The intervertebral discs undergo more dramatic alterations with age than any other musculoskeletal soft tissue structure or component of spine. All discs eventually develop similar changes, but within the same person and among persons they vary in rate and extent. In particular, in one person degeneration of one or more discs advances more rapidly than other discs or in the discs of other persons on the same age. (1) Degenerative disc disease most frequently involves the C5-6, C6-7, and C4-5 motion segments, in decreasing order of occurrence. (2) The age-related alterations in disc tissue after skeletal maturity appear to decrease structural integrity of the disc and thereby contribute to changes in disc volume and shape and the increased probability of disc herniation. (1,3)
Mechanisms leading to the diffuse bulging and a decrease in the disc height include declining nutrition, decreasing proteoglycan and water concentration, and fatigue failure of the matrix. Associated changes occur in the vertebral endplate. Sclerosis and reduced number of vascular communications between marrow space of the vertebral body and the intervertebral disc are also observed. Decreased disc height, declined elasticity, and fissures of annulus fibers may lead to segmental laxity. (1,3)
Segmental spinal hypermobility results in when passive and active dynamic stabilizers are not able to control segmental motions allowing excessive tilting or more often shearing to take place. Disc degeneration has an important role in this process. Cuts and tears in annulus layers allow nucleus material to occupy larger area. Internal changes of annulus and nucleus result in nucleus to loose its ball like form and to flatten out as to a shape of a pancake. These changes are decreasing the height of the disc letting vertebral bodies to get closer to each other. The disc is losing its ability, as an important intervertebral stabilizing structure, to stabilize a movement segment. This allows increased shearing movement between vertebrae that may over stretch ligaments creating receptor disturbance. Receptor disturbance, tissue overload and effects of gravity may “shut down” deep muscles in and around hypermobile movement segment. This results in progressively increasing muscle imbalance between phasic and tonic muscles leading to poor posture and disturbed movement patterns. These changes are leading to even further tissue load in the hypermobile movement segment enhancing its degeneration. (3,4) Osteophyte formation, arthritis of facet joints and joints of Luschka, and thickening of ligamentum flavum often occurs. (3)
Soft disc herniation or hard disc degeneration may irritate cervical nerve mechanically or chemically. (2,3,5) Several studies have demonstrated that the nucleus pulposus has strong inflammatogenic properties. It has shown to produce intraleukin-1 α, which increases prostaglandin E2 production; to increase local vascular permeability; to create ischemic injury of nerve roots exposed; and to produce expansion of the Schwann cell cytoplasm and intracellular edema in nerve fibers with normal axons. (6,7,8,9) Therefore, mechanisms other than mechanical pressure alone may often be involved in producing inflammation resulting in cervical nerve irritation. A discogram could be a means of demonstrating the clinical existence of a nuclear leak through the annulus fibrosus.
On that account, is it time to challenge the traditional clinical thinking that nerve irritation is resulted from constant compression of neural tissues and to promote the idea of chemical irritation as a primary reason to cause cervical nerve irritation. In my opinion this ”chemical thinking” should not stop just to nucleus pulposus leakage, but to continue into an occasional mechanical irritation resulting in a chemical reaction. This could often be a case with the degenerative disc with decreased stability but without direct chemical leak of nucleus material. Segmental dysfunction, muscle imbalance, poor posture, and disturbed movement patterns are increasing the possibility to this kind of cervical nerve irritation.
Irritation of cervical nerve and nerve root could alter local circulation including intraneural microcirculation, intrude on axonal transport system, disturb excitation and conduction, and produce pain and sensory changes. The role of the axonal transportation in the maintenance of the plasticity of the nervous system and health of the innervated tissues is often forgotten. This axonal transport system is bi-directional. Through the antegrade transport system materials produced in the cell body are transported along the axon to the tissues innervated. This is essential for their development, growth and very survival. Any factor that causes derangement of transport mechanisms in the axon or that alters the quality or quantity of the axonally transported substances could cause trophic influences to become adverse and detrimental. This in turn would produce aberrations of structure, function, and metabolism, thereby contributing to dysfunction and disease. Retrograde transport from target tissues to the cell body carries messages about the status of the axon, the synapse and the general environment around the synapse, including target tissues. If the retrograde flow is altered by physical constriction or from loss of blood flow, nerve cell reactions are induced. (10,11)
Radicular pain varies from a deep, aching pain to sharp superimposed on a dull, aching background. It is often common for radicular pain to be felt proximally and sensory changes to be felt distally. (5) Pain from cervical nerve irritation is not just dermatomal, but often myotomal, sclerotomal, or some combination thereof. (2,12) The fact that the pain do not follow a particular dermatome map, does not exclude the existence of a symptomatic nerve root. Motor deficit, change in deep tendon reflexes, and sensory changes may or may not be present in the case of cervical nerve irritation. (2,3) And because of the cervical movements are not always capable of reproducing the radiating symptoms, traditional clinical testing is not comprehensive enough to detect cervical nerve irritation. However, direct palpation or mechanical pressure over the exiting nerve root provokes patient’s radiating symptoms. Radicular pain is also exacerbated by any maneuver that stretches the involved nerve root. (2,3) Arm movements that increase tension of the affected nerve and nerve root are easy way to provoke the symptom.
Pain in the shoulder could be difficult to differentiate from that of cervical nerve root origin. Pain provoked by active arm abduction and felt only in the shoulder is too often concluded to originate in the shoulder structures. However, careful examination would often demonstrate an irritated cervical nerve root. Testing of the cervical nerve irritation should include nerve tension and movement testing, cervical nerve root palpation, specific traction test, and neurological tests. The neural tension tests introduced by R.L. Elvey is performed with patient lying supine on an examination table with the head and neck supported in a resting position and the shoulder girdle comfortably supported by the table. (13) David Butler begins his upper limb tension testing with shoulder girdle depression creating movements to all of the shoulder structures. (10) However, based on my experience, the successful differentiation testing between shoulder structures and cervical nerve irritation utilizing nerve tension tests should be done just out of symptomatic arm position and without movement of the glenohumeral or shoulder girdle tissues.
Therefore, I propose that nerve tension tests should be done using the defined symptomatic movement or position. Patient moves arm towards symptomatic direction into the starting symptoms. At the point of the minimal symptoms, the extremity is supported by therapist and minimal movement away from symptoms is performed to relief or to decrease patient’s symptoms. Passive movement in and out of symptoms, or in the case of constant symptoms, to increasing / decreasing symptoms may be repeated in order to find the final testing position just out of the symptoms or just out of the increasing symptoms. Tightening up one peripheral nerve at the time increasing the tension from distal end using forearm and wrist movements increases tension of selected neural structures. Movement is continued till the symptoms are provoked or the end of range of motion is reached. Neural tissues are then tighten up proximally by the neck flexion or side bending to increasing symptoms / to maximal tension tolerated. The nerve tension test is positive if the test of any one of the peripheral nerves provokes the symptoms patient was initially complaining of. This indicates that patient’s symptoms are coming from of neural structures. To differentiate between the neural irritation with or without entrapment/ adhesion the nerve movement tests are performed. (4)
Cervical nerve root palpation enables localization of the irritated cervical nerve root. Medial-caudal pressure on the top of the distal end of transversal processes above the nerve root is used to provoke patient’s symptoms. The cervical spine nerve root palpation defines the level of the specific manual traction test. Segmental axial traction is applied to decrease patient’s symptoms. Test is performed in the most comfortable neck position arm in minimal symptom position created by the tension of the affected nerve. Three-dimensional positioning is used to find the most effective position to alleviate patient’s symptoms. Alleviation of the patient’s symptoms confirms that the neural irritation is the origin of the symptoms and indicates that the intermittent three-dimensional pre-positioned axial manual traction should be used for successful treatment results. Neuromuscular tests should be done to assess the strength of the key muscles, possible sensory changes, and changes in deep tendon reflexes. (4)
Although neural mechanisms underlying manual cervical traction are traditionally linked to joint receptors, review of the literature suggests that stretch generated in cervical muscles and skin has the potential to influence the excitability of α-motoneurons. (14) On the other hand repeated cervical retractions has shown to alter H reflex amplitude and to be effective reducing radicular pain causing immediate reduction or relief. (15) Manual intermittent traction results in the same effect. On a daily basis I see how patients’ symptoms are decreased, pain centralized, movement of the pain free nerve tension test movement increased and functional ability enhanced by simple treatment of gentle intermittent manual traction and pain free neural gliding.
The mechanisms underlying these positive changes are not well understood. Facilitative movements are probably increasing nutrition and circulation bringing more oxygen to the tissues, pushing and pulling fluids in and out of tissues, alternating internal tissue pressure, activating mechanoreceptors to modulate pain and muscle tension, and facilitating axonal transportation. Further research is needed to fully understand the mechanisms involved. However, increasing number of studies and excellent clinical treatment outcomes are supporting this experimental assessment and treatment model.
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