Category: Advanced

Terminology Update

The terminology pertaining to lumbar spinal disk herniations has been confusing, inconsistent, and contradictory. Consequently, in 2014, the North American Spine Society, the American Society of Spine Radiology, and the American Society of Neuroradiology convened a combined task force to agree upon the nomenclature. The results were published in the Spine Journal, and titled (1):

Lumbar Disc Nomenclature:
Version 2.0

    In summary, and based on CT or MRI imaging, a herniated lumbar spine intervertebral disk has four categories:

• Bulging Disk
• Protrusion Disk
• Extrusion Disk
• Sequestration Disk

The Normal Disk

The Bulging Disk

If any part of the annulus extends beyond the normal disc space, it is considered to be a bulging disk.

The Protrusion Disk

In the protrusion disk, the base of the displaced material is greater than the distance the disk material had moved towards the intervertebral foramen and/or the central neural canal.

The Extrusion Disk

In the extrusion disk, the greatest measure of the displaced disk material is greater than the measure of the base of the displaced material.

The Sequestration Disk

In the sequestration disk, the disk material has lost all connection with the original disk material.

••••••••••

    A disk herniation that compresses, irritates or inflames a single nerve root is called discogenic radiculopathy. Nerve root compression/irritation/inflammation can cause radiating leg pain down the course of the sciatic nerve. Consequently, this radiating leg pain is often referred to as sciatica. If this sciatica is initiated by the intervertebral disk, it is referred to as discogenic sciatica.

Technically, the sciatic nerve is made up of nerve roots L4, L5, S1, and as such a problem with any of these nerve roots can cause sciatica.

If the intervertebral disk is the cause of the nerve root compression/irritation/inflammation, the single most important clinical test is the straight-leg-raising test. While supine, the subject is asked to raise their straight leg as far as possible. Normally this causes the lower lumbar nerve roots to slide out of the intervertebral foramen by approximately ½ inch (12 mm). If the nerve root is compressed/irritated/inflamed, pain may start at about 30 degrees from the horizontal (2, from Kapandji).

Important questions pertaining to herniated lumbar intervertebral disc with radiculopathy/sciatica include:

• What are the typical presenting symptoms for patients suffering from discogenic radiculopathy/sciatica?
• What are the most important clinical tests for the patient with suspected discogenic radiculopathy/sciatica?
• Are spinal x-rays required or helpful in establishing the diagnosis of discogenic radiculopathy/sciatica?
• When is computed tomography (CT) and/or magnetic resonance imaging (MRI) advisable for a patient with suspected discogenic radiculopathy/sciatica?
• For how long is it advised and/or safe for the patient with discogenic radiculopathy/sciatica to have their signs and symptoms managed conservatively?
• How effective is conservative treatment for the discogenic radiculopathy/sciatica patient, as compared to surgical treatment?
• Is chiropractic spinal adjusting (specific manipulation) safe and effective for patients suffering from discogenic radiculopathy/sciatica?

The answers to many of these questions are thoroughly explored in an important article published May 5, 2016 in The New England Journal of Medicine, titled (3):

Herniated Lumbar Intervertebral Disk

    The authors are Richard A. Deyo, MD, MPH, and Sohail K Mirza, MD, MPH. Dr. Deyo is from the Oregon Institute of Occupational Health Sciences. A search of the United Stated National Library of Medicine (June 12, 2016) shows he is an author or contributing author to 378 indexed publications. Dr. Mirza if from the Department of Orthopedic Medicine, Dartmouth School of Medicine. A search of the United Stated National Library of Medicine (June 12, 2016) shows he is an author or contributing author to 87 indexed publications. These men are leading experts on the clinical guidelines pertaining to the lumbar spine and intervertebral disk syndromes.

In this article, Drs. Deyo and Mirza make the following points:

• 2/3 of adults have back pain at some time in their lives.
• 10% of adults have back pain that has spread below their knees within the previous 3 months. Often, the sciatica occurs with “no specific precipitating event.”
• “The prevalence of herniated disks as the cause of back and leg pain may be approximately 10% in primary care.”
• Lumbar radiculopathy refers specifically to pain and motor and sensory disturbances in a nerve-root distribution.
• “Disk herniation does not necessarily cause pain; MRI commonly shows herniated disks in asymptomatic persons.”
• Genetic factors related to the structure of collagen may predispose the disk to degeneration.
• Strenuous activity and smoking are environmental factors that increase the risk of disk herniation.
• “Disk-related radiculopathy is both a biochemical and a biomechanical process.” “Contact of the nucleus pulposus with a nerve root provokes inflammation that may be necessary for mechanical compression to cause pain.” This inflammatory component to radiculopathy is recognized, and anti-inflammatory therapy is proposed. [This is important as it indicates that some patients will benefit or perhaps require anti-inflammatory adjuncts in the management of their discogenic radiculopathy/sciatica].
• 95% of herniated disks occur between L4-L5 (L5 nerve root) and L5-S1 (S1 nerve root).“The L5 nerve root affects neither the Achilles tendon nor the patellar reflex and is one of the two most commonly affected nerve roots.” Consequently in a person with L5 radiculopathy, tendon reflexes may convey no information.
• A “massive midline disk herniation may compress the cauda equina, causing cauda equina syndrome.” Cauda Equina Syndrome symptoms include sciatica, motor weakness, urinary incontinence or retention, saddle anesthesia, and diminished anal sphincter tone. [Cauda Equina Syndrome is a surgical emergency].
• “Electromyography is usually unnecessary.”
• The use of opioid drugs should be limited to patients with severe pain and should be time limited from the outset because of the lack of evidence of benefit and the “growing concern regarding serious long-term adverse effects.”
• Glucocorticoid injections for lumbar herniation with radiculopathy shows no significant advantage over placebo for pain relief or reduced rate of subsequent surgical intervention, nor does it show an advantage with respect to improvement in physical function.
• “In patients with acute disk herniations, avoidance of prolonged inactivity in order to prevent debilitation is important.”
• Most patients with acute disk herniations “can be encouraged to stand and walk.”
• “The ability to sit comfortably is a sign of improvement in the patient’s condition” and suggests more structured exercise may begin.
• Lifestyle modifications, including smoking cessation, weight loss, and regular exercise may prevent sciatica or help reduce its recurrence.

What are the typical presenting symptoms for
patients suffering from discogenic radiculopathy/sciatica?

    Drs. Deyo and Mirza note that approximately 85% of patients with sciatica have a herniated intervertebral disk. Hence, sciatica is the single most important presenting symptom of discogenic radiculopathy/sciatica.

What are the most important clinical tests
for the patient with suspected discogenic radiculopathy/sciatica?

    Drs. Deyo and Mirza note that the majority of patients “with back and leg pain and a positive straight-leg-raising test suggests a herniated disk.” Straight-leg-raising is positive for nerve root compression if sciatica occurs by elevating the leg to between 30 and 70 degrees.

Other helpful tests include deep tendon reflexes, superficial sensation, myotomal strength, and Valsalva tests.

Are spinal x-rays required or helpful in establishing
the diagnosis of discogenic radiculopathy/sciatica?

    Spinal x-rays are not required or helpful in establishing the diagnosis of discogenic radiculopathy/sciatica. Spinal x-rays may show levels of disc degeneration of varying degrees, but are non-revealing as to the presence or type of disc herniation and compressive neuropathology. Spinal x-rays may show the presence of other complications to discogenic radiculopathy/sciatica, such as birth anomalies (tropism, lumbosacral transitional segments, scoliosis, leg length inequality, etc.) and/or acquired syndromes (degenerative osseous central canal stenosis, spondylolisthesis, fracture, etc.). Spinal x-ray may also show evidence of tumor and/or infection. As such, exposing spinal x-rays is dependent upon the clinical judgment of the provider.

When is computed tomography (CT) and/or magnetic resonance imaging (MRI) advisable for a patient with suspected discogenic radiculopathy/sciatica?

    Drs. Deyo and Mirza do not recommend routine use of CT or MRI because “on imaging, disk bulging is common among asymptomatic persons (in approximately 60% of persons at 50 years of age).” They state:

“CT or MRI is necessary only in a patient whose condition has not improved over 4 to 6 weeks with conservative treatment.”

“The use of CT or MRI should be discouraged unless the symptoms do not decrease over 4 to 6 weeks” of conservative treatment.

For how long is it advised and/or safe for
the patient with discogenic radiculopathy/sciatica
to have their signs and symptoms managed conservatively?

    Drs. Deyo and Mirza state:

Six weeks of conservative therapy is generally recommended in patients with herniated lumbar disks, in the absence of a major neurological deficit.

    “Unless patients have major neurologic deficits, surgery is generally appropriate only in those who have nerve root compression that is confirmed on CT or MRI, a corresponding sciatica syndrome, and no response to 6 weeks of conservative therapy.”

In the absence of severe neurologic deficits, discogenic sciatica patients should have conservative treatment for 6 weeks before agreeing to more invasive approaches (glucocorticoids injections, surgery).

The mean time for resolution of discogenic sciatica symptoms with conservative care is 12 weeks.

Patients who first use conservative treatment for discogenic sciatica and later opt for surgery still do well, indicating an “absence of a therapeutic window for surgery that closed quickly.”

How effective is conservative treatment for the discogenic radiculopathy/sciatica patient, as compared to surgical treatment?

    Drs. Deyo and Mirza state that most patients with radicular sciatica who do not undergo surgery will improve. They further note:

Conservative treatment does not change the natural history of disk herniation, but offers relief of symptoms. Most herniated disks will shrink with resolution of symptoms over 3-12 months.

Minor motor deficits will resolve in most patients who are treated conservatively.

“Elective surgery is an option for patients with congruent clinical and MRI findings and a condition that does not improve within 6 weeks.”

“Patients with severe or progressive neurologic deficits require a referral for surgery.”

There is “no significant advantage of surgery over conservative treatment for sciatica relief at 1 to 4 years of follow-up.”

“By 1 year, outcomes of early surgery generally do not differ from those of prolonged conservative therapy.”

Is chiropractic spinal adjusting (specific manipulation) safe and effective for patients suffering from discogenic radiculopathy/sciatica?

    Drs. Deyo and Mirza clearly indicate that chiropractic spinal manipulation is both safe and usually effective in the management of patients suffering with discogenic radiculopathy/sciatica, stating:

A randomized trial of chiropractic manipulation for subacute or chronic back related leg pain “showed that manipulation was more effective than home exercise with respect to pain relief at 12 weeks.”

“A randomized trial involving patients who had acute sciatica with MRI-confirmed disk protrusion showed that at 6 months, significantly more patients who underwent chiropractic manipulation had an absence of pain than did those who underwent sham manipulations (55% vs. 20%).”

    In addition, for many decades, published studies have supported the effectiveness and safety of spinal manipulation for the management of discogenic radiculopathy/sciatica (4, 5, 6, 7, 8, 9). A recent study adding to the evidence is presented here (10).

In 2006, physicians Valter Santilli, MD, Ettore Beghi, MD, Stefano Finucci, MD published a study in the Spine Journal, titled (10):

Chiropractic manipulation in the treatment of
acute back pain and sciatica with disc protrusion:
A randomized double-blind clinical trial of
active and simulated spinal manipulations

    The purpose of this study was to assess the short- and long-term effects of spinal manipulations on acute back pain and sciatica with disc protrusion. It is a randomized double-blind trial comparing active and simulated manipulations for these patients. The study used 102 patients. The manipulations or simulated manipulations were done 5 days per week by experienced chiropractors for up to a maximum of 20 patient visits, “using a rapid thrust technique.” Re-evaluations were done at 15, 30, 45, 90, and 180 days. Sixty-four men and 38 women were randomized to manipulations (n=53) or simulated manipulations (n=49).
The aim of the thrust side-posture chiropractic manipulations of the spinal column was to restore the physiological motor unit movement. Rationales for using spinal manipulation in the treatment of low back pain and sciatica include:

• Reduction of a bulging disc
• Correction of disc displacement
• Release of adhesive fibrosis surrounding prolapsed discs or facet joints
• Release of entrapped synovial folds
• Inhibition of nociceptive impulses
• Relaxation of hypertonic muscles
• Unbuckling displaced motion segments

The study noted that:

“Active manipulations have more effect than simulated manipulations on pain relief for acute back pain and sciatica with disc protrusion.”

“At the end of follow-up a significant difference was present between active and simulated manipulations in the percentage of cases becoming pain-free (local pain 28% vs. 6%; radiating pain 55% vs. 20%).”

Active manipulations resulted in reduction of radiating pain and by a lower number of days on, and prescriptions of, nonsteroidal anti-inflammatory drugs.

“Patients receiving active manipulations enjoyed significantly greater relief of local and radiating acute LBP, spent fewer days with moderate-to-severe pain, and consumed fewer drugs for the control of pain.”

“No adverse events were reported.”

The authors concluded that chiropractic spinal “manipulations may relieve acute back pain and sciatica with disc protrusion.”

••••••••••

CONCLUDING POINTS

       As a rule:

• Unless there are signs/symptoms of severe nerve compression, and/or cauda equina syndrome, patients suffering with discogenic radiculopathy/sciatica should be managed conservatively for a period of 4-6 weeks.
• If there is no improvement after a period of 4-6 weeks of conservative treatment, a CT and/or MRI is clinically warranted.
• If decompressive surgery is indicated, a delay of 4-6 weeks with conservative treatment does not adversely affect the surgical clinical outcome.
• Spinal x-rays are non-revealing for patients with discogenic radiculopathy/sciatica, and exposing them is the clinical discretion of the provider.
• If after 4-6 weeks of conservative treatment there is acceptable clinical improvement to justify continued conservative treatment, maximum conservative treatment benefit may not be achieved for a period of 3-12 months.
• Chiropractic spinal manipulation (adjusting) is as a rule both safe and effective in the treatment of discogenic radiculopathy/sciatica.

REFERENCES

1. Fardon DR, Williams LA, Dohring EJ, Rothan SL, Sze GK; Lumbar Disc Nomenclature: Version 2.0: Recommendations of the Combined task forces of the North American Spine Society, the American Society of Spine Radiology, and the American Society of Neuroradiology; Spine Journal; 14; pp. 2525-2545.
2. Kapandji IA; The Physiology of the Joints; Volume Three, The Trunk and the Vertebral Column; Churchill Livingstone; 1974.
3. Deyo R, Mirza S; Herniated Lumbar Intervertebral Disk; New England Journal of Medicine; May 5, 2016; Vol. 374; No. 18; pp. 1763-1772.
4. Ramsey RH; Conservative Treatment of Intervertebral Disk Lesions; American Academy of Orthopedic Surgeons, Instructional Course Lectures; Volume 11, 1954, pp. 118-120.
5. Mathews JA, Yates DAH; Reduction of Lumbar Disc Prolapse by Manipulation; British Medical Journal; September 20, 1969; No. 3; pp. 696-697.
6. Edwards BC; Low back pain and pain resulting from lumbar spine conditions: a comparison of treatment results; Australian Journal of Physiotherapy; 15:104, 1969.
7. Turek S; Orthopaedics, Principles and Their Applications; JB Lippincott Company; 1977; page 1335.
8. Kuo PP and Loh ZC; Treatment of Lumbar Intervertebral Disc Protrusions by Manipulation; Clinical Orthopedics and Related Research; No. 215, February 1987, pp. 47-55.
9. Cassidy JD, Thiel HW, Kirkaldy-Willis WH; Side posture manipulation for lumbar intervertebral disk herniation; Journal of Manipulative and Physiological Therapeutics; February 1993; Vol. 16; No 2; pp. 96-103.
10. Santilli V, Beghi E, Finucci S; Chiropractic manipulation in the treatment of acute back pain and sciatica with disc protrusion: A randomized double-blind clinical trial of active and simulated spinal manipulations; The Spine Journal; March-April 2006; Vol. 6; No. 2; pp. 131–137.

BACKGROUND CONCEPTS

Upright posture is a first class lever mechanical system, such as a teeter-totter or seesaw:

Fulcrum       

By mechanical definition, the fulcrum is where the forces are the greatest. In human spinal posture, the fulcrum is the intervertebral disc and facet joints.

When the human head is bent forward, as in looking down, the loads on the fulcrum (disc and facet joints) would be the weight of the head multiplied by the distance from the fulcrum, added by the counter-balancing contraction of the posterior spinal muscles. This counterbalance contraction of the cervical spine muscles is fatiguing to the muscle, increases the compressive loads on the fulcrum tissues, and causes a constant increased tension in the muscles. This can cause headaches.

Rene Cailliet, MD, uses an example where a patient has unbalanced forward head posture (1). Dr. Cailliet assigns the head a weight of 10 lbs. and displaces the head’s center of gravity forward by 3 inches. The required counter balancing muscle contraction on the opposite side of the fulcrum (the vertebrae) would be 30 lbs. (10 lbs. X 3 inches):

Kenneth K. Hansraj, MD, is Chief of Spine Surgery at the New York Spine Surgery & Rehabilitation Medicine center. In 2014 he published an article in the journal Surgical Technology International, titled (2):

Assessment of Stresses in the Cervical Spine Caused by Posture and Position of the Head

In this article, Dr. Hansraj points out that the ubiquitous use of cellular devices are creating an epidemic incidence of joint and muscular problems in the upper thoracic and lower cervical spines. He notes that billions of people are using cell phone devices on the planet, essentially in poor posture. The purpose of his study was to assess the forces incrementally seen by the cervical spine as the head is tilted forward, into a worsening posture.

Dr. Hansraj created a cervical spine model to calculate the forces experienced by the cervical spine when in incremental flexion (forward head position). His mathematical analysis used a head weight of 13.2 pounds.

Dr. Hansraj made the following observations:

“Poor posture invariably occurs with the head in a tilted forward position and the shoulders drooping forward in a rounded position.”
        
“The weight seen by the spine dramatically increases when flexing the head forward at varying degrees.”

“Loss of the natural curve of the cervical spine leads to incrementally increased stresses about the cervical spine. These stresses may lead to early wear, tear, degeneration, and possibly surgeries.”

An average person spends 2-4 hours a day with their heads tilted forward reading and texting on their smart phones / devices, amassing 700-1400 hours of excess, abnormal cervical spine stress per year. “A high school student may spend an extra 5,000 hours in poor posture” per year.

Nikolai Bogduk, from the University of Newcastle, Australia, is a Doctor of Medicine and a Doctor of Science. Dr. Bogduk pioneered research into the neuroanatomical basis for spinal pain, beginning in 1972. Through today (May 2016), he has authored numerous book chapters, books, and 254 articles located using a PubMed search of the US National Library of Medicine.

Perhaps the best article ever written pertaining to headaches was by Dr. Bogduk. It appeared in the journal Biomedicine and Pharmacotherapy in 1996, and is titled (3):

Anatomy and Physiology of Headache

This article is based on an extensive review of neuroanatomy. The key concept explained by Dr. Bogduk is that all headaches synapse in the upper cervical spine (Trigeminal-Cervical Nucleus) before being relayed to the cortical homunculus for perception. This anatomical fact supports the plausibility and the anecdotal observations that people with a variety of headaches (migraine, cluster, cervicogenic, muscle tension, etc.) may obtain relief from manual therapy and/or manipulation of the upper cervical spine. Explanations for this relief tend to center around the 1965 Gate Theory of Pain (4). The Gate Theory is succinctly stated by Eric Kandel, MD, and colleagues (5):

“Pain is not simply a direct product of the activity of nociceptive afferent fibers but is regulated by activity in other myelinated afferents that are not directly concerned with the transmission of nociceptive information.”

“The idea that pain results from the balance of activity in nociceptive and non-nociceptive afferents was formulated in the 1960s and was called the gate control theory.”

The non-nociceptive afferents that close the Pain Gate are primarily mechanoreceptors (proprioceptors). When the joints and tissues of the upper cervical spine are not functioning optimally, the Pain Gate is “open,” and more pain signals arrive to the cortical brain. Spinal manipulation and other mechanical therapeutic interventions at the upper cervical spine “close” the Pain Gate (by initiating a neurological sequence of events). This will reduce the perception of any type of headache. This premise is well stated by orthopedic surgeon William H. Kirkaldy-Willis and colleague (6):

“Spinal manipulation is essentially an assisted passive motion applied to the spinal apophyseal and sacroiliac joints.”
   
Melzack and Wall proposed the Gate Theory of Pain in 1965, and this theory has “withstood rigorous scientific scrutiny.”

“The central transmission of pain can be blocked by increased proprioceptive input.” Pain is facilitated by “lack of proprioceptive input.” This is why it is important for “early mobilization to control pain after musculoskeletal injury.”

The facet capsules are densely populated with mechanoreceptors. “Increased proprioceptive input in the form of spinal mobility tends to decrease the central transmission of pain from adjacent spinal structures by closing the gate. Any therapy which induces motion into articular structures will help inhibit pain transmission by this means.”

Stretching of facet joint capsules will fire capsular mechanoreceptors that reflexively “inhibit facilitated motor neuron pools” which are responsible for the muscle spasms that commonly accompany low back pain.

Restating the above, there is a potential that manual/manipulative can improve any headache as a consequence of improved proprioceptive/mechanoreceptive afferent input into the Trigeminal-Cervical Nucleus, “closing” the Pain Gate. Chiropractors and other providers of this type of manual intervention are particularly versed in Cervicogenic Headaches. Cervicogenic Headaches are referred pain to the head, where the actual primary nociceptive afferent arises in the joints and/or soft tissues of the upper cervical spine.

Although there may be some overlap, Cervicogenic Headaches and Tension-Type Headaches can be distinct. Tension-Type Headaches result from increased tension in the muscles of the upper back and neck, the head, and the temporomandibular joints. Hence, Tension-Type Headaches are often referred to as Muscle Tension Headaches:

••••••••••

Tension-type headache is the most common form of benign, primary headache (7). Tension-Type Headaches have been known by other names, such as Muscle Tension Headache and Muscle Contraction Headache; yet, the International Headache Society officially classified this type of headache as Tension-Type Headaches in 1988 (8).

The features of Tension-Type Headache include (9):

• The headache is bilateral
• The intensity is mild to moderate
• The pain quality is aching, tightening, or pressing
• The duration is from 30 minutes to 7 days
• The headache is not accompanied by nausea or vomiting
• Either photo- or phonophobia may be experienced, but not both

More detailed criteria for Tension-Type Headache appeared in the journal Cephalalgia in 1983, including  (10):

• A minimum of at least 10 previous headache episodes meeting the criteria below:
  • Headache lasting from 30 minutes to 7 days.
  • At least two of the following:

• • • Pressing, Tightening, but Non-Pulsating quality
    • Mild or Moderate intensity that may inhibit but does not prohibit activity
    • Bilateral location
    • Not aggravated by walking, stairs, or other similar routine physical activities

• • Both of the following:
    • No Nausea or Vomiting
    • One of either photo- or phonophobia may be present, but not both

There are two forms of Tension-Type Headache (8):

• Episodic

The headaches are experienced no more than 180 days per year.

• Chronic

The headaches are experienced more than 180 days per year.

The prevalence of Tension-Type Headache varies between 10-65% of the population, depending upon the country and the other classification features. A review of the literature in 2003 concluded that, “slightly more than one-third of the adult population suffers from this problem (9).”

••••••••••

A number of studies have assessed the effectiveness of spinal manipulation and other manual techniques of the cervical spine for the treatment of Tension-Type Headache. Several are presented below:

A 1979 study published in the Journal of the American Osteopathic Association, titled (11):

Osteopathic Manipulation in the Treatment of Muscle-Contraction Headache

The authors evaluated the benefit of a single manipulative session on nine subjects suffering with muscle contraction headaches. The authors found this manipulation to be helpful.
•••••

A 1995 study published in the Journal of Manipulative Physiological Therapeutics, titled (12):

Spinal Manipulation vs. Amitriptyline for the Treatment of Chronic Tension-Type Headaches: A Randomized Clinical Trial

The authors compared the effectiveness of chiropractic spinal manipulation to the drug amitriptyline for chronic tension-type headache. The study design was a randomized controlled trial with a 6-week treatment period and a 4-week post-treatment, follow-up period. The study involved 150 patients. The authors concluded:

 “The spinal manipulation group showed a reduction of 32% in headache intensity, 42% in headache frequency, 30% in over-  the-counter medication usage and an improvement of 16% in functional health status. By comparison, the amitriptyline therapy group showed no improvement or a slight worsening from baseline values in the same four major outcome measures.”

“The results of this study show that spinal manipulative therapy is an effective treatment for tension headaches.”

“Four weeks after the cessation of treatment, the patients who received spinal manipulative therapy experienced a sustained therapeutic benefit in all major outcomes in contrast to the patients that received amitriptyline therapy, who reverted to baseline values.”

“The sustained therapeutic benefit associated with spinal manipulation seemed to result in a decreased need for over-   the-counter medication.”

It is also noteworthy that 82% of the subjects in the amitriptyline group reported side effects that included drowsiness, dry mouth and weight gain; 4% in the spinal manipulation group reported neck soreness and stiffness.

•••••

A 2005 study (from Harvard Medical School) published in the journal Headache, titled (13):

Physical Treatments for Headache: A Structured Review

The author in the study reviewed published clinical trial evidence, systematic reviews, and case series regarding the efficacy of selected physical modalities in the treatment of primary headache disorders. He noted, “Chiropractic manipulation demonstrated a trend toward benefit in the treatment of Tension-Type Headaches.”

A 2012 study (from Peninsula Medical School, Exeter, United Kingdom) published in the journal Complimentary Therapies in Medicine, titled (14):

Spinal Manipulations for Tension-Type Headaches: A Systematic Review of Randomized Controlled Trials

The objective of this systematic review was to assess the effectiveness of spinal manipulations as treatment option for tension-type headaches. Eight databases were searched and all randomized trials were considered if they investigated spinal manipulations performed by any type of healthcare professional for treating tension type headaches in human subjects. The authors concluded:

“Four randomized clinical trials suggested that spinal manipulations are more effective than drug therapy, spinal manipulation plus placebo, sham spinal manipulation plus amitriptyline or sham spinal manipulation plus placebo, usual care or no intervention.”

“The evidence that spinal manipulation alleviates tension type headaches is encouraging.”

•••••

A 2014 study (from the University of Valencia, Spain) published in the Journal of Chiropractic Medicine, titled (15):

Efficacy of Manual and Manipulative Therapy in the Perception of Pain and Cervical Motion in Patients with Tension-Type Headache: A Randomized, Controlled Clinical Trial

The purpose of this study was to evaluate the efficacy of manipulative and manual therapy treatments with regard to pain perception and neck mobility in patients with tension-type headache. The study was a randomized clinical trial assessing 84 subjects diagnosed with tension-type headache. Four treatment sessions were administered over 4 weeks, with post-treatment assessment and follow-up at 1 month.

The intervention showed significant improvements in pain perception and ranges of motion, as well as reduced frequency of headache.

•••••

Another 2014 study (from the University of Milano-Bicocca, Milan, Italy) published in the Journal of the American Osteopathic Association, titled (16):

Pilot Trial of Osteopathic Manipulative Therapy for Patients with Frequent Episodic Tension-Type Headache

The purpose of this study was to explore the efficacy of spinal manipulation for pain management in frequent episodic tension-type headache. It was a single-blind randomized placebo-controlled pilot study, involving 44 subjects. Treatment was given over a period of 1-month, and there was a 3-month follow-up period.

The manipulation group had a significant reduction (40%) in headache frequency. The authors concluded:

“Manipulative therapy may be preferred over other treatment modalities and may benefit patients who have adverse effects to medications or who have difficulty complying with pharmacologic regimens.”

•••••

A third 2014 study (and the second study from the University of Valencia, Spain) published in the journal European Journal of Physical Rehabilitation Medicine, titled (17):

Effect of Manual Therapy Techniques on Headache Disability in Patients with Tension-Type Headache. Randomized Controlled Trial

The aim of this study was to assess the effectiveness of manual therapy techniques, applied to the suboccipital region, on aspects of disability in a sample of patients with tension-type headache. It was a randomized controlled trial using 67 subjects. Patients were randomly divided into four treatment groups: 1) suboccipital soft tissue inhibition; 2) occiput-atlas-axis manipulation; 3) combined treatment of both techniques; 4) control. Four sessions were applied over 4 weeks.

The authors found that headache frequency was significantly reduced with the manipulative and combined treatment. When manipulation was combined with suboccipital soft tissue techniques, there was improvement in photophobia, phonophobia and pericranial tenderness.

•••••

In 2016, a third study from the University of Valencia, Spain group, also published in the European Journal of Physical Rehabilitation Medicine, titled (18):

Do Manual Therapy Techniques Have a Positive Effect on Quality of Life in People with Tension-Type Headache? A Randomized Controlled Trial

The aim of this study was to specifically look at the effect of manual/manipulative therapy on the tension-type headache patient’s quality of life. Seventy-six subjects were treated for 4 weeks with manual therapy techniques. The authors concluded:

“Manual therapy techniques applied to the suboccipital region, for as little as four weeks, offered a positive improvement in some aspects of quality of life of patient’s suffering with Tension-Type Headaches.”

•••••

SUMMARY

Tension-Type Headache is the most common headache in society, affecting about one-third of the population. The studies presented here are often critical of the need for more and better studies, with more subjects, to thoroughly evaluate the benefit of manipulation and adjunct manual therapies for the treatment of these common headaches. However, there is clear support indicating that cervical spine manipulation and adjunct manual therapies are helpful for many suffering from these headaches. Cervical spine manipulation and adjunct manual therapies are particularly beneficial when compared to other treatment approaches, such as drugs and placebo interventions.

Additionally, long-term improvement of Tension-Type Headache may require postural improvement, especially of the Forward Head Syndrome (19). As noted above, when the head is bent forward, the posterior neck muscles must contract, resulting in “muscle contraction headache.” Chiropractic spinal adjusting (specific manipulation) is designed to both improve segmental spinal function and to also improve postural alignment. Both will benefit patients suffering from Tension-Type Headaches. 

REFERENCES

• Cailliet R; Soft Tissue Pain and Disability; 3rd Edition; F A Davis Company, 1996.
• Kenneth K. Hansraj K; Assessment of Stresses in the Cervical Spine Caused by Posture and Position of the Head; Surgical Technology International; November 2014; Vol. 25; pp. 277-279.
• Bogduk N; Anatomy and Physiology of Headache; Biomedicine and Pharmacotherapy; 1995; Vol. 49; No. 10; pp. 435-445.
• Melzack R, Wall PD; Pain mechanisms: a new theory; Science; November 19, 1965;150(3699); pp. 971-9.
• Kandel E, Schwartz J, Jessell T; Principles of Neural Science; McGraw-Hill; 2000.
• Kirkaldy-Willis WH, Cassidy JD; Spinal Manipulation in the Treatment of Low back Pain; Canadian Family Physician; March 1985, Vol. 31, pp. 535-540.
• Silberstein SD; Tension-type headaches; Headache; September 1994; Vol. 34; No. 8; pp. S2-7.
• International Headache Society; Classification and Diagnostic Criteria for Headache Disorders, Cranial Neuralgias and Facial Pain; Cephalalgia; 1988; Supplemental 7.
• Vernon HT; “Tension-type and cervicogenic headaches, Part 1, Clinical descriptions and methods of assessment”; In The Cranio-Cervical Syndrome; Edited by Howard Vernon; Butterworth Heinemann; 2003.
• Sjaastad O, Saunte C, Hovdahl H, Breivik H, Grønbaek E; “Cervicogenic” headache, An hypothesis; Cephalalgia; December 1983; Vol. 3; No. 4; pp. 249-256.
• Hoyt WH, Shaffer F, Bard DA, Benesler JS, Blankenhorn GD, Gray JH, Hartman WT, Hughes LC; Osteopathic manipulation in the treatment of muscle-contraction headache; Journal of the American Osteopathic Association; January 1979; Vol. 78; No. 5; pp. 322-325.
• Boline PD, Kassak K, Bronfort G, Nelson C, Anderson AV; Spinal manipulation vs. amitriptyline for the treatment of chronic tension-type headaches: a randomized clinical trial. Journal of Manipulative Physiological Therapeutics; March-April 1995;Vol. 18; No. 3; pp. 148-154.
• Biondi DM; Physical treatments for headache: a structured review; Headache; June 2005; Vol. 45; No. 6; pp. 738-746.
• Posadzki P, Ernst E; Spinal manipulations for tension-type headaches: a systematic review of randomized controlled trials; Complimentary Therapies in Medicine; August 2012; Vol. 20; No. 4; pp. 232-239.
• Espí-López GV, Gómez-Conesa A; Efficacy of manual and manipulative therapy in the perception of pain and cervical motion in patients with tension-type headache: a randomized, controlled clinical trial; Journal of Chiropractic Medicine; March 2014; Vol. 13; No. 1; pp. 4-13.
• Rolle G, Tremolizzo L, Somalvico F, Ferrarese C, Bressan LC; Pilot trial of osteopathic manipulative therapy for patients with frequent episodic tension-type headache; Journal of the American Osteopathic Association; September 2014; Vol. 114; No. 9; pp. 678-685.
• Espí-López GV, Rodriquez-Blanco C. Oliva-Pascual-Vaca A, Benitez-Martinez JC, Lluch E, Falla D; Effect of manual therapy techniques on headache disability in patients with tension-type headache. Randomized controlled trial; European Journal of Physical Rehabilitation Medicine; December 2014; Vol. 50; No. 6; pp. 641-647.
• Espi-Lopez GV, RODRíGUEZ-Blanco C, Oliva-Pascual-Vaca Á, Molina-Martinez FJ, Falla D; Do manual therapy techniques have a positive effect on quality of life in people with tension-type headache? A randomized controlled trial; European Journal of Physical Rehabilitation Medicine; February 29, 2016. [Epub ahead of print]
• Fernández-de-las-Peñas C, Alonso-Blanco C, Cuadrado ML, Pareja JA; Forward head posture and neck mobility in chronic tension-type headache: a blinded, controlled study; Cephalalgia; March 2006; Vol. 26; No. 3; pp. 314-319.

Introduction

Vertigo is defined as “a condition in which somebody feels a sensation of whirling or tilting that causes a loss of balance.” To describe the sensation of vertigo, patients often use words such as dizziness, giddiness, unsteadiness, or lightheadedness. The neurological vertigo center is called the vestibular nucleus. The vestibular nucleus is located in the brainstem. It extends from the caudal portion of the pons through the caudal portion of the medulla.

The afferent information that enters the vestibular nucleus to initiate the sensation of vertigo arises primarily from four sources:
1)    Labyrinthine Inner Ear (1)
2)    Cerebellum (2)
3)    Temporomandibular Joint (TMJ) (3, 4, 5)
4)    Cervical spine afferents, especially from C1 – C3 (6)

All health care providers should also be aware that vertigo could result as a consequence of vascular compromise of the posterior circulation of the brainstem (the vertebral and basilar arteries, and their branches) (7).

Pathology

The first study to link problems in the cervical spine to vertigo was published in the journal Lancet in 1955 (8). Today (October 12, 2015), a search of the National Library of Medicine with PubMed, using the words “cervical vertigo” locates 2,211 citations.

It was established in 1977 that the injection of saline irritants into the deep tissues of the upper cervical spine would create the sensation of vertigo in normal human volunteers (6).

Clinicians have documented a relationship between cervical spine trauma and the symptoms of vertigo (9). In her chapter titled “Posttraumatic Vertigo”, Dr. Linda Luxon (10) notes that this vertigo can be explained by “disruption of cervical proprioceptive input.” She notes that the major cervical spine afferent input to the vestibular nuclei “arises from the paravertebral joints and capsules, with relatively minor input from paravertebral muscles.” Dysfunctional upper cervical spinal joints and their capsules can alter the proprioceptive afferent input to the vestibular nucleus resulting in the symptoms of vertigo. Treatment would be to improve the mechanical function of these joints.

In 2001, an article appeared in the Journal of Neurology, Neurosurgery, and Psychology titled (11):

Cervical Vertigo

This article reviews the theoretical basis for cervical vertigo. These authors note:

“Proprioceptive input from the neck participates in the coordination of eye, head, and body posture as well as spatial orientation,” and this is the basis of the of cervical vertigo syndrome. Cervical vertigo is when the suspected mechanism is proprioceptive.

“Degenerative or traumatic changes of the cervical spine can induce altered sensory input causing vertigo.

“Dizziness and unsteadiness suspected to be of cervical origin could be due either to loss or inadequate stimulation of neck receptors in cervical pain syndromes.”

“Section or anesthesia of cervical roots or muscles causes an asymmetry in somatosensory input, unilateral irritation or deficit of neck afferents could create a cervical tone imbalance, thus disturbing integration of vestibular and neck inputs.”

“As somatosensory cervical input converges with vestibular input to mediate multisensory control of orientation, gaze in space, and posture, the clinical syndrome of cervical vertigo could theoretically include perceptual symptoms of disorientation, postural imbalance, and ocular motor signs.”

“A convincing mechanism of cervical vertigo would have to be based on altered upper cervical somatosensory input associated with neck tenderness and limitation of movement.”

“In summary, vertigo can be accompanied by cervical pain, associated with head injury, whiplash injury, or cervical spine disease.”

“If cervical vertigo exists, appropriate management is the same as that for the cervical pain syndrome.”

In 2002, an article appeared in the Journal of Whiplash & Related Disorders, titled (12):

A Cross-Sectional Study of the Association Between Pain and Disability in Neck Pain Patients with Dizziness of Suspected Cervical Origin

In this article, these authors state:

“The term ‘cervical vertigo’ was introduced to describe dizziness and unsteadiness associated with cervical spine pain syndromes.”

“Increasing evidence suggests that dizziness and vertigo may arise from dysfunctional cervical spine structures.”

“Whiplash patients are likely to suffer from dizziness, vertigo and associated neck pain and disability resulting from traumatized cervical spine structures.”

“Cervicogenic dizziness, especially in whiplash patients, may result from disturbed sensory information due to dysfunctional joint and neck mechanoreceptors.”

“Dizziness and vertigo are common complaints of neck pain patients with 80 to 90% of whiplash sufferers reporting these symptoms.”

“Dysfunction or trauma to connective tissues such as cervical muscles and ligaments rich in proprioceptive receptors (mechanoreceptors) may lead to sensory impairment.”

“Emerging evidence suggests that dizziness and vertigo may commonly arise from dysfunctional cervical spine structures such as joint and neck mechanoreceptors, particularly from trauma.”

In this study, the authors evaluated 180 consecutive neck pain patients over the age of 18 who were recruited from an outpatient clinic. Of these, 71 patients (40.57%) reported neck pain resulting from trauma and 60 patients (33.5%) were suffering from dizziness. Pain intensity was measured using the Numerical Rating Scale while disability was measured with the Neck Disability Index (NDI).

The authors note that dizzy patients also describe their symptoms with “lightheadedness, seasickness, instability, rotatory vertigo, etc.” Regarding dizziness, females were significantly more likely to report dizziness compared to males while no significant difference was found for dizziness versus age. Patients experiencing dizziness also reported greater intensity of neck pain compared to those without dizziness. Increasing duration of neck pain was significantly associated with increasing reports of dizziness.  Subjects who reported dizziness were significantly more likely to have been involved in an injury. Neck pain patients with dizziness reported significantly more disability (total NDI score) compared to neck pain patients without dizziness.

The authors concluded that neck pain patients with dizziness were significantly more likely to have suffered a traumatic injury, experienced greater pain intensity and disability levels, and experienced for a longer period of time, compared to neck pain patients without dizziness.

This “study results reinforce the concept of neck pain and disability leading to cervicogenic dizziness/vertigo due to dysfunction of the somatosensory system of the neck.” The basic model presented in this article is that trauma causes “dysfunctional cervical spine structures” resulting in altered “joint and neck mechanoreceptor” function, causing both pain and dizziness.

In 2003, a group from the University of Queensland, Brisbane, Australia, published a study in the Journal of Rehabilitative Medicine titled (13):

Dizziness and Unsteadiness Following Whiplash Injury: Characteristic Features and Relationship with Cervical Joint position Error

These authors note that dizziness and/or unsteadiness are common symptoms of chronic whiplash-associated disorders, and that if the cervical spine injury is the suspected origin of these complaints that it can be assessed with “joint position error.” Joint position error is the accuracy to return to the natural head posture following extension and rotation. Consequently, these authors measured joint position error in 102 subjects with persistent whiplash-associated disorder and 44 control subjects. These authors found:

“The results indicated that subjects with whiplash-associated disorders had significantly greater joint position errors than control subjects.”

“Within the whiplash group, those with dizziness had greater joint position errors than those without dizziness following rotation.”

“Cervical mechanoreceptor dysfunction is a likely cause of dizziness in whiplash-associated disorder.”

“When there is no traumatic brain injury, abnormal cervical afferent input from damaged or functionally impaired neck joint and muscle receptors is considered the likely cause.”

Dizziness of cervical origin “originates from abnormal afferent activity from the extensive neck muscle and joint proprioceptors, which converges in the central nervous system with vestibular and visual signals, confusing the postural control system.”

These authors “contend that our results support a likely cervical cause of dizziness and or unsteadiness rather than other causes of dizziness in these subjects with persistent whiplash associated disorders and the joint position error findings highlight the role of cervical mechanoreceptor dysfunction.”

“The study highlights the role of cervical mechanoreceptor dysfunction and the importance of assessment and management of this impairment in persistent whiplash     associated disorders, particularly in those complaining of dizziness and unsteadiness.”

These authors also noted that the most common words used were “lightheaded”, “unsteady” and “off-balance”. Other descriptions were clumsy, giddy, imbalance, motion sickness, falling/veering to one side, imbalance in the dark, vision jiggle (disturbance), faint feeling, might fall. Unsteadiness was the most common description, being stated by 90% of the subjects.

In 2012, neurological investigators from Buenos Aires, Argentina, and from the Chicago Dizziness and Hearing Center confirmed the existence and pathophysiology of post-traumatic cervical vertigo, and cervicogenic proprioceptive vertigo. Their article appeared in the journal Neurologia, and is titled (14):

Cervical Vertigo:
Myths, Facts, and Scientific Evidence

These authors note that aspects of “cervical vertigo” have “survived the test of time and may be found in the literature today.” They recommend that the provider rule out “rotational vertebral artery syndrome,” and state:

“Once potentially severe causes of the symptoms have been ruled out, the most appropriate strategy seems to be use of manipulative and vestibular physical therapy.”

In 2014, researchers from the University of Montreal assessed 25 subjects with cervicogenic dizziness and 25 subjects with labyrinthine dizziness to determine which clinical tests were best able to distinguish between the two groups. Their study was published in the journal Otology & Neurotology, and titled (15):

Evaluation of Para-clinical Tests in the Diagnosis of Cervicogenic Dizziness

          These authors concluded subjects with cervicogenic dizziness were more likely to:

• Have a sensation of drunkenness and lightheadedness.
• Have pain induced during the physical examination of the upper cervical vertebrae.
• Have an elevated joint position error during the cervical relocation test.

Treatment

There is strong evidence spanning decades, arising from multiple countries, and published in a variety of well-respected peer reviewed medical journals indicating that the reason for cervical vertigo is a mechanical lesion/dysfunction of the cervical spine. This lesion may be articular, capsular, ligamentous, muscular, or a combination there of. The strongest evidence is that the lesion/dysfunction is in the upper cervical spine, from C1-C3. Consequently, a variety of mechanical approaches to treatment of cervical vertigo have been assessed and the results are usually quite favorable.

These mechanical therapies include physiotherapy, varieties of passive joint mobilizations, manipulation, and muscle work. This same type of mechanical therapeutic approach is also effective in treating spinal pain conditions. The explanation for this is that the improvement in mechanical function creates a neurological sequence of events that closes the “Pain Gate.” (16)

The studies below review some of these mechanical approaches and their effectiveness is duly noted:

In 1996, providers from the Department of Oto-Rhino-Laryngology, University Hospital, Lund, Sweden, completed a prospective, randomized, controlled trial of 17 individuals with dizziness of suspected cervical origin and 17 healthy control subjects. The study was published in Archives of Physical Medicine and Rehabilitation and titled Postural and symptomatic improvement after physiotherapy in patients with dizziness of suspected cervical origin (17).

The subjects in this study suffered from both dizziness and neck pain. The treatment targeted their neck pain, yet measurement outcomes assessed their pain and dizziness, specifically using posturography body sway, the Visual Analog Scale ratings, and intensity/frequency of dizziness score. The authors concluded:

“Physiotherapy significantly reduced neck pain and intensity and the frequency of dizziness, and significantly improved postural performance.”

“Patients with dizziness of suspected cervical origin are characterized by impaired postural performance. Physiotherapy reduces neck pain and dizziness and improves postural performance. Neck disorders should be considered when assessing patients complaining of dizziness.”

In 1998, an article appeared in the European Spine Journal titled Vertigo in Patients with Cervical Spine Dysfunction(18). The authors defined “dysfunction” as a reversible, functional restriction of motion of an individual spinal segment or as articular malfunction presenting with hypomobility. The authors also state that upper cervical spine dysfunctions can cause vertigo, and they cite 13 references to support the premise. They explain vertigo may occur as a consequence of disturbances of proprioception from the neck. They cite an additional 4 references to claim that only dysfunctions of the upper cervical spine can cause vertigo, noting that anatomical studies identify links between upper cervical spine receptors and the vestibular nuclei.

In this study the authors used 50 patients who were referred to rule out a cervical spine problem as a cause of vertigo. All patients displayed symptoms of dizziness. Labyrinthine ear examination and neurology examination were equivocal. A reproducible manual palpation examining technique was used to diagnose segmental cervical spine dysfunction.

The cervical spine dysfunctions were treated with mobilization and manipulative techniques over a period of 3 months. Seventy-seven percent of the patients reported meaningful improvement in their vertigo, including 16% whose symptoms completely resolved. The authors state the following conclusions:

“Physical therapy is more likely to succeed in reducing vertigo symptoms if these patients present with an upper cervical spine dysfunction that is successfully resolved by manual medicine prior to physical therapy.”

“In the presence of vertigo, our presented data suggests consideration of cervical spine dysfunctions, requiring a manual medicine examination of upper motion segments.”

“A non-resolved dysfunction of the upper cervical spine was a common cause of long-lasting dizziness in our population.”

In 2005, researchers from the University of Newcastle, Australia, published an article in Manual Therapy titled Manual therapy treatment of cervicogenic dizziness: A systematic review (19). The authors note, “in some people the cause of their dizziness is pathology or dysfunction of upper cervical vertebral segments that can be treated with manual therapy.” They proceeded to review 7 electronic databases to locate both randomized controlled trials and non-randomized controlled clinical trials, finding 9 studies that met their inclusion criteria. They concluded:

“A consistent finding was that all studies had a positive result with significant improvement in symptoms and signs of dizziness after manual therapy treatment.”

“Manual therapy treatment of cervicogenic dizziness was obtained indicating it should be considered in the management of patients with this disorder.”

There is a manual therapy mobilization technique called “sustained natural apophyseal glides” (SNAGs) that is often used to treat cervical vertigo patients. In 2008, the journal Manual Therapy published a study titled Sustained natural apophyseal glides (SNAGs) are an effective treatment for cervicogenic dizziness (20). This aim of the study was to determine the efficacy of sustained natural apophyseal glides (SNAGs) in the treatment of cervical vertigo.

The authors performed a double-blind randomized controlled clinical trial involving 34 participants with cervicogenic dizziness who were randomized to receive four to six treatments of SNAGs (n=17) or a placebo (n=17). All were followed at 6- and 12-weeks. The authors concluded:

“The SNAG treatment had an immediate clinically and statistically significant sustained effect in reducing dizziness, cervical pain and disability caused by cervical dysfunction.”

This same group continued to assess the sustained natural apophyseal glides (SNAGs) protocol for patients with cervical vertigo and have reported similar conclusions (#21 in 2014 and #22 in 2015).

In 2013, chiropractors from the University of Zürich and Orthopaedic University Hospital Balgrist, Zürich, Switzerland, published a study in the journal Chiropractic Manual Therapy, titled Comparison of outcomes in neck pain patients with and without dizziness undergoing chiropractic treatment (23). The purpose of this study was to compare clinical outcomes of neck pain patients with and without dizziness undergoing chiropractic treatment. It was a prospective cohort study comparing neck pain patients with dizziness (n = 177) to neck pain patients without dizziness (n = 228).

Eighty percent of patients with dizziness and 78% of patients without dizziness were improved at 6 months. The authors concluded:

“Neck pain patients with dizziness reported significantly higher pain and disability scores at baseline compared to patients without dizziness. A high proportion of patients in both groups reported clinically relevant improvement.”

In 2015, physicians Yongchao Li, MD, and Baogan Peng, MD, PhD, from Liaoning Medical University, Beijing, China, published a study in the journal Pain Physician titled Pathogenesis, Diagnosis, and Treatment of Cervical Vertigo (24). In this article they detail a syndrome they call “Proprioceptive Cervical Vertigo,” in which abnormal afferent input to the vestibular nucleus from damaged joint receptors in the upper cervical region alter vestibular function resulting in cervical vertigo. They note that this syndrome often occurs from whiplash trauma, noting:

“In whiplash-associated disorder, pain, limitation of movement, and strains of joint capsules, paravertebral ligaments, and cervical musculature could modify the proprioceptive cervical balance in a sustained way and produce mild but chronic vertigo.”

There are “close connections between the cervical dorsal roots and the vestibular nuclei with the neck receptors (such as proprioceptors and joint receptors), which played a role in eye-hand  coordination, perception of balance, and postural adjustments. With such close connections between the cervical receptors and balance function, it is understandable that traumatic, degenerative, inflammatory, or mechanical derangements of the cervical spine can affect the mechanoreceptor system and give rise to vertigo.”
“Evidence leads to the current theory that cervical vertigo results from abnormal input into the vestibular nuclei from the proprioceptors of the upper cervical region.”

 “Manual therapy is recommended for treatment of proprioceptive cervical vertigo.”
 
“Manual therapy is effective for cervical vertigo.”

“Cervical spondylosis and cervical muscle spasms can also cause vertigo.”

These authors note that if a patient has a chief complaint of vertigo, but no neck pain, a diagnosis of cervical vertigo is excluded. Cervical vertigo patients usually have pain in the back of the neck and occipital region, sometimes accompanied by neck stiffness. Cervical vertigo is often increased with neck movements or neck pain and decreased with interventions that relieve neck pain. The vertigo symptoms can be reproduced with head/neck movement. Pain is often elicited with palpation of the suboccipital region, cervical transverse processes of C1 and C2, cervical spinous processes of C2 and C3, levator scapulae, upper trapezius muscle, splenius, rectus, and semi-spinalis muscles.

The neck torsion nystagmus test may identify cervical vertigo: the head of the patient is stabilized while the body is rotated underneath.

Since cervical vertigo originates from proprioceptive dysfunction of the upper cervical spine, treatment should be to the upper cervical spine. Chiropractic and other manual spinal therapies have been shown to be effective in treating cervical vertigo, typically with around 80% acceptable clinical outcomes.

Another effective technique for treating cervical vertigo is a type of spinal mobilization known as “sustained natural apophyseal glides” (SNAGs), often resulting in significant immediate and sustained effect in reducing dizziness and neck pain. It restores “normal movement of the zygapophyseal joints, reducing pain and muscle hypertonicity, and thereby restoring normal proprioceptive and biomechanical functioning of the cervical spine.”

Summary

Hundreds of studies over the past 60 years have established that dysfunctions of the joints and/or muscles of the cervical spine, especially the upper cervical spine, can cause the sensation of vertigo. Neuroanatomical evidence shows that upper cervical spine mechanoreceptors/proprioceptors fire to the vestibular nucleus as a portion of our human upright balance mechanisms. These studies also link the functional neurophysiology of upper cervical spine mechanoreceptors/proprioceptors to the vestibular nucleus.

The upper cervical spine is anatomically unique, with great mobility coupled with reduced stability. Hence, it is especially vulnerable to trauma, especially whiplash-type trauma, and capable of initiating cervical vertigo.

Chiropractors are exceptionally trained in the diagnosis and treatment of cervical vertigo. This includes ruling out other potential causes for the vertigo symptoms. The safe and appropriate management of cervical vertigo requires training and skill, issues that are stressed in the education of the modern chiropractor. Chiropractic spinal adjusting (specific manipulation), and other treatment adjuncts, are safe and very effective in treating patients with cervical vertigo.

REFERENCES

• Epley JM; The canalith repositioning procedure: for treatment of benign paroxysmal positional vertigo; Otolaryngology Head Neck Surgery; September 1992; Vol. 107; No. 3; pp. 399-404.
• Baloh R, Honrubia V; Clinical Neurophysiology of the Vestibular System; Third edition; Oxford University Press; 2001.
• Jordan P, Ramon Y; Nystagmus and Vertigo Produced by Mechanical Irritation of the Temporomandibular Joint-space; J Laryngol Otol; August  1965;79; pp. 744-8.
• Morgan DH; Temporomandibular joint surgery. Correction of pain, tinnitus, and vertigo; Dent Radiogr Photogr; 1973;46(2); pp. 27-39.
• Wright EF; Otologic symptom improvement through TMD therapy; Quintessence International; October 2007;38(9):e564-71.
• de Jong PT, de Jong JM, Cohen B, Jongkees LB; Ataxia and nystagmus induced by injection of local anesthetics in the Neck; Annals of Neurology; March 1977; Vol. 1; No. 3; pp. 240-246.
• NCMIC Chiropractic Solutions; Current Concepts in Spinal Manipulation and Cervical Arterial Incidents; 2006
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• Hinoki M; Vertigo due to whiplash injury: a neurotological approach; Acta Otolaryngology; Supplement 1984;419; pp. 9-29.
• Luxon L; “Posttraumatic Vertigo” in Disorders of the Vestibular System; edited by Robert W. Baloh and G. Michael Halmagyi; Oxford University Press; 1996.
• Brandt t, Bronstein M; Cervical Vertigo; Journal of Neurology, Neurosurgery, and Psychiatry; July 2001; Vol. 71; No. 1, pp. 8-12.
• Humphreys KM, Bolton J, Peterson C, Wood A; A Cross-Sectional Study of the Association Between Pain and Disability in Neck Pain Patients with Dizziness of Suspected Cervical Origin; Journal of Whiplash & Related Disorders, Vol. 1; No. 2; 2002, pp. 63-73.
• Treleaven J, Jull G, Sterling M; Dizziness and Unsteadiness Following Whiplash Injury: Characteristic Features and Relationship with Cervical Joint position Error; Journal of Rehabilitative Medicine; January, 2003; 35; pp. 36–43.
• Yacovino DA; Cervical vertigo: myths, facts, and scientific evidence; Neurologia; September 13, 2012.
• L’Heureux-Lebeau B, Godbout A, Berbiche D, Saliba I; Otology & Neurotology; Evaluation of para-clinical tests in the diagnosis of cervicogenic dizziness; December 2014; Vol. 35; No. 10; pp. 1858-1865.
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Why is Chronic Low Back Pain So Prevalent and Often so Treatment Resistant?

The Concept of Hyper-innervation, Neoneuralisation, Receptive Field Enlargement

Pain, like all perceptions, is a cortical event. Pain is experienced in the brain. Pain perception in the brain begins in a peripheral tissue and is transmitted to the brain via a nerve. Thus, the peripheral tissue source of pain must have a nerve supply (be innervated by sensory nociceptive nerves).

Eight decades of evidence (since 1934) argues that the primary peripheral tissue source for chronic low back pain is the intervertebral disc (1, 2, 3, 4, 5, 6, 7). Several lines of investigation support this evidence, including:

“Investigations have been performed in which thin nylon threads were surgically fastened to various structures in and around the nerve root. Three to four weeks after surgery these structures were irritated by pulling on the threads, but [lower back] pain resembling that which the patient had experienced previously could be registered only from the outer part of the annulus” of the disc.

[Nachemson in reference #4, describing the primary research of Smyth and Wright, reference #3).

In 1991, Dr. Stephen Kuslich and colleagues published a study titled (6):

The Tissue Origin of Low Back Pain and Sciatica:
A Report of Pain Response to Tissue Stimulation During
Operations on the Lumbar Spine Using Local Anesthesia

The authors performed 700 lumbar spine operations using only local anesthesia to determine the tissue origin of low back and leg pain. They presented the results on 193 consecutive patients they studied prospectively. The authors concluded:

“Back pain could be produced by several lumbar tissues, but by far, the most common tissue of origin was the outer layer of the annulus fibrosis.”

As noted above, accepting that the intervertebral disc is the primary source of chronic low back pain, it would mandate that the intervertebral disc has a sensory nociceptive nerve supply. Although there are respected authors of the modern era continuing to claim the intervertebral disc is aneural (8), the evidence is largely against them (1, 7, 9, 10, 11). As an example, the 1987 text edited by rheumatology professor Malcolm Jayson, MD, titled The Lumbar Spine and Back Pain, states “the mature human spine has no nerve endings of any description in the nucleus pulposus or annulus fibrosis of the intervertebral disc in any region of the vertebral column.” (8)

In summary, there is good evidence that the annulus of the intervertebral disc is innervated with sensory nociceptive nerves, and the annulus of the intervertebral disc is “the site” of chronic low back pain:

• The intervertebral disc is innervated with nociceptors.
• The intervertebral disc itself is capable of producing low back and leg pain.
• The intervertebral disc is probably the most frequent source of chronic low back pain.

••••••••••

The Magnitude of the Chronic Low Back Pain Problem

Chronic pain in America is epidemic. Recent evidence suggests that of the 238 million adults in the US, 116 million suffer from chronic pain (12, 13). Quantifying the anatomical regions for American’s chronic pain shows that more than a quarter of chronic pain is located in the low back (14):

Hip Pain 07.1%
Finger Pain 07.6%
Shoulder Pain 09.0%
Neck Pain 15.1%
Severe Headache 16.1%
Knee Pain 19.5%
Lower-Back Pain 28.1%

Low back pain is one of the most thoroughly investigated health problems worldwide. Suffering with low back pain is almost a universal human experience. The United Stated Government’s National Institutes of Health (NIH) has the National Institute of Neurological Disorders and Stroke, which has a Low Back Pain Fact Sheet (15). The Fact Sheet makes the following key points:

• Nearly everyone at some point will have back pain.
• Americans spend at least $50 billion each year on low back pain.
• Back pain is the most common cause of job-related disability and a leading contributor to missed work.

Public Health statistics add the following key points (16):

• Low back pain (LBP) is a major public health problem worldwide.
• All age groups are affected with low back pain, including children and adolescents.
• 1%–2% of adults in the United States are disabled with low back pain.
• The morbidity toll attributed to low back pain is enormous from both personal and societal perspectives.
• Direct back pain health-care expenditures in the United States were $90.7 billion in 1998. The burden is even greater when indirect costs such as productivity losses, indemnity pay, litigation, retraining and other administrative costs are considered.
• Only heart disease and stroke have substantially higher medical expenditures than spine disorders in the United States.
• LBP is presently the leading cause of disability in the world.
• LBP is the leading cause of activity limitation and workplace absence in most parts of the world.
• Most people will experience LBP at some point in their lifetime, with two-thirds having a recurrence and one third having periods of disability.
• Cases in which LBP never recurs are rare.
• A previous episode of back pain is the primary risk factor for a new LBP episode.

••••••••••

For decades, conventional wisdom pertaining to Low Back Pain (LBP) has been that the great majority (90%) of those suffering with it will resolve quickly (within two months) with no treatment or with any form of treatment. This “wisdom” was published early on by the spine care pioneer Alf Nachemson, MD, PhD, in the debut issue of the journal SPINE in 1976. Dr. Nachemson stated (4):

“Irrespective of treatment given, 70% of [back pain] patients get well within 3 weeks, 90% within 2 months.”

A few years later (1979 first edition, 1990 second edition), the reference text Clinical Biomechanics of the Spine, was published and stated (17):

“There are few diseases [low back pain] in which one is assured improvement of 70% of the patients in 3 weeks and 90% of the patients in two months, regardless of the type of treatment employed.”

This “quick recovery regardless of treatment conventional wisdom” pertaining to low back pain was challenged in 1998 by Peter R. Croft, PhD, and colleagues. Dr. Croft is a Professor of Primary Care Epidemiology at Keele University in Staffordshire, UK. Dr. Croft and colleagues published their work in 1998 in the British Medical Journal in an article titled (18):

Outcome of Low back Pain in General Practice: A Prospective Study

These authors evaluated the statistics on the natural history of low back pain, noting that it is widely believed that 90% of episodes of low back pain seen in general practice resolve within one month. They consequently investigated this claim by prospectively following 463 cases of acute low back pain for a year.

These researchers discovered that 92% of these low back pain subjects ceased to consult their primary physician about their low back symptoms within three months of onset; they were no longer going to their doctor for low back pain treatment. Yet, most of them still had substantial low back pain and related disability. Only 25% of the subjects who consulted about low back pain had fully recovered 12 months later; 75% had progressed to chronic low back pain sufferers, but they were no longer going to their doctor!

Dr. Croft and colleagues note that NOT seeing a doctor for a back problem does NOT mean that the back problem has resolved. This study showed that 75% of the patients with a new episode of low back pain have continued pain and disability a year later, even though most are not continuing to go to the doctor. They conclude that the belief that 90% of episodes of low back pain seen in general practice resolve within one month is false.

In 2003, Lise Hestbaek, DC, PhD, and colleagues from the University of Southern Denmark published a study in the European Spine Journal, titled (19):

Low back pain: what is the long-term course? A review of studies of general patient populations

These authors performed a comprehensive review of the literature on this topic, noting “it is often claimed that up to 90% of low back pain (LBP) episodes resolve spontaneously within 1 month.” They used 36 articles that met their criteria. The tabulated results showed that 62% on average (range 42-75%) still experienced pain after 12 months. The authors concluded:

“The overall picture is that LBP does not resolve itself when ignored.”

“The overall picture is clearly that LBP is not a self-limiting condition. There is no evidence supporting the claim that 80–    90% of LBP patients become pain free within 1 month.”

Ronald Donelson, MD, is a Board Certified Orthopedic Surgeon and the current Vice President of the American Back Society. Dr. Donelson is associated with the State University of New Youk, in Syracuse. In 2102, Dr. Donelson and colleagues published a study in the journalPhysical Medicine and Rehabilitation, titled (20):

Is It Time to Rethink the Typical Course of Low Back Pain?

The purpose of this study was to determine the frequency and the characteristics of low back pain (LBP) recurrences. Questionnaires were given to 589 LBP patients from 30 clinical practices (primary care [7%], physical therapy [67%], chiropractic [19%], and surgical spine [7%]) in North America and Europe. The results were:

1) Are low back pain (LBP) recurrences common?: [rounded]

73% had suffered a previous episode of LBP

54% had experienced ≥10 episodes of prior LBP in their lifetime

20% had experienced >50 episodes of prior LBP in their lifetime

27%  with a previous episode of LBP had 5 or more episodes of LBP per year

2) Do LBP episodes worsen with multiple recurrences?: [rounded]

61% reported in the affirmative

Dr. Donelson and colleagues are critical of clinical practice guidelines that characterize the typical course of LBP as benign and favorable, stating:

“It is often stated that LBP is normal; has an excellent prognosis, with 90% of individuals recovering within 3 months of onset in most cases; and is not debilitating over the long term.”

“In any one year, recurrences, exacerbations, and persistence dominate the experience of low back pain in the community. This clinical picture is very different from what is typically portrayed as the natural history of LBP in most clinical guidelines.”

“Consistent with many other published studies, the recurrence rate among our respondents with LBP was 73%.”

“Many patients with chronic LBP had prior recurrent episodes that had become longer and more severe until the most recent episode did not resolve and thus became chronic.”

“Collectively, our findings, and those of other studies, indicate that it may be inaccurate to characterize LBP as having an excellent prognosis. Recurrences are frequent and are often progressively worse over time. Recovery from acute LBP is not as favorable as is routinely portrayed.”

“Eventually, there may be no recovery, and the underlying condition may become chronically painful. In light of these characteristics, it seems inappropriate to characterize the natural history of LBP as benign and favorable.”

••••••••••

In 2013, Coen J. Itz, PhD, and colleagues from the Department of Health Service Research, Maastricht University, The Netherlands, published a study in the European Journal of Pain, titled (21):

Clinical Course of Non-Specific Low Back Pain: A Systematic Review of Prospective Cohort Studies set in Primary Care

Dr. Itz and colleagues performed a systematic literature review investigating the clinical course of pain in patients with non-specific acute low back pain that obtained treatment in primary care. All included studies were prospective studies, with follow-up of at least 12 months. Proportions of patients still reporting pain during follow-up were pooled. A total of 11 studies were eligible for evaluation. The pooled proportion of patients still reporting pain after 1 year was 71%. These authors state:

“Non-specific low back pain is a relatively common and recurrent condition for which at present there is no effective cure.”

“In current guidelines, the prognosis of acute non-specific back pain is assumed to be favorable.”

“The findings of this review indicate that the assumption that spontaneous recovery occurs in a large majority of patients is not justified.”

Kate Dunn, PhD, is an epidemiologist working at the Arthritis Research UK Primary Care Centre, Keele University, Staffordshire, UK. In 2013, Dr Dunn and colleagues published a study in the journal Best Practice & Research Clinical Rheumatology, titled (22):

Low Back Pain Across the Life Course

Dr. Dunn and colleagues note that people with back pain continue to have it on and off for years. They state:

“Back pain episodes are traditionally regarded as individual events, but this model is currently being challenged in favor of treating back pain as a long-term or lifelong condition. Back pain can be present throughout life, from childhood to older age, and evidence is mounting that pain experience is maintained over long periods.”

Dr. Dunn and the other articles referenced above all make the same central points. They are, as a rule, acute non-specific low back pain is not self limiting, it is more likely than not to become chronic, when it becomes asymptomatic recurrences are very common, each recurrence tends to become worse, and the solution is to administer a long-term management strategy that alters the pathophysiological process.

••••••••••

Hyper-innervation, Neoneuralisation, Receptive Field Enlargement

So, what is going on? What is happening? Why is the intervertebral disc not following the “rules” of healing that other tissues of the body follow?

Undoubtedly, chronic and recurrent low back pain is multifactorial, involving genetics, inflammatory profile, uniqueness and number of injuries, occupation, recreational activities, age, gender, nutrition, etc. Starting about 2 decades ago, a unique explanation for back pain and chronicity began to emerge: more pain nerves grow into the disc.

Today there is almost universal acceptance that the annulus of the intervertebral disc is innervated with pain afferents and the annulus of the disc is the most probable source for low back pain. There was also 100% agreement that these nerves are only found in the annulus, and that the nucleus was aneural (has no nerve supply and therefore cannot initiate a pain response to the brain). However, an important addition to these concepts arose in 1997.

•••••

In 1997, AJ Freemont and colleagues published a study in the journal Lancet, titled (23):

Nerve Ingrowth Into Diseased Intervertebral Disc in Chronic Back Pain

Using samples of the intervertebral discs from 38 humans, these authors were able to show that when the disc degenerates, the nerves in the annulus can migrate into the nucleus. Histologically, these nerves in the nucleus were judged to be pain afferents. Thus the nucleus itself could be a source of discogenic pain. These authors used these anatomical findings to explain why low back pain can be so chronic, and continue to add to the evidence that the disc is the primary source of low back pain.

•••••

Also in 1997, in the journal Spine, another study was published on the topic of nucleus innervation by MH Coppes and colleagues from the Department of Neurosurgery, Groningen University, The Netherlands. Their article was titled (24):

Innervation of “Painful” Lumbar Discs

These authors note that the innervation of intervertebral discs has been extensively described in fetal and adult animals and humans. However, little is yet known about the innervation of severely degenerated human lumbar discs. They question whether a disc that has been removed for low back pain possesses an increased innervation compared with normal discs.

They investigated the innervation of discographically confirmed degenerated and “painful” human intervertebral discs to determine the type and distribution patterns of nerve fibers present. Their investigation used immunocytochemistry from 10 degenerated and 2 control human discs.

In all specimens, nerve fibers of different diameters were found in the anterior longitudinal ligament and in the outer region of the disc. In 8 of 10 degenerated discs, fibers were also found in the inner parts of the disc. The authors concluded:

“Findings indicate a more extensive disc innervation in the severely degenerated human lumbar disc compared with normal discs. The nociceptive properties of at least some of these nerves are highly suggested by their substance P immunoreactivity, which provides further evidence for the existence of a morphologic substrate of discogenic pain.”

•••••
In 2002, AJ Freemont and colleagues from Manchester University, UK, published a study in the Journal of Pathology, titled (25):

Nerve Growth Factor Expression and Innervation of the Painful Intervertebral Disc

In this study, the authors used immunohistochemistry analysis of painful human intervertebral discs to determine the presence of nerve growth factor. Such a finding would support the growth of nociceptors into deeper layers of the annulus, accounting for increased discogenic pain. The authors concluded:

“These findings show that nociceptive nerve ingrowth into painful intervertebral disc is causally linked with nerve growth factor production.”

•••••

In 2002, J. Melrose and colleagues from the University of Sydney, published a study in the journal Spine, titled (26):

Increased Nerve and Blood Vessel Ingrowth Associated with Proteoglycan Depletion in an Ovine Annular Lesion Model of Experimental Disc Degeneration

These authors note that following intervertebral disc injury, there is a loss of disc proteoglycans and disc degeneration ensues. The aim of this study was to evaluate whether disc nerve ingrowth was associated with proteoglycans depletion and disc degeneration. They used a sheep injury model, and like other studies assessed the injured tissues using immunohistochemistry. The injured discs were assessed at 3, 6, 12, and 26 months. They confirmed that disc injury results in degeneration, a loss of proteoglycans, and an ingrowth of nerve fibers. Importantly, nerve ingrowth could take 12 months to achieve a meaningful level; this may explain why increased or chronic back may be delayed following an disc injury. The authors concluded:

“Nerve and blood vessel ingrowth into the annulus fibrosis were strongly associated with proteoglycan depletion.”

•••••

In 2005, B. Peng and colleagues from the Department of Orthopaedics, 304th Hospital, Beijing, China, published a study in the journal Journal of Bone and Joint Surgery, British, titled (27):

The Pathogenesis of Discogenic Low Back Pain

These authors note that discogenic low back pain is a common cause of disability. They state, “discogenic low back pain is non-radicular and occurs in the absence of spinal deformity, instability and signs of neural tension. It arises from the disc itself.” They collected 19 specimens of lumbar intervertebral discs from patients with discogenic low back pain. Once again they used immunohistochemistry to evaluate disc fibers.

The authors found a distinct histological characteristic of the painful disc: there were more nerve fibers in the painful discs than in the control discs. Importantly, the painful discs showed ingrowth of nerve into the nucleus pulposus in 32% of specimens. The authors state:

“Our findings suggest that pain may arise from the nucleus pulposus due to innervation accompanying the ingrowth of granulation tissue.”

•••••

In 2012, Manos Stefanakis, PT, PhD, and colleagues from the Centre for Comparative and Clinical Anatomy, University of Bristol, Bristol, United Kingdom, published a study in the journal Spine, titled (28):

Annulus Fissures Are Mechanically and Chemically Conducive to the Ingrowth of Nerves and Blood Vessels

These authors note that it has long been suspected that lumbar intervertebral discs are a common source of the most severe symptoms of chronic low back pain. They state, “discogenic back pain is closely associated with fissures in the annulus fibrosus, and with the ingrowth of nerves and blood vessels.”

These authors completed a mechanical and biochemical analyses of human cadavers and surgically removed discs to test the hypothesis that fissures in the annulus of degenerated human discs are mechanically and chemically conducive to the ingrowth of nerves and blood vessels. They conclude:

“The two features most strongly associated with discogenic back pain—annulus fissures and nerve ingrowth—may themselves be causally related. It has long been supposed that discogenic back pain can arise from nerves growing into radial fissures.”

“Nerves do grow into fissures in patients with back pain.” 

“The present study has shown that annulus fissures are conducive to the ingrowth of nerves and blood vessels.”

It appears that “annulus fissures are indeed essential for nerve ingrowth into degenerated discs.”

•••••

Summary

The intervertebral disc is innervated with an extensive array of pain nerves. With disc degeneration, there is an increase in the number of pain nerve fibers migrating deeper into the disc, including into the nucleus itself. The increase in the number of pain nerve fibers increases the likelihood that stress and injury will produce low back pain.

Improving mechanical integrity of the spine initiates a neurological sequence that inhibits chronic low back discogenic pain; it “closes the pain gate.” This is the clinical goal of chiropractic spinal manipulation (adjusting) (29). Many studies show that chiropractic spinal adjusting is both effective and has long-lasting clinical improvement in the management of the chronic low back pain patient (29, 30, 31, 32, 33).

REFERENCES

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• Inman VT, and Saunders JMB; Anatamico-physiological aspects of injuries to the intervertebral disc; Journal of Bone and Joint Surgery; 29 (1947); pp. 461–468.
• Smyth MJ, Wright V; Sciatica and the intervertebral disc. An experimental study; Journal of Bone and Joint Surgery [American]; Vol. 40; No. 6; December 1958, pp. 1401-1418.
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• Mooney V; Where Is the Pain Coming From?; Spine; Vol. 12; No. 8; 1987; pp. 754-759.
• Kuslich S, Ulstrom C, Michael C; The Tissue Origin of Low Back Pain and Sciatica: A Report of Pain Response to Tissue Stimulation During Operations on the Lumbar Spine Using Local Anesthesia; Orthopedic Clinics of North America; Vol. 22; No. 2; April 1991; pp. 181-7.
• Izzo R, Popolizio T, D’Aprile P, Muto M; Spine Pain; European Journal of Radiology; May 2015; Vol. 84; pp. 746–756.
• Jayson M, Editor; The Lumbar Spine and Back Pain, Third Edition, Churchill Livingstone, 1987, p. 60.
• Bogduk N, Tynan W, Wilson AS, The nerve supply to the human lumbar intervertebral discs, Journal of Anatomy; 1981, 132, 1, pp. 39-56.
• Bogduk N, The innervation of the lumbar spine; Spine. April 1983;8(3): pp. 286-93.
• Ozawa, Tomoyuki MD; Ohtori, Seiji MD; Inoue, Gen MD; Aoki, Yasuchika MD; Moriya, Hideshige MD; Takahashi, Kazuhisa MD; The Degenerated Lumbar Intervertebral Disc is Innervated Primarily by Peptide-Containing Sensory Nerve Fibers in Humans; Spine; Vol. 31; No. 21; October 1; 2006; pp. 2418-2422.
• Foreman J; A Nation in Pain, Healing Our Biggest Health Problem; Oxford University Press; 2014.
• Pho, K; UST TODAY, The Forum; September 19, 2011; pg. 9A.
• Wang S; Why Does Chronic Pain Hurt Some People More?; Wall Street Journal; October 7, 2013.
• www.ninds.nih.gov; Low Back Pain Fact Sheet; accessed May 12, 2014.
• Vassilaki M, Hurwitz EL; Insights in Public Health: Perspectives on Pain in the Low Back and Neck: Global Burden, Epidemiology, and Management; Hawaii J Med Public Health; Apr 2014; 73(4): 122–126.
• White AA, Panjabi MM; Clinical Biomechanics of the Spine; Lippincott; 1979 and 1990.
• Croft PR, Macfarlane GJ, Papageorgiou AC, Thomas E, Silman AJ; Outcome of Low back Pain in General Practice: A Prospective Study; British Medical Journal; May 2, 1998; Vol. 316, pp. 1356-1359.
• Hestbaek L, Leboeuf-Yde C, Manniche C; Low back pain: what is the long-term course? A review of studies of general patient populations; European Spine Journal; April 2003; Vol. 12; No 2; pp. 149-65.
• Donelson R, McIntosh G; Hall H; Is It Time to Rethink the Typical Course of Low Back Pain?; Physical Medicine and Rehabilitation (PM&R); Vol. 4; No. 6; June 2012, Pages 394–401.
• Itz CJ, Geurts JW, van Kleef M, Nelemans P; Clinical course of non-specific low back pain: a systematic review of prospective cohort studies set in primary care; European Journal of Pain; January 2013;Vol. 17; No. 1; pp. 5-15.
• Dunn KM, Hestbaek L, Cassidy JD; Low back pain across the life course;Best Practice & Research Clinical Rheumatology; October 2013; Vol. 27; No. 5; pp. 591-600.
• Freemont AJ, Peacock TE, Goupille P, Hoyland JA, O’Brien J, Jayson MI; Nerve ingrowth into diseased intervertebral disc in chronic back pain; Lancet; Jul 19, 1997;350(9072):178-81.
• Coppes MH, Marani E, Thomeer RT, Groen GJ; Innervation of “painful” lumbar discs; Spine; October 15, 1997; Vol. 22; No. 20; pp. 2342-2349.
• Freemont AJ, Watkins A, Le Maitre C, Baird P, Jeziorska M, Knight MT, Ross ER; O’Brien JP, Hoyland JA; Nerve growth factor expression and innervation of the painful intervertebral disc; Journal of Pathology; July 2002; Vol. 197; No. 3; pp. 286-92.
• Melrose J, Roberts S, Smith S, Menage J, Ghosh P; Increased nerve and blood vessel ingrowth associated with proteoglycan depletion in an ovine anular lesion model of experimental disc degeneration; Spine; June 15, 2002; Vol. 15; No. 12; pp. 15; pp. 1278-1285.
• Peng B, Wu W, Hou S, Zhang C, Li P, Yang Y; The pathogenesis of discogenic low back pain; Journal of Bone and Joint Surgery (Br); January 2005; Vol. 87-B; No. 1; 62-67.
• Stefanakis M, Al-Abbasi M, Harding I; Pollintine P, Dolan P, Tarlton J, Adams MA; Annulus Fissures Are Mechanically and Chemically Conducive to the Ingrowth of Nerves and Blood Vessels; Spine; October 15, 2012; Vol. 37; Number 22; pp. 1883–1891
• Kirkaldy-Willis WH, Cassidy JD; Spinal Manipulation in the Treatment of Low Back Pain; Canadian Family Physician, March 1985, Vol. 31, pp. 535-540.
• Meade TW, Dyer S, Browne W, Townsend J, Frank OA; Low back pain of mechanical origin: Randomized comparison of chiropractic and hospital outpatient treatment; British Medical Journal; Volume 300, June 2, 1990, pp. 1431-7.
• Giles LGF, Muller R; Chronic Spinal Pain: A Randomized Clinical Trial Comparing Medication, Acupuncture, and Spinal Manipulation; Spine, July 15, 2003; 28(14):1490-1502.
• Muller R, Lynton G.F. Giles LGF, DC, PhD; Long-Term Follow-up of a Randomized Clinical Trial Assessing the Efficacy of Medication, Acupuncture, and Spinal Manipulation for Chronic Mechanical Spinal Pain Syndromes; Journal of Manipulative and Physiological Therapeutics; January 2005, Vol. 28; No. 1; pp. 3-8.
• Keeney BJ, Fulton-Kehoe D, Turner JA, Wickizer TM, Chan KCG, Franklin; Early Predictors of Lumbar Spine Surgery after Occupational Back Injury: Results from a Prospective Study of Workers in Washington State; Spine; May 15, 2013; Vol. 38; No. 11; pp. 953-964

When a force is applied to a joint, increased motion and “joint separation” occur. This can be done without causing any injury to the joint tissues (bones, cartilage, ligaments, muscles, tendons, nerves, etc.). This increased motion has a number of proposed benefits, including (1):

• The disruption of intra-articular and peri-articular adhesions.
• The remodeling of peri-articular fibrosis.
• Generating spinal cord reflexes that inhibit muscle tone and spasm.
• Improving proprioception to inhibit pain by closing the pain gate.

The classic joint cavitation process was initially described by Sandoz in 1976 (2). In this initial publication, Sandoz categorizes joint motion into three categories:

• Active Motion
• Passive Motion
• Peri-articular Paraphysiological Space Motion

This model of joint cavitation is supported by others (1, 3), and is explained as follows:

There are three categories of joint motion:

1)     Active Range of Motion.

This is the motion that occurs as a consequence of performing exercise.

2)     Passive range of Motion.

This is the motion that occurs as a consequence of stretching and/or through mobilization techniques.

“Beyond the end of the active range of motion of any synovial joint, there is a small buffer zone of passive mobility.” A joint can only move into this zone with passive assistance, and going into this passive range of motion “constitutes mobilization.” [not manipulation.]

3)     Peri-articular Paraphysiological Space Motion

“At the end of the passive range of motion, an elastic barrier of resistance is encountered.”

“If the separation of the articular surfaces is forced beyond this elastic barrier, the joint surfaces suddenly move apart with a cracking noise.”

“This additional separation can only be achieved after cracking the joint and has been labeled the paraphysiological range of motion. This constitutes manipulation.”

“The cracking sound on entering the paraphysiological range of motion is the result of sudden liberation of synovial gases—a phenomenon known to physicists as cavitation.”

Following cavitation, a synovial bubble can be observed on x-rays, which is reabsorbed over the following 30 minutes.  During this “refractory period” there is no resistance between the passive and paraphysiological zones.

“At the end of the paraphysiological range of motion, the limit of anatomical integrity is encountered.  Movement beyond this limit results in damage to the capsular ligaments.”

Joint manipulation [adjusting] “requires precise positioning of the joint at the end of the passive range of motion and the proper degree of force to overcome joint coaptation” [to overcome the resistance of the joint surfaces in contact].

•••••

Physicians JB Roston and R Wheeler Haines from St. Thomas’s Hospital Medical School, London, UK, published the first study in the literature to investigate the cavitation of a joint leading to an audible “cracking” of the joint in 1947. It was published in the Journal Of Anatomy and titled (4):

Cracking in the Metacarpal-Phalangeal Joint

In this study, the subject’s middle digit was wrapped with adhesive plaster, and a stout string was tied tightly over this, around the proximal phalanx. The string was then attached to an immovable object through a tensiometer. A preliminary x-ray was taken. The subject was instructed to draw his hand away until the metacarpal-phalangeal (MC) joint “cracked”, and the tensiometer recorded the degree of traction. After “cracking,” while still under tension, a second x-ray was taken, and the degree of joint separation was measured.

When the “crack” occurred, an immediate and significant increase in joint separation also occurred, from 1-3 mm. (Picture after 1, 2, 5)

These authors noted that a tractional tension of about 6 kg is insufficient to produce a “crack,” but will slightly separate the adjacent joint surfaces. After a tension of about 7 kg or more, a “crack” will occur and there is an immediate significant separation of the joint surfaces.

After the joint “cracks” and the increased joint separation is achieved, the increased separation can be repeated for the next 17-22 minutes without having to recavitate the joint. Further direct tension on the joint will not produce a second crack; the joint is in a “refractory phase.”

After about 20 minutes (17-22 minutes), the whole cycle of joint “cracking” can be repeated. “The minimum time recorded between two cracks produced by direct tension was 17 minutes, and never more than 22 minutes rest was required before a second crack could be produced.”

After “cracking” the joint, a tractional x-ray shows a gas shadow bubble in the joint. These authors suggest that the refractory phase after cracking corresponds to the time required for the gas bubble to pass back into solution.

These authors found that some joints were difficult (or impossible) to cavitate (“crack”). They propose that the explanation for this “is inability to relax the muscles whose tendons pass across the joint.” This has clinically practical importance.

•••••

Decades later, a second, more detailed study investigating the joint cavitation and “cracking” phenomenon appeared in the Annals of Rheumatic Diseases in 1971. The investigators were from the Bioengineering Group for the study of Human Joints, at the University of Leeds in the United Kingdom. Their study is titled (5):

‘Cracking Joints’ A Bioengineering Study of Cavitation in the Metacarpal-phalangeal Joint

The authors used a similar investigational approach as the prior study (Roston/Haines, 4) on 17 test subjects. Interestingly, on 5 of their test subjects they were not able to cavitate their joints because they could “not relax sufficiently to allow a test to be performed properly.” In agreement with the prior study (4), increased muscle tension appears to impair the ability of a joint to cavitate and “crack.”

These authors largely agree with the finding of Roston/Haines (4) above. With increased joint traction, they state:

“The joint separation increases at a high rate, allowing the net flow of fluid into the low pressure regions. This results in collapse of the vapor phase of the cavities with consequent energy release as noise (the ‘crack’ heard externally).”

The gas removed during the period of low pressure “does not   reabsorb for 20 to 30 minutes.”

“This gas is readily visible on the radiograph, but is not responsible for causing the crack; it is there as a consequence of the cracking phenomenon.”

“The results support the view that ‘cavitation’ is responsible for the phenomenon of cracking.”

These authors extracted the post-cavitation gas bubble and analyzed it. They found it to be composed of carbon dioxide.

•••••

The most recent study investigating joint cavitation and “cracking” was published April 15, 2015, in the journal Public Library of Science One (PLOS ONE). Gregory N. Kawchuk from the Department of Physical Therapy, Faculty of Rehabilitation Medicine, University of Alberta, CAN, and colleagues titled their study (6):

Real-Time Visualization of Joint Cavitation

The objective of this study was to characterize the events associated with joint cracking within the joint itself using real-time cine-magnetic resonance imaging (cine-MRI). This article presents direct evidence from real-time magnetic resonance imaging that the mechanism of the sound obtained is from joint cavitation. The authors applied a slowly increasing long-axis traction manually to 10 metacarpal-phalangeal joints while imaging the joints with rapid cine-magnetic resonance images at a rate of 3.2 frames per second until the cracking event occurred.

This cine-MRI study, in agreement with prior x-ray studies, showed that joint cracking following joint distraction followed this sequence of events:

• The process begins with the resting phase where joint surfaces are in close contact.
• “As traction forces increased, real-time cine magnetic resonance imaging demonstrated rapid cavity inception at the time of joint separation and sound production after which the resulting cavity [gas bubble] remained visible.”

The evidence shows that the mechanism of joint cracking is related to cavity (gas shadow) formation. These authors make the following observations:

“Our results offer direct experimental evidence that joint cracking is associated with cavity inception.”

“Cracking” sounds require time to pass before they can be repeated despite ongoing joint motion. This is called the refractory period.

“A light distraction force will barely separate the joint surfaces. With a greater distraction force, the surfaces resist separation until a critical point after which they separate rapidly. It is during this rapid separation phase that the characteristic cracking sound is produced. Following cracking, the joint is in a refractory phase where no further cracking can occur until time has passed (approximately 20 minutes).”

“Cine-MRI demonstrated minimal joint surface separation in the resting phase prior to joint cracking followed by rapid joint separation during the crack itself.”

“Cine-MRI revealed rapid cavity inception associated with concurrent sound production and joint separation.”

These authors also observed that joint separation with cavity formation does not occur at the same traction force in each finger. This implies that some joints are easier and some joints are harder to cavitate. Other research, noted above, attribute this to tension of the muscles that cross a particular joint that one is attempting to cavitate.

These authors end their study by stating: “Habitual knuckle cracking has not been shown to increase joint degeneration.”

•••••

Is Frequent Joint “Cracking” Harmful to Joints?

Several studies have investigated as to whether habitual joint cracking is harmful to the cavitated joint, especially with respect to the incidence of degenerative joint disease (osteoarthritis). In 1975, researchers for the Departments of Medicine and Rehabilitation Medicine at the University of Southern California School of Medicine in Los Angeles, CA, published a study in the Western Journal of Medicine, titled (7):

The Consequences of Habitual Knuckle Cracking

The authors note that habitual knuckle cracking has been considered to be a cause of arthritis. Knuckle cracking appears to cause some comfort or satisfaction to the person doing it; however, it has been claimed, “arthritis would be an inevitable outcome.” As a consequence, many children with this habit are chided to stop cracking their knuckles lest arthritis or enlarged knuckles or both develop.

Knuckle cracking appears to be a habit that begins in childhood and persists into adult life.

In this study, 28 (average age 78.5 years) patients were examined clinically and by x-ray; 15 were habitual knuckle crackers and 13 were not (controls).

The authors found that only one subject with a history of knuckle cracking showed metacarpal-phalangeal degenerative joint disease (DJD). In contrast, 5 of the control subjects (non-knuckle crackers) had metacarpal-phalangeal degenerative joint disease.

Elderly people (average 78.5 years) and knuckle cracking / osteoarthritis

These authors observed that every patient with metacarpal-phalangeal degenerative joint disease, whether or not they were knuckle crackers, also had radiographic evidence of distal hand degenerative joint disease, suggesting that “metacarpal-phalangeal degenerative joint disease is a function of whatever the predisposing factors are to osteoarthritis” and that

“metacarpal-phalangeal degenerative joint disease is not a consequence of knuckle cracking.”

These authors also made these comments:

This survey of a “geriatric patient population with a history of knuckle cracking failed to show a correlation between knuckle cracking and degenerative changes of the metacarpal phalangeal joints.”

“The data fail to support evidence that knuckle cracking leads to degenerative changes in the metacarpal phalangeal joints in old age.”

“The chief morbid consequence of knuckle cracking would appear to be its annoying effect on the observer.”

This study concludes that habitual knuckle cracking does not increase the incidence of cracked knuckle osteoarthritis. However, in reviewing the data, their findings could have been interpreted differently:

1/15 knuckle crackers had knuckle DJD, = 6.7%

5/13 who did NOT crack their knuckles had knuckle DJD, = 38.5%

An alternative interpretation could be that habitual knuckle cracking significantly reduces the incidence of knuckle degenerative joint disease. Mathematically, it is an 82% reduction.

•••••

 A more recent investigation of knuckle cracking and osteoarthritis was published in the journal American Board of Family Medicine in 2011 by military physicians Kevin deWeber,  Mariusz Olszewski, and Rebecca Ortolano. Their article is titled (8):

Knuckle Cracking and Hand Osteoarthritis

These physicians note that the characteristics of hand osteoarthritis include:

• It increases in prevalence and severity with age.
• 22% of those aged between 71 to 100 years have symptomatic hand osteoarthritis.
• Risk factors include prior joint trauma, family history of hand osteoarthritis, and history of heavy labor involving the hands.
• Those with hand osteoarthritis have reduced grip strength, difficulty writing, difficulty handling small objects, and difficulty carrying objects.

Consequently, they state:

“Given this burden of suffering from hand osteoarthritis and the lack of curative or disease-modifying treatments, factors that potentially protect against osteoarthritis warrant further investigation. One such factor is knuckle cracking.”

Knuckle cracking is a behavior that involves manipulation of the finger joints that results in an audible crack, and it is often done habitually. It is estimated that 25% to 54% of people habitually crack their knuckles:

• 25% in adults older than 45 years
• 34% in 11-year-old children
• 54% among nursing home residents with a mean age of 78 years

This study assessed 215 individuals; 135 with osteoarthritis, and 80 controls. Their mean age was 62 years (50 to 89 years). Twenty percent habitually cracked their knuckles. Participant’s hands were assessed radiographically.

Study subjects quantified the frequency of their daily knuckle cracking:

• None
• 1–5 times/day
• 6–10 times/day
• 10–20 times/day
• >20 times/day

Study participants described how frequently each day they crack each knuckle and for how many years they have been doing it. This was the first study to correlate the duration and the total volume of previous knuckle cracking with osteoarthritis.

The mechanics of knuckle cracking was described as follows:

“During an attempt to crack a knuckle, the joint is manipulated by axial distraction, hyperflexion, hyperextension, or lateral deviation. This lengthens part or all of the joint space and greatly decreases intra-articular pressure, causing gases that have dissolved in the synovial fluid to form microscopic bubbles, which coalesce. When the joint space reaches its maximum distraction (up to 3 times its resting joint space distance), joint fluid rushes into the areas of negative pressure. The larger bubbles suddenly collapse into numerous microscopic bubbles, leading to the characteristic cracking sound. The maneuver leaves the joint space wider than it had been and synovial fluid more widely distributed. The stretching of joint ligaments required to produce the widened joint space also leaves the joint with greater range of motion. It typically takes at least 15 minutes for the joint to be able to be cracked again because of the time required for the microscopic bubbles to fully dissolve into solution and for the joint space to retract back to its resting position.”

Findings include:

“This study represents the most comprehensive evaluation to date of habitual knuckle cracking and any association with hand osteoarthritis. Our findings support the conclusions of 2 previous studies that the presence of knuckle cracking is not associated with hand osteoarthritis.”

“The duration of knuckle cracking has no correlation to the presence of osteoarthritis.” There was “no significant correlation of knuckle cracking ‘crack-years’ with osteoarthritis in the respective joint.”

These authors conclude, “a history of habitual knuckle cracking—including the total duration and total cumulative exposure to knuckle cracking—does not seem to be a risk factor for hand osteoarthritis.”

These authors note that some people crack their knuckles because of the sense of relief it can bring, some do so because of habit, and some for both reasons. After knuckle cracking, there is an “immediate joint tension release and increased joint range of motion.” A “common urban legend suggests that knuckle cracking will lead to arthritis of the hand joints,” but this is not “supported in the medical literature.”

•••••

A lay and/or cynical argument against regular chiropractic care is that the regular cavitation of the joints increases the risk of osteoarthritis. The reviewed articles investigated a clinically relevant number of individuals who cavitated their knuckle joints multiple times daily for years and suffered no increased risk of joint osteoarthritis. One study suggests that regular cavitation of joints may in fact reduce the risk of joint osteoarthritis.

There appears to be no controversy that joint cavitation improves joint range of motion and reduces articular symptomatology.

REFERENCES 

• Kirkaldy-Willis WH, Cassidy JD; Spinal Manipulation in the Treatment of Low back Pain; Canadian Family Physician; March 1985, Vol. 31, pp. 535-540.
• Sandoz R. Some physical mechanisms and effects of spinal adjustment. Ann Swiss Chiropractic Association; 1976; 6: 91–141.
• Fischgrund, Jeffrey S, Neck Pain, monograph 27, American Academy of Orthopaedic Surgeons, 2004.
• Roston JB, and R. Wheeler-Haines R; Cracking in the Metacarpo-Phalangeal Joint; Journal Of Anatomy; Vol. 81; Part 2; 1947; pp. 165-173.
• Unsworth A, Dowson D, Wright V. ‘Cracking joints’ A bioengineering study of cavitation in the metacarpophalangeal joint. Ann Rheum Dis. 1971; 30: 348–358.
• Gregory N. Kawchuk GN, Jerome Fryer J, Jacob L. Jaremko JL, Hongbo Zeng H, Lindsay Rowe L, Richard Thompson R; Real-Time Visualization of Joint Cavitation; Public Library of Science One (PLOS ONE); April 15, 2015; Vol. 10; No. 4; pp. e0119470.
• Robert L. Swezey RL, MD, and Stuart E. Swezey SE; The Consequences of Habitual Knuckle Cracking; Western Journal of Medicine; May 1975; Vol. 122; pp. 377-379.
• Kevin deWeber K, MD; Mariusz Olszewski M, MD; Rebecca Ortolano R; Knuckle Cracking and Hand Osteoarthritis; American Board of Family Medicine; March-April 2011; Vol. 24; No. 2; pp. 169-174.

The escalation in health care spending in the United States has mandated an approach for cost containment. The contemporary approach in this effort is called “Evidenced-Based Medicine.” Proponents of Evidence Based Medicine have become increasingly organized, beginning in the 1990s. As an example, in 1996, the British Medical Journal published an editorial titled (1):

Evidence Based Medicine: What it is and What it isn’t

This article describes Evidence Based Medicine as:

“Evidence based medicine is the conscientious, explicit, and judicious use of current best evidence in making decisions about the care of individual patients. The practice of evidence based medicine means integrating individual clinical expertise with the best available external clinical evidence from systematic research.”

A necessary component for the implementation of Evidence Based Medicine is the development and use of Clinical Practice Guidelines. As stated in the journal Health Affairs in 2005 (2):

“One common implementation of Evidence Based Medicine involves the use of clinical practice guidelines during medical decision making to encourage effective care.”

A central theme in Evidence Based Guidelines is that treatment should be reasonable and necessary. To establish that treatment is reasonable and necessary, the treating clinician should be using measurement outcomes.

Measurement Outcomes measure the health status of a patient before treatment, and then again after treatment (or a series of treatments) is/are performed. If the post treatment measurement outcome shows improvement, it is classically interpreted that the treatment was both reasonable and necessary. When measurement outcomes stop improving, it means that the patient’s clinical status has reached maximum improvement, or that a different clinical approach may be warranted.

There are literally hundreds of measurement outcomes available for health care providers. Each discipline of health care has developed recognized measurement outcomes that best serve their disciplines and patient’s needs. Chiropractors and other musculoskeletal disciplines often use the same measurement outcomes. These same measurement outcomes that are used clinically are often used in musculoskeletal research. Musculoskeletal health care providers, including chiropractors, commonly use these measurement outcomes:

• Oswestry Back Pain Disability Index (ODI)
• Roland-Morris Low Back Pain Disability Questionnaire
• Neck Disability Index (NDI)
• Functional Rating Index (FRI)
• Whiplash Disability Questionnaire
• Headache Disability Index

A sample of each of these is included below.

Clinically, measurement outcomes are primarily used for two purposes:

• To show that the treatment given was reasonable and necessary.
• To determine when the patient’s clinical status has reached maximum improvement.

Essentially, if measurement outcomes show progressive improvement in a patient’s clinical status, it means that the treatment given was reasonable and necessary, and that continued treatment is warranted. Additional treatment is warranted as long as the patient’s clinical status continues to improve.

In contrast, if measurement outcomes no longer show improvement, it is often interpreted as meaning that the patient’s clinical status has reached maximum improvement, and additional scheduled treatment may not be warranted. Often, maximum improvement is determined to be when there is no significant change in symptoms and measurement outcomes for approximately 8 weeks (3).

Secondary reasons to use measurement outcomes include:

• To document long-term or permanent symptoms and/or disabilities for a particular patient.
• To help apportion treatment, residual symptoms and permanent disabilities.
• The frequency of the use of measurement outcomes is at the discretion of the treating doctor, but here are a few suggestions:
• Appropriate measurement outcomes should be used as a component of initial patient intake.
• For patients under active care, measurement outcomes should be completed at least once per month.
• For patients under maintenance care, measurement outcomes should be completed at least once every 10-12 patient visits.

Measurement outcomes are a standard component of contemporary clinical practice, including for chiropractors. Using measurement outcomes is an invaluable tool for the modern health care provider. Failure to use measurement outcomes invites criticism and conflict. Future health providers will be increasingly judged by their use of measurement outcomes and their results.

••••••••••

OSWESTRY LOW BACK DISABILITY QUESTIONNAIRE

The Oswestry Low Back Disability was first published in the journal Physiotherapy in 1980 by orthopedic surgeon Jeremy Fairbank, MD, and colleagues from Nuffield Orthopaedic Centre, Oxford, United Kingdom (4).

The Oswestry was revised in 2000 and published in the journal Spine (5).

The Oswestry has become the gold standard for measuring the degree of disability and estimating quality of life in a people with low back pain. The Oswestry is a valid and vigorous outcome measurement (5).

Scoring the Oswestry is as simple as adding the number value on the left side of the form. The total number is the disability index for that patient. The Oswestry disability index is categorized as follows:

0 – 20: Minimal disability

21- 40: Moderate Disability

41 – 60: Severe Disability

61 – 80: Crippling back pain

81 – 100: These patients are either bed-bound or have an exaggeration of their symptoms

••••••••••

Roland-Morris LOW BACK PAIN DISABILITY QUESTIONNAIRE

The Roland-Morris Questionnaire was first published in the journal Spine in 1983 (6, 7). Professor Martin Roland and colleague R. Morris from the Institute of Public Health at the University of Cambridge developed it. It is longer than the Oswestry, having 24 questions instead of 10. Similarly to the Oswestry, it is considered to be valid and sensitive.

The Roland-Morris Questionnaire is a self-administered. Each of the 24 questions that are checked off is assigned a value of 1. Higher numbers on the 24-point scale reflects greater levels of disability. Clinical improvement over time is graded based on the analysis of serial questionnaire scores. If, for example, at the beginning of treatment, a patient’s score was 18 and, at the conclusion of treatment, his/her score was 8 (10 points of improvement), we would calculate a 55% improvement. [(18-8)/18 x 100]

••••••••••

NECK DISABILITY INDEX

The Neck Disability Index was created by chiropractor Howard Vernon, DC, from Canadian Memorial Chiropractic College, Toronto, Ontario, CAN. It was initially published in the Journal of Manipulative ad Physiological Therapeutics in 1991 (8). The initial purpose of the Neck Disability Index was to determine the disability of individuals who had been injured in motor vehicle collisions.

In the construction of the Neck Disability Index, Dr. Vernon modified the Oswestry. It is now the gold standard for measuring the degree of disability and estimating quality of life in a person with neck pain caused my motor vehicle collisions. Similar to the Oswestry, it has been shown to be valid, reliable ad sensitive.

The Neck Disability Index is scored identically to the Oswestry.

••••••••••

FUNCTIONAL RATING INDEX

The Functional Rating Index is newer, first published in the journal Spine in 2001 (9). The primary authors of the Functional Rating Index are chiropractors Ron Feise, DC, and J. Michael Menke, DC. Dr. Menke is from Palmer Chiropractic College West, located in San Jose, CA.

The Functional Rating Index combines the concepts of the Oswestry Low Back Disability Questionnaire and the Neck Disability Index. It has a total of 10 questions, improving clinical utility (time required for administration).

Their initial study assessed 139 subjects. Their conclusions are:

“The Functional Rating Index appears to be psychometrically sound with regard to reliability, validity, and responsiveness and is clearly superior to other instruments with regard to clinical utility. The Functional Rating Index is a promising useful instrument in the assessment of spinal conditions.”

The Functional Rating Index has 10 questions, and each response is given a value of 0 – 4. Adding up the total score and dividing by 40 determines the percent of disability. If, for example, the summed score is 30, the total disability would be 75%. [30/40 = .75]

If, for example, the Functional Index Score was 10 on a follow-up assessment, the total disability would be 25% [10/40 = .25], and the clinical improvement would be [(30-10)/30 = 67%]

••••••••••

WHIPLASH DISABILITY QUESTIONNAIRE

        The Whiplash Disability Questionnaire was first published in the journal Spine in 2004 (10). It was designed by Melanie Pinfold and colleagues from the School of Physiotherapy, La Trobe University, Victoria, Australia. Its reproducibility and responsiveness was further assessed by the same group and published in the journal Pain (11).

• The Whiplash Disability Questionnaire measures functional limitations and psychometrics associated with whiplash injury. It was developed from the Neck Disability Index, but it consists of 13 questions rather than 10. The authors concluded:

“The Whiplash Disability Questionnaire has excellent short- and medium-term reproducibility and responsiveness in a population seeking treatment for Whiplash Associated Disorders.”

The Whiplash Disability Questionnaire has 13 questions with a possible of 10 points per question. Scoring is done by adding the total points and dividing by 130.

••••••••••

HEADACHE DISABILITY INDEX

The Headache Disability Index was developed at the Department of Otolaryngology-Head and Neck Surgery, Henry Ford Hospital, Detroit, Michigan. It was first published in the journal Neurology in 1994 (12), and further validated in the journal Headache in 1995 (13).

The Headache Disability Index is 25 questions, and is designed to quantify the impact of headaches on daily living. Each question has only 3 possible responses: YES = 4;  SOMETIMES = 2; NO = 0

The authors determined that a 29 point change or greater in the total score from test to retest must occur before the change can be attributed to treatment effects. The authors found the Headache Disability Index to have strong consistency and reliability. They concluded:

“The Headache Disability Index is useful in assessing the impact of headache, and its treatment, on daily living.”

Two Viable, Overlapping Models

Anecdote

Sports Team Doctor Calls the Shots
Portola Valley Physician Aims for Zero Pain

San Francisco Chronicle
October 7, 2000

Friends of Dr. Mark Sontag of Portola Valley, CA, like to joke that he’s “a man for all seasons.”

A specialist in sports medicine and rehabilitation, Sontag is a team doctor for the San Francisco Giants, the San Jose Sharks, and the San Jose SaberCats, as well as is a consulting spinal physician for the Oakland Raiders and Menlo Colleges athletic programs. He has also treated players for the San Francisco 49ers.

In July 2000, Dr. Sontag and colleagues opened the Sports, Pain, and Rehabilitative Care Center in Menlo Park for the treatment of chronic and acute pain sufferers. Their patients are not elite athletes, but people with chronic pain syndrome who have undergone previous medical or surgical treatment with little or no relief.

Sontag has developed a theory about the levels of pain tolerance among athletes that now forms this center’s treatment model.

Sontag, a certified physiatrist, said “neurological studies show that motion tends to block pain impulses to the brain.” In the case of some athletes, this enables them to perform at almost superhuman levels.

Sontag has established a pecking order of pain tolerance that puts hockey players at the highest pain threshold and baseball players at the lowest, with football players somewhere in the middle.

Eventually, he came to believe that there was a correlation between pain thresholds and how much continuous movement a particular sport demands of an injured athlete. “The more action, the less pain is likely to be felt, and I’ve observed that this applies not only to athletes but for others too.”

As examples, football has a relatively brief burst of action wrapped around lengthy strolls back to the huddle, timeouts and other and scheduled delays.

By comparison, hockey matches are 60 minutes of almost continuous action, while in baseball, players, may not do much for several innings at a time.

Introduction

In 1970, Princeton educated physiologist Irvin M. Korr, PhD, emphasized the importance of motion for life and health, stating (1):

What does human life consist of? What does man do?

Man does all the things that we see each other do. He moves, runs, works, plays tennis, builds buildings, paints pictures, makes music, makes love — to paraphrase the flower children, he makes love and war. He is creative. He teaches, learns, writes, educates, practices medicine, does surgery, and gives osteopathic manipulations.

If you look at these activities objectively, you will see that in all of them the body as a whole is moved or some part of the body is moved; and the common feature, the indispensable substratum, is the contraction of skeletal musculature. Human life is expressed through the contractile processes of striated muscle. Every aspect of human life is acted out by the body’s muscles and joints. Everything man does to express his aspirations and convictions can be perceived by others only through his bearing and demeanor and utterances, and these are composites of myriads of finely controlled motions.

Education itself is sometimes defined as a change in behavior and behavior is produced by muscles acting on joints.

Here then is an important conclusion which I think is implicit in the total osteopathic perspective: that the musculoskeletal system is the primary machinery of life. These are the body parts that act together to transmit and modify force and motion through which man acts out his life. But since machinery must be supplied with motor power in order to function, our concept of the primary biologic machinery should include its direction by the nervous system acting in response to the continual sensory input that reports what is going on in the outside environment and what is going on in the body itself; hence, the “neuromusculoskeletal” system.

If the musculoskeletal system and the nervous system that directs it comprise the primary machinery of life, then what is the function of all the rest of the bodily machinery with which medicine is so much concerned? As the title suggests, their function is entirely supportive. Their concern is with the care and maintenance of the primary machinery of life, which means supplying fuels and building materials, disposing of wastes and end products, taking care of the defense and repair and regeneration of components and in general maintaining regulation of the internal environment in which the cells of the primary machinery carry out their function.

The musculoskeletal system is the largest mass of the body and the main consumer. Muscles consume more energy, more rapidly and in wider ranges, than any other tissues in the body.

•••••••••

As noted by Dr. Korr, motion is critical for human life and its expression. The motion of the spine is dependent upon the integrity of the intervertebral disc. The intervertebral disc gives the spine its mobility (2). The intervertebral disc also acts as a shock absorber, and is primarily responsible for carrying all of the compressive loads to which the trunk is subjected (3).

The adult intervertebral disc is void of blood vessels (4, 5). Above and below each intervertebral disc is the vertebral body. The vertebral body is quite vascular (it has a well developed blood supply). Between the disc and the vertebral body is a porous cartilaginous end plate. Disc cell nutrition, health, water binding and hydrostatic properties are dependent upon motion. Deleterious consequences are inevitable following anything that impairs intervertebral disc motion.

(Picture from reference #6)

Reviews of pathology and the evolutionary basis for survivability links infection, inflammation, and excessive-harmful tissue fibrosis, resulting in impaired motion. Succinctly stated by James Cyriax, MD, in 1982 (7):

“The excessive reaction of tissues to an injury is conditioned by the overriding needs of a process designed to limit bacterial invasion. If there is to be only one pattern of response, it must be suited to the graver of the two possible traumas. However, elaborate preparation for preventing the spread of bacteria is not only pointless after an aseptic injury, but is so excessive as to prove harmful in itself. The principle on which the treatment of post-traumatic inflammation is based is that the reaction of the body to an injury unaccompanied by infection is always too great.”

Many others support this perspective (8, 9, 10, 11, 12, 13). In summary, for more than half a century, experts in pathology, physiology, orthopedics, sports injuries, and wound healing have suggested this model:

Inflammation is a paradox. Inflammation can directly kill pathogens. Inflammation also triggers a fibrous response that walls-off infection so that the pathogens are less likely to spread and kill the host. Without inflammation we would die of infection. All who are alive today had ancestors that could successfully initiate an inflammatory response, kill pathogens, and wall off the pathogens.

Infection can kill the young before they can reproduce. Hence, a strong inflammatory response is genetically selected, giving those with such a response a survivability advantage. Our ancestors genetically handed down these traits and we possess them. In a world prior to the availability of antibiotics, inflammation, with reactive walling-off fibrosis to contain pathogens, is desirable because it increases host survivability.

Infections were the primary cause of death for humans for millennias. Infections remained the primary cause of human death until very recent history, only a few decades ago.

Infection is not the only cause of inflammation. Inflammation is also triggered by trauma, excessive tissue stress, chemicals, and immunologic responses. Apparently, the body cannot distinguish the different causes of inflammation from each other, and they all trigger a fibrous response. “The resolution of inflammation in the body is fibrosis.”

This fibrosis response is necesasary when there is an infection, it is life-saving. However in an aseptic sterile injury or tissue stress, the fibrous response is excessive and it creates adverse mechanical deficits. These adverse mechanical deficits create tissue stiffness and limit the mobility of joints. These mechanical deficits impair local biomechanical function, affecting performance, generating pain, and accelerating degenerative changes.

For 40 years it has been understood that the structure primarily responsible for back pain, especially for chronic back pain, is the intervertebral disc (14, 15, 16, 17, 18, 19, 20). It is proposed that there is a connection between discogenic back pain and lack of intervertebral disc movement.

Model #1: Mechanics Influences Chemistry

The United States of America is plagued with chronic pain. Of the 238 million adults in America, approximately half of them have chronic daily pain (21). The conservative estimate of the direct costs and lost productivity resulting from this pain is up to $635 billion yearly (22).

Chronic pain affects every region of the body. Quantifying the anatomical regions for American’s chronic pain shows that the most significantly affected region is the lower back (23):

Hip Pain 07.1%

Finger Pain 07.6%

Shoulder Pain 09.0%

Neck Pain 15.1%

Severe Headache 16.1%

Knee Pain 19.5%

Lower-Back Pain 28.1%

Most pain is a chemical event. Inflammatory chemicals irritate pain nerves. The understanding of the inflammatory chemical nature of pain was awarded the Nobel Prize in Physiology or Medicine in 1982. In 2007, the journal Medical Hypothesis states (24):

“Every pain syndrome has an inflammatory profile consisting of the inflammatory mediators that are present in the pain syndrome.”

“The key to treatment of Pain Syndromes is an understanding of their inflammatory profile.”

“Our unifying theory or law of pain states: the origin of all pain is inflammation and the inflammatory response.”

“Irrespective of the type of pain whether it is acute or chronic pain, peripheral or central pain, nociceptive or neuropathic pain, the underlying origin is inflammation and the inflammatory response.”

“Activation of pain receptors, transmission and modulation of pain signals, neuro-plasticity and central sensitization are all one continuum of inflammation and the inflammatory response.”

“Irrespective of the characteristic of the pain, whether it is sharp, dull, aching, burning, stabbing, numbing or tingling, all pain arises from inflammation and the inflammatory response.”

The most common treatment of inflammatory pain is consumption of drugs, specifically non-steroidal anti-inflammatory drugs (NSAIDs). However, when these drugs (NSAIDs) are taken for chronic pain, there are many serious side effects. In 2003, the journal Spine states (25):

“Adverse reactions to non-steroidal anti-inflammatory (NSAID) medication have been well documented.”

“Gastrointestinal toxicity induced by NSAIDs is one of the most common serious adverse drug events in the industrialized world.”

“The newer COX-2-selective NSAIDs are less than perfect, so it is imperative that contraindications be respected.”

There is “insufficient evidence for the use of NSAIDs to manage chronic low back pain, although they may be somewhat effective for short-term symptomatic relief.”

In 2006, the journal Surgical Neurology states (26):

Blockage of the COX enzyme inhibits the conversion of arachidonic acid to the very pro-inflammatory prostaglandins that mediate the classic inflammatory response of pain.

“More than 70 million NSAID prescriptions are written each year, and 30 billion over-the-counter NSAID tablets are sold annually.”

“5% to 10% of the adult US population and approximately 14% of the elderly routinely use NSAIDs for pain control.”

Almost all patients who take the long-term NSAIDs will have gastric hemorrhage, 50% will have dyspepsia, 8% to 20% will have gastric ulceration, 3% of patients develop serious gastrointestinal side effects, which results in more than 100,000 hospitalizations, an estimated 16,500 deaths, and an annual cost to treat the complications that exceeds 1.5 billion dollars.

“NSAIDs are the most common cause of drug-related morbidity and mortality reported to the FDA and other regulatory agencies around the world.”

One author referred to the “chronic systemic use of NSAIDs to ‘carpet-bombing,’ with attendant collateral end-stage damage to human organs.”

Vert Mooney, MD (d. 2009), was a renowned and respected orthopedic surgeon. He was trained at Columbia University College of Physicians and Surgeons (Medical Doctor) and at the University of Pittsburgh (Orthopedic Surgeon).

Dr. Mooney was a founding member of the North American Spine Society (NASS), and he served as NASS President from 1987-1988. He also received the Lifetime Achievement Award in Lumbar Spine Research from the International Society for the Study of Lumbar Spine in 2008. His area of specialty was in advocating for non-surgical approaches to the management of acute and chronic lumbo-pelvic pain, and the promotion of interdisciplinary approaches to the prevention, diagnosis and treatment of lower back spinal problems.

In his 1986 Presidential Address of the International Society for the Study of the Lumbar Spine, Dr. Mooney made these comments in the journal Spine, in an article titled (16):

Where Is the Pain Coming From?

“In the United States in the decade from 1971 to 1981, the numbers of those individuals disabled from low-back pain grew at a rate 14 times that of the population growth. This is a greater growth of medical disability than any other. Yet this growth occurred in the very decade when there was an explosion of ergonomic knowledge, labor-saving mechanical assistance devices, and improved diagnostic equipment. We apparently could not find the source of pain.”

“Anatomically the motion segment of the back is made up of two synovial joints and a unique relatively avascular tissue found nowhere else in the body – the intervertebral disc. Is it possible for the disc to obey different rules of damage than the rest of the connective tissue of the musculoskeletal system?”

“Mechanical events can be translated into chemical events related to pain.”

“Mechanical activity has a great deal to do with the exchange of water and oxygen concentration” in the disc.

An important aspect of disc nutrition and health is the mechanical aspects of the disc related to the fluid mechanics.

The pumping action maintains the nutrition and biomechanical function of the intervertebral disc. Thus, “research substantiates the view that unchanging posture, as a result of constant pressure such as standing, sitting or lying, leads to an interruption of pressure-dependent transfer of liquid. Actually the human intervertebral disc lives because of movement.”

“The fluid content of the disc can be changed by mechanical activity.”

“In summary, what is the answer to the question of where is the pain coming from in the chronic low-back pain patient? I believe its source, ultimately, is in the disc. Basic studies and clinical experience suggest that mechanical therapy is the most rational approach to relief of this painful condition.”

This model supports this perspective:

• The intervertebral disc is the primary source of chronic low back pain.
• The disc in anatomically unique. Its lack of blood supply makes disc health dependent upon motion.
• All things that impair disc motion alter disc biochemistry. Altered disc biochemistry is inflammatory.
• Inflammatory disc biochemistry causes discogenic pain.
• Mechanical therapy that improves disc motion will mitigate disc inflammatory biochemistry, reducing pain.
• Anti-inflammatory drugs (NSAIDs), passive treatment modalities, and prolonged rest are not the solution to chronic low back pain.

Model #2: Motion “Closes” the Pain Gate

Melzack and Wall’s Gate Control Theory of Pain was originally published in the journal Brain in 1962 (27), and later updated and published in the journal Science in 1965 (28). Ronald Melzack, PhD, is a Canadian psychologist. Patrick Wall, MD (d. 2001), was a British neuroscientist and pain expert, as well as the first editor of the journal Pain. An oversimplified explanation of their Gate Control Theory of Pain is that the pain electrical signal to the cortical brain (small diameter afferents) can be inhibited by non-painful electrical signals arising from other sensory afferents (large diameter afferents). Representative reference book comments include:

The perception of pain is dependent upon the balance of activity in large (mechanoreceptor) and small (nociceptive) afferents. (29)

If large myelinated fibers (mechanoreceptors) were selectively stimulated, then normal “balance” of activity between large (mechanoreceptor) and small (nociceptive) fibers would be restored and the pain would be relieved. (29)

“Pain is not simply a direct product of the activity of nociceptive afferent fibers but is regulated by activity in other myelinated afferents that are not directly concerned with the transmission of nociceptive information.” (30)

“The idea that pain results from the balance of activity in nociceptive and nonnociceptive afferents was formulated in the 1960s and was called the gate control theory.” (30)

“Simply put, non-nociceptive afferents ‘close’ and nociceptive afferents ‘open’ a gate to the central transmission of noxious input.” (30)

“The balance of activity in small- and large-diameter fibers is important in pain transmission…” (30)

Melzack and Wall’s Gate Control Theory of Pain was reviewed and confirmed in 2002 in the British Journal of Anaesthesia in an article titled (31):

Gate Control Theory of Pain Stands the Test of Time

This article reiterates that the Gate Theory “has stood the test of time.” The electrical transmission and perception of pain is subject to modulation by non-nociceptive neurological electrical signals. These non-nociceptive neurological electrical signals emanate from large diameter nerve fibers, such as mechanoreceptors. Consequently, the author notes that pain can be modulated through 2 mechanisms (as noted above):

• Reducing excitation. This approach is commonly achieved by reducing inflammation.
• Increasing Inhibition. This approach is commonly achieved by improving mechanical function and mechanical afferentation, firing inhibitory large diameter mechanoreceptors.

The application of chiropractic spinal adjusting for pain control using

Melzack and Wall’s Gate Control Theory of Pain was first done by Canadian orthopedic surgeon Kirkaldy-Willis in 1985 (32). Dr. Kirdaldy-Willis notes:

“Spinal manipulation is essentially an assisted passive motion applied to the spinal apophyseal and sacroiliac joints.”

Melzack and Wall proposed the Gate Theory of Pain in 1965, and this theory has “withstood rigorous scientific scrutiny.”

“The central transmission of pain can be blocked by increased proprioceptive input.” Pain is facilitated by “lack of proprioceptive input.” This is why it is important for “early mobilization to control pain after musculoskeletal injury.”

The facet capsules are densely populated with mechanoreceptors. “Increased proprioceptive input in the form of spinal mobility tends to decrease the central transmission of pain from adjacent spinal structures by closing the gate. Any therapy which induces motion into articular structures will help inhibit pain transmission by this means.”

Stretching of facet joint capsules will fire capsular mechanoreceptors which will reflexly “inhibit facilitated motoneuron pools” which are responsible for the muscle spasms that commonly accompany low back pain.

In chronic cases, there is a shortening of periarticular connective tissues and intra-articular adhesions may form; manipulations [adjustments] can stretch or break these adhesions.

“In most cases of chronic low back pain, there is an initial increase in symptoms after the first few manipulations [probably as a result of breaking adhesions]. In almost all cases, however, this increase in pain is temporary and can be easily controlled by local application of ice.”

“However, the gain in mobility must be maintained during this period to prevent further adhesion formation.”

These patients were given a “two or three week regimen of daily spinal manipulations by an experienced chiropractor.”

“No patients were made worse by the manipulation, yet many experienced an increase in pain during the first week of treatment. Patients undergoing manipulative treatment must therefore be reassured that the initial discomfort is only temporary.”

“In our experience, anything less than two weeks of daily manipulation is inadequate for chronic low back pain patients.”

•••••••••

Conclusions

The study by Dickenson (31), published in the British Journal of Anaesthesia, notes that successful pain suppression should apply two approaches:

• Reducing excitation
• Increasing Inhibition

Both approaches are addressed with spinal manipulation. The increased segmental motion achieved with spinal manipulation will improve disc biochemistry, reducing inflammation and pain excitation.

The increased segmental motion achieved with spinal manipulation will also increase proprioception, leading to a neurological sequence of events that inhibits pain by “closing” the Pain Gate.

These models support the evidence showing that spinal manipulation is both safe and effective in the treatment of chronic low back pain.

REFERENCES

• Korr IM; The Sympathetic Nervous System as the Mediator Between the Somatic and Supportive Processes; The Collected Papers of Irvin M. Korr; The American Academy of Osteopathy; 1979; pp. 170-175.
• Turek SL; Orthopaedics: Principles and Their Applications; JB Lippincott Company; 1977; p. 1324.
• White AA, Panjabi MM; Clinical Biomechanics of the Spine; Second edition; JB Lippincott Company; 1990; p. 3.
• Harris RI, MacNab I; Structural changes in the lumbar intervertebral discs; their relationship to low back pain and sciatica; Journal of Bone and Joint Surgery, British; May 1954;36-B(2):304-22.
• Hassler O; The human intervertebral disc. A micro-angiographical study on its vascular supply at various ages; ACTA Ortho Scand; 1969; 40(6):765-72.
• Kapandji IA; The Physiology of the Joints; Volume 3; The Trunk and the Vertebral Column; Churchill Livingstone; 1974.
• Cyriax, James; Textbook of Orthopaedic Medicine, Diagnosis of Soft Tissue Lesions; Bailliere Tindall; Volume 1; eighth edition; 1982.
• Boyd W; PATHOLOGY: Structure and Function in Disease; Eighth Edition; Lea & Febiger; Philadelphia; 1970.
• Anderson WAD, Scotti TM; Synopsis of Pathology; Ninth Edition; The CV Mosby Company; 1976.
• Robbins SL, Cotran RS; PATHOLOGIC BASIS OF DISEASE; Second Edition; WB Saunders Company; Philadelphia; 1979.
• Roy, Steven; Irvin, Richard; Sports Medicine: Prevention, Evaluation, Management, and Rehabilitation; Prentice-Hall; 1983.
• Guyton A; Textbook of Medical Physiology; Saunders; 1986.
• Cohen, Kelman; Diegelmann, Robert F; Lindbald, William J; Wound Healing, Biochemical & Clinical Aspects; WB Saunders; 1992.
• Nachemson AL; The Lumbar Spine, an Orthopedic Challenge; Spine; Volume 1, Number 1, March 1976, pp. 59-71.
• Bogduk N, Tynan W, Wilson AS; The nerve supply to the human lumbar intervertebral discs; Journal of Anatomy; 1981; Vol. 132; No. 1; pp. 39-56.
• Mooney V; Where Is the Pain Coming From?; Spine; Vol. 12; No. 8; 1987; pp. 754-759.
• Kuslich S, Ulstrom C, Michael C; The Tissue Origin of Low Back Pain and Sciatica: A Report of Pain Response to Tissue Stimulation During Operations on the Lumbar Spine Using Local Anesthesia; Orthopedic Clinics of North America; Vol. 22; No. 2; April 1991; pp. 181-187.
• Ozawa T, Ohtori S, Inoue G, Aoki Y, Moriya H, Takahashi; The Degenerated Lumbar Intervertebral Disc is Innervated Primarily by Peptide-Containing Sensory Nerve Fibers in Humans; Spine Volume 31; Number 21; October 1, 2006; pp. 2418-2422.
• DePalma MJ, Ketchum JM, Saullo T; What is the source of chronic low back pain and does age play a role?; Pain Medicine; Feb 2011; Vol. 12; No. 2; pp. 224-233.
• Izzo R, Popolizio T, D’Aprile P, Muto M; Spine Pain; European Journal of Radiology; May 2015; Vol. 84; pp. 746–756.
• Foreman J; A Nation in Pain, Healing Our Biggest Health Problem; Oxford University Press; 2014.
• Pho, K; USA TODAY, The Forum; September 19, 2011; pg. 9A.
• Wang S; Why Does Chronic Pain Hurt Some People More?; Wall Street Journal; October 7, 2013.
• Sota Omoigui S; The biochemical origin of pain: The origin of all pain is inflammation and the inflammatory response: Inflammatory profile of pain syndromes; Medical Hypothesis; 2007, Vol. 69; pp. 1169–1178.
• Giles LGF;Reinhold Muller R; Chronic Spinal Pain: A Randomized Clinical Trial Comparing Medication, Acupuncture, and Spinal Manipulation; Spine; July 15, 2003; 28(14):1490-1502.
• Maroon JC, Bost JW; Omega-3 Fatty acids (fish oil) as an anti-inflammatory: an alternative to nonsteroidal anti-inflammatory drugs for discogenic pain; Surgical Neurology; 65 (April 2006); pp. 326–331.
• Melzack R, Wall PD; On the nature of cutaneous sensory mechanisms; Brain; June 1962; 85:331-56.
• Melzack R, Wall PD; Pain mechanisms: a new theory; Science; November 19, 1965; 150(3699):971-9.
• John Nolte, The Human Brain; Mosby Year Book, 1993.
• Eric Kandel, James Schwartz, Thomas Jessell, Principles of Neural Science. McGraw-Hill, 2000.
• Dickenson AH; Gate Control Theory of pain stands the test of time; British Journal of Anaesthesia, 88, No. 6, June 2002, pp. 755-757.
• Kirkaldy-Willis WH, Cassidy JD; Spinal Manipulation in the Treatment of Low back Pain; Canadian Family Physician; March 1985; Vol. 31; pp. 535-540.

America’s Pain Crisis

Judy Foreman was educated at Harvard, and has been a Lecturer on Medicine at Harvard’s Medical School. In 2014, she published a book titled (1):

A Nation in Pain
Healing Our Biggest Health Problem

Ms. Foreman notes that of the 238 million adults in America, approximately half of them have chronic daily pain. The conservative estimate of the direct costs and lost productivity resulting from this pain is up to $635 billion yearly.

Americans pay $113 billion yearly for Social Security Disability benefits (2), and it’s not enough. Our Social Security Disability program is paying out $200 billion yearly. Political newspapers are buzzing about the prediction that the Social Security Disability Trust Fund will go broke next year (2016) (3). Fifteen million Americans are on Social Security Disability, and new applications average 200,000 monthly (2). The primary condition for which Americans apply for and are granted Social Security Disability is “musculoskeletal system and connective tissue” disorders, primarily back pain (2).

The drugs used to treat chronic pain are themselves creating yet another crisis. The political magazine, Time published a cover article titled (4):

They’re the most powerful painkillers ever invented;
And they’re creating the worst addiction crisis America has ever seen;
The price of Relief; Why America can’t kick its painkiller problem

This article makes these points:

• “Around the nation, doctors so frequently prescribe the drugs known as opioids for chronic pain conditions like arthritis, migraines and lower back injuries that there are enough pills prescribed every year to keep every American adult medicated around the clock for a month.” “The result is a national epidemic.”
• “Now, 4 of 5 heroin addicts say they came to the drug from prescription painkillers.”
• “By 2011 the number of opioid prescriptions written for pain treatment had tripled to 219 million.”
• “By 2011, 17,000 Americans were dying every year from prescription opioid overdoses.”
• “The American Academy of Neurology last year concluded that the risks of long-term opioid treatment for headaches and chronic low back pain likely outweighed the benefits.”

Also in 2015, the newspaper the Wall Street Journal reviewed a booked titled Dreamland in an article titled The Great Opiate Boom (5). This article makes these points:

• “Children of the most privileged group in the wealthiest country in the history of the world were getting hooked and dying in almost epidemic numbers from substances meant to, of all things, numb pain.”
• These “prescriptions [opioids] for chronic pain rose from 670,000 in 1997 to 6.2 million in 2002.”

In June 2015, the front page of the newspaper USA Today published an article titled Heroin use surges among women, middle-class (6). This article makes these points:

• “Heroin use is reaching into new communities—addicting more women and middle-class users—as people hooked on prescription painkillers transition to cheaper illegal drugs.”
• “About 75% of new heroin users first became hooked on prescription opiates.”

In 2013, the Wall Street Journal quantifies chronic pain location by citing the Centers for Disease Control and Prevention, and the World Health Organization (7):

28.1% Low Back Pain
19.5% Knee Pain
16.1% Severe Headache or Migraine
15.1% Neck Pain
09.0% Shoulder Pain
07.6% Finger pain
07.1% Hip Pain

Back pain is at the center of America’s pain and disability crisis. It has been know for 40 years that the structure primarily responsible for back pain, especially for chronic back pain, is the intervertebral disc:

• In 1976, internationally respected orthopedic surgeon Alf Nachemson published his detailed review on back pain in the journal Spine (8), in which he states:

“The intervertebral disc is most likely the cause of the pain.”

• In 1981, anatomist and physician Nikoli Bogduk published an extensive review of the literature on the topic of disc innervation, along with his own primary research in the Journal of Anatomy (9). Dr. Bogduk states:

“The lumbar intervertebral discs are supplied by a variety of nerves.”

“Clinically, the concept of ‘disc pain’ is now well accepted.”

• In 1987, the journal Spine published Dr. Vert Mooney’s Presidential Address of the International Society for the Study of the Lumbar Spine (10). In this article, Dr. Mooney states:

“We know that 10% of back ‘injuries’ do not resolve in 2 months and that they do become chronic.”

“Persistent pain in the back with referred pain to the leg is largely on the basis of abnormalities within the disc.”

“Where is the pain coming from in the chronic low-back pain patient? I believe its source, ultimately, is in the disc. Basic studies and clinical experience suggest that mechanical therapy is the most rational approach to relief of this painful condition.”

• In 1991, Stephen Kuslich and colleagues published an article in the journal Orthopedic Clinics of North America (11). The authors performed 700 lumbar spine operations using only local anesthesia to determine the tissue origin of low back and leg pain, and they present the results on 193 consecutive patients studied prospectively. They state:

“Back pain could be produced by several lumbar tissues, but by far, the most common tissue or origin was the outer layer of the annulus fibrosis.”

• In 2006, researchers from Japan published an article in the journal Spine showing the results of a sophisticated immunohistochemistry study of the sensory innervation of the human lumbar intervertebral disc (12). These authors note:

“Many investigators have reported the existence of sensory nerve fibers in the intervertebral discs of animals and humans, suggesting that the intervertebral disc can be a source of low back pain.”

“Both inner and outer layers of the degenerated lumbar intervertebral disc are innervated by pain sensory nerve fibers in humans.”

Pain neuron fibers are found in all human discs that have been removed because they are the source of a patient’s chronic low back pain.

The nerve fibers in the disc, found in this study, “indicates that the disc can be a source of pain sensation.”

• In 2011, researchers from the University/Medical College of Virginia published a study in the journal Pain Medicine in which they quantified the structural source of low back pain in which diagnostic procedures were performed on 170 back pain patients (13). The authors note:

“Our data confirm the intervertebral disc as the most common etiology of chronic low back pain in adults.”

• In 2015, a team from Naples, Italy, published a study in the European Journal of Radiology, in which they present an extensive review of the literature pertaining to spinal pain (14). The authors note:

“Spinal pain, and especially low back pain (LBP), represent the second leading cause for a medical consultation in a primary care setting and is a leading cause of disability worldwide.”

The most frequent cause of LBP is “internal disc disruption and is referred to as discogenic pain.” “Internal disc disruption refers to annular fissures, disc collapse and mechanical failure, with no significant modification of external disc shape, with or without endplates changes.”

Discogenic pain is “considered as the most frequent cause of chronic low back pain.” Discogenic pain secondary to internal disc disruption is the main cause of chronic LBP and disability.

•••••

A central theme in the back pain literature is that discogenic back pain is prevalent, and probably accounts for the majority of back pain complaints within the American Society. Chiropractic / manipulative management of patients with back and/or leg pain secondary to nerve compression has a long and impressive history of good clinical outcomes with very low risks. Representative studies include:

• In 1954, RH Ramsey, MD published a study in the Instructional Course Lectures of the American Academy of Orthopedic Surgeons (15). Dr. Ramsey states:

“The conservative management of lumbar disk lesions should be given careful consideration because no patient should be considered for surgical treatment without first having failed to respond to an adequate program of conservative treatment.”

“From what is known about the pathology of lumbar disk lesions, it would seem that the ideal form of conservative treatment would theoretically be a manipulative closed reduction of the displaced disk material.”

• In 1969, physicians JA Mathews and DAH Yates from the Department of Physical Medicine, St. Thomas’ Hospital, London, published a study in the British Medical Journal (16). These authors evaluated a number of patients that presented with an acute onset of low back and buttock pain who did not respond to rest. Diagnostic epidurography showed a clinically relevant small disc protrusion, along with antalgia and positive lumbar spine nerve stretch tests. These patients were then treated with manipulations of the lumbar spine. The manipulations were repeated until abnormal symptoms and signs had disappeared. Following the manipulations there was resolution of signs, symptoms, antalgia, and reduction in the size of the protrusions.

•  Also in 1969, BC Edwards compared the effectiveness of heat/massage/exercise to spinal manipulation in the treatment of 184 patients that were grouped according to the presentation of back and leg pain. The study was published in the Australian Journal of Physiotherapy (17). This study was considered to be “a well-designed, well executed, and well-analyzed study.” (18)

“This study certainly supports the efficacy of spinal manipulative therapy in comparison with heat, massage, and exercise. The results (80 – 95% satisfactory) are impressive in comparison with any form of therapy.”

• In 1977, the third edition of Orthopaedics, Principles and Their Applications was published (19). The author, Samuel Turek, MD (d. 1986), was a Clinical Professor, Department of Orthopedics and Rehabilitation at the University of Miami School of Medicine. In the section pertaining to the protruded disc, Dr. Turek makes the following observations:

“Manipulation. Some orthopaedic surgeons practice manipulation in an effort at repositioning the disc. This treatment is regarded as controversial and a form of quackery by many men. However, the author has attempted the maneuver in patients who did not respond to bed rest and were regarded as candidates for surgery. Occasionally, the results were dramatic.

Technique. The patient lies on his side on the edge of the table facing the surgeon, and the uppermost leg is allowed to drop forward over the edge of the table, carrying forward that side of the pelvis. The uppermost arm is placed backward behind the patient, pulling the shoulder back. The surgeon places one hand on the shoulder and the other on the iliac crest and twists the torso by pushing the shoulder backward and the iliac crest forward. The maneuver is sudden and forceful and frequently is associated with an audible and palpable crunching sound in the lower back. When this is felt, the relief of pain is usually immediate. The maneuver is repeated with the patient on the opposite side.”

• In 1985, Dr. Kirkaldy-Willis, a Professor Emeritus of Orthopedics and director of the Low-Back Pain Clinic at the University Hospital, Saskatoon, Canada, published an article in the journal Canadian Family Physician (20). In this study, the authors present the results of a prospective observational study of spinal manipulation in 283 patients with chronic low back and leg pain. All 283 patients in this study had failed prior conservative and/or operative treatment, and they were all totally disabled. These patients were given a two or three week regimen of daily spinal manipulations by an experienced chiropractor. Eighty-one percent of the patients with referred pain syndromes subsequent to joint dysfunctions achieved a good result. Forty-eight percent of the patients with nerve compression syndromes achieved a good result.
• In 1987, physicians Paul Pang-Fu Kuo and Zhen-Chao Loh published a study pertaining to lumbar disc protrusions and spinal manipulation in the journal Clinical Orthopedics and Related Research (21). Drs. Paul Pang-Fu Kuo and Zhen-Chao Loh are from the Department of Orthopedic Surgery, Shanghai Second Medical College, and Chief Surgeon, Department of Orthopaedic Surgery, Rui Jin Hospital, Shanghai, China. They note that manipulation has been used in Chinese healthcare for thousands of years, and by the Tang Dynasty (618-907 AD), “manipulation was fully established and became a routine for the treatment of low back pain.”

In their study, they performed a series of eight manipulations on 517 patients with protruded lumbar discs and clinically relevant signs and symptoms. Their outcomes were quite good, with 84% achieving a successful outcome and only 9% not responding. Only 14 % suffered a reoccurrence of symptoms at intervals ranging from two months to twelve years. Based upon their results, Drs. Kuo and Loh make these statements:

“Manipulation of the spine can be effective treatment for lumbar disc protrusions.”

“Most protruded discs may be manipulated. When the diagnosis is in doubt, gentle force should be used at first as a trial in order to gain the confidence of the patient.”

• In 1989, the Journal of Manipulative and Physiological Therapeutics published a case study of a patient with an “enormous central herniation lumbar disc” who underwent a course of side posture manipulation (22). The patient improved considerably with only 2 weeks of treatment. The authors state:

“It is emphasized that manipulation has been shown to be an effective treatment for some patients with lumbar disc herniation.”

• In 1990, Dr. TW Meade published the results of a randomized comparison of chiropractic and hospital outpatient treatment in the treatment of low back pain. This trial involved 741 patients and was published in the British Medical Journal (23). The patients were followed for a period between 1–3 years. Key points presented in this article include:

“Chiropractic treatment was more effective than hospital outpatient management, mainly for patients with chronic or severe back pain.”

“There is, therefore, economic support for use of chiropractic in low back pain, though the obvious clinical improvement in pain and disability attributable to chiropractic treatment is in itself an adequate reason for considering the use of chiropractic.”

“Patients treated by chiropractors were not only no worse off than those treated in hospital but almost certainly fared considerably better and that they maintained their improvement for at least two years.”

“The results leave little doubt that chiropractic is more effective than conventional hospital outpatient treatment.”

• In 1993, chiropractor J. David Cassidy, chiropractor Haymo Thiel, and physician William Kirkaldy-Willis published a “Review Of The Literature” pertaining to side posture manipulation for lumbar intervertebral disk herniations. Their article appeared in the Journal of Manipulative and Physiological Therapeutics (24). Based upon their review of the literature and their own experiences, these authors state:

“The treatment of lumbar disk herniation by side posture manipulation is not new and has been advocated by both chiropractors and medical manipulators.”

“The treatment of lumbar intervertebral disk herniation by side posture manipulation is both safe and effective.”

• In 1995, chiropractors PJ Stern, Peter Côté, and David Cassidy published a study in the Journal of Manipulative and Physiological Therapeutics (25). They retrospectively reviewed the outcomes of 59 consecutive patients complaining of low back and radiating leg pain, and were clinically diagnosed as having a lumbar spine disk herniation. Ninety percent of these patients reported improvement of their complaint after chiropractic manipulation. They concluded:

“Based on our results, we postulate that a course of non-operative treatment including manipulation may be effective and safe for the treatment of back and radiating leg pain.”

• In 2003, the journal Spine published a randomized clinical trial involving the nonsteroidal anti-inflammatory COX-2 inhibiting drugs Vioxx or Celebrex v. needle acupuncture v. chiropractic manipulation in the treatment of chronic neck and back pain (26). Chiropractic was better than 5 times more effective than the drugs and better than twice as effective as needle acupuncture in the treatment of chronic spine pain. Chiropractic was able to accomplish the clinical outcome without any reported adverse effects. One year after the completion of this 9-week clinical trial, 90% of the original trial participants were re-evaluated to assess their clinical status. The authors discovered that only those who received chiropractic during the initial randomization benefited from a long-term stable clinical outcome (27).
•  In 2006, physicians Valter Santilli, MD, Ettore Beghi, MD, Stefano Finucci, MD, published an article in The Spine Journal (28). Their study was a randomized double-blind clinical trial of active and simulated chiropractic spinal manipulations in the treatment of acute back pain and sciatica with disc protrusion. The study used 102 patients. The manipulations or simulated manipulations were done 5 days per week by experienced chiropractors for up to a maximum of 20 patient visits, “using a rapid thrust technique.” The authors noted the following:

“Active manipulations have more effect than simulated manipulations on pain relief for acute back pain and sciatica with disc protrusion.”

“At the end of follow-up a significant difference was present between active and simulated manipulations in the percentage of cases becoming pain-free (local pain 28% vs. 6%; radiating pain 55% vs. 20%).”

“Patients receiving active manipulations enjoyed significantly greater relief of local and radiating acute LBP, spent fewer days with moderate-to-severe pain, and consumed fewer drugs for the control of pain.”

“No adverse events were reported.”

• In 2014, a group of multidisciplinary researchers and chiropractic clinicians from Switzerland presented a prospective study involving 148 patients with low back and leg pain. The study was published in the Journal of Manipulative and Physiological Therapeutics (29). The purpose of this study was to document outcomes of patients with confirmed, symptomatic lumbar disc herniations and sciatica that were treated with chiropractic side posture high-velocity, low-amplitude, spinal manipulation to the level of the disc herniation. Evaluations were performed at 2 weeks, 1 month, 3 months, 6 months, and 12 months. The authors make the following statements:

“The proportion of patients reporting clinically relevant improvement in this current study is surprisingly good, with nearly 70% of patients improved as early as 2 weeks after the start of treatment. By 3 months, this figure was up to 90.5% and then stabilized at 6 months and 1 year.”

“A large percentage of acute and importantly chronic lumbar disc herniation patients treated with chiropractic spinal manipulation reported clinically relevant improvement.”

“Even the chronic patients in this study, with the mean duration of their symptoms being over 450 days, reported significant improvement, although this takes slightly longer.”

“A large percentage of acute and importantly chronic lumbar disc herniation patients treated with high-velocity, low- amplitude side posture spinal manipulative therapy reported clinically relevant ‘improvement’ with no serious adverse events.”

“Spinal Manipulative therapy is a very safe and cost-effective option for treating symptomatic lumbar disc herniation.”

In America, it is not uncommon for persistent back pain to be treated surgically. An analysis of America’s low back surgery rate compared internationally to other nations was published in the journal Spine in 1994 (30). The authors were from the Department of Health Services, University of Washington in Seattle. They compared rates of back surgery in eleven developed countries to determine if back surgery rates are higher in the United States than in other developed countries. Their findings include:

“The rate of back surgery in the United States was at least 40% higher than in any other country and was more than five times those in England and Scotland.”

“Back surgery rates increased almost linearly with the per capita supply of orthopaedic and neurosurgeons in the country.”

In this regard, an interesting article was published in the journal Spine in 2013, designed to predict the major reason for back surgery as compared to the utilization of less invasive approaches (31). A team of investigators from Dartmouth Medical School, the University of Washington School of Medicine, and Ohio State University College of Public Health, completed a prospective cohort study to identify early predictors of lumbar spine surgery within 3 years after occupational back injury.

The authors note that back injuries are the most prevalent occupational injury in the United States, and that back pain is the most costly and prevalent occupational health condition among the U.S. workers. After adjustment for medical and general inflation, costs for occupational back pain increased over 65% from 1996 through 2002, and spine surgeries represent a significant proportion of these costs. Yet, they note:

“Spine surgeries are associated with little evidence for improved population outcomes, yet rates have increased dramatically since the 1990s.”

“Reducing unnecessary spine surgeries is important for improving patient safety and outcomes and reducing surgery complications and health care costs.”

Previous studies have shown that those with occupational back injuries who first saw a chiropractor had lower odds of chronic work disability, and that those seeing chiropractors for occupational back pain had “higher rates of satisfaction with back care.”

In this study, after controlling for injury severity, workers with an initial visit for the injury to a surgeon had almost nine times the odds of receiving lumbar spine surgery compared to those seeing primary care providers, and workers whose first visit was to a chiropractor had significantly lower odds of surgery (by 78%). The authors stated:

“42.7% of workers who first saw a surgeon had surgery, in contrast to only 1.5% of those who saw a chiropractor.”

“Approximately 43% of workers who saw a surgeon had surgery within 3 years, in contrast to only 1.5% of those who saw a chiropractor.”

“There was a very strong association between surgery and first provider seen for the injury, even after adjustment for other important variables.” [such as symptom severity]

“It is possible that these findings indicate that who you see is what you get.”

Seeing a chiropractor as the first provider for a back complaint significantly reduced odds of surgery.

These authors suggest that it is wise to use a “gatekeeper” for patients who suffer occupational back injury. This article presents substantial reason for why such a gatekeeper should be a chiropractor. The reduction of back surgeries in those consulting chiropractors for back pain represents a substantial costs savings, and also the highest levels of back care satisfaction.

REFERENCES

1. Foreman J; A Nation in Pain, Healing Our Biggest Health Problem; Oxford University Press, 2014.
   www.ssa.gov (the Official Social Security Website): “December 2011, diseases of the musculoskeletal system and connective tissue were the primary reason disabled workers and disabled widow(er)s received benefits.”
2. Associated Press; STEPHEN OHLEMACHER and RICARDO ALONSO-ZALDIVAR; July 22, 2015.
3. Calabresi M; They’re the most powerful painkillers ever invented; And they’re creating the worst addiction crisis America has ever seen; The price of Relief; Why America can’t kick its painkiller problem; Time; June 15, 2015; pp. 26-33.
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6. Wall Street Journal, October 7, 2013.
7. Nachemson AL; The Lumbar Spine, an Orthopedic Challenge; Spine; Volume 1, Number 1, March 1976, pp. 59-71.
8. Bogduk N, Tynan W, Wilson AS; The nerve supply to the human lumbar intervertebral discs; Journal of Anatomy; 1981; Vol. 132; No. 1; pp. 39-56.
9. Mooney V; Where Is the Pain Coming From?; Spine; Vol. 12; No. 8; 1987; pp. 754-759.
10. Kuslich S, Ulstrom C, Michael C; The Tissue Origin of Low Back Pain and Sciatica: A Report of Pain Response to Tissue Stimulation During Operations on the Lumbar Spine Using Local Anesthesia; Orthopedic Clinics of North America; Vol. 22; No. 2; April 1991; pp. 181-187.
11. Ozawa T, Ohtori S, Inoue G, Aoki Y, Moriya H, Takahashi; The Degenerated Lumbar Intervertebral Disc is Innervated Primarily by Peptide-Containing Sensory Nerve Fibers in Humans; Spine Volume 31; Number 21; October 1, 2006; pp. 2418-2422.
12. DePalma MJ, Ketchum JM, Saullo T; What is the source of chronic low back pain and does age play a role?; Pain Medicine; Feb 2011; Vol. 12; No. 2; pp. 224-233.
13. Izzo R, Popolizio T, D’Aprile P, Muto M; Spine Pain; European Journal of Radiology; May 2015; Vol. 84; pp. 746–756.
14. Ramsey RH; Conservative Treatment of Intervertebral Disk Lesions; American Academy of Orthopedic Surgeons, Instructional Course Lectures; Volume 11; 1954; pp. 118-120.
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21. Quon JA, Cassidy JD, O’Connor SM, Kirkaldy-Willis WH; Lumbar intervertebral disc herniation: treatment by rotational manipulation; Journal of Manipulative and Physiological Therapeutics; 1989 Jun;12(3):220-7.
22. Meade TW, Dyer S, Browne W, Townsend J, Frank OA; Low back pain of mechanical origin: Randomized comparison of chiropractic and hospital outpatient treatment; British Medical Journal; Volume 300; June 2, 1990; pp. 1431-7.
23. Cassidy JD, Thiel HW, Kirkaldy-Willis WH; Side posture manipulation for lumbar intervertebral disk herniation; Journal of Manipulative and Physiological Therapeutics; February 1993;16(2):96-103.
24. Stern PJ, Côté P, Cassidy JD; A series of consecutive cases of low back pain with radiating leg pain treated by chiropractors; Journal of Manipulative and Physiological Therapeutics; 1995 Jul-Aug;18(6):335-42.
25. Giles LGF, Muller R; Chronic Spinal Pain: A Randomized Clinical Trial Comparing Medication, Acupuncture, and Spinal Manipulation; Spine July 15, 2003; 28(14):1490-1502.
26. Muller R, Lynton G.F. Giles LGF, DC, PhD; Long-Term Follow-up of a Randomized Clinical Trial Assessing the Efficacy of Medication, Acupuncture, and Spinal Manipulation for Chronic Mechanical Spinal Pain
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28. Santilli V, Beghi E, Finucci S; Chiropractic manipulation in the treatment of acute back pain and sciatica with disc protrusion: A randomized double-blind clinical trial of active and simulated spinal manipulations; The Spine Journal; March-April 2006; Vol. 6; No. 2; pp. 131–137.
29. Leemann S, Peterson CK, Schmid C, Anklin B, Humphreys BK; Outcomes of Acute and Chronic Patients with Magnetic Resonance Imaging–Confirmed Symptomatic Lumbar Disc Herniations Receiving High-Velocity, Low Amplitude, Spinal Manipulative Therapy: A Prospective Observational Cohort Study With One-Year Follow-Up; Journal of Manipulative and Physiological Therapeutics; March/April 2014; Vol. 37; No. 3; pp. 155-163.
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