The Progression of Cervical Stenosis Toward Cervical Spondylotic Myelopathy(CMS)
By Dale G. Alexander
LMT, MA, PhD
The Progression of Cervical Stenosis Toward Cervical Spondylotic Myelopathy(CMS)
By Dale G. Alexander
LMT, MA, PhD
In my previous article you were invited to consider the following points regarding the potential for cervical stenosis to progress toward cervical spondylotic myelopathy (CMS):
- There is a relationship between upper- and lower-extremity somatic difficulties mediated by the cervical reflex arc of C5-6.
- Cervical stenosis (narrowing of the spinal canal) progressing toward CMS may underlie many of the chronic somatic complaints our clients bring to us.1
- The prevalence of this progression is estimated to express itself functionally in approximately 80 percent of the general population over 55 years of age.
- Becoming familiar with the early indications of this progression may assist us in making timely referrals of our clients for appropriate medical testing, especially encouraging consideration of a cervical MRI.1
This article expands on the clinical indications with which we need to become more familiar, the theories that exist describing why and how this progression may occur, and some hands-on suggestions for what I have found to be effective in assisting clients exhibiting the early and moderate stages of the progression of CMS.
However, at a certain point in this pathological progression, surgery does appear to be the best remedy. I have worked with two clients who needed surgery for advanced CMS, with positive results. I was unable to stem the tide for both of them. My best efforts and all the research I have done failed to prevent its progression. Many other clients have now identified this progression and are proactively adjusting their lives with common sense and grace to maintain their quality of life. They have been my teachers.
Let's begin by further elaborating the many possible somatic indications that might highlight this progression. The number-one tipoff to my sensibilities is when a client presents with a history of same-sided somatic complaints of the neck, and upper- and lower-extremity pain or dysfunction, including sciatica. The possible somatic combinations are quite varied. When the pain or dysfunction is on the same side, this is my clinical flag. Another subtle clue a client might not volunteer is occasional or frequent urgency or difficulty with urination.
Just today, a client (an orthopedist specializing in knees, shoulders, and sports medicine) who underwent surgery for CMS recounted that his fellow spinal surgeons have suggested to him that when an individual experiences an inability to stop their urinary stream, this is one of the reliable indicators the progression of CMS has become clinically significant.2 The following paragraphs offer three different sets of symptomatic indicators that might trigger your perceptions as to the varied functional expressions of this progression.
One medical journal article offers the following concise description of CMS: "Patients will generally report neck stiffness, a unilateral or bilateral deep aching of the neck, arm or shoulder and possibly stiffness or clumsiness while walking. CMS usually develops insidiously. Other common complaints include crepitus in the neck with movement, occasional stabbing pain into the arm, elbow, wrist, or fingers or report a dull achy feeling into the arm with intermittent numbness or tingling into the hands. The hallmark symptom of CMS is weakness or stiffness in the legs. Patients with CMS also might present unsteadiness of gait. Weakness or clumsiness of the hands in conjunction with the legs also is characteristic of CMS. Loss of sphincter control or frank incontinence is rare, however, some patients complain of slight hesitancy on urination."3
Another medical article references the following additional symptoms:
Myelopathy is distinguished from the many forms of radicular pain in that the discomfort is more generalized and doesn't necessarily follow the established, generally accepted sensory and motor maps for dermatomes (skin) and myotomes (muscles).
Finally, another medical article references the typical symptoms in yet a different fashion:
- weakness, numbness or clumsiness of the upper extremities (arms, hands, fingers);
- altered walking ability, perceived as poor balance, weakness, heaviness or numbness in the legs; and
- variable degrees of radicular arm pain.
Alhough CMS is painless in more than 50 percent of patients, when pain is present, it might be described as a stabbing, burning sensation or a persistent dull ache radiating throughout the arms to the forearms. At times, the pain will extend into the fingers, associated with "pins and needles" paresthesias. Patients often comment about dropping objects accidentally or having trouble fastening their clothes. If prolonged, there might be associated muscle wasting and overt loss of sensation to vibration, pinprick sensation, pain and thermal sensation. As the impairment to spinal cord function progresses, both legs weaken and become progressively spastic. Bowel and bladder control subsequently may be altered. In advanced cases, gait will become progressively more difficult without aid by a cane or walker.5
The above descriptions reflect some of my own somatic complaints. You may find they describe some of yours as well. Let's be real. A fair number of us within our profession are going to be part of that 80 percent of the population who experience somatic complaints of this progression. Some of these indications began popping up for me in my mid-30s, whereas now, at age 55, I experience them more often. To the best of my memory, the occasional clumsiness in my general balance was the first indication to attract my attention at about age 35. Admittedly, my accumulated trauma history is well beyond the average and yes, I have scheduled a cervical MRI.
Obviously, these identical somatic complaints might be indications of other forms of pathological progressions. I have listed these in the Appendix for your further consideration. More acute presentations of CMS often include visual disturbances and bilateral pain symptoms, similar to the early and moderate stages of multiple sclerosis.2
We all know our role as massage therapists is not to diagnose anything, but rather to encourage our clients to seek medical attention that might provide them with the timely opportunity to make appropriate lifestyle or medical choices. We are part of our clients' early detection and prevention team. Aging occurs within all of us and injury strikes some of us. Not everyone is dealt an equal hand in the genetic shuffle of the cards. Early detection and prevention are our best hedges to maintain quality of life.
According to Rene Calliet, MD, cervical spondylotic myelopathy (CMS) was distinguished from myelopathy in 1956, based on the presence of acute disk prolapse. The principal pathology is encroachment of bony protrusion(s) into the spinal canal, the intervertebral foramen or foraminae, or both. The resulting encroachment might apply direct pressure to the spinal cord itself and/or to one or both of the exiting spinal nerves.6
Let's now review the general theories offered to explain how the progression of CMS might occur. Most common among the references I have gathered is the notion of a congenitally narrow spinal canal. Such a diminished diameter for the spinal cord accentuates the probability of eventual stenosis and myelopathy, and hastens its clinical expression.
The second most offered theory, which builds on the first, is that nearly all of us eventually develop some degree of arthritis (spondylosis) between our cervical vertebrae, most commonly between the C4-7 levels of the spinal cord. Such spondylosis often is accompanied by varying degrees of osteophyte/spur formation, disc thinning and desiccation, disc protrusions/herniations, vertebral remodeling, and compression of the foraminal openings through which the spinal nerves deliver their electrochemical vitalization to their somatic and visceral end organs.
The third most cited reason for this central compression of the spinal cord is related to traumatic cranial/cervical events with their resulting vertebral subluxations and scar-tissue formation. The effects of wear and tear of repetitive head/neck movements also are cited as contributing to and hastening the clinical expression of symptoms.
Additionally, the thickening of the ligaments surrounding the spinal canal, including the pleating of the ligamentum flavum and the ossification of the anterior or posterior ligaments, is proposed as a contributor to spinal cord compression. The latter notion of ossification of the posterior longitudinal ligament has a particular designation of OPLL and more often is appreciated in the non-Asian population.5,6
Vascular insufficiency and edema also are considered part of the degenerative progression, usually thought to be associated with this fibrosis of ligaments, as they might affect the anterior and posterior spinal arteries that supply the spinal cord.7
All of these notions have obvious merit and make sense logically, yet, in my opinion, there seem to be missing pieces of the puzzle. It is a "both/and" rather than an "either/or." Not a right or wrong. The body is both complex and quite simple, simultaneously. In my experience, there rarely is a singular causative agent in chronic somatic profiles. Rather, there are multiple streams flowing into a river of unrelenting somatic expression. My next article will propose some additional streams I believe also contribute to the progression of CMS.
Clinically, what has made the most sense to me is that most of our internal visceral organs are anatomically suspended forward and down from the spine and cranium. I owe a debt of gratitude to Dr. Jean Pierre Barral, DO, the developer of visceral manipulation, and to Jon Zahourek, the developer of the manikin style of anatomy study, for illuminating this elegantly simple aspect of human anatomy.8,9
Thus, what I have consistently observed is that relieving the forward and downward pull of the head and neck upon the trunk can assist clients. This might be accomplished by releasing the tensions associated with the suspension of the viscera themselves and by attending to the musculoskeletal flexor muscles, especially those whose attachments span from the posterior aspect of the body to an anterior mooring.
I would encourage you, by whatever style of bodywork and massage is your training base, to release the tension and enhance the fascial ease of the SCMs, the scalenes, the longus colli, the muscles of the jaw, the subclavius muscles, the pectoralis minor muscles, both sides of the diaphragm muscle, the rectus abdominus, the iliopsoas muscles, the piriformis muscles and the rectus femoris muscles, and to enhance the range of motion of your clients' ankles.
Releasing any existing tension of muscular contracture and enhancing the fascial ease of these flexor muscles will reduce the forward and downward pressure on the neck, and will soften the need for the extensor musculature of the posterior neck and upper back to develop varying states of contracture or spasm. Additionally, I recommend attending to the ease of the body's transverse diaphragms at C0-1/2, C7, T1-2, T12-L1 and L4-5/S1. It is through these transverse diaphragms that lymphatic and circulatory flow most often is impeded.10 Also, apply your experience and knowledge of enhancing blood flow to the cervical vertebrae. This is a significant approach through which we might offer some assistance. It is not about technique, per se, but rather where we place our attention and intention, mediated by the quality of our touch. Place your attention and intention inside the body. Work from the "inside-out."
Appendix: Conditions That Mimic Cervical Spondylotic Myelopathy on Presentation2
- Amyotrophic lateral sclerosis (Lou Gehrig's disease, a progressive neurodegenerative disease that affects nerve cells in the brain and the spinal cord).
- Extrinsic neoplasia (metastatic tumors).
- Hereditary spastic paraplegia (also called familial spastic paraplegia or Strumpell-Lorrain disease) is not a single disease, but rather a heterogeneous group of genetic disorders, the main feature of which is progressive spasticity in the lower limbs due to pyramidal tract dysfunction.
- Intrinsic neoplasia (tumors of spinal cord parenchyma).
- Multiple sclerosis (asymmetric paraparesis with sensory ataxia and hyper-reflexia).
- Normal-pressure hydrocephalus (cerebral spinal fluid congestion).
- Spinal cord infarction. (Spinal cord infarction is a stroke within either the spinal cord or the arteries that supply it. It is caused by arteriosclerosis or a thickening or closing of the major arteries to the spinal cord.)
- Syringomyelia (a condition in which fluid-filled cysts form within the spinal cord).
- Vitamin B12 deficiency (central to the body's ability to make new red blood cells).
- Rheumatoid arthritis and myelopathy (this condition usually afflicts the hands first).6
- Alexander DG. "The Progression of Cervical Stenosis Toward Cervical Spondylotic Myelopathy." Massage Today, April 2008.
- Dr. Kurt Chambless, MD, orthopedic surgeon.
- Young WF. Cervical spondylotic myelopathy: a common cause of spinal cord dysfunction in older persons. American Family Physicians, Sept. 1, 2000;62:5.
- Ullrich PF. "Cervical Stenosis With Myelopathy." www.spine-health.com.
- "Understanding Cervical Spondylotic Myelopathy," Thomas M. Wascher, MD, FACS. www.spine-health.com, Aug. 31, 2001.
- Calliet R. Neck and Arm Pain. F.A. Davis Company, 1988.
- Durrant DH, True JM. Myelopathy, Radiculopathy, and Peripheral Entrapment Syndromes. CRC Press LLC, 2002.
- Barral J-P. Visceral Manipulation I and II and Trauma. Eastland Press, 1988, and class notes from 1986-1993.
- Zahourek J. Atlas of Human Musculature in Clay, Books 1-5. Zahourek Systems Incorporated, 1995 and class notes from 1986-1991.
- CranioSacral Therapy courses with Dr. John Upledger, DO, and Dr. Richard MacDonald, DO, at the Upledger Institute, 1986-1991.