In all of these diseases, the underlying problem is the same: The body’s immune system becomes misdirected and attacks the very organs it was designed to protect. The greatest percentages of those affected with this disease are women, with autoimmune conditions representing the fourth-largest cause of disability among women in the United States.1,2
Research indicates that autoimmune diseases are linked to a dominant genetic trait that is very common (20 percent of the population), and that they may occur as different autoimmune diseases, even within the same family. For example, a mother may have systemic lupus erythematosus (SLE); a daughter, diabetes; and a grandmother, rheumatoid arthritis.
These studies are very clear, however, that the genetic predisposition alone does not cause the development of autoimmune diseases. It seems that other factors need to be present in order to initiate the disease process.1, 3-5
The following report outlines the clinical observation of a patient presenting with a chronic severe paralytic autoimmune disease. Alleviation of signs and symptoms is noted subsequent to corrections of aberrant arthrokinematic function of the occipito-atlanto-axial complex. A relationship between biomechanical faults in the upper cervical spine and the manifestation of abnormal autonomic neurophysiology is suggested as the initiating and maintaining factor in the pathophysiologic process of this patient’s autoimmune disease.
Case Report
A 33-year-old female was referred to our center with the chief complaints of stocking-glove numbness, bilateral upper and lower extremity weakness and twitching and overall fatigue over a three-month period. Her symptoms began six years earlier when she awoke with numbness in the left fifth finger. The symptoms progressed quickly over the next eight weeks, resulting in two hospitalizations and finally complete quadriplegia. She became terrified by the severity of her condition and wondered if she was going to die.
The patient sought care from several specialists and underwent a battery of tests, including several magnetic resonance imaging (MRI) and computed tomography (CT) scans, spinal taps and lab exams, all without conclusive results. A trial of prednisone was initiated with some improvement noted. This led to a suspected inflammatory disease process. Intravenous immunoglobulin (IVIG) therapy was tried, with subsequent cessation of all signs and symptoms. From the success of the treatment, a diagnosis of autoimmune disorder with associated peripheral neuropathy was made.
Since the onset of her condition, the patient had been receiving IVIG treatments, followed with a 10-day regimen of prednisone to counteract the side effects, every three months in order to alleviate the progressive symptoms and weakness. After each IVIG treatment, her symptoms would eventually progress to complete paralysis, unless she received another IVIG treatment. She noted that having her condition return to its initial state was terrifying.
At this time of her visit, she was due for another round of IVIG, since her upper extremity dexterity and ambulation were quickly deteriorating. Since her occupational demands included sensitive manual dexterity, the patient was very concerned about whether she should wait to see what the chiropractic care would do or begin another round of IVIG and prednisone.
Upon examination, the patient presented with a mild limp and slight shuffling gait. Vital signs and ear, nose and throat examinations were unremarkable. Orthopedic examination revealed significant palpatory hypertonicity of the paraspinal musculature from the occiput to C4 bilaterally, with a marked increase on the left. Bilateral palpatory hypertonicity was also noted in the anterior cervical musculature, with a significant increase on the left. The patient demonstrated a reduction in active and passive right cervical rotation and lateral flexion. Her thoracic and lumbosacral evaluation was unremarkable.
Gross neurologic examination revealed a moderate loss of pain and light touch sensations in a stocking-glove distribution. Muscle strength deficits, with gradings of 4 to 4- of 5, were found in most of the muscles of the upper and lower extremities. A computerized paraspinal infrared analysis (neurologic imaging via a TyTron C-3000 paraspinal infrared imaging system) was performed in accordance with thermographic protocol.6-8
A continuous paraspinal neurologic scan consisting of approximately 350 infrared samples was taken from the level of S1 to the occiput (Figure 1). The data were analyzed against established normal values and found to contain thermal asymmetries indicating abnormal autonomic regulation (Figure 2).9-12 Since the cervical spine displayed abnormal thermal asymmetries, a focused neurologic scan was performed with approximately 85 infrared samples taken from T1 to the occiput (Figure 3). When interpreting these neurologic scans, you will note the mild Delta-T findings (Figures 2-3, center graph field, or pre bar graph, Figures 4-5).
In some patients with severe conditions, the degree of temperature differential is not excessive. As a minimum, a plotted graph denoting mild repeatable anatomic location differentials objectively indicates a lack of normal neurologic homeostasis. Since the neurologic scans in this patient showed objective findings of neuropathophysiology, existence of the vertebral subluxation complex was suspected.
The information gained from the above examinations indicated a high probability of abnormal upper cervical arthrokinematics. Consequently, a precision radiographic series of the upper cervical spine was performed for an accurate analysis of specific segmental biomechanics.13 Neutral lateral, AP, APOM and BP views were taken using an on-patient laser-optic alignment system in order to precisely align the patient to the central ray.
An analytical radiographic method consisting of mensuration combined with arthrokinematics was performed.13 Noticeable biomechanical abnormalities were found at the atlanto-occipital and atlanto-axial articulations.
Chiropractic Management
From the accumulated degree of aberrant biomechanics noted in the upper cervical spine, the atlanto-occipital subluxation was chosen as the first to undergo adjustive correction. Before care was rendered, the patient was counseled that she might expect exacerbations in symptomatology as part of the normal response to care due to the global impact of neural reintegration.
To correct the subluxation, the patient was placed on a specially designed knee-chest table with the posterior arch of atlas as the contact point (Figure 6). An adjusting force was introduced using a specialized upper cervical adjusting procedure.14 The patient was then placed in a post-adjustment recuperation suite for 15 minutes as per thermographic protocol.6-8 Correction of the subluxation was determined from the post-adjustment neurologic image noting resolution of the patient’s presenting neuropathophysiology (Figure 4).
All subsequent office visits included an initial cervical neurologic scan, and if care was rendered, another scan was performed to determine if normal neurophysiology was restored. Since the focus of the patient’s care was in the upper cervical spine, neurologic scans were made only in this region during normal visits, with full spine scans performed at 30-day re-evaluation intervals.
The patient was adjusted once weekly during the first three months of care. After the first adjustment, the patient noted an increase in stocking-glove numbness for two days. By the end of the week she reported a significant decrease in symptoms and a mild increase in muscle strength. She also noticed a mild improvement in her levels of fatigue. The patient mentioned that this change left her very hopeful, but that her condition was so severe and debilitating that she would have to see greater improvement to discontinue her IVIG treatment.
During the second week of care, the patient reported continued improvement in both symptoms and strength. She noted having complete days without any stocking-glove numbness. Her upper extremity strength had improved so dramatically that she was able to take on a greater workload. The lower extremity weakness was also improving with a noticeable gait change, but the improvement was much less than in the upper extremities. The patient expressed disbelief in the amount of change in her condition and the speed at which it was occurring.
Between the third and fourth week of care, the patient reported an increase in her stocking-glove numbness. Her upper extremity strength, however, had continued to improve. She noted that her lower extremity strength had been waxing and waning. Despite her increased workload, she continued to report an increase in energy. By the fourth week of care, the patient had not received an IVIG treatment for four months. In the past six years, she had never been able to avoid medical treatment for this long.
A re-evaluation was performed at this time. The examination revealed normal cervical muscle tone and ranges of motion, normal sensation findings in the upper and lower extremities, and a mild limp without shuffling. A full spine neurologic scan was performed noting total resolution of the patient’s presenting autonomic neuropathophysiology (Figure 5).
Weeks five through twelve showed continued improvement. There were two mild increases in stocking-glove numbness that lasted for two to three days. The patient noted that she was now having days completely without symptoms or muscle weakness. She also reported that the lower extremity weakness was noticeable mostly with stair use only. A re-examination was performed at eight weeks with no remarkable findings.
Adjustments were made to the upper cervical spine at four and eleven months of care. At this time, the patient had not received any IVIG, prednisone or other medical treatment for one year.
The patient has continued to improve with mild changes over time. She notes that some lower extremity weakness still shows up with stair use. Other than this, her lifestyle remains active and symptom-free.
In consideration of the chronicity and severity of this autoimmune condition, permanent neurologic damage cannot be ruled out with regard to the residual weakness in the lower extremities. Complete resolution of this residual finding, however, may be possible over time considering the drastic improvements seen in this case.
Neurobiologic Mechanisms
Current autoimmune disease research clearly indicates that genetic predisposition alone does not cause the development of autoimmune diseases, but that other factors need to be present in order to initiate the disease process.
There are two extensively studied neurophysiologic mechanisms which may explain the genesis of this patient’s condition—central nervous system facilitation and cerebral penumbra. Both of these conditions are thought to arise from an initiating trauma (birth, falls, etc.), which causes entrapment of intra-articular meniscoids, resulting in segmental hypomobility and compensatory hypermobility. As a result of this hypermobility, hyperexcitation of intra and periarticular neuroreceptors occurs causing afferent bombardment of the CNS.
Over time, this can result in facilitation, which is a state of neuronal conditioning where an exponential rise in afferent signals to the cord and/or brain occurs. This may cause a loss of central neural integration due to direct excitation, or a lack of normal inhibition, of pathways or nuclei at the level of the cord, brainstem and/or higher brain centers. The upper cervical spine is uniquely suited to this condition, as it possesses inherently poor biomechanical stability along with the greatest concentration of spinal mechanoreceptors.
This same mechanism is the genesis of cerebral penumbra. Hyperafferent activation of the central regulating center for sympathetic function in the brain may cause differing levels of cerebral ischemia. A second route via the superior cervical sympathetic ganglia may also cause higher center ischemia. When a certain threshold of cerebral ischemia is reached, a neuronal state of hibernation occurs; the cells remain alive but cease to perform their designated purpose. Entire functional areas of the cerebral cortex or cerebellum may be affected.
Propagation of these mostly non-adapting signals to the CNS may have systemic autonomic ramifications. Local and long-tract autonomic manifestations are readily seen with neurologic imaging, as the scans are a direct reflection of sympathetic nervous system function (Figure 5). It is suggested that one of the secondary effects of upper cervical hyperafferency may be global autonomic pathophysiology, specifically the sympathetic division. Sympathetic dysregulation would be capable of maintaining the autoimmune disease process through direct affects on the immune response.
The role that the sympathetic nervous system plays in the regulation of immune function is paramount to understanding the possible relationship between aberrant upper cervical biomechanics and autoimmune disease. Direct sympathetic innervation of the thymus, spleen, pineal gland, Peyer’s patches, lymph nodes, lymphocytes and bone marrow is well understood in the regulation of immune responses.27-29
It has been discovered that biochemical messengers, in the form of cytokines and neurokines (the signal molecules of the immune and nervous system respectively), are expressed and perceived by both systems. Since both systems are capable of acting on terminal immune response tissues and receiving feedback from the same, is there any difference between the two? The sharp delineation of the two systems has become blurred as research has uncovered their homeostatic interrelationship.
Historically viewed as separate, the two systems are now considered as a single integrated mechanism—the neuroimmune system.27-29 Consequently, sympathetically mediated immune dysfunction may be implicated in the maintenance of autoimmune diseases. Correction of pathologic central sympathetic regulation, secondary to aberrant upper cervical biomechanics, may lead to a return of normal immune function. Considering this mechanism, the potential for the improvement of any autoimmune disease is tremendous.
Conclusion
Autoimmune diseases remain among the most poorly understood and poorly recognized of any category of illnesses. A myriad of chronic and severe disease states can result from the dysfunction of the body’s immune system. As discussed, the controlling ability of the nervous system on the immune response cannot be ignored in the pathophysiology of autoimmune diseases.
The most important factor in this case was our ability to objectively monitor the adjustment’s affects on the patient’s autonomic neurophysiology. By using thermal neurologic imaging, our center has been able to consistently determine the correct adjustive procedures that produce reproducible and dramatic neurophysiologic improvements in our patients.
To what magnitude the upper cervical spine is involved in the genesis of autoimmune disease remains to be seen. In an atmosphere where much of the public sees our profession as useful for neck and back pain treatment at most, patients with complex disorders are left unaware of the possible benefits of care.
The body of literature detailing a possible upper cervical etiology, or at least contribution, to organic disorders is substantial. Further research into this area of the spine, combined with objective monitoring of neurophysiology, may reveal that chiropractic does indeed offer consistent conservative management of autoimmune disorders.
[References are available from the author upon request.]
About the author: William C. Amalu, D.C., is vice president of the International Academy of Clinical Thermology and research director for the International Upper Cervical Chiropractic Association. Inquiries should be directed to him at the Pacific Chiropractic and Research Center, 621 Middlefield Rd., Redwood City, CA. 94063; call (650) 361-8908, or e-mail info@pacificchiro.com.