Question
I am being treated with physical therapy for a work related injury in Oct 08. I had a lumbar xray that was negative. I then had a lumbar CAT scan that showed mild disc bulges at L3-4, L4-5, and L5-S1. My PCP doesnt seem to think that these disc bulges are the cause of my pain. Can you please explain what a mild disc bulge is? Are they tears in the disc? If so can they heal/repair themselves? Should I be worried about these bulges? I dont have any sharp shooting leg pain, only central and right sided low back pain, difficulty with forward bending with increased pain. I was improving with therapy after 2 months, but then 1.5 weeks ago I used my snowblower and my back went into severe spasm afterward and I feel like Im back to square 1. Any ideas?

Answer
Dear Joseph,

Print this out, it is lengthy!!  Now, I get so sick of hearing people tell me that their medical doctor doesn't think that disk bulges can cause pain...this is a ridiculous assumption...even if the disk bulges are "mild".  Not to mention that your x-rays were "negative" tells me nothing...negative for what?  Did your medical doctor actually give you a diagnosis other than back pain? Did they discuss nerve supply, referred pain or muscular stabilization?  Lastly, a CT scan is not the best imaging to evaluate the disk an MRI is, and tears in the outer portion of the disc (annulus) would be better visualized and documented with an MRI than CT.

Medical doctors look at things much differently than do chiropractic physicians.  They are trained to look for serious signs of pathology such as fractures and tumors that may require surgery or advanced pharmacological management such as cancer.  They really do not get the importance of spinal structure or degeneration in the pain experience, nor do they understand what to do for it...it just isn't part of their training.  Most of the time they do not even perform a physical examination of your low back, and if they do, it usually consists of a nurse taking your vital signs, and you bending over to touch your toes and laying flat on your back while the doctor raises your leg.  A functional orthopedic examination of the low back should include a broad family and personal medical history, focused history of the low back pain, all ranges of motion for the low back and pelvis (measured with instrumentation), manual palpation of the spine and soft tissues of the low back, multiple orthopedic tests for the disk, facet joints, tendons/muscle, sacroiliac joints, ligaments/fascial sheaths, grading of muscle strength and deep tendon reflexes.  To be the most complete balance, and sensory testing should also be performed, and then radiographic tests if needed.  I doubt this was actually done.

Concerning the disc bulge, when one is found on MRI it should be measured to ascertain the magnitude of the problem, but this is often not done.  What does minor, moderate, or severe really mean without quantification.  The most appropriate way to document a disc bulge is to list the millimeters of bulge and in what direction.  Such as: a 4mm posterior disc protrusion was found at L5/S1 without cord impingement or foraminal encroachment...that description is specific and means that no neurological structures are being impinged by the bulge. However, chemical irritation due to inflammation can still occur locally to the muscle, disc, and nerve roots. I have often seen that a 3mm protrusion is called a bulge while more than 5mm protrusion would be called a herniation, but there is often no consensus on this and that is why the MRI results can be confusing.

Now disk protrusions can and do cause pain due to the nerve supply that actually goes into the outer portion of the disc.  It used to be thought that the disk had no nerve supply and some practitioners still believe this.  I will copy down some research oin this for your appreciation.  See end of document.

I would encourage you to continue with the exercises you learned in physical therapy since you had improved, but realize that you may need more care.  I would also recommend that you seek out the advice and care of a local chiropractic physician to help you with this condition.  Disk healing take a long time and will never be complete.  It's structure has a poor blood supply and this makes recovery slow and incomplete.   

揟he spinal injury weakens the spine and predisposes the patient to further injury, regardless of type and extent of damage. This phenomenon is especially true when protection of the injured part is not adequate. Ligaments and muscles heal only by scar formation, and the annulus fibrosis of the disk is almost powerless to heal tears of its substance.?David B. Levine, M.D., The Painful Back, Page 451, Chapter 92

However, decompression types of care will help to restore fluid exchange with the disk which increases healing...chiropractors often use decompression types of therapy in office for low back disk injury:  cox flexion/distraction tables, posture pumps, intervertebral decompression tables, not to mention that spinal adjustments designed to take pressure off the disk while increasing joint motion.  Find a good chiropractor and get an examination, also make sure that you are taught exercises to help train the multifidus muscle which helps to stabilize the low back and disks.

Respectfully,
Dr. J. Shawn Leatherman
www.suncoasthealthcare.net

Nerve Ingrowth Into Diseased Intervertebral Disc in Chronic Back Pain
The Lancet:  July 19, 1997, Vol. 350, pp. 178-181

AJ Freemont, TE Peacock, P Goupille, JA Hoyland, J O払rien, MIV Jayson
Authors associated with the Departments of Rheumatology and Pathological Sciences, University of Manchester, UK.

FROM ABSTRACT:

BACKGROUND:
In the healthy back only the outer third of the annulus fibrosus of the intervertebral disc is innervated.
Nerve ingrowth deeper into diseased intervertebral disc has been reported, but how common this feature is and whether it is associated with chronic pain are unknown. We examined nerve growth into the intervertebral disc in the pathogenesis of chronic low back pain.

METHODS:
We collected 46 samples of intervertebral discs from 38 patients during spinal fusion for chronic back pain. 30 samples were from pain levels clinically established by discography and 16 samples were from adjacent vertebral levels with no pain. We obtained 34 control samples of intervertebral disc from previously healthy individuals with normal histology within 8 h of recorded death. We used standard immunohistochemical techniques to test for a general nerve marker, a nociceptive neurotransmitter (substance P), and a protein expressed during axonogenesis (growth-associated protein 43 [GAP43]).

FINDINGS:
We identified nerve fibers in the outer third of the annulus fibrosus in 48 (60%) of the 80 samples of intervertebral discs. Nerves were restricted to the outer or middle third of the annulus fibrosus in the 34 control samples. Among the patients with chronic low back pain, nerves extended into the inner third of the annulus fibrosus in 46% and into the nucleus pulposus in 22% of samples.

Deep nerve ingrowth into the inner third of the annulus fibrosus, the nucleus pulposus, or both was seen in four (25%) of 16 biopsy samples from non-pain levels and in 17 (57%) samples from pain levels.

Of the 16 paired samples from both pain and non-pain levels, five pain-level samples and one non-pain-level sample showed deep nerve ingrowth.

INTERPRETATION:
Our finding of isolated nerve fibers that express substance P deep within diseased intervertebral discs and their association with pain suggests an important role for nerve growth into the intervertebral disc in the pathogenesis of chronic low back pain.

THESE AUTHORS ALSO NOTE:
These authors cite 5 studies that indicate the intervertebral disc is often the source of back pain and, 揷hronic back pain is one of the leading causes of morbidity and loss of work.?br>
The pathogenesis of chronic back pain is poorly understood, and chronic low back pain is not caused by nerve root compression. Moreover, leg pain / sciatica can be caused by mechanisms other than nerve root compression.

Immunohistochemical staining techniques show that in healthy human intervertebral discs nerves extend no deeper than the outer third of the annulus fibrosis. These authors 搈easured nerve ingrowth in terms of how deep within the annulus nerve fibers were seen and whether nerves had penetrated the nucleus pulposus.?br>
Two studies have shown the nerves extend deeper into the annulus fibrosis and into the nucleus pulposus in diseased intervertebral discs. Deep nerve ingrowth was defined as growth into the inner third of the annulus or into the nucleus.  In this study, the overall disruption of the normal architecture of the disc was greatest in the samples taken from painful discs.

DISCUSSION:
Substance P is a nociceptive neurotransmitter and pain mediator.  This study shows that there is an association between substance P and disc degeneration, and the 揺xtent of neoneuralization is greatest at intervertebral disc levels at which the patient experiences pain.?揑t is noteworthy that these neural elements did not occur in any of the control discs but were found commonly in intervertebral discs from pain levels.? Most of the nerves identified in this study accompanied blood vessels, indicating both a nociceptive and vasoregulatory role for these nerves.

揟he presence of these neural elements within the nucleus pulposus was a feature only of intervertebral discs from the pain level.? 揙ur findings strongly implicate these fibrils in the pathogenesis of chronic low back pain.?br>
揥hy such nerve fibrils should also be present within a small proportion of the anatomically deranged non-pain level intervertebral discs [12% into the inner third of the annulus; 3% into the nucleus] is open to conjecture. One possible explanation is that pain perception requires a nociceptive trigger as well as innervation.?Studies have shown that discal chondrocytes are capable of producing nociceptive triggers including prostaglandins [PGE2]. [Very Important]

In this study, no control discs showed nerve ingrowth into the nucleus pulposus. Every time nerve ingrowth was found in the nucleus, it was a painful disc. However, not all painful discs had nerve ingrowth into the nucleus pulposus; 30 ?38% did, and not all painful discs had nerve ingrowth into the inner third of the annulus; about 60% did.

揝o what is the biological purpose of nerve ingrowth into intervertebral discs? By analogy with other connective tissues, nerve ingrowth into damaged intervertebral discs could mediate various tissue events, notably healing. Initially, an immobilizing might be beneficial, but because the healing process is thought to be poor in this tissue, unproductive nerve ingrowth and pain may result.?br>
揥e have shown an association between the frequency and site of back pain and nerve ingrowth into the intervertebral disc, or more specifically the nucleus pulposus.?揘erve ingrowth may be part of the process of disturbed repair, and is therefore of little value.?br>
KEY POINTS FROM SUNCOAST HEALTHCARE:
1)      揅hronic back pain is one of the leading causes of morbidity and loss of work.?br> 2)      Chronic low back pain is not caused by nerve root compression.
3)      Leg pain / sciatica can be caused by mechanisms other than nerve root compression.
4)      The intervertebral disc is often the source of back pain.
5)      The normal healthy human disc has nerves into the outer third of the annulus.
6)      Painful discs have the greatest amount of histological degeneration.
7)      Substance P is a nociceptive neurotransmitter and pain mediator. There is an association between substance P and disc degeneration. It is noteworthy that these neural elements did not occur in any of the control discs but were found commonly in intervertebral discs from pain levels.?br> 8)      The 揺xtent of neoneuralization is greatest at intervertebral disc levels at which the patient experiences pain.?
19)    揟he presence of these neural elements within the nucleus pulposus was a feature only of intervertebral discs from the pain level.?br> 10)    揙ur findings strongly implicate these fibrils in the pathogenesis of chronic low back pain.?br> 11)    揥hy such nerve fibrils should also be present within a small proportion of the anatomically deranged non-pain level intervertebral discs [12% into the inner third of the annulus; 3% into the nucleus] is open to conjecture. One possible explanation is that pain perception requires a nociceptive trigger as well as innervation.?[Important]
12)    In this study, no control discs showed nerve ingrowth into the nucleus pulposus. Every time nerve ingrowth was found in the nucleus, it was a painful disc.
13)    In this study, not all painful discs had nerve ingrowth into the nucleus pulposus; 30 ?38% did. Not all painful discs had nerve ingrowth into the inner third of the annulus; about 60% did.
14)    Discal chondrocytes are capable of producing nociceptive triggers including prostaglandins [PGE2]. [Important]
15)     Nerve ingrowth into damaged intervertebral discs mediates tissue healing, which might be beneficial because of initial immobilization, but because the disc is poor in healing 搖nproductive nerve ingrowth and pain may result.?br> 16)      These authors 揾ave shown an association between the frequency and site of back pain and nerve ingrowth into the intervertebral disc, or more specifically the nucleus pulposus.?

The nerve supply of the lumbar intervertebral disc
Journal of Bone and Joint Surgery -British Volume, Vol. 89-B, Issue 9, September 2007, pp. 1135-1139
M. A. Edgar, MChir, FRCS, Retired Orthopedic Surgeon

FROM ABSTRACT:
The anatomical studies, basic to our understanding of lumbar spine innervation through the sinu-vertebral nerves, are reviewed.

1980s Research suggested that pain sensation was conducted in part via the sympathetic system. These pathways have now been clarified using sophisticated experimental and histochemical techniques confirming a dual pattern. One route enters the adjacent dorsal root segmentally, whereas the other supply is non-segmental ascending through the paravertebral sympathetic chain with re-entry through the thoracolumbar white rami communicantes.

Sensory nerve endings in the degenerative lumbar disc penetrate deep into the disrupted nucleus pulposus, they do not in the normal lumbar spine. Complex as well as free nerve endings appear to contribute to pain transmission.

The nature and mechanism of discogenic pain is still speculative but there is growing evidence to support a 憊isceral pain?hypothesis, unique in the musculoskeletal system. This mechanism is open to 憄eripheral sensitization?and possibly 慶entral sensitization?as a potential cause of chronic back pain.

THIS AUTHOR ALSO NOTES:
The sinuvertebral nerve is 揻ormed by a fine sympathetic branch, usually arising from the grey ramus communicans, and a fine sensory spinal branch from the ventral ramus.?揟hese conjoined sinuvertebral nerves re-entered the vertebral canal through each intervertebral foramen to lie anterior to the nerve root in association with the segmental vessels.? 揟he sympathetic fibers were considered as vasomotor efferents and the sensory fibers as proprioceptive and nociceptive.?Sinuvertebral nerve branches innervate the posterior longitudinal ligament, the outer layers of the annulus fibrosus, and the anterior dura.  揟he lumbar sinuvertebral nerves had up to three segmental levels of overlap, which might explain the poor localization of low back pain.?br>
The anterior part of the disc annulus is innervated solely from sympathetic nerves. Other parts of the disc are 90% innervated by sympathetic nerves. It is probable that these sympathetic nerves are conveying pain afferent information to the central nervous system, indicating, 搇ow back pain is a kind of visceral pain.?br>
Studies indicate, 揳fferent nerve fibers from the annulus pass into the sympathetic chain to re-enter the sensory nerve roots at L1 and L2.? Other studies state 搕his experiment has confirmed the presence of a clear nociceptive pathway of sympathetic afferent discharge from the dorsal aspect of the lower lumbar intervertebral discs to the dorsal roots of L2,?indicating that 搇umbar discogenic pain is indeed a variety of visceral pain.?

Electrical stimulation to the annulus of an upper lumbar disc produces multilevel bilateral motor unit action potentials in the lumbar multifidus musculature. 揑t is reasonable to propose that the annular stimulus was transmitted via the widespread non-segmental sympathetic afferents.?The pattern of response suggests a spinal reflex to the anterior horn cells.

Electrical stimulus to an adjacent facet joint caused only a localized, unilateral response multifidus contraction. 揇istension of the adjacent facet joint with saline depressed the motor unit action potentials.?[Important for chiropractors-spinal adjustments distend the facet and facet capsule卪ay reduce multifidus spasm]




揘ormal nucleus pulposus and inner annular zones are devoid of nerves.?The three outer lamellae of the disc are innervated with nociceptive afferents.  However, nerves can extend to the inner third in 50% of painful degenerative discs. These nerves arise from granulation tissue growing into the degenerative disc, 搉eo-innervation.?Disc and/or facet inflammation can sensitize local mechanoreceptors into becoming pain afferents, resulting in chronic discogenic pain. [Important]

揟he authors of a number of recent papers suggest that the sensory nerve supply of the disc is similar to that of certain enteric structures and represents a form of visceral pain. 揟here is growing evidence that these pain receptors are peripherally sensitized by the activity of sympathetic efferents.?br>
Disc nociceptive afferents 搈ay initiate a pain impulse in response to ischemia, pressure changes (mechanoreceptors) or inflammatory irritation.? [Important for Chiropractors, Vertebral fixation can cause pressure changes affecting mechanoreceptors, while spinal joint cavitation increase mechanoreception from the joint capsules and muscle spindles of the multifidus which inhibits nociception.]

Psychological stress can activate the 慶entral sensitization?of the descending autonomic nerves which may lower the threshold for disc nociception, adding to chronic discogenic pain.

揟here is something unique about the nerves related to the spine and the spinal canal, which makes the source of pain different from the rest of the musculoskeletal parts of the body. Could the answer be that the disc, unlike other joints, is uniquely provided with a predominantly visceral-type of nerve supply??[May be why disc pain is often chronic and requires more treatment than does pain arising from other musculoskeletal tissues]

KEY POINTS FROM SUNCOAST HEALTHARE PROFESSIONALS
1) sympathetic nerves innervate Viscera.
2) The intervertebral disc is also innervated primarily (90%) by sympathetic nerves.
3) Disc sympathetic nerves are capable of sending nociceptive information to the sympathetic nervous system.
4) Disc pain is different than all other musculoskeletal pain because it is a form of 搗isceral pain.?br> 5) The sympathetic component of disc innervation is found in the sinuvertebral nerve. The lumbar sinuvertebral nerves have up to three segmental levels of overlap, 搘hich might explain the poor localization of low back pain.?br> 6) Degenerated discs are more extensively innervated than normal discs.
7)  Sensory nerve endings in the degenerative lumbar disc penetrate deep into the disrupted nucleus pulposus, which is insensitive in the normal lumbar spine.
8) The sympathetic nerve fibers that innervate the lower lumbar discs inter the central nervous system through the sensory nerve roots at L1 and L2.
9) 揕umbar discogenic pain is indeed a variety of visceral pain.?
10) Disc irritation produces bilateral contraction of the lumbar multifidus.
11) Facet joint irritation produces unilateral multifidus contraction.
12) Distension of the facet joint inhibits the multifidus muscle contraction. [Important for chiropractors]
13) Disc and/or facet inflammation can sensitize local mechanoreceptors into becoming pain afferents, resulting in chronic discogenic pain. [Important]
14) Pain receptors are sensitized by the activity of sympathetic efferents.
15) Disc nociceptive afferents 搈ay initiate a pain impulse in response to ischemia, pressure changes (mechanoreceptors) or inflammatory irritation.擺Important for Chiropractors]
16) Psychological stress can activate the 慶entral sensitization?of the descending autonomic nerves which may lower the threshold for disc nociception, adding to chronic discogenic pain.
17) 揟here is something unique about the nerves related to the spine and the spinal canal which makes the source of pain different from the rest of the musculoskeletal parts of the body. Could the answer be that the disc, unlike other joints, is uniquely provided with a predominantly visceral-type of nerve supply??