QuestionHello. I was in a motor vehicle accident two years ago. I was stopped at a stop light and rear ended by a full size pickup pulling an enclosed trailer. From day one I have told the Dr. about my upper neck pain, shoulder pain, back pain and sternum chest pain. They ignored everything but the upper back pain. I had an MRI done which states: mild diffuse disk bulge at C5-6, an annular tear in the posterior annulus fibrosis. Also a disk protrusion at T8-9. I have had constant pain in my upper back, left shoulder blade, neck and down shoulder to elbow. I constantly have pins and needles or crawling feelings going on in shoulder area and feels like electrical shock shooting down shoulder. Left hand tingles and goes numb at times. I have had trigger point injections done for the back area and two cervical injections. They did not last long. I am still doing physical therapy which I think is making it worse. I am so tired of being in pain and taking medications. I can't get the Dr. to listen to me and feel like they think I'm imagining this. I think it's because it's a workmans comp injury. Because of this I felt like I had to quit my job. I could no longer wear my bullet proof vest or reach for my hand cuffs. Do you think I need an MRI done on my neck and shoulder? I have never had any problems until this accident. I want to know how you can diagnose someone as 5% impairment but not look at the shoulder and neck.
AnswerDear Janeal,
First thing...the fact that you were hit by a truck pulling a trailer alone makes your risk for initial injury and chronic injury more likely. This is simple physics...as the impacting force becomes larger, the transmitted force into your vehicle is larger. If you would like a more in-depth explanation of this concept with the equations to actually compute forces generated, e-mail me from my website and I will send you the information.
Second your doctors probably have no education in regards to vehicle crash kinematics, occupant kinematics, soft tissue acceleration injuries, or the management of them. If your care has been directed by a medical doctor, I can virtually guarantee those facts, because medical doctors do not complete these training programs and it is not taught in medical school. They are largely unaware of risk factor analysis which actually provides the best prognostic value, and do not know how to manage these injuries. Not to mention that workers compensation docs are often more interested in serving the interests of the insurance carrier rather than the patient...this is an unfortunate reality.
I cannot understand why the doctors will not listen to you for the simple reason that the disk bulge an annular tears can account for the pain you are describing. It has been well established in the medical literature that disk pathology can create radicular pain and symptoms into the arms as well as pain patterns into the upper back. Not to mention muscle spasm, trigger points and chronic inflammation are common with disk pathology. This should be common knowledge in the medical community...unfortunately it is often not. Please read the addendum at the bottom of this response on sclerotogenous pain referral.
Now, specifically concerning the vehicle crash, rear impact crashes can be debilitating, and they often cause disk bulges/herniation/annular tears. Along with this the most common injury is to the facet joint and surrounding ligaments. This is another well documented fact in the scientific literature. The docotrs should have also performed flexion extension stress views in the neck to look for instability (ligament tearing)around the facet joints. This is easy to quantify and I find these in juries on car crash patients all the time. As a matter of fact, the American Medical Associations 5th edition guidelines to impairment states that a 25-28% whole body impairment results form 3.6 mm of instability of one spinal segment to the next in the neck. You can only find this instability on flexion/extension x-ray views or a DMX motion x-ray study. Your 5% impairment is likely inadequate, and based on conjecture rather than the appropriate guidelines.
As far a a shoulder MRI is concerned, a functional orthopedic examination of the shoulder should be performed first to ascertain what exactly is causing the shoulder pain. The C5/C6 nerve root is responsible for pain transmission to the shoulder...so the shoulder may or may not be damaged. Although shoulder injuries are also common in car crashes, pain can originate locally from damaged shoulder tissue or be referred from the neck.
Listen Janeal. I think you should be evaluated by another doctor...one interested in trying to resolve this issue and get you back to work. You should also try to find a doc who has been properly educated in vehicle crash injuries...these are largely chiropractic physicians only.(again very few medical doctors have completed this training) I would encourage you to go the Spine Research Institute of San Diego's website: www.srisd.com, and read the information. While you are there, you can check your state to see if there are any properly trained doctors in your area to consult with.
Hope this helps Janeal..feel free to e-mail me at my office if you would like more information. Much of this is just too in depth for the allexperts format as I cannot attach Word or PDF documents.
Respectfully,
Dr. J. Shawn Leatherman
www.suncoastehalthcare.net
ADDENDUM: 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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