Erik Dalton, PhD

As discussed in earlier e-newsletters and in newly-released articles on my website, the “joint receptor concept” attempts to override the idea that pain is primarily a consequence of “pinched nerves” that could ultimately be freed by removing bony obstructions. Many manual therapists and neurophysiologists now believe that restoration of proper postural alignment and range of motion successfully reduces pain by encouraging normal functioning of 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. This will eventually inhibit the chemical activation of pain at the site of its peripheral stimulation.


Pinched Nerves, Sensory Receptors and Joint Pain

If not pinched nerves–where is the pain coming from? Many manual therapists still view pinched nerve pain as emanating from “bones out of place” that if returned to their proper position, will reduce painful drag on the spinal nerve root. Misaligned bones (facet joints stuck open or closed) such as those shown in Figure 1 are definitely a major concern, but nerve root occlusion does not appear to be the primary factor leading to the client’s pain and dysfunction. As new alternatives to the pain puzzle have surfaced due to scientific advances in nerve-staining techniques, imino-histochemistry and histologic sectioning, researchers are able to dig deeper into the neurological complexities of myoskeletal innervation.

facet joints

Figure 1. The facet joints on the left demonstrate a person in a normal upright position. Note how the facets have not completely approximated their inferior neighbors. This free movement between joint surfaces is termed “joint-play”. In the figure on the right, the superior vertebra is attempting to glide forward on its inferior neighbor (spinal flexion) but the right facets don’t want to open which causes the top transverse process to rotate posteriorly. Mechanoreceptors embedded in joint capsules, spinal ligaments, intervertebral discs and the deep transversospinalis muscles become aroused when normal flexion and extension movements are disrupted. They immediately bombard the spinal cord with proprioceptive information regarding changes in the joint’s axis of rotation and center of gravity. Prolonged joint misalignment leads to protective spasm as seen in the short right intertransversaria.

Open-Minded Holistic Approach

To understand the neuropathophysiology of joint misalignment and the pinched nerve theory, one needs to look more closely at the innervation of all spine-related structures….not just the nerve root. Nociceptors and mechanoreceptors are the primary sensory receptors that innervate spinal tissues such as joint capsules, ligaments, intervertebral discs, tendons, muscles, fasciae, bone, and blood vessels. Always remember that the predominant receptor is the nociceptor–especially in context that more than 90 percent of joint innervation is nociceptive. These theories were originally determined by animal studies, 1 then confirmed in studies with human spinal joint capsules. 2

The fact that there is a relative scarcity of mechanoreceptor innervation of joint capsules and spinal ligaments compared to nociceptive innervation should lead pain management therapists into further study of the nature of nociception. Since there is less nociceptive innervation of the muscular system than other joint-related tissues, today’s manual therapist must begin thinking outside the traditional “muscle-pain, trigger point, fibromyalgia” box and include soft tissue techniques which focus on restoring joint-play through proper myoskeletal alignment. According to John Mennell, M.D., all the body’s synovial joints must have at least 1/8th inch of movement not directly controlled by voluntary muscle contraction. The term “joint-play” was coined to describe this fundamental rule essential for normal, pain-free, non-restricted movement of each vertebral segment. 3 Deep tissue myoskeletal techniques focus on breaking reflexogenic pain/spasm/pain cycles caused by loss of joint-play.


Are we designed to experience joint pain?

Compared with nociceptors, significantly fewer mechanoreceptive afferents leave our joints. This heavy concentration of nociceptive fibers in joints suggests that humans are basically built to experience joint pain; which bears itself clinically when considering how many people suffer joint-related neck and back pain during their lifetime.

If asked why back pain is so common, the therapist must state the simple truth: spine-related tissues are densely populated with nerve receptors designed to deliver pain signals warning of possible tissue damage due to overuse, misuse and abuse. It only makes sense that Mother Nature would place the greatest number of damage-detecting nociceptors in and around vital structures that house the spinal cord and nerve roots.

Clearly, the afferent innervation of the spinal joint complex favors nociceptive receptors. At this point, readers should appreciate that nociceptors are not always pain-generators and nociception does not always equate with pain. This misinterpretation is common throughout the extent of health care professions, as texts such as Guyton’s Physiology use “pain receptor” and “nociceptor” interchangeably.

When they die…they’re done?

Nociceptors may be activated by tissue injury and the chemical mediators that cause inflammation while mechanoreceptors are primarily stimulated by normal movements. Joint misalignment that leads to sustained compressional loading in joint capsules, spinal ligaments and intervertebral discs initially causes an increased rate of mechanoreceptive firing into the spinal cord. However, prolonged compression combined with the natural process of aging, produces reduced mechanoreceptive activity. As large diameter mechanoreceptors die off, they can’t inhibit the small diameter unmyelinated nociceptive free nerve endings (Fig. 2). The result is more pain. Bottom line: As we age, we lose mechanoreceptors (some permanently) and, thus, experience more pain.

dowagers hump

Figure 2. A common finding in clients presenting with a Dowager’s hump is C-7 forward-bent on T-1. As C-7’s facets glide forward, they often get stuck there. In time, large-diameter (dynamic) mechanoreceptors such as the Pacinian corpuscle (located deep in joint capsules and ligaments) sense the loss of normal motion which results in a decrease in normal mechanoreceptive input. Prolonged loss of mechanoreceptor input (due to joint dysfunction) allows the tiny nociceptors (free nerve endings shown above) to squeeze through and fast-track information to the thalamus (the brain’s sorting and switching station). The thalamus routes the information to three areas of the cortex (sensing, thinking & feeling) for interpretation. Usually the brain reacts by developing pain syndromes and nociceptive reflexes that alter myoskeletal tone and up-regulate the sympathetic nervous system. Pain/spasm/pain cycles begin as the brain layers the cervicothoracic junction with protective muscle guarding to protect vital neural and vascular structures. These “Catch 22” cycles can only be broken by manually restoring balance and symmetry to all spine-related tissues, correcting the forward head posture and closing the C7-T1 facets. As normal mechanoreceptive flow returns, nociceptive pain is blocked (gated). The brain sensing that everything is now OK releases the protective muscle guarding.

Regrettably, nociceptors and mechanoreceptors cannot be seen.

Although spinal nerves travel through small intervertebral foraminal 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. Researchers suggest that only 10 to 15% of spine related problems are caused by direct pressure of bone on nerve tissue. Clients with this type of nerve occlusion usually report numbness, burning or a “pins and needles” feeling.

More frequently, nerve roots become agitated from prolonged exposure to chemical or mechanical irritation. This condition develops slowly as the nerve’s dural sheath is rubbed, scraped or over-stretched. However, when such neurocompression does exist, referrals should be made to appropriate medical professionals for an orthopedic work-up. Nerve-stretching techniques developed by David Butler 4 are sometimes helpful in releasing slightly-restricted neural structures. Contraindications for nerve mobilization techniques include irritable conditions, inflammation, spinal cord signs, malignancy, severe nerve root compression, peripheral neuropathy, and complex regional pain syndromes. As with all manual therapy procedures, the goal remains the same: “To restore maximal pain-free movement within postural balance”.

What makes the bone-on-nerve or foot-on-the-hose “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.

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


  1. McLain RF. Mechanoreceptor endings in human cervical facet joints. Spine 1994; 19:495-501.

  2. Burt AM. Textbook of Neuroanatomy. Philadelphia: WB Saunders; 1993:p.311.

  3. Mennell, J MCM. Joint Pain. Boston, Little Brown & Company., 1964.

  4. Butler D. Mobilization of the Nervous System, 1995, Churchill Livingstone

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