QuestionHello
I was in an auto accident in 2006. I was diagnosed with a c1 neck fracture at that time and wore a hard cervical collar for 3 months. At that time I also had severe swelling over the right scapula area and pain in the thoracic spine between t5 and t7. My doctors have called this a trigger point however it continues to be extremely painful and I am unable to maintain my posture correctly. A cat scan of the T spine was never done and MRI was and that was negative but there was an area on that that my doctor question however no follow up was done. I was also diagnosis with a TBI in October following the accident. I have made great progress in this area. I have had significant vision and auditory problems as a result of the head injury. Finally, my cervical MRI revealed an ruptured disc at c5-c6 and a pinched nerve. Surgery has been recommended my two neuro surgeons although they want to complete a rhzotomy before doing surgery. I consented to this because I do understand that surgery is risky however I have new symptoms as a result of the Left sided cervical rhzotomy that was done for example severe dizziness and numbness in my left arm during the night. This numbness wakes me 3-4 times a night. I am wondering if MRI of my brain and cervical spine as well as a cat scan of my thoracic spine should be done prior to any more procedures including the rhysotomy. I say a thoracic cat scan because that test was never done of this area. I appreciate any information that you can offer and thank you kindly for reading this long e-mail. Sincerely, Mia M.
AnswerDear Mia,
First...you should probably print this out! Most thoracic pain post car crash is actually referred pain from the cervical spine. When the soft tissue structures of the neck are damaged, the pain referral is the entire neck, shoulders and upper back to the shoulder blades. This type of pain is called sclerotogenous pain and has been clinically documented and well known for over 70 years. Therefore, I do not think you absolutely need the thoracic CT. If any occult fractures are suspected in the thoracic spine, a SPECT scan would be preferable to regular CT.
An additional MRI of your neck may be a viable source of new information, but I would ask that a FLAR with proton density (T1 and T2) be performed. This is to look at the upper cervical ligament structures as well as the disk. You are very likely to have significant damage to the capsular ligament, crucifrom ligament, and alar ligaments of the neck...not all radiologists read these correctly though...you need to have one who reads these views regularly.
I doubt that an MRI of the brain will give you more information. MTBI and TBI often do not show up on an MRI unless there has been a bleed in the brain or large focal area of necrosis (tissue death). The injuries are usually at the cellular level of the neuron and axon which cannot be imaged by MRI. SPECT and PET (positron emission tomography) scans have been found useful in imaging the brain as well to help determine metabolic avtivity either increased or reduced. Another study that may be of help is called BEAM, Brain electrical activity mapping, or brain mapping, was developed to detect more electrophysiological abnormality than could be detected by the usual EEG alone, however they are not used frequently in trauma cases.
Concerning the rhizotomy, it is my experience that these are not really performed just to eliminate pain unless other measures have failed, and usually there are other issues such as spacticity or previously diagnosed neurological disease. Usually, facet or epidural injections are utilized for pain reduction first. Anyway some reading you might be interested in below:
http://www.spineuniverse.com/article/radiofrequency-rhizotomy-4306.html
http://en.wikipedia.org/wiki/Rhizotomy
Lastly I am going to include some information I compliled on sclerotogenous pain referral and out MTBI protocols in this office. Although you have a TBI injury which is more severe, the information should be helpful for understanding. Please read.
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 illustartion to visualize the pain patterns, copy and past the link below into your web browser to reach my online glossary of terms. Then click on the letter "s" which will take you to sclerotome.
http://suncoasthealthcare.net/glossaryofterms/
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.
E/M Counseling Supplement for Patient Treatment
Traumatic Brain Injury/Mild Traumatic Brain Injury/Concussion
Motor vehicle trauma is the single most important factor in both fatal and mild brain injuries. Early reports ranged from 40% to 60% caused by motor vehicle crash (MVC) with concussion being the most common diagnosis given. (15,27,57) More recent accounts report MVC as the origin of 60% to 67% of all occurrences. (1,21) Many of these MVC-related injuries are the result of blunt head injury, which describes contact with some object without penetration of the skull, such as striking the steering wheel, dash board or the B pillar of the doorframe. However, it has been shown that non-contact concussion is a common result of acceleration type injuries. The term of choice today is traumatic brain injury (TBI) or mild traumatic brain injury (MTBI). (15)
Mechanism of Injury: Previously thought to be a direct shearing of axons, the actual mechanism is from abrupt acceleration and deceleration of brain tissue. (39) The initial shear effect creates the activation of a degenerative cascade. During a low speed whiplash injury, (7 mph) the head may be accelerated at 9-18g. (58) Since the brain is a soft structure, shear strains are created as the outer part of the brain moves at a different pace than the inner part of the brain. This is intensified as the momentum of the head changes rapidly in a sagittal direction during a whiplash trauma, and when head impact occurs inside the vehicle. The most important factors in whiplash-induced concussion are angular acceleration, flexion/extension of the neck, and increased intracranial pressure gradients. (40,41,52)
Animal studies confirm the real issue of induced concussion from acceleration/deceleration even though animals did not lose consciousness. (32,33) Portnoy et al. reported that significant increases in intracranial pressure were measured in baboons exposed to whiplash. Examination discoveries included suprascapular intramuscular hemorrhages. (47) Hemorrhages were not from contact. Acceleration, deceleration, and shear were mechanisms of injury. Non-centroidal motion in the coronal plane was found to be the most injurious and non-centroidal acceleration in the sagital plane to be least injurious concerning brain injury. (22,38,56) Although this infers that lateral whiplash motions of the head are more likely to produce concussion or diffuse axonal injury (DAI) than frontal or rear impacts, MTBI and DAI have been found in both types of collisions.
According to the work of Hinoki, the integrity of the brainstem reticular formation is largely responsible for maintaining levels of consciousness. A study by Jane et al. proved conclusively that non-centroidal accelerations of the head (without contact) could produce damage to axons in the inferior colliculus, pons, and dorsolateral medulla, which are in close proximity to the reticular formation. (25) The authors discussed the previous work of Povlishock et al., who presented the pathogenesis of DAI. Their proposed mechanism of trauma is not necessarily an immediate shearing of axons, but rather a reactive degeneration secondary to trauma. (48,49) Others have corroborated this concept of continuing degeneration, such as Gennerelli, in statements that MTBI should be considered a process rather than an event. (21). In addition we know that the spinal cord becomes stiffer as rates of strain increase, therefore creating a higher susceptibility to injury. (5)
Pathophysiology: The precise nature of DAI is thought to be a reactive swelling of damaged axons and capillaries throughout the brain (29,48,49) 揇irect brain trauma results in intra-axonal changes in the 68-kd neurofilament subunit which then loses its alignment and interferes with axoplasmic transport. This causes axonal swelling and eventual disconnection. The neurofilament change may be the result of either direct damage to the cytoskeleton or a biomechanical event that results in neurofilament disassembly. The temporal progression of those events is related to the severity of the injury? (16,42)
At time of injury, the brain is subjected to massive depolarization from acceleration/deceleration, and tissues are damaged due to shear currents/forces that increase intracranial pressure and mechanically deform axons. It is postulated that such events terminate with neuronal death involving the production of free radicals, and tissue acidosis. (6,7,53) In 1997, Connor and Connor showed in the American Journal of Clinical Nutrition that free radicals amplify inflammation by up regulation of genes that encode for pro-inflammatory cytokines and adhesion molecules. It is known that free radicals damage lipids, proteins, membranes and DNA. (2,8,13,18,19,28)
Micro hemorrhages develop between 12 and 96 hours post injury, arachadonic acid is released, CSF lactic acidosis is present, and lipid peroxidation occurs from membrane disruption and squalor. Free radical scavengers such as large doses of antioxidants and iron chelators have been proposed as therapeutic devices. (59) Antioxidant supplementation as well as Omega III fatty acid supplementation, (DHA-docosahexanoic acid & EPA-eicosapentanoic acid), inhibit the degradation of tissue by the reduction of oxidative stress. Oxidative stress is due to free radical damage, arachadonic acid production, lipid peroxidation/degradation, prostaglandins (pge2), and leukotrienes. (9,10,11,20,24,31,34,46,51,54) In particular, bioflavonoids play a significant role as they have been proven to act as intracellular and extra cellular antioxidants, reduce platelet aggregation, repair damage in vessel walls and have anti-inflammatory action. (12,14,17,30,35,36,44,45,50)
Even in relatively mild brain injuries, an excessive release of excitatory neurotransmitters such as acetylcholine and glutamate, contribute to the pathologic neuronal apoptosis (cell death) in the brain. The results are permanent deficits! MTBI can produce diffuse reactions in cerebral metabolic activity and can disrupt the blood brain barrier allowing an increase of excitotoxic effects. (6,7,23) Recent research affirms that brain injury leads to increased glutamate release, which in turn activates the NMDA (N-methyl d-aspartate) receptor in cortical neurons allowing an increased calcium influx. (26) This channel complex contributes to excitatory synaptic transmission at sites throughout the brain and the spinal cord, and is responsible for neuronal plasticity. When continually activated neuronal death and chronic pain may result. Specific areas known to be vulnerable to injury include the parieto-occipital lobe, the temporal lobe, amygdala, anterior frontal lobe, and para-sagital sinuses. (43) Antioxidants, magnesium and omega III fatty acid supplementation all inhibit circulating Excitotoxins and down-regulate the NMDA receptor.
Post concussion syndrome (PCS) can develop after MTBI. Posttraumatic headaches are exceedingly common residuals, and may last for years. (55) First headaches begin with a concussion and can continue for weeks or months. The head usually hurts where the head is struck if blunt force trauma was the mechanism of injury. Etiological factors in posttraumatic headaches are blunt head trauma, 57.3%, whiplash, 43.6%, Object hit head, 13.7%, other, 13.7%, and body shaken, 9.4%. (3) It has been suggested by one of the preeminent experts in this area that patients suffering from recurrent post-traumatic headaches or other elements of the PCS should be treated for migraine. (37) Other symptoms of PCS are as follows: Dizziness: Light headedness, vertigo and nausea, which is caused by injury to the semicircular canals, changes in endolymph or perilymph pressure, or direct damage to the vestibular cochlear nerve. Serious symptoms of hearing loss such as hyperacusis may occur as the result of damage to the actual hearing mechanism. Cranial nerve and brain dysfunction: Disruption of smell and taste, information speed and processing, attention, articulation, memory, new information acquisition, reaction time and sleep disturbances such as lethargy, drowsiness, and fatigue are common sequelae. (4)
**In relation to the research above, Suncoast Healthcare Professionals uses nutritional supplementation to decrease the cyto-toxic attack on neuronal tissue after resultant concussive episodes. Due to the fragile nature of brain tissue as well as the physiological makeup, it is evident that nutritional supplementation is paramount in the treatment of mild traumatic brain injury post motor vehicle trauma. The application of ant-inflammatory and antioxidant agents should be utilized initially and sequentially for a minimum period of 6 months post injury. Our office procedures and this supplementation is in line and adapted from protocols used in hospitals for the preservation of brain tissue after concussion, coma, transient ishemic attack and strokes, as well as brain surgery.**
REFERENCES
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Hope this helps Mia.
Respectfully,
Dr. J. Shawn Leatherman
www.suncoasthealthcare.net
