QuestionI will try to explain this the best way I can and with as much detail possible. In 96 I was a passenger in a car accident, struck from behind which severely damaged my entire back T1 - L6. I went to a chiropractor and he corrected the T and the C areas. Unfortunately, the chiropractor needed to continue treatment on the Lumbar areas due to the severity of damage.
I continued with treatment for long as possible however stopped due to legal proceedings and settlement which I never should have. Anyway. Years went by and my back healed incorrectly. I did begin experiencing a few times of when there were sudden "blow outs" and my back would give out for no reason. I just assumed it was going through the healing process and continued on.
Years later, when I was actually walking okay, I had a bone density test. During the test, my lower back was damaged again after the technician attempted to assist me instead of allowing me to move on my own. Not being able to move on a flat surface it was quite a sight that started two long years of terror.
It began with a visit to ER the following day then a visit to my primary doctor who requested x-rays and after seeing them then said there was something going on which required a specialist.
I then went to a back specialist who tested my back, asked me questions, did a CAT Scan, and discovered I had one disc that was fissured and a nerve that was bulged. The nerve that was bulged was workable however the disc that was fissured was questionable as to what it looked like. I didn't say much else other than, how are you going to fix it?
He proceeded to send me to a pain management doctor who then checked my back by poking, looked at the x-rays and the MRI results then said okay we can start by giving you epidurals and go from there. To wrap everything up in a bow, I had EPIs, I had Bilateral shots, I had the Facet joint shots, I also went through the ambulatory surgery that is the Z formation which felt like labor. I had attempted different types of pain medication which worked for awhile and that seemed to help the most. As for the cortisone shots, they did not.
I went through almost 2 years of physical therapy and nothing worked, if anything, it made my back worse because I had more difficulty walking. I was becoming weaker as what was being done was more stretching than strengthening. I went through the nerve stimulation at physical therapy which worked for awhile but it was only brief.
At the end of those two years, I basically said, enough is enough. As I was ready to walk out, the pain management doctor said to me the next step was looking at surgery. He called a surgeon and I called on one of my own choice because I believed in 2nd opinions. What it all came down to is the first surgeon did not want to give me the time of day let alone speak to me yet he saw me long enough to say I didn't need surgery. The second surgeon spent 45 minutes with me, did an actual exam on my back and determined I have myofascial trigger point damage in the lower lumbar area and the only way to correct it is through PT. *sigh*
Being already strained from it, I needed a break so I took his recommendation on where to go and went home. When my back was healed, I went to the person suggested and was given thoughts on attending swimming classes.
Now, up to this point I did not think that chronic migraines had anything to do with back pain however what I have read is showing lower back damage can cause chronic migraine issues. I did have them for some time, they went away and now they have returned again (as of September 2008)
I am a professional executive and just earned my MBA in Business Administration. I don't know if I can go back into the executive office stream safely because of this issue now and it is quite scary. Please help! Sorry so long but I am nervous and unsure if I can ever go back to work. Thank you so much for any and all information you can provide me. Oh one more thing, I am in the Omaha Metropolitan area but when I looked on your web site I did not see anyone. Does anyone work out of the Univ of NE at Omaha hospital?
Regards,
S. Elvins
AnswerDear Sue,
Sorry it has taken me a few days to get back in touch with you, I had to leave town for a few days on short notice. You should print this out Sue...it is long and you will likely need to read it over a few times.
First, sorry to hear of all the trouble you are having. Unfortunately I hear of people like you all the time. People who are injured in a car crash, are forced to settle claims for low money, have difficulty at work and home, and then experience unrelenting problems and pain for years afterward as their health care cost spiral out of control. The insurance industry has basically branded all auto injury patients as fakers and continue to propagandize the public and lawmakers so that they can take away your rights to resolution, even in the face of clinical research that completely refutes their approach.
To top all of this off, the medical approach to these patients is often failed pain management techniques because the source of the pain is directly from the soft tissue structures such as the disk, ligament, fascial structures etc...not specific nerve damage. This is called sclerotogenous pain, and can be very difficult to treat.
The Misunderstood Pain: Sclerotogenous Referral Pain
Presenting Situation: The patient states, 揑 have back pain that shoots into my leg? but the neurologist states the NCV (Nerve Conduction Velocity) EMG (Electromyogram) and MRI (Magnetic Resonance Imaging) are all normal. The treating doctor states, "I have no reasonable medical explanation for this continued pain." Is the patient embellishing? The answer is probably no. While it is true that some patients magnify their symptoms, they are usually not sophisticated enough to feign symptoms into a specific reproducible pattern. Why then were the imaging and electrodiagnostic tests negative? The answer is simple. The tests are either not sensitive enough to demonstrate the lesion, not designed to find the existing lesion or improperly performed and interpreted. For example, a negative MRI may suggest that there is no visualized compression of neural structures by discs or bone spurs. Negative NCV抯 and EMG抯 may suggest that there was insufficient compression or no compression of the large diameter nerves, which would result in a measurable abnormality. But what about the small diameter sensory nerves, what about ligament tearing, is there fatty infiltration of the muscle fibers that surround the spine for support and function, what about the other soft tissue structures? The truth is that researchers have shown an association between low back pain or leg pain and the lumbar facet joints many times, which is not generated by the disc, spinal nerve or spinal cord (1,2,3).
In fact, patients with referred pain often do not have nerve compression. Sounds good, right? Unfortunately it抯 not that simple. The most common referred pain seen in trauma cases are vascular, neurologic, visceral and sclerotomal. Neurologic pain (dermatomal pain), such as seen with disc herniations and nerve root compression, is the most frequently looked for type of pain. Less common are the vascular referred pains such as those seen with thoracic outlet syndromes (pain and numbness down the arms), and visceral referred pain that can happen with contusion to the body抯 organ systems. However, the most common and frequently overlooked origin of referred pain is from the soft tissues of the spine, also known as sclerotomal or sclerotogenous pain. An example: referred pain experienced with myofascial trigger points. While trigger points are common they are only one of the many sources of sclerotomal pain. Other sources would include the disc itself, facet joint capsules, facet joint cartilage, tendons, ligaments, etc?br>
Sclerotomal: The name suggests pain can come from any tissue of the same embryonic origin. A sclerotome is an embryonic region, which during fetal development differentiates into a variety of different body structures. These parts may or may not be neurologically connected but are understood to have some physiological relationship. Researchers have demonstrated these relationships repeatedly over the years and mapped out their referral distributions quite well. In fact, sclerotomal referral patterns have been published in many indexed medical journals beginning with the early work of Kellgren in 1939, Inman and Saunders in1944, and Feinstein et al. in 1954. One of the most well respected anatomical researchers, Bogduk, confirmed earlier findings in 1988.
Sclerotomal/referred pain has some unique characteristics. For example, in the lumbar spine (lower back) a Sclerotomal pain is usually more severe than dermatomal pain. Sclerotomal pain may not radiate down the entire leg and will usually stop at the knee or calf. There is no weakness or muscle atrophy with scerotomal pain. Referred pain can often be reproduced by applying pressure to the tissue site. In the cervical spine (neck) referral patterns to the cranium, chest, upper extremities and thoracic spine (upper and middle back) are common.
Referred pain has been overlooked as a source of pain by many clinicians because of the difficulty in treatment and diagnosis. Defense doctors, independent medical examiners, file reviewers, and insurance carriers, who have little or no experience with managing these types of injuries, often classify patients as malingerers or symptom magnifiers, and limit their treatment by cutting insurance benefits. Over time these patients may become chronic pain patients and eventually develop symptoms consistent with Fibromyalgia and Chronic Fatigue Syndrome.
Early Discovery: Many years ago Kellgren (4) conducted his now-classic research into the nature of referred pain. He injected hypertonic saline into paraspinal and other soft tissues and observed that the volunteers felt not only a local pain at the site of injection, which was to be expected, but also a pain radiating some distance away. Volunteers often complained of deep somatic pain or autonomic symptoms such as sweating, pallor, or palpitations. Kellgren mapped these referred patterns and found that there was a fair amount of consistency from one person to the next.
Rediscoveries: Some time later, Inman and Saunders (5) conducted similar research, again injecting fluid into the paraspinal tissues and documenting the patterns and nature of the resultant referred pain. In both instances they found that fairly consistent patterns of referred pain could be reproduced. Usually this referred pain began shortly after the injection and grew gradually. Most volunteers described it as gripping, aching, burning, heavy, or cramp-like. The important findings of Inman and Saunders are listed below.
Findings of Inman and Saunders
1. A time lag of minutes to several hours between injection and referred pain existed.
2. Volunteers had difficulty localizing the stimulus.
3. Periosteum and its attachments were most sensitive; muscle was least sensitive.
4. Greatest radiation occurred when periosteum or attachments were stimulated.
5. Muscles in referral areas were tender and sore.
6. Autonomic symptoms occurred when thoracic areas were stimulated.
7. The pain could last for several days.
Refinements: In an elegant experiment, Feinstein et al. replicated the earlier work of Kellgren, Inman and Saunders (6). They injected the brachial plexus of one volunteer with procaine. The complete regional block that resulted also included the autonomic nervous system (ANS), as evidenced by the temporary Horner's syndrome that was produced. In this way they had removed both the peripheral nervous system (PNS) and the autonomic nervous system from the list of contributors to the pain. Another paraspinal injection of saline solution into this volunteer's neck resulted in the same referred arm pain experienced before the regional block. Therefore, this mechanism of referral was not mediated or conveyed by either the ANS or the PNS, but was in fact a central phenomenon. The findings of Feinstein et al. are summarized below.
Findings of Feinstein et al.
1. Upper cervical stimulation resulted in head pain.
2. A segmental relationship existed, whereby injection of a muscle whose innervation was C5-6 would result in soreness in other muscles innervated by those levels.
3. Muscle soreness and spasm was noted in referred pain areas.
4. Hypesthesia was noted over referred areas.
5. Phantom limb pain could be reproduced in amputees (even in those who had not experienced it at the time of their amputation).
6. **The ANS and PNS are not mediators of the pain.
Perhaps most interesting about this referred or sclerotogenous pain, is the observation that the levels of referral, while reproducible from patient to patient, do not seem to follow known dermatomal or myotomal patterns. In fact, the body maps created by Feinstein and coworkers are re-created in Foreman and Croft抯 Textbook: Whiplash Injuries: the cervical acceleration/deceleration syndrome [3rd edition, pp 396-404]. These body maps demonstrate that, very often, injection at one spinal level results in pain referral to areas innervated two to four spinal segments away. And often, referral is to not one, but several segment levels. This serves to confuse the issue all the more. For example, an injection at C7 may result in referred pain in areas innervated by C5, C6, C7, C8 and T1.
Since it is most common for clinicians to view the human body with the neurogenic pain model, a ligamentous injury at C7, resulting in the above referred pain pattern, might confuse the uneducated physician. Diagnostic options may include: multiple disc lesions, brachial plexopathy, thoracic outlet syndrome, or outright malingering, which is often the impression many doctors arrive at. The patient is branded a faker, and left without answers.
Non-classical neurological findings in CAD/whiplash trauma are common (7) and should not be used to suggest that patients are disingenuous. These non-dermatomal sensory abnormalities, as common as they are, qualify one for a DSM-III psychiatric diagnosis! Some have argued that they are common in Multiple Personality Disorder. As stated previously, anatomical studies and electrodiagnostic studies will generally be normal, although plain films often demonstrate some instability. Again, this only serves to confound the uneducated physician, and muddle diagnosis.
Recent Corroboration: Bogduk and Marsland (8,9) demonstrated that cervical facet joints could be the source of neck pain. Over 50% of their chronic CAD injury group had facet pain (8,10). Dwyer et al. (11) injected the cervical facet joints of human volunteers with saline solution and dye and recorded their responses. They found that the upper cervical joints, C2-3, were associated with suboccipital headaches when injected (they did not inject C1-2 or OCC-C1, but presumably these would have resulted in headaches as well). Lower levels were productive of neck and shoulder pain, not surprisingly. In part II of their study (12), they used the pain maps created from injecting normal volunteers to predict the spinal levels involved in a group of patients who complained of neck and/or shoulder pain. Their success rate with this method was 100% (Limitations- fairly small study group).
Although this work by Bogduk and Marsland (9) and Dwyer et al. (11) seems to suggest that discrete scleratomes exist in the cervical region, the high degree of overlap at lumbar levels noted by some observers precludes the description of such a construct there. Kellgren (4) and Inman and Saunders (5) described discrete scleratomes at lumbar levels, but more recent researchers have been unable to confirm such consistency (13,14). McCall et al. (15), for example, injected facet joints at L1-2 and L4-5 and found much overlap even though a general pattern of flank pain was seen at upper levels, whereas buttock and groin pain was seen at lower levels. In essence, these studies argue against 搕rue scleratomes," in the lumbar spine while the phenomenon of scleratogenous pain is still very real. Scleratomal pain, it turns out, was a poor term for the phenomenon. Nevertheless, Bogduk and Lord (16) continue to use the term and give a good review of pain and whiplash injury. The figure below points to the differences between dermatomal and scleratomal pain.
The broadly referring pattern of facet joints is at least partially explained by a recent set of experiments. Ohtori et al. (17) used retrograde neurotracing methods with Fluoro-Gold (FG), to trace the level of dorsal root ganglions (DRGs) innervating the C1-C2, C3-C4, and C5-C6 facet joints and their pathways in rats. Neurons labeled with FG were present in the DRGs from C1 through C8 in the C1-C2 group, from C1 to T2 in the C3-C4 group, and from C3 to T3 in the C5-C6 group, which illustrates the redundancy of innervation at multiple levels. No wonder an injured facet joint may refer pain so broadly.
The prognosis for sclerotogenous pain from traumatic insult is dependent upon many factors. The extent of damage, pre-exiting illnesses, compliance with care and early detection by the physician, all contribute to the potential outcome. Damaged soft tissues tend to heal in a disorganized manner even with regular management. Active care protocols applied in a controlled manner are essential in managing the resultant scar formation in sclerotogenous structures and reducing chronic pain. The fibrotic replacement tissue is never as competent as the original tissue and is prone towards re-injury and hypersensitivity. Even with prompt attention the prognosis for complete recovery may be only fair to poor.
References:
1. Carrera GF: Lumbar facet joint injection in low back pain and sciatica. Neuroradiology 137:665-667, 1980
2. Fairbank JCT, Park WM, McCall IW, O'Brien JP: Apophyseal injection of local anesthetic as a diagnostic aid in primary low-back pain syndromes. Spine 6(6):598-605, 1981.
3. Destouet JM, Gigula LA, Murphy WA, Monsees B: Lumbar facet joint injection: indication, technique, clinical correlation, and preliminary results. Radiology 145:321-325, 1982.
4. Kellgren JH: On distribution of pain arising from deep somatic structures with charts of segmental pain areas. Clin Sci 4:35-46, 1939.
5. Inman VT, Saunders JBdeCM: Referred pain from skeletal structures. J Nerv Ment Dis 99:660-667, 1944.
6. Feinstein B, Langton JNK, Jameson RM, Schiller F: Experiments of pain referred from deep somatic tissues. J Bone Joint Surg 36A(5):981-997, 1954.
7. Bogduk N: Post whiplash syndrome. Aust Fam Phys 23(12):2303-2307, 1994.
8. Barnsley L, Lord S, Wallis BJ, Bogduk N: The presence of chronic cervical zygapophyseal joint pain after whiplash. Spine 20(1):20-26, 1995.
9. Bogduk N, Marsland A: The cervical zygapophyseal joints as a source of neck pain. Spine 13(6):610-617, 1988.
10. Lord SM, Barnsley L, Wallis BJ, Bogduk N: Chronic cervical zygapophyseal pain after whiplash. Spine 21(15):1737-1745, 1996.
11. Dwyer A, Aprill C, Bogduk N: Cervical zygapophyseal joint pain patterns I: a study in normal volunteers. Spine 15(6):453-457, 1990.
12. Aprill C, Dwyer A, Bogduk N: Cervical zygapophyseal joint pain patterns II: a clinical evaluation. Spine 15(6):458-461, 1990.
13. Hockaday JM, Whitty CWM: Patterns of referred pain in the normal subject. Brain 90(3):481-496, 1967.
14. Sinclair DL Jr, Feindel WH, Weddell G, et al.: The intervertebral ligaments as a source of pain. J Bone Joint Surg 30B:515-525, 1948.
15. McCall IW, Park WM, O'Brien JP: Induced pain referral from posterior lumbar elements in normal subjects. Spine 4(5):441-446, 1979.
16. Bogduk N, Lord SM: Cervical spine disorders. Cur Opin Rheumatol 10:110-115, 1998.
17. Ohtori S, Takahashi K, Chiba T, Yamagata M, Sameda H, Moriya H. Sensory innervation of the cervical facet joints in rats. Spine 26:147-150, 2001.
Moving on...The continuation of pain can in itself become a neurological phenomena where pain is now generated centrally inside the nervous system rather than at the injured tissue site: central sensitization, synaptic arborization, wind-up, neoneuralization are terms you should research to understand this concept better.
Concerning the migraine type headaches, there is an direct anatomical connection from the low back (lumbar spine and sacrum)to creating headache pain. As a matter of fact, I often adjust a patients sacrum when they have headaches and get good results in eliminating pain. Here is how it works:
A specific structure called the meninges covers the brain and spinal cord. It contains the cerebrospinal fluid that keeps the brain/cord nourished and protected from trauma. The meninges is composed of three distinct layers called the Pia, Arachnoid and Dura matter which is richly innervated with pain sensing fibers...if the meninges is disrupted/injured or inflamed it can result in appreciable pain transmission This is the reason that post-partum mothers often get severe headaches after giving birth with an epidural placement. The meninges attaches to the inside of the skull, to all the vertebra in the spine, and anchors itself at the sacrum and coccyx at the base of the spine. So if you have an injury in the lower back which either direct affects the dural sheaths of the nerve roots, or indirectly affects them by inflammation or scar tissue formation, this can result in headache pain.
That being said, you must realize that the headache symptoms could also be completely independent of your low back injury...so the best approach to this is to have the upper cervical spine/occiput examined for dysfunction as well as the lower back anatomy. Even though you stated that the chiropractic care after your crash fixed your neck pain issues, over time the original injury can continue to create pain. It has been well established in the clinical literature on car crash soft tissue injuries as well as the anatomical literature, that the neck structures are a prime site for dysfunction which directly relates to headache pain. One of the most well respected anatomical researchers, Nikoli Bogduk, MD published a paper on this a few years back, which is one of the best representations of headache pain generation. Below is a synopsis of that paper:
N Bogdu. Anatomy and Physiology of Headache. Biomedicine and Pharmacotherapy, 1995, Vol. 49, No. 10, 435-445
FROM ABSTRACT:
All headaches have a common anatomy and physiology.
All headaches are mediated by the trigeminocervical nucleus, and are initiated by noxious stimulation of the endings of the nerves that synapse on this nucleus, by irritation of the nerves themselves, or by disinhibition of the nucleus.
DR. BOGDUK ALSO NOTES:
The brainstem contains a region of grey matter called the trigeminocervical nucleus. This nucleus is causally continuous with the grey matter of the dorsal horn of the spinal cord. The trigeminocervical nucleus is 揹efined by its afferent fibers.?[Key Point: afferent fibers are sensory fibers that send information to the brain]
The trigeminocervical nucleus receives afferents from the following sources:
1) Trigeminal Nerve (Cranial Nerve V)
2) Upper three cervical nerves
3) Cranial Nerve VII (Facial Nerve)
4) Cranial Nerve IX (Glossopharyngeal Nerve)
5) Cranial Nerve X (Vagus Nerve)
All of these sources of afferents terminate on common second-order neurons in the trigeminocervical nucleus.
Trigeminal Nerve afferents will descend to the level of C3 and perhaps as low as C4. The trigeminocervical nucleus is the sole nociceptive nucleus of the head, throat and upper neck. 揂ll nociceptive afferents from the trigeminal, facial, glossopharyngeal and vagus nerves and C1-C3 spinal nerves ramify in this single column of grey matter.?br>
Because the ophthalmic branch of the trigeminal nerve extends the farthest into the trigeminocervical nucleus, cervical afferent stimulation is most likely to refer pain to the frontal-orbital region of the head.
The stimulation of any neurons that activate the trigeminocervical nucleus can cause headache, which includes cranial nerves V, VII, IX, X, and C1-C3. 揂ny structure innervated by these nerves is capable of causing headache.?br>
揟he C1 and C2 spinal nerves are distinctive in that they do not emerge through intervertebral foramina.?br>
The C1 spinal nerve passes across the posterior arch of the atlas behind its superior articular process, descending in front of the C1 transverse process to descend as a part of the cervical plexus.
C1 spinal nerve does not supply the skin, but does supply sensory innervation to the suboccipital muscles. The sensory root of C1 can be found with the motor roots of the spinal accessory (cranial nerve XI) nerve.
The C2 spinal nerve crosses the posterior aspect of the C1-C2 facet joint; its dorsal root ganglion is opposite the midpoint of the C1-C2 facet joint.
The anterior primary rami of C1-C2-C3-C4 join and form the cervical plexus to innervate the prevertebral muscles: longus capitis, longus cervicis, rectus capitis anterior, rectus capitis lateralis, sternocleidomastoid and trapezius.
The anterior primary rami of C1-C2-C3 form the recurrent meningeal branches of the sinuvertebral nerves. These nerves innervate the anterior surface of the upper cervical dura mater, and then pass through the foramen magnum to innervate the dura mater between the pituitary gland to the anterior occiput (the clivus). They also innervate the medial portion of the C1-C2 joint capsule, the transverse and alar ligaments.
In the posterior cranial fossa, C1-C3 sinuvertebral nerves add components to cranial nerve X (vagus) and XII (hypoglossal). [Important...also gives rationale why we get stomach upset with bad headache pain...the vagus nerve send information to the digestive tract]
The anterior primary rami from C1-C3 join the vertebral nerve, the plexus of nerves that travels with the vertebral artery, and supplies sensory branches to the fourth part of the vertebral artery.
The posterior primary rami of C1 innervate the 4 suboccipital muscles: inferior oblique, superior oblique, rectus capitis posterior major, rectus capitis posterior minor.
The motor component of the C2 posterior primary rami innervates the longissimus capitis and splenius.
The sensory component of the C2 posterior primary rami becomes the greater occipital nerve. It winds under the inferior oblique muscle, ascends and pierces the shared aponeurosis of the trapezius and sternocleidomastoid muscle to supply the posterior scalp.
The motor components of the C3 posterior primary rami also innervate the longissimus capitis and splenius muscles as well as the C2-C3 multifidus muscle.
The sensory component of the C3 posterior primary rami runs across the posterior aspect of the C2-C3 facet joint (which it innervates) and ascends as the third occipital nerve to supply the suboccipital region.
Stretch on the dura mater can initiate mechanical pain. [Important...remember how I explained this connection above]
The posterior cranial fossa and its contents are innervated by cervical nerves.
揤ertebral artery disease, such as an aneurysm becomes an important differential diagnosis of what otherwise might seem to be neck pain with referred pain to the head.?br>
Arthritis of the upper cervical synovial joints (including C2-C3) can cause neck pain and headache.
Injury and damage to the alar ligaments can cause upper cervical pain and headache. The diagnosis is made with upper cervical rotational CT scanning, showing significant greater unilateral rotation. [Important: I actually utilize FLAR study MRI's to find this damage in my patients with chronic headaches after car crashes...I find it all the time due to the acceleration injury experienced, especially after rear impact crashes]
Posterior cervical muscle tears are not a cause of chronic headache.
C2 neuralgia is a neurogenic headache that can be caused by 搒car tissue following trauma to the lateral atlanto-axial joint.?[Important]
[Fibrosis of the C1-C2 facet joint affecting the adjacent C2 root]
So...what does all of this mean Sue. Well in my humble opinion, I would suggest that you try chiropractic care again for these issues. The chiropractor can adjust the upper cervical spine if fixated to allow proper movement which will help to remodel any abnormal scar tissue in that area, as well as affect the dural structures at the base of the skull, and at the base of the spine. Mechanical neurological input to the spine (adjustments) actually send signals to the brain to reduce pain processing in the brain, brain stem, spinal cord and at the spinal cord level nerve roots. Bottom line, what do you have to lose at this point.
Hope this helps Sue...I know it was long and dense, but I wanted you to have as much information as possible. Feel free to share the information with your doctors and good Luck.
Respectfully,
Dr. J. Shawn Leatherman
www.suncoasthealthcare.net
