to be effective in the reduction of falls and fractures that are the result of this disease in the most of cases. The indication to maintain a constant physical activity adapted to the possibilities of each osteoporotic patient should form and inexcusable part of their treatment.

Artículo

INTRODUCCION
La osteoporosis constituye un enorme problema de salud pública, por lo que es necesario difundir el conocimiento de las posibles causas de la misma, así como las medidas utilizadas para su diagnóstico, prevención y tratamiento. Este último debe ser enfocado de una manera multidisciplinaria para obtener los mejores resultados.
La osteoporosis afecta a una de cada cinco mujeres mayores de 45 años y a cuatro de cada diez mayores de 75 años.
La osteoporosis es la disminución de masa ósea y de la resistencia mecánica del hueso lo que le lleva a sufrir fracturas. Es la principal causa de fracturas óseas en mujeres después de la menopausia y en ancianos en general.
La osteoporosis no tiene un comienzo bien definido, y hasta hace poco, el primer signo visible de la enfermedad acostumbraba a ser una fractura de cadera, muñeca o de los cuerpos vertebrales que originaban dolor o deformidad.
Los factores predisponentes a tener en cuenta en la osteoporosis son: la menopausia precoz, el consumo de alcohol o cafeína, el tabaquismo, la amenorrea, el uso prolongado de corticoesteroides, los procesos que bloquean la absorción intestinal del Calcio, la dieta pobre en calcio durante la adolescencia y juventud y una vida sedentaria.
El caminar y los ejercicios de extensión de columna pueden estabilizar e incluso aumentar ligeramente la masa ósea y mejorar el equilibrio y la fuerza muscular previniendo, por tanto, caídas y fracturas.

ESTRATEGIA DE BUSQUEDA
Con el objetivo de ver si la actividad física y el deporte son efectivos o no para la prevención y tratamiento de la osteoporosis, y si tiene efecto sobre la masa ósea, se ha realizado una revisión bibliografica desde el año 1999 al año 2005 utilizando las palabras clave como "osteoporosis", "osteoporosis and exercise", "exercise", "falls and fractures", "osteoporotic fractures" y "postmenopausal osteoporosis", en las bases de datos PubMed ­ Medline, Cochrane Database of Systematics Reviews (CSDR), JANO Online, Sports Medicine y OVID.
Los criterios de inclusión considerados fueron la característica de estudio clínico en humanos, el cumplimiento de los años de revisión y que las muestras analizadas por los autores, contuvieran sujetos de mas de 45 años, tanto hombres como mujeres.
Sobre un total de 432 estudios, se seleccionaron para esta revisión 80, que cumplían los citados criterios.

RESULTADOS
Existen numerosos trabajos y revisiones que muestran la correlación entre el grado de actividad física desarrollado y la Densidad Mineral Ósea (DMO) a cualquier edad biológica.
Los primeros artículos encontrados ¹ nos indican los beneficios de la actividad física diciendo que es esencial para el desarrollo y mantenimiento de la salud del esqueleto, que los ejercicios de fuerza pueden resultar beneficiosos, aumentando la masa muscular pero sin ser sustitutivo de la terapia hormonal sustitutiva.
Hay estudios ^2,3 que indican que el mejor y mayor estímulo para remodelar el hueso es el ejercicio con carga. Éste aumenta en mujeres mayores de 50 años la DMO de la zona lumbar entre un 9,2 % y 35 % más que en mujeres que no hacen ejercicio.
En un trabajo realizado ⁴ en individuos de 86-96 años que participaron de un programa de entrenamiento de ocho semanas para fortalecer los miembros inferiores se mostró la mejora de un 174 % de la fuerza y un 48 % de la velocidad al andar. Sin embargo, tras cuatro semanas de suspensión se disminuyó un 32 % la fuerza.
Los músculos que deben ser trabajados son aquellos utilizados en las actividades de la Vida Diaria (AVD) con repeticiones realizadas con 2-3 segundos para levantar el peso y 4-6 segundos para bajarlo, aumentando la carga cada dos o tres semanas y realizando el ejercicio dos veces por semana. El uso de máquinas es preferible al de pesos libres porque evitan lesiones y protegen la columna vertebral.
En el año 2000 Seeman et al ⁵ muestran que la Densidad Mineral Ósea (DMO) es mayor en una persona que hace ejercicio y menor en los que hacen ejercicio leve o no lo practican. El estudio con 49 mujeres gimnastas de entre 7 y 11 años que practicaban ejercicio moderado (5-10 horas por semana) o a altos niveles (más de 10 horas por semana). Se vio que tenían más masa ósea que aquellas que lo practicaban a baja frecuencia (2-5 horas por semana). Los autores concluyeron que cinco o más horas por semana de ejercicio de alto impacto aumenta la DMO en la pubertad. En adultos el incremento es del 1-3 % y éste se pierde con el cese del ejercicio. Pero aún quedaban preguntas sin resolver como si hay alguna ventaja al hacer ejercicio durante el crecimiento, los efectos del ejercicio en cuanto a forma y tamaño, el efecto del ejercicio en fracturas y caídas y la cantidad necesaria para evitar la pérdida de masa ósea.
Ese mismo año Sharkey et al ^6,7 dicen que el ejercicio y la actividad física ayuda a disminuir los factores de riesgo y síntomas de la osteoporosis aportando un buen estado en general y mayor calidad de vida. Los resultados de la conferencia sobre la prevención, diagnóstico y tratamiento de la osteoporosis nos muestran a los profesionales de los distintos campos de la medicina que la osteoporosis es una enfermedad de grandes consecuencias físicas, psicológicas y económicas. El ejercicio regular, especialmente de resistencia y alto impacto, contribuye a desarrollar el pico de masa ósea y a reducir el riesgo de caídas en personas mayores.
Otros artículos de Curl et al ^8-10 indican los beneficios del ejercicio en la prevención de la osteoporosis. Recomiendan los autores andar 30 minutos a intensidad moderada todos los días de la semana.
Además del ejercicio ^11-13 otros factores de riesgo como la edad, raza, tabaquismo, nutrición y estado de salud están asociados con la osteoporosis y deben ser evaluados y modificados para prevenir la pérdida de masa ósea. El tratamiento de la osteoporosis influye además del ejercicio el aporte de calcio y vitamina D, los estrógenos, biofosfanatos y calcitonina. Aunque sólo se han visto sus efectos en mujeres, promete ser beneficioso también para los hombres.
A finales del año 2000, unos estudios muy similares con triatletas ^14,15 incluye a 94 hombres y 58 mujeres de 40 años de edad en adelante y hasta los 52. La masa ósea del cuello femoral y de las vértebras lumbares era igual en hombres y mujeres, había diferencias en la cantidad de calcio en el cuerpo y en la masa ósea del pecho, pelvis, piernas y brazos.
En 2001 un estudio de profesionales del Consejo Superior de Deportes de Madrid ¹⁶ relaciona la actividad física y la masa ósea. El grado de esta influencia y el tipo de programa que induce al estímulo osteogénico más eficaz todavía no se conocen con profundidad; mientras que se sabe con certeza que una disminución en la actividad física produce una gran pérdida de masa ósea, el aumento de la misma por un incremento de la actividad es menos concluyente. Los resultados varían según la edad, el estado hormonal, la nutrición y el tipo de ejercicio.
La mayoría de los estudios sobre la influencia del ejercicio en el hueso adulto señalan marcadas diferencias de la DMO en las diferentes regiones entre los deportistas y el grupo control en un amplio rango de actividades deportivas.
Los efectos del ejercicio sobre el músculo están bien claros. A través del entrenamiento se produce una adaptación funcional que capacita al sistema muscular para funcionar a un nivel superior. En el entrenamiento de tipo aeróbico, aunque se ha observado aumento de fuerza de algunos grupos musculares, no se alcanza la misma magnitud que del producido por entrenamiento con pesas ^16-19.
Las investigaciones de los últimos años indican que la DMO vertebral en las deportistas amenorreicas es baja. Algunas presentan una DMO vertebral significativamente menor que la de las mujeres amenorreicas en general; lo cual indica la existencia de osteopenia. Este estudio deja claro que el ejercicio intenso puede reducir el impacto que la amenorrea provoca en la DMO aunque las corredoras amenorreicas continúan teniendo alto riesgo de fracturas relacionadas con el ejercicio^20,21.
En contraposición aparecen otros estudios ²² que nos dicen que la conducta sedentaria es un factor de riesgo para enfermedades crónicas; esto puede evitarse con la práctica de ejercicio durante los años de crecimiento dando lugar a un esqueleto más maduro.
Es clara pues la relación entre la práctica habitual de ejercicio con la adquisición y mantenimiento del hueso, las consecuencias sobre el esqueleto y la evaluación clínica del paciente con huesos frágiles que se puede hacer con el ejercicio.
Burrows et al ²³ exploraron los factores que podían estar asociados con la disminución de la DMO en mujeres corredoras. Estudiaron a 52 mujeres corredoras (desde los 1.500 metros a la maratón), con edades comprendidas entre 18 y 44 años, midiendo en porcentajes la DMO de la columna vertebral lumbar y del cuello femoral usando la densitometría.
En el Congreso Mundial sobre Osteoporosis del año 2002 ²⁴ se mostraron los efectos positivos del ejercicio de alto impacto sobre la salud de los huesos en un estudio que duró tres años y que utilizó a mujeres postmenopáusicas. Se encontró un interesante papel del ejercicio sobre la masa ósea y la calidad de vida en mujeres postmenopáusicas que participaban de una rutina diaria de ejercicios. Estos datos se comprobaron con otro estudio que examinaba la relación entre la actividad física diaria (incluyendo el andar, nadar, pedalear, actividades cotidianas de la casa y algunos deportes) y el riesgo de caídas en 1.383 sujetos de los cuales 705 fueron mujeres y 678 hombres con edades comprendidas entre 65 y 88 años.
Además de la práctica de actividad física ^25-29 se vio que una prevención y tratamiento óptimos para la osteoporosis requerían la modificación de factores de riesgo como el abandono del tabaco, tener una dieta equilibrada y la intervención farmacológica. Dentro de ésta última se incluyen los biofosfanatos y la calcitonina entre otros.
Según Torstveit ³⁰ la actividad física es mejor durante los años premenopáusicos. Ejercicios de alta magnitud pueden incrementar la DMO en mujeres premenopáusicas, ejercicios de menor intensidad muestran menos efectos. Para mantener o aumentar la DMO en mujeres jóvenes se deben incluir ejercicios rápidos y dinámicos que reducirán el riesgo de fracturas osteoporóticas más adelante ³¹.
Todd y Robinson ³² vieron diferencias en cuanto a los estudios que había sobre el ejercicio y la osteoporosis hasta entonces. La mayoría de estudios han demostrando una buena correlación entre los niveles de ejercicio y la masa ósea. Sin embargo, estudios de grupo demuestran una asociación simple que no implica causalidad. Además la asociación está basada en el ejercicio durante la vida que no significa que el ejercicio previo en individuos sedentarios pueda prevenir o revertir la osteoporosis.
El ejercicio tiene beneficios como el aumento de fuerza muscular, mejora de la coordinación, disminución de fracturas traumáticas osteoporóticas; además en otro tipo de pacientes, disminuye el riesgo de enfermedad cardiovascular, diabetes y depresión ^33-36.
Un grupo de científicos de la universidad de Harvard ^37-38 evaluó los niveles de actividad de más de 61.000 mujeres con edades comprendidas entre los 44 y 70 años. Los científicos concluyeron que aquellas mujeres que caminaban al menos una hora a la semana podían reducir en un 6 % el riesgo a sufrir una fractura de cadera. En el caso de las mujeres más activas, con un nivel de ejercicio cercano a las ocho horas semanales, la reducción aumenta a un 55 % en comparación con las participantes sedentarias. Los beneficios fueron apreciables incluso entre las mujeres sedentarias que comenzaron a realizar algún tipo de ejercicio a intensidad moderada, mientras que el riesgo de fractura se incrementó en aquellas mujeres activas que dejaron de practicar ejercicio.
Sin embargo, un trabajo de los científicos de la Universidad Johnn Hopkins de Estados Unidos publicado en el Journal of Internal Medicine ³⁹ concluye que el ejercicio leve no basta para fortalecer los huesos. En el estudio participaron 38 hombres y 46 mujeres sanos sedentarios. No se observó un efecto significativo de la actividad física sobre la DMO. Por ello, concluyen que para fortalecer los huesos o prevenir la pérdida de DMO asociada a la edad es necesario un ejercicio vigoroso.
A. Gustavsonn et al ⁴⁰ hicieron un estudio longitudinal en el que concluyeron que el entrenamiento del hockey sobre hielo durante la niñez y adolescencia no prevenía el desarrollo de la osteoporosis en el cuello femoral si no se mantenía dicha actividad.
El estudio estaba formado por 43 jugadores de hochey sobre hielo y 25 sujetos control que se controlaron durante el juego y después del juego se controlaron en un período entre 30 y 70 meses. Los jugadores de hockey tenían más DMO en el cuello femoral mientras que los sujetos controles no. Entre la primera y segunda temporada, 21 jugadores detuvieron su actividad deportiva. Durante este mismo período, estos sujetos perdieron mucha DMO del cuello femoral comparados con los 22 jugadores que seguían entrenando; los cuales tenían mayor DMO en el cuello femoral y columna vertebral comparados con el grupo control. Luego, de aquí la conclusión de los autores de este estudio.
Estudio similares ^41,42 vio la relación entre el ejercicio físico y el aporte de Calcio en chicas adolescentes entre 16 y 18 años. Los resultados fueron que sí aumentaba la DMO pero para ver si disminuía el riesgo de fractura y mejorar el pico de masa óseo habría que realizar otro tipo de estudios. Como el de CH Turner et al que demuestran los efectos del ejercicio y la actividad física en la niñez y la adolescencia ⁴³.
En la Universidad de Heidelberg en Alemania ^44,45 se estudiaron los primeros atletas internacionales en levantamiento de peso, boxeo y ciclismo. Encontraron que la DMO de los deportistas levantadores de pesos era superior en un 24 % al grupo control y los boxeadores en un 17 %. La DMO de la zona vertebral lumbar en los ciclistas sin embargo era un 10 % más bajo que el del grupo control. Actividades de alto rendimiento como el sprint y tenis tienen un aumento de la DMO similar a la de los levantadores de peso. Andar, caminar y pedalear están asociados con un buen condicionamiento muscular que no implica un aumento de la DMO. Algunos casos de pérdida de DMO se deben a factores nutricionales o en mujeres atletas a desórdenes hormonales.

La prevención y tratamiento de la osteoporosis debería enfatizar una adecuada cantidad de calcio, vitamina D y ejercicio ^46-48. Además de un suplemento de estrógenos y receptores moduladores de los estrógenos (antagonistas de éstos) que puedan aumentar la DMO y disminuir el riesgo de fractura. Biofosfanatos orales e intravenosos también disminuyen la incidencia de fracturas de cadera.
La utilización del ejercicio en el tratamiento de la osteoporosis ^49-63 se debe a la maximización del pico de masa ósea; mantener o reducir la pérdida de la DMO y mantener la fuerza muscular y estabilidad postural para reducir el riesgo de fractura y caídas en los últimos años de vida del paciente.
Por eso, mientras el ejercicio da estos beneficios, hay riesgos asociados con el ejercicio intenso en mujeres atletas según MP Warren y LR Goodman ^64,65. La triada de la mujer atleta aumenta estos riesgos debido a la amenorrea, osteoporosis y desórdenes alimenticios.
Consecuentemente la causa de desarreglos hormonales no se debe sólo al ejercicio pero inadecuadas o restrictivos aportes de calorías no compensan el desgaste energético. El riesgo más peligroso asociado con la amenorrea es el impacto sobre el esqueleto. Complicaciones que incluyen una comprometida DMO, fallos en el pico de masa ósea durante la adolescencia y aumento del riesgo de fracturas por estrés.
El tratamiento más efectivo es la disminución de la intensidad del ejercicio y el aumento de los aportes nutricionales junto con opciones farmacológicas como es la terapia hormonal sustitutiva, calcitonina, biofosfanatos y la hormona paratifoidea.
Gary y Vogin ⁶⁶ indica que los ejercicios acuáticos mejoran el equilibrio en mujeres postmenopáusicas y esto ayuda a prevenir las caídas.
Las mujeres del grupo acuático trabajaban más seguras pues no estaban preocupadas por caerse mientras realizaban la actividad; en el grupo que hacía los ejercicios en el gimnasio, dos de las mujeres se cayeron durante el programa de entrenamiento.
Según Peña ⁶⁷ la Fisioterapia puede ser útil al paciente osteoporótico estimulando el ejercicio físico en general y previniendo las actividades que conllevan riesgo de caídas y disminución del dolor entre otras cosas ^{68 69} También puede actuar proporcionando normas posturales que ayuden a aliviar el dolor del paciente junto con la aplicación de numerosos agentes físicos como la electroterapia, masoterapia, órtesis, hidrocinesiterapia y otras técnicas del ámbito de la Fisioterapia que pueden ayudar a la mayor y más precoz recuperación funcional de los pacientes osteoporóticos.
Rodríguez ⁷⁰ complementa lo anterior diciendo que la sesión durará entre quince y sesenta minutos de tres a cinco veces por semana donde se trabajará de manera incremental y en grupo a ser posible con ejercicios variados o no repetitivos. Se pueden usar pelotas, cuerdas, palos y música siempre con órdenes sencillas.
Según Tamaki et al ⁷¹ correr a 0,7 km/h durante diez minutos cada día inhibe el desarrollo de la osteoporosis debida a la insuficiencia proteica. Un marcador de formación ósea en la osteoporosis no está elevado en esta deficiencia proteica cuando se ha inhibido al correr.
Asikainen et al ⁷² estudiaron a mujeres postmenopáusicas de entre 50 y 65 años en cuanto a su composición muscular y ósea, flexibilidad y fuerza muscular, control postural, presión sanguínea y control metabólico.
Mujeres postmenopáusicas precoces pueden beneficiarse de treinta minutos de caminata diaria combinada con ejercicios de resistencia dos veces por semana.
Para las personas sedentarias, el andar se puede incluir fácilmente en su rutina diaria. Para comenzar, se pueden hacer de ocho a diez repeticiones de cada ejercicio comenzando con ejercicios al 40 % del máximo. El entrenamiento de resistencia requiere profesional cualificado.
En cada sesión hay que estirar y combinarlo con una dieta adecuada lo que nos ayudaría a mejorar el equilibrio, la coordinación, la fuerza, disminuir la hipertensión arterial y la dislipidemia.
Kelley ⁷³ estudió la eficacia de los ejercicios de resistencia en la zona lumbar y en el cuello femoral a efectos de la DMO. Fueron incluidos en el estudio 143 sujetos, 74 en el grupo de ejercicio y 69 en el control. Más cambios en la DMO de la zona lumbar y cuello femoral en el grupo de ejercicio que en el grupo control pero no muy significativos; luego, los resultados del estudio no soportan la eficacia del ejercicio de resistencia sobre la DMO en mujeres postmenopáusicas.
Barclay y Lie ⁷⁴ estudiaron a 50 mujeres postmenopáusicas en un programa de ejercicios durante veintiséis meses con dos sesiones grupales de sesenta o setenta minutos por semana y dos sesiones no supervisadas en su cada de al menos veinticinco minutos por semana. Las mujeres tenían 55 años y estaban exentas de toma de medicamentos y de enfermedades conocidas.
Kemper et al ^75-78 estudiaron la fuerza y resistencia en un programa de ejercicios, que duraba mínimo dieciséis semanas, definido entre el porcentaje de DMO por año en el grupo de entrenamiento y el control. Los ejercicios de fuerza mostraron menores efectos que los ejercicios de resistencia. Éstos últimos, según este estudio, pueden prevenir o revertir la pérdida de masa ósea en al menos un 1 % por año ⁷⁹.

CONCLUSIONES
El mayor efecto del ejercicio sobre la Densidad Mineral Ósea (DMO) se produce durante el crecimiento pero tenemos la difícil tarea de motivar desde niños a ancianos el hábito de adoptar una disciplina para que se mantengan activos toda la vida. Cuánto más precozmente se comience a realizar ejercicio físico vigoroso, mayor será el desarrollo óseo y la mineralización.
Abandonar la actividad revierte las ganancias obtenidas a cualquier edad.
En casi todos los estudios analizados hay una relación directa entre el ejercicio y la actividad física y la DMO a todas las edades. Además ayuda a la reducción de caídas, prevención de fracturas, mejora de la coordinación y equilibrio entre otras cosas.
Los ejercicios aeróbicos, con carga y de resistencia son los más efectivos para aumentar la DMO. La actividad física no puede recomendarse como sustitutivo de la terapia hormonal sustitutiva en el período de menopausia.
Un programa de actividad general que haga énfasis en la fuerza, flexibilidad, coordinación y condición cardiovascular podría reducir el riesgo de fractura.
Se ha visto que por lo menos caminar treinta minutos tres veces a la semana es beneficioso para la DMO incluso en un paciente sedentario.
Se recomiendan también ejercicios de tonificación y estiramiento muscular, que son ejercicios de bajo impacto evitando así los de alto impacto e hiperflexiones que no son nada beneficiosas para el paciente con osteoporosis.
Todo esto hay que combinarlo con una dieta adecuada y un aporte de Calcio evitando hábitos tóxicos como pueden ser por ejemplo el alcohol o el tabaco

Bibliografía

1.Erickson SM, TL. Sevier. Osteoporosis in Active Women: Prevention, Diagnosis and Treatment. The Physician and SportsMedicine. 1997; vol. 25 n.º 11.
2.Katz C. Sherman. Exercise for Osteoporosis. The Physician and SportsMedicine. 1998; vol. 26 n.º 2.
3.Drug Ther Perspect. Female Osteoporosis: Taking Regular Exercise Constitutes Good Advice 1999 Medscape General Medicine. 13(7):8-9.
4.Mahecha Matsudo SM. Osteoporosis y Actividad Física. 2003 PubMed (artículo completo).
5.Seeman E. The Role of Exercise in Osteoporosis Prevention World Congress on Osteoporosis 2000, Chicago, Illinois (Abstract, PubMed).
6.Sharkey NA, Williams Ni, Guerin JB. The role of exercise in the prevention and treatment of osteoporosis and osteoarthritis. Nurs Clin North Am. 2000;35(1):209-21.
Medline
7.No Authors Listed. National Institutes of Health, EEUU. Osteoporosis prevention, diagnosis and therapy. NIH Consens Statement. 2000;17(1):1-45.
Medline
8.Curl WW. Aging and exercise: Are they compatible in women? Clin Orthop Relat Res. 2000;(372):151-8.
9.Taafe DR, Marcus R. Musculoskeletal health and the older adult. J Rehabil Res Dev. 2000;37(2):245-54.
Medline
10.Woo J. Relationships among diet, physical activity and other lifestyle factors and debilitating diseases in the elderly. Eur J Clinic Nutr. 2000;54 Suppl 3:S143-7.
11.Kenny AM, Prestwood KM. Osteoporosis. Pathogenesis, diagnosis and treatment in older adults. Rheum Dis Clin North Am. 2000;26(3):569-91.
Medline
12.Watts NB. Focus on primary care postmenopausal osteoporosis: an update. Obstetric and Gynecology Survey. 2000;55(12 Suppl):S49-55.
13.Ohta H. Lifestyle management approaches in postmenopausal osteoporosis. Clin Calcium. 2004;14(11):63-8.
14.Gregg EW, Pereira MA, Caspersen CJ. Physical Activity, falls and fractures among older adults: a review of the epidemiologic evidence. J Am Geriatr Soc. 2000;48(8):883-93.
Medline
15.Medscape Medical News. Spine and upper thigh bone strength equalized with physical activity training; 2000.
16.Palacios N, Santaella O, Sainz L. Relación entre la masa ósea y la fuerza muscular: un nuevo campo en la aplicación de la vibroestimulación en el deporte; 2001 (artículo completo).
17.Marcus R. Role of exercise in preventing and treating osteoporosis. Rheum Dis Clin North Am. 2001;27(1):131-41.
Medline
18.Vuori IM. Dose-response of physical activity and low back pain, osteoarthritis and osteoporosis. Medical Science Sports Exercise. 2001;33(6 Suppl):S551-86; discussion 609-10.
19.American Journal of Public Health 2001. Ejercicio moderado y osteoporosis. 2001;91:1056-9.
20.Karlsson M, Bass S, Seeman E. The evidence that exercise during growth or adulthood reduces the risk of fragility fractures is weak. Best Pract Res Clin Rheumatol. 2001;15(3):429-50.
Medline
21.Hertel KL, Trahiotis MG. Exercise in the prevention and treatment of osteoporosis: the role of physical therapy and nursing. Nurs Clin Nort Am. 2001;36(3):441-53, VIII-IX.
22.DIPietro L. Physical Activity in aging: Changes in patterns and their relationship to health and function. J Gerontol A Biol Sci Med Sci. 2001;56 Spec n.º 2:13-22.
23.Burrows M, Nevill AM, Bird S, Simpson D. Physiological factors associated with low bone mineral density in female endurance runners. The Physician and SportsMedicine; 2002.
24.Susan A. Bone Health: Nutricional and Lifestyle factors International Osteoporosis Foundation World Congress on Osteoporosis; 2002 (abstract PubMed).
25.Prestwood KM, Raisz LG. Prevention and treatment of osteoporosis. Clin Cornerstone. 2002;4(6):31-41.
Medline
26.Delmas PD. Treatment of postmenopausal osteoporosis. Lancet. 2002;359(9322):2018-26.
27.Turkoski B. Treating osteoporosis without hormones. Orthop Nurs. 2002;21(5):80-5.
Medline
28.Sirola J, Rikkonen T. Muscle performance after the menopause. J Br Menopause Soc. 2005;11(2):45-50.
Medline
29.Siddiqui NI, Rahman S, Mia AR, Shamsuzzaman AK. Evaluation of hormone replacement therapy. Mymensingh Med J. 2005;14(2):212-8.
Medline
30.Torstveit MK. Does exercise improve the skeleton of young women? Tidsskr Nor Laegeforen. 2002;122(21):2112-5.
31.Lillelund HK, Jorgensen HL, Hendriksen C, Lauritzen JB. Effect of physical exercise on bone mass in the elderly. Ugeskr Laeger. 2002;164(39):4522-8.
32.Tood JA, Robinson RJ. Osteoporosis and exercise. The Physician and SportsMedicine; 2002.
33.Karlsson M. Exercise increases muscle strength and probably prevents hip fractures Lakartidningen. 2002;99(35):3408-13.
34.Cacho del Amo A, Fernández de Santiago FJ. Ejercicio físico en el anciano institucionalizado. Revista Fisioterapia. 2003;25 (3):150-8.
35.Medline. Haga ejercicios para tener huesos saludables; 2003.
36.Bean JF, Vora A, Frontera WR. Benefits of exercise for community-dwelling older adults. Arch Phys Med Rehabil. 2004;85 (7 Suppl 3):S31-42; quiz S43-4.
37.Medscape. Caminar una hora a la semana previene fractura de cadera. JAMA. 2002;288:2300-6.
Medline
38.Beitz R, Doren M. Physical Activity and postmenopausal health. J Br Menopause Soc. 2004;10(2):70-4.
Medline
39.Ejercicio leve y densidad mineral ósea. Journal of Internal Medicine. 2002;252:1-8.
Medline
40.Gustavsson A, Olsson T, Nordström P. Rapid loss of bone mineral density of femoral neck after cessation of ice hockey training: A 6-year longitudinal Study In males. The Physician and SportsMedicine. 2003;18:1964-9.
41.Kemmler W, Engelke K, Weineck J, Hensen J, Kalender WA. The Erlangen fitness osteoporosis prevention study: a controlled exercise trial in early postmenopausal women with low bone density ­ first year results. Arch Phys Med Rehabil. 2003;83:679-82.
42.Stear SJ, Prentice A, Jones SC, Cole TJ. Effect of a Calcium and exercise intervention on the bone mineral status of 16-18 Years old adolescent girls. Am J Clin Nutr. 2003;77:985-92.
Medline
43.Turner CH, Robbing AG. Designing exercise regimens to increase bone strength. Exercise Sport Science Rev. 2003;31(1):45-50.
44.Cyclist may risk bone loss. The Physician and SportsMedicine; 2003.
45.Harvey B, Simon MD. Diet and Exercise. Section CE Clinical Essentials; 2003 (Abstract).
46.No authors listed. Osteoporosis-Prevention, diagnosis and treatment. A systematic literature review. SBU conclusions and summary. Lakartidningen. 2003;100(45):3590-5.
47.How can osteoporosis be prevented? Medscape; 2005 (abstract).
48.Lane JM, Garfin SR, Sherman PJ, Poyton AR. Medical management of osteoporosis. Instr Course Lect. 2003;52:785-9.
Medline
49.Mora S, Gilsanz Y. Establishment of peak bone mass. Endocrinol Metab Clin North Am. 2003;32(1):39-63.
Medline
50.Passeri G, Passeri M. Clinical surveillance of osteoporotic patients Recenti Prog Med. 2003;94(5):211-6.
51.Wed GS, Jackson JL, Hatzigeorgion C, Tofferi JK. Osteoporosis management in the new millennium. Prim Care. 2003; 30(4):711-41, VI-VII.
Medline
52.Kessenich C. An approach to postmenopausal osteoporosis treatment: a case study review. J Am Acad Nurse Pract. 2003; 15(12):539-45.
53.Imanishi Y, Nishizawa Y. The effect of lifestyle factors on osteoporotic fractures. Clin Calcium. 2004;14(2):298-301.
Medline
54.Chilibeck PD. Exercise and estrogens or estrogen alternatives (phytoestrogens, bisphosphonates) for preservation of bone mineral in postmenopausal women. Can J Appl Physiol. 2004; 10(2):70-4.
55.Wallace L, Boxall M, Riddick N. Influencing exercise and diet to prevent osteoporosis: lessons from three studies. Br J Community Nurse. 2004;9(3):102-9.
56.Dargent-Molina P. Epidemiology and risk factors for osteoporosis. Rev Med Interne. 2004;25 Suppl 5:S517-25.
57.Borer KT. Physical Activity in the prevention and amelioration of osteoporosis in women: interaction of mechanical, hormonal and dietary factors. The Physicians and Sports Medicine. 2005;35(9):779-830.
58.Kannus P, Uusi-Rasi K, Palvanen M, Parkkari J. Non-pharmacological means to prevent fractures among older adults. Ann Med. 2005;37(4):303-10.
Medline
59.Cassidv A. Diet and menopausal health. Nurs Stand. 2005; 19(50):67.
60.Yoshimura N. Intervention in lifestyle factors for the prevention of osteoporosis and osteoporotic fractures. Clin Calcium. 2005; 15(8):1399-408.
Medline
61.Ishiwaka-Takata K, Ohta T. Nonpharmacological prevention and treatment for osteoporosis. Clin Calcium. 2005;15(9): 1463-6.
Medline
62.Wilkins CH, Birge SJ. Prevention of osteoporotic fractures in the elderly. Am J Med. 2005;118(11):1190-5.
63.Beck BR, Snow CM. Bone Health across the lifespan­exercising our options. Exercise Sport Science Revist. 2003;31(3): 117-22.
64.Warren MP, Goodman LR. Exercise induced endocrine pathologies. J Endocrinol Invest. 2003;26(9):873-8.
Medline
65.Prather H, Hunt D. Issues unique to the female runner. Phys Med Rehabil Clin North Am. 2005;16(3):691-709.
66.Medscape. Aquatic and land exercise improve balance, function in older women with osteoporosis. 2003 (abstract).
67.Peña Arrebola A. Efectos del ejercicio sobre la masa ósea y la osteoporosis. Doyma. 2003;37(6):339-53.
68.Warden SJ, Fuchs RK, Turner CH. Osteoporotic patient rehabilitation. The Physician and Sports Medicine. 2004;40(3):223.
69.Lynn A, Kohlmeier MD. Osteoporosis; Risk factors, screening and treatment. Medscape; 2005 (abstract).
70.Female osteoporosis: Taking regular exercise constitutes good advice. Drugs and Therapy Perspectives; 1999 (abstract).
71.Tamaki H, Sun L, Ohta Y, Katsuyama N, Ishimary T, Chinen I. Running inhibits osteoporosis induced by protein-deficient (PD) food intake Biosci Biotechnol Biochem ISBA. 2004; 68(7):1578-80.
72.Asikainen TM, Kukkonen-Harjula K, Miilunpalo S. Exercise for health for early postmenopausal women: a systematic review of randomised controlled trials. The Physician and Sports Medicine. 2004;34(11):753-78.
73.Kelley GA, Kelley KS. Efficacy of resistance on lumbar spine and femoral neck bone mineral density in premenopausal women: a meta-analysis of individual patient data. Journal of Women's Health. 2004;13(3):293-300.
Medline
74.Barclay L, Lie D. Exercise program improves osteoporosis. Archives of Internal Medicine. 2004;161:1047-8, 1084-91.
Medline
75.Kemper HC.G, Wolff I, Croonenborg JJV. Can exercise prevent osteoporosis in postmenopausal women? Meta-analysis of (R)CT's on the effects of endurance and strength training on bone mass. The Cochrane Database of Systematic Reviews; 2004.
76.Bonaiuti D, Shea B, Lovine R, Cranny A, Welch V, Cagnana A, et al. Exercise therapy for osteoporosis in postmenopausal women. The Cochrane Database of Systematic Reviews; 2004.
77.Bonaiuti D. Exercise for preventing and treating osteoporosis in postmenopausal women. Medscape 2005; (abstract).
78.Bonaiuti D, Cranney A, Iovine R, Kremper HHC.G, Negrini S, Robinson VA, et al. Exercise for preventing and treating osteoporosis in postmenopausal women. The Cochrane Database of Systematic Reviews; 2005.
79.FCosman. The prevention and treatment of osteoporosis. A review Medscape; 2005.
80.Pagés Bolívar E, Climent Barrera JM, Iborra Urios J, Rodríguez-Piñeiro Durán M, Peña Arrebola A. Taichi, caídas y osteoporosis. Trainmed Com. 2005;39(5):230-45.