QuestionI was in a MVA accident 12 months ago; someone ran a stop sign and I T-boned them going about 30-40 kms (car was a write off).I automatically had whiplash pain the day after, including headaches, I thought this was normal and it will go away. Well a few months down the road I started having severe arm pain which would make my pinkies and ring fingers tingle and go numb, and severe back pain (upper) and sharp leg pain in my left leg which would stop me from walking on it. My doctor checked and said no nerve damage.
It has been 12 months now and I have had headaches every single day (I've never had headaches in my life until this accident), horrid wrist and arm pain and when it gets very bad I can't close my hands or grip anything, dizziness that is everyday. I've had CT Scans on my neck and brain - nothing showed up, I've had a EEG - nothing, X-rays on my neck - nothing but a bit out of place which my doctor says it's from muscles pulling.
But my doctor won't send me to any therapy, he keeps saying time will tell and that it's too late for any type of therapy.
Any advice will help, I've tried to get other doctors opinions but no one will see me because I've been in a MVA.
Thank you in advance!
AnswerDear Kristin,
Please print this out to read. It is a bit lengthy and in some places technical. By the way, you are not crazy, and your complaints are normal.
You have unfortunately been given the runaround by a physician who does not know what he is talking about. He may have the best intentions, but just not the training to deal effectively with your injuries. I often wonder why patients even bother to see their medical doctors after a car crash, especially when they can find no explanation for your symptomatology...no matter how many tests they run. It isn't really the medical professionals fault - they just haven't been trained to deal with these types of injuries - they are more concerned with focal blood loss, fractures, and significant blunt trauma injuries.
However, your case is very similar to all the rest....you are exhibiting some of the most common problems patients face after a whiplash mechanism trauma. Medical physicians just don't seem to get it...they do not really understand soft tissue injuries, and they don't understand whiplash mechanism injuries either. If they can't find it on a CT or MRI scan, they just tell you to go home and that nothing is wrong. Not to mention if they do find an bulging disk etc...medication, surgery or pain management is frequently all they ever offer. [Read the attachment at the end on sclerotogenous pain]
Car crashes, [especially rear impacts] cause very specific injuries, and these are often overlooked by the medical community. Specifically, we see torn ligaments (posterior longitudinal ligament, anterior longitudinal ligament), capsular ligament, in the neck and structural derangement of the disk without focal herniations. The best way to visualize this damage is with stress radiographic views in the neck or DMX-dynamic motion x-rays, (both diagnostic tools are not commonly utilized by medical doctors or hospitals) or a special high field MRI view called a FLAR study (fluid attenuation).
Also common is cartilage damage in the facet joints, and the lack of motion in the neck after injury makes the problems worse over time leading to degeneration and chronic pain. Often torn muscles accompany this, but their healing rates are better than ligament or disk tissue (muscles have a better blood supply, therefore a better repair capacity).
I see this in my practice all the time. As a matter of fact I was just referred a patient from her neurosurgeon who has been in chronic pain for the last year with almost the exact symptoms you have, but with the addition of radiating pain and numbness in both of her legs. She was non-surgical, had head and neck MRI's that were negative, and he could do nothing for her. Within 2 months I had her completely pain free and on vacation hiking in the northwest.
The first thing you need to do here is find a better doctor. He is absolutely wrong about the fact that time will heal this, and you should have been in active types of care long ago. Not to mention that "bones out of place on and x-ray" do not result from muscles pulling. While it is true that muscle spasm can slightly change the shape of the neck, this is transient. It takes trauma or long term biomechanical stress to make permanent changes in the shape of the spine. Again, the most common injuries to the neck is to the ligaments and the facet joints of the spine, which has been documented in the clinical literature many times. The kinematics of the acceleration/deceleration injury has been well documented too.
Whiplash injuries are most frequently treated by chiropractic physicians because we have the only world renowned training programs designed to teach doctors about the mechanisms of injury as well as how to effectively treat these injuries. The programs are taught by the Spine Research Institute of San Diego (SRISD) , and The International Chiropractic Association's Counsel on Spine Trauma (ICA)...I am a graduate of both programs, and I would recommend that you find a chiropractor close to you that has been certified by one of them if you can. The treating doctor need to understand the mechanism of injury, the involved anatomy, as well as the symptomatology, thereby underscoring what the care program will entail. If you go to the ICA or Spine Research websites, you can find a listing of the doctors who have graduated from their respective programs:
www.srisd.com
www.chiropractic.org
Lastly if you would like more detailed information about whiplash injury, please read over the SRISD website as well. Please feel free to write me back with additional questions about "specific symptoms" and I will be more than happy to explain it in more detail. I stress specific, because the realm of information is actually quite large on this subject. Good Luck Kristin.
Respectfully,
Dr. J. Shawn Leatherman
www.suncoastehalthcare.net
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:
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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.
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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.
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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.
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