Mark Twain loathed exercise. “Whenever I get the urge to exercise,” he is said to have remarked, “I lie down until it goes away.” He did acknowledge that his approach was not right for everyone. Beyond the intended humor of his remarks, we now understand that complete inactivity has tremendously deleterious effects on the body, even for patients in intensive care units. Early mobilization of even the sickest hospitalized patients is now being undertaken to reduce the high rates of fatigue, muscle weakness, and tachycardia after severe critical illness . The ability to tolerate exercise is a key component of good health, and few would argue with the observation that regular exercise is an important part of a healthy lifestyle. But there is a paradox about exercise for those with chronic fatigue syndrome (CFS). While most studies show a modest benefit of graded increases in exercise on CFS symptoms (at least for those healthy enough to participate in the studies), a defining feature of the illness is worsening of fatigue and other symptoms after activity. For many with CFS, especially those who have more severe impairment, a major challenge is to find a way to bridge the gap between their post-exertional worsening of symptoms and being able to tolerate the kinds of activities that common sense and the available evidence tell us should be helpful.
Over the past 20 years, we have tried to bridge that gap, first by using treatments directed at orthostatic intolerance in those with CFS to help improve exercise tolerance and activity. In our early work, patients improved after treatment with medications like fludrocortisone, beta-blockers, and midodrine, noting that they felt better and then began to tolerate exercise, usually not vice versa. That approach, however, has not been universally helpful, prompting a search for additional ways to improve function in our patients.
In the last decade, a series of observations has helped us develop a new approach that derives from advances in neurophysiology and the fields of physical therapy and osteopathic medicine. Manual treatment methods developed in Australia by Robert Elvey, P.T., and David Butler, P.T., and by Jean-Pierre Barral, D.O., and Alain Croibier, D.O. in France have formed the basis for much of our therapeutic intervention [2-5]. The observations from these individuals and from related literature have focused on nerve tissue as a source of spinal and limb pain and other related symptoms. While our research on this topic continues, we have been invited to sketch out the general concepts here.
The nervous system as a continuum
The nervous system is a continuum electrically, chemically, and mechanically—electrically by virtue of its conducting properties, chemically because of the method of communication at the junctions between two or more nerves in series, and, more importantly for our purposes, mechanically, due to the extensive connective tissue investment of each fiber in a series of fibers, and its blending with the connective tissue of other structures in the body . The nerve tissue of the brain and spinal cord constitutes the central nervous system. The nerve fibers found within the cranial nerves and the spinal nerves and their branches form the peripheral nervous system. Most peripheral nerves are mixed nerves, that is, they consist of various proportions of motor fibers to skeletal muscles such as the biceps or the abdominal muscles, and sensory fibers that convey information about touch, pressure, pain, proprioception (position sense), temperature, and vibration from the limbs, head, neck and body wall to the brain and spinal cord. Peripheral nerves may also contain another set of motor and sensory fibers called autonomic fibers that serve the smooth muscle in blood vessel walls throughout the body, including those of the skin. They also serve cardiac muscle and the smooth muscle in the walls of various hollow tubes and organs in the body, secretory glands such as sweat glands of the skin, and other structures.
Placing a mechanical strain on the peripheral nerves in the limbs and trunk can affect more distant tissues including the central nervous system tissue in the brain and spinal cord, and vice versa. This obviously is not a new concept. One of the oldest ways to assess for inflammation in the central nervous system is the straight leg raise test, during which the subject is lying flat on the examining table, and the leg is raised by the examiner. In those with meningitis, raising the legs exerts traction on the nerve roots and the dural membrane, the dense, outer connective tissue investment of the spinal cord and brain, resulting in neck pain.
In health, our bodies must be able to move freely and comfortably through extensive arcs of motion without provoking pain or other symptoms. As we move, our nervous system and its associated connective tissues must be capable of moving and functioning independently of potential restrictions imposed by other adjacent tissues and of the successive angular changes of the joints over which it passes. Similarly our bones, joints and muscles must be able to move into any position without excessively pulling on or compressing our nervous system. The brain and spinal cord and all the peripheral nerves and their coverings must be able to change lengths and slide freely throughout the body without symptoms and yet, regardless of position, be able to conduct electrical impulses properly to or from other parts of the nervous system as well as the skin, joints, muscles, body organs, and blood vessels.
Neural tension and neurodynamics
This interaction of nerve mechanics and nerve function has been termed neurodynamics. As an example of the principles of neurodynamics, the median nerve elongates approximately 20% as the upper extremity moves from a position of full wrist and elbow flexion to one of full wrist and elbow extension. If the median nerve loses the ability to adjust to angular changes at the joints—due to movement restrictions in tissues adjacent to the median nerve and its branches, or due to swelling or adhesions within the median nerve itself—the result is an increase in mechanical tension within the nerve or within its connective tissue. This adverse neural tension, in turn, is thought to contribute to pain and other symptoms through mechanical sensitization and altered pain signaling, altered proprioception (positional sense), adverse patterns of muscle recruitment and force of muscle contraction, reduced blood flow within the nerve, and release of inflammatory neuropeptides. Nerve endings which are in and around the coverings of the nerves cause reflex behaviors to manifest in the tissues innervated by those nerves. Most commonly, muscles crossing joints where the nerve is abnormally tensioned will reflexly shorten or guard. On careful clinical examination by experienced clinicians, the muscles will appear firm, tense, and can be tender to deep touch. These muscles will lose their extensibility and may contribute to reduced joint mobility. The range of motion of those joints can become limited and they too can become tender to touch and lack resilience. The skin and underlying soft tissues that are served by the involved nerve will become restricted in their ability to glide, and will demonstrate temperature changes and changes in sweat activation. A person may feel very cold or may sweat profusely. These tissues will likewise lack resilience and will usually be tender to touch, even painful.
Certain “neural provocation maneuvers” can assess for adverse tension and other behaviors within the nervous system. Signs of altered neurodynamics include reduced joint range of motion, increased resting muscle tone, and increased pain sensation or hyperalgesia along the course of the involved nerve tissue. The most notable examples of these provocation maneuvers are the various passive straight leg raise tests, the upper limb tension (or neurodynamic) tests, and the seated slump test.
In the past, when our CFS patients had received an exercise-based treatment program by physical therapists, many would report that their symptoms had been made much worse, even though the activities selected and the intensity of the exercise program seemed otherwise quite suitable. In reality, it appeared to be a case of too much, too soon.
One insight into why this might have occurred was the observation that many of the symptoms experienced by people with CFS could be reproduced by selectively placing tension on the spinal cord and its coverings, or on certain nerves in the trunk, arms, and legs. We noted that fatigue, cognitive fogginess, light-headedness, nausea, reflux, sweating and flushing, many types of vision changes, headache, and other symptoms can be aggravated, or in many cases eased, by changing the way tension is applied to or removed from nerves in the body. In CFS patients with symptoms that had not responded as completely as expected to medical treatment, these nerve tensions appeared to contribute to the persistent symptoms.
As an illustration of the potential for neurodynamic abnormalities to provoke symptoms, two young adult males with CFS were placed supine and a sustained passive straight leg raise (SLR) was performed. A therapist held one leg elevated in SLR at 10° of hip flexion for two minutes and then raised it to 20° for two minutes, adding 10° incremental increases in SLR every 2 minutes until the 12 minute point, at which time the leg was returned to the horizontal plane. The Figure shows symptom responses to this maneuver in one subject:
Although blood pressure, heart rate, skin temperature, and pulse oximetry did not change over the 12 minutes, both subjects became progressively more symptomatic, and by the end of 12 minutes, they were having difficulty answering basic questions. They remained sluggish and more fatigued than usual for 12-24 hours. Notably, this supine neuromuscular strain provoked lightheadedness, a symptom usually observed with individuals upright, even though more blood should have returned to the heart from raising the leg. We also noted increased fatigue and cognitive disturbance, in a pattern entirely consistent with their daily symptoms. Such severe responses do not occur in all CFS subjects, but the changes experienced by these young men illustrate the concept. Thus far, very little work has documented the typical extent of neural tension and neurodynamic abnormalities in CFS.
We have not yet published formal studies, but our physical therapy colleagues find that there are many common abnormalities on the physical exam in persons with CFS. Most obvious is a stiff upper and middle thoracic spine with rounded shoulders and a forward head. Patients find that it is difficult to straighten up and tuck the chin. The rib cage is often very tight, and rotational range of motion is markedly limited. Pressure on the rib cage can give rise to diverse symptoms including vision changes, lightheadedness (to the point of near-fainting) and other autonomic nervous system sensations. These and the various neural provocation tests are not maneuvers typically performed by physicians, and often had been missed in the past when a more conventional medical examination was performed.
What about joint hypermobility? We have noticed that as many as two-thirds of adolescents with CFS have increased mobility of the joints, and first noted that there was an increased prevalence of Ehlers-Danlos syndrome, a heritable form of joint hypermobility, among those with CFS. Do those with hypermobile joints also have neurodynamic dysfunctions? Our clinical experience has been that this is the case, possibly because nerves are exposed to greater mechanical tension as they traverse hypermobile joints, and possibly because the ligamentous laxity leads to greater instability or excessive motion of the spine. While treatment of those with hypermobility needs to avoid increasing the mobility of the joints, treating altered neurodynamics, postural dysfunctions in the spine, and soft tissue dysfunctions has seemed to provide symptomatic benefit.
In Part 2 of this two-part article we will describe our current research to better understand how manual therapy in CFS can help explain features of the condition and contribute to clinical improvements for CFS patients.
Peter C. Rowe, M.D., is professor of pediatrics at Johns Hopkins Children’s Center where he directs the Chronic Fatigue Clinic. Kevin R. Fontaine, Ph.D., is a professor at University of Alabama at Birmingham; and Richard L. Violand, Jr., is a physical therapist in private practice at Violand and McNerney Physical Therapists, in Ellicott, MD. Dr. Rowe’s research project, “Neuromuscular Strain in CFS,” is being funded by the Solve ME/CFS Initiative under its Research Institute Without Walls. Dr. Rowe was part of a Johns Hopkins team that was the first to identify orthostatic intolerance as a key feature of CFS. He has cared for CFS patients in his medical practice and conducted research on CFS for nearly 20 years.
1. Needham DM. Mobilizing patients in the intensive care unit: improving neuromuscular weakness and physical function. JAMA 2008;300:1685- 90.
2. Elvey RL. Physical evaluation of the peripheral nervous system in disorders of pain and dysfunction. J Hand Therapy 1997;10:122-9.
3. ButlerDS. Mobilisation of the nervous system. London:Churchill-Livingstone, 1999.
4. Walsh MT. Interventions in the disturbances in the motor and sensory environment.J Hand Therapy 2012;25:202-19.
5. Barral J-P, Croibier A. Manual therapy for the peripheral nerves. London: Churchill-Livingstone, 2007.
6. Barral J-P, Croibier A. Visceral vascular manipulations. London: Churchill-Livingstone, 2011.
“Seated Slump Test Testing Procedure” figure reprinted with permission from J. Walsh from Walsh J, Flatley, M, Johnson N, Bennett K. Slump test: sensory responses in asymptomatic subjects. J Man Manip Ther; 2007; 15(4): 231-238. Link: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2565641/
“Upper Limb Neural Tension Testing” figure reprinted with permission from Walsh MT. Upper limb neural tension testing and mobilization. Journal of Hand Therapy; 2005; 9(2): 241–258. Link: http://www.sciencedirect.com/science/article/pii/S0894113005000505