FHN Complementary Medicine Monthly Newsletter September 2001
“WHAT’S IN A BULGE”
This month we will talk about Low Back Pain (LBP). There can be many reasons for LBP , we will look at the bulging intervertebral disc(IVD) as one of the causes.
First we need to look at the anatomy of the IVD to understand its role in back pain. The IVD is composed of an outer layer ( annulus) of tough connective tissue , and an inner layer ( nucleus pulposis) of a jelly like substance. The connective tissue annulus holds the nucleus in place and the nucleus acts as a shock absorber for movement and stress in the spine. The annulus of the disc has been shown by Bogduk and others to be well innervated with both sensory and autonomic/sympathetic fibers of the sinuvertebral nerve. There are mechanoreceptors (stretch), nociceptors (pain), and chemoreceptors that can detect all types of mechanical and biomechanical changes occurring in the periphery of the disc.
A disc bulge is the protrusion of the jelly-like substance into the space where the nerve sits. A disc herniation is when a bulge ruptures. With either of these conditions, you may experience pain or numbness in your back or down your leg. Most commonly, a disc will herniate from repetitive strain over time. A person will bend a certain way with little problems for years. Then, one day, you sneeze and your back is killing you!! The backaches that you get from time to time are giving you a warning signal.
Are disc bulges or central disc herniations clinically significant findings when revealed on anatomical studies such as MRI or CT scanning, when there is clinical correlation on physical examination? While this is a controversy in some circles, clearly the scientific literature supports that central/paracentral disc herniation or bulge without neural impingement as significant when there is clinical correlation. Recent studies with CT/discography have shown that there is an entity of internal disc disruption that can cause the patient pain, prior to a disc protrusion that is evident on MRI or CT scans. Bogduk has published similar work where he describes "internal disc disruption" based on CT discography studies. The symptoms of nerve irritation can also be caused by inflammation from the breakdown products from a degenerate but not bulging disc. So patients may be suffering intense back and leg pain where no protrusion is visible on MRI scans. Disc degeneration is caused by the watertight endplates of the vertebra above and below the disc, squeezing water from within the disc causing it to dry out during the day, when it is under pressure from the upright spine. Consequently the disc contents are less able to conduct oxygen and other nutrients into the disc and this results in the cells dying and disrupting. This destruction liberates acids and enzymes which effectively dissolve the proteins that form the healthy disc material and these breakdown products leak and the disc gradually looses bulk. These chemical irritants affect the surrounding disc and the posterior longitudinal ligament, which are abundantly supplied with nerves (remember?) and as it is linked to the levels above and below the affected disc, the pain is felt over a much wider area than just the level concerned.
So what can you do about that back pain?
First of all determining the extent of the disc involvement / bulge is imperative. CT/MRI, while not perfect , are helpful in this area. If we have a bulge that is causing a space occupying lesion , we need to reduce the bulge! If we have neurological deficits ( weakness, numbness, radiating pain, etc.) That may need a surgical procedure . However if not severe there are some conservative measures that have proven effective. An osteopathic procedure that has been refined by a chiropractor (Cox) called
flexion/ distraction (F&D) has proven very effective in reducing/retracting the disc. ( We have two very special F&D tables exactly for that purpose.)
Exercise
Research shows that recurrence rates for low back pain soar as high as 50% in the 12 months following the initial episode. And although patients are encouraged to return to normal activities as soon as possible, many fear that movement or activity will only make their pain worse. In July 2000 , the British Medical Journal published a study that evaluated the effectiveness of an exercise program for dealing with back pain. One hundred and eighty-seven patients with low back pain of 1-6 months duration were divided into an exercise group or a control group. The exercise group participated in eight one-hour classes that included muscle strengthening, stretching, relaxation techniques and a brief education on back care. The control group continued under the care of their doctor.
Questionnaires completed six months and one year after the program revealed that patients in the exercise group reported less back pain and associated disability than the control group. The exercise group also took less days off work than the control group in the 12-month follow-up period (378 days by the exercise group vs. 607 days by the control group).
Rest has been standard recommendation for low back pain (LBP) for years . This recommendation persists despite research evidence suggesting that prolonged rest serves no purpose and may delay return to work and resumption of normal activities.
A report from the International Paris Task Force on Back Pain outlines the role of activity in the treatment of back pain. In addition to presenting numerous recommendations and summaries, the authors offer the following key points as summary to their findings:
· Bed rest is contraindicated in subacute and chronic cases of LBP.
· In acute cases, bed rest should neither be enforced nor prescribed.
· If authorized (based on pain indication), bed rest should be for the shortest duration possible.
· Patients whose pain is intense enough to justify bed rest should be referred for a specialized back pain evaluation if daily activities have not been resumed after 10 days of strict bed rest (defined as getting up only to go to the bathroom) and adequate pain therapy.
Acupuncture is a wonderful modality in the treatment of LBP and assist in the healing of the area by increasing blood perfusion, increasing lymph drainage, and helping to shunt prostaglandin( one pain producing hormone) production form the proinflammatory type to the antiinflammatory type.
Nutritional Support for the disc include:
· Hydrolyzed gelatin - Gelatin provides the components of collagen, which is the basis of connective tissue found in skin, ligaments, cartilage, vertebral discs, joint linings, capillary walls, and the bones and teeth.
· Glucosamine sulfate - Glucosamine is a major component of cartilage. It helps the body make synovial fluid—an important joint lubricant—and proteoglycans—the large, shock absorbing molecules found in cartilage.
· Chondroitin sulfate - Chondroitin is a derivative of glucosamine that supports the strength and flexibility of all connective tissues in the body.
· MSM (methylsulfonylmethane) - MSM is a natural, nutritional source of biologically active sulfur. MSM provides the body with the raw materials it requires to remanufacture protein and connective tissues. MSM also has an anti-inflammatory effect on injured joints.
· Vitamin C (ascorbic acid) - Ascorbic acid is essential for the synthesis of collagen and the reconstruction of connective tissues in the body.
. Bromelain, a highly effective anti-inflammatory enzyme from pineapple. This enzyme has been extensively tested and found to have prostaglandin regulating properties. Prostaglandin cascades are centrally involved in inflammation, and by helping to shift the prostaglandin balance away from pro-inflammatory and towards anti-inflammatory, bromelain can moderate the process and speed recovery time.
• N-acetyl glucosamine (NAG), an activated metaboliteof glucosamine..
The enzymes that assemble connective materials from precursors readily utilize NAG “downstream” from glucosamine. NAG bypasses the acetylation of glucosamine that in vivo is known to be sensitive to blockage by aspirin and ethanol. NAG also may help to heal the “leaky gut” that sometimes accompanies connective tissue dysfunctions. NAG has antioxidant efficacy – it is an effective quencher of superoxide, one of the oxygen radicals that are abundantly produced during inflammation. NAG also partially blocks the release of elastase enzyme from immune cells, a phenomenon that normally contributes to spreading inflammation.
• Silicon and boron. These dietarily essential minerals are involved in crosslinking the primary connective strands to generate a final material that has great tensile strength
• Vitamin B6/pyridoxine.
Vitamin B6 helps recycle homocysteine, which when accumulating in excess will
interfere with collagen hydroxylation.
• Magnesium and calcium,
In this “yin-yang”mineral pair, magnesium is involved in connective tissue renewal and calcium if included for balance.
. Manganese is included as a mineral cofactor for SOD.
Molybdenum is another mineral essential for tissue homeostasis.
• Proanthocyanidin flavonoids, standardized.
This class of bioflavonoids is proven to enhance the tonicity of the microcapillaries and other small vessel beds.
Sincerely
Dr. Julie and Glenn Smith
PS Past copies of the newsletter can be found on the “P” drive in the Complementary Medicine folder.
