QuestionDr. Leatherman,
I have an issue. I was involved in a car accident at the age of 15, I was seated in the front passenger seat with my seatbelt buckled when a car slammed into my mothers car. We were practically stationary merging onto the highway in traffic and the car flew forward. Since then I've seen neurologists, general physicians, orthopedic surgeons, a chiropractor...I've done multiple Xrays, MRI's, CT Scans, etc of my neck, back and brain..but none of these doctors can diagnose a problem. I experience pain/discomfort daily in all areas of my back but the pain relocates whenever it pleases. The tests show nothing!...According to my doctors there is nothing physically wrong so they don't know where to take this. I cant sit, stand or walk for too long. I'm 19 and my body won't allow me to dance like I used to, if I try I end up in pain for 2 days. I'm not much of an athlete so I haven't aggravated anything playing sports. I am really running out of options here and I have no proof that I am actually experiencing pain. I know its not in my head, but someone as young and healthy as I am should have no problem healing. My back and shoulders tense up and feel like rocks on my worst days.
I'm forced to do the dishes in intervals because I cant stand over the sink too long without experiencing muscle spasms.
At one point I had to wear sunglasses in the class because certain lights triggered a ridiculous headache that lead to overheating and a drastic raise in blood pressure and pulse.
I saw a chiropractor for a year and there has been minimal change if any.
I recently tried physical therapy which made the situation worse. The massage I was given after the back strengthening exercises put me in more pain (2 days after therapy) than I was without the therapy.
Help!
Thank You in advance
Kimberly
AnswerDear Kimberly,
You are not alone and I have seen numerous cases such as yours in the past. What most physicians fail to realize is that just because you cannot find a problem doesn't mean it ceases to exist. For instance, chronic degnerative diseases such as cancer and heart disease often go undiagnosed for years before they become symptomatic. Moreover, it is widely accepted in the clinical literature that pain can become chronic and be centralized in the central nervous system after the offending intial injury should have resolved. Even though this is well known, there are misconceptions about soft tissue injuries and whiplash type injuries where as a majority of people (physicians included) think they are trivial and will subside in 6-8 weeks. The research and clinical literature absolutely refutes that notion and we know patients can have chronic pain and undiagnosed brain injuries from these crashes....this is well documented across disciplines and in studies all over the world.
Converse to the above, you can have initial and ongoing pain and dysfunction in the soft tissue due to trauma, acute or chronic inflammation, scar tissue formation and adhesion formation between the layers of soft tissue (muscle and fascial tissue)...this is often called sclerotogenous pain or referred pain. I have found this to be poorly understood as well by many physicians and need to explain it further.
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. 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, 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. Visceral referred pain 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.
For an illustration of these cervical scleratomal patterns of referred pain, compared to the classic dermatomal patterns, look up the word SCLEROTOME on the glossary page of my website www.suncoasthealthcare.net. Illustration is posted with permission from The Spine Research Institute of San Diego, 1998.
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.
Now, I hope this gives you a more complete understanding of the types of pain that you may be experiencing as well as why. Chronic pain is no laughing matter especailly when nobody seems to understand why or where it is comming from. To learn more about whiplash injury and chronic pain, I would suggest that you contact the Spine Research Institute of San Diego (SRISD) and purchase the latest book written by Dr. Arthur C. Croft (the director of the institute). His newest text was written primarily for patients and is superb in the quality and presentation of information as well as the research documentation...worth double the purchase price, in fact I recommend it for all my crash patients. TITLE: "Whiplash and Mild Traumatic brain injuries: a guide for patients and practitioners" (2009). The book is quite literally the best text ever published on the subject in my opinion. His older text, "Whiplash Injuries, The cervical acceleration deceleration syndrome" is far too complex for most readers in the general public and was geared towards doctors and researchers. To contact SRISD check out thier website, www.srisd.com, or give them a call at 1(619) 423-9867.
I hope this helpd Kimberly. In addition to the above information, I would suggest that you seek out the opinion of a chiropractic neurologist. They are not easy to find however as few chiropractors have compelted the requisiet coursework of this rigorous program. Chiropractic neurologists frequently only see the hard cases in thier offices and take a completely different approach to the diagnosis and treatment of pain ans neurological disorders than a regular chiropractor would. I have seen some dramatic results with some of my patients utilizing the neurological techniques taught by the institute. For more information on functional neurology and chiropractic neurologists, check out the Carrick Institute. They should be able to help you find one closest to your location. If you have any further comments or questions, please feel free to write me back with some specifics and I would be more than happy to follow-up with you. Good Luck!
Respectfully,
Dr. Shawn leatherman
www.suncoastehalthcare.net
Spine Research Institute of San Diego
826 Orange Avenue, Suite 633
Coronado, CA 92118
Phone (619) 423-9867
Fax (619) 423-3084
www.srisd.com
Carrick Institute for Graduate Studies
203-8941 Lake Drive
Cape Canaveral, FL 32920
(321) 868-6464, Fax (321) 868-6468
www.carrickinstitute.org
