QuestionI was in a rear end collision on Monday Nov 10, 2008. There was no injuries so I did not go to the ER. The next day, I had a sore neck and a bad headache, took some OTC meds and chopped it up to being in the accident. By Wednesday I had this throbbing pain that nothing would help in two spots. Being that I was just out of the military I had not been to a doctor, so I called and made a appointment and because I was a new patient I had to wait a week. The throbbing pain was all over my head by then, neck really stiff, tried heat and cold packs, with no luck. Also when I look up at the sky I get this sharp pain. Dealt with that for a week and went to see the doctor. He said I had severe whiplash and gave me vicoden and flexorel. Told me if it wasn抰 better in a week to see a chiropractor. After taking the meds for about 3 days the pain went away. I quit taking the vicoden on Friday, and then on Sat I quit taking the flexorel. By Monday I wanted to chop my head off the pain hurt so bad. It starts behind my ears and grows all the way to my forehead and eyes sometimes constant pain, throbbing. I start taking my meds again, and call a chiro and get in right away. He sends me for X-rays and says that I have pulled muscles between C2-C3 and a straight neck. I see him for three weeks and I the pain in my neck and head is gone so he has me quit taking my flexoral. Within in 6 hours pain is back, its bearable. I go through the day and in pain because he wants to do a exam. I see him and he says he doesnt know why I am getting the pain but that we will work on the occipital muscles and to take my meds again and that we will do exercises next week. Two treatments of exercises and I am in pain on my medicine. This time he adjusts my head. Wow, within minutes I get relief with the sharp pain. Still have the numbness, tenseness behind my ears on both sides. We did this for three visits and the sharp pain is gone altogether. I still have this tenseness and numb feeling on both sides behind my ears. He tells me he is not sure what is causing this and that he will see me on Monday and we will go from there.
I guess my questions are, is there something else we should be doing. Would a MRI show anything? I know I cant live without taking this medicine, but yet I don抰 like taking it either. Is their anything you can suggest that I can suggest. Please help!!!
Thanks
Jennifer
AnswerDear Jennifer,
First and foremost, I would recommend that you print this out...it is a bit lengthy, and contains some technical information. Additionally, I would encourage you to continue reading more about your injuries online as it can be a great resource. Learn as much as you can...it will help your recovery.
You are experiencing the normal and expected pain patterns after being in a motor vehicle collision. Neck pain and headache are the #1 and #2 pain complaints after whiplash type injury mechanisms. For instance: whiplash patients with resulting mild-to-moderate head trauma were evaluated for headache type. The 112 patients experienced headaches at least twice per week, and had experienced the injury an average of two-and-a-half years previously.
Tension-type headache was the most common (37 of patients), followed by migraine (27) and cervicogenic headache (18). Regarding migraine, there was no significant difference between genders, and patients who had suffered loss of consciousness were not more likely to experience migraine. Pain was usually bilateral (59 of cases), but 25 of cases had pain on one side only and 16 had pain that alternated between sides. Neck pain occurred concurrently in 93 of whiplash sufferers.
Source: Radanov BP, Stefano GD, Augustiny KF. Symptomatic approach to posttraumatic headache and its possible implications for treatment. European Spine Journal 2001:10, pp. 403-407.
That being said, the diagnosis of pulled muscles at the c3/c3 area is over simplistic. However, I do agree with the chiropractor that your pain distribution matches the clinically proven pain distribution patterns of the c2, and c3 joints of the neck....as well as higher spinal regions. This has been proven in numerous clinical research papers on headache distribution by a researcher by the name of BOGDUK.
Whiplash trauma often injures the cartilagenous surfaces of the "facet joints" in the neck, along with tears in the joint capsule and the associated ligaments. The pain that results does not follow a nerve root generated pain path, but is more broad and generalized. This is called sclerotogenouis pain or referred pain. **Please read bottom of response which details the mechanism of referred pain.**
To document these injuries, flexion and extension stress radiographs should have been ordered of the neck. This will allow the doctor to measure for instability caused by ligamentous tearing. Additional imaging that would be appropriate would be Dynamic Motion X-rays (DMX) which is actually more comprehensive that just the flexion and extension views. And lastly if you have persistent and severe headache pain, an MRI called a fluid attenuation study (FLAIR) is helpful to visualize any tearing of the ligaments in the upper cervical complex of the spine which is the occiput, C1 and C2 vertebra articulations. The ligaments that need to be checked are the Alar and Accessory ligaments, which when injured cause chronic headache pain.
As far as treatment is concerned, the chiropractor you are seeing is on the right track. Although he does not seem to have advanced knowledge on the intricacies of whiplash trauma, he is doing the right things thus far. The fact that he recognized and adjusted your head (occiput) and the pain levels quickly went away actually corroborates injury higher in the spine other than just the c2 and c3 areas. You may wish to have him check out more information from the Spine Research Institute of San Diego online: www.srisd.com
They have great information for patients as well.
I would suggest that you continue with adjustments to the neck and upper back regions of the spine, and you do need to do exercises to help strengthen the muscular system while scarring takes place in the ligaments. This is not a quick process depending on the grade of injury you have sustained. I would also suggest that you look up the CROFT GUIDELINES to whiplash diagnosis so that you can get a better understanding of how to grade your injury and understand the amount of time that may be required for recovery. I have pasted two links for you below.
http://www.nationalinjurydiagnostics.com/Crofttxguides.html
http://www.nationalinjurydiagnostics.com/Croft.htm
Listen Jennifer, Keep positive and realize that this is a healing process not an event. Healing takes time. While muscle tears usually heal in 6-8 weeks, cartilage and ligament injures take much longer. It has been reported in the clinical literature that complete resolution of cartilage and ligament injury takes more than 500 days (this is in regard to fibrotic repair-scar tissue formation) This is because the tissue has a poor blood supply and an unspecified form of collagen forms the scar.
It is very important that you complete a rehab program to facilitate the best resolution possible. This should include specific active range of motion, stretching and exercises along with spinal adjustments. Ask your chiropractor to explain all of this to you, and instruct you on proper techniques. If he cannot, and if he is unwilling to learn, it may be advantageous to seek out the care of another chiropractor who does understand the injury better as well as the rehab. The SRISD website has a national listing of chiropractors who have been through the training program, and may be helpful to you.
Hope this helps Jennifer. Please feel free to write back if you have further comments, questions, or would like to have a copy of my office treatment protocols. Best of luck.
Respectfully,
Dr. J. Shawn Leatherman
www.suncoasthealthcare.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:
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.
