Professional Papers
By DR. W.N. DUDLEY, D.C., D.A.B.C.T,
Dr. Dudley is a postgraduate Iecturer at Palmer and Texas Chiropractic Colleges. He has been using thermography since 1970. He is a past president of the International Thermographic Society and is also a diplomate of tile American Board of Clinical Thermology and a member of the board. Dr. DudIey is board certified in Thermography by the ACA. He has authored numerous articles on thermography and related subjects. Currently, Dr. Dudley practices in Howell, MI.
The use of thermography for the detection of sensory nerve loss is growing in the chiropractic profession. The evaluation of sensory nerves by thermography provides an index for discovery of the loss of dermatome function. Thermography further provides an index of possible dermatome recovery and long-term residual loss, both quantitatively and qualitatively, but only if critical measurement is done.
For example, if a case presents with dermatome loss, and that loss is quantified by thermography, followed by adjustment to the spine and therapy to peripheral region, recovery may be anticipated. However, subjective examination of the initial dermatome loss may be negative after therapy, but the thermographic scan may reveal residual asymmetry. The most distal portion of the dermatome seems to be the prevalent residual loss area.2 This discussion examines a possible mechanism for these findings, along with a case study of a patient with residual thermal loss, following treatment. For the purpose of this discussion. neuropathies initiated by diabetes, uremia, cold exposure, peritoneal dialysis,4-8 galactorrhea9 and pregnancy10-15 are excluded. Cases with a history of fracture or surgery must be excluded due to alteration of the vascular beds that render the thermographic scan of that portion not interpretable when compared to the opposite side.
Upton and McComas16 proposed the concept of "double crush" of a nerve as a mechanism by which are thought of as independent lesion,17-21 but may not be such, and these lesions should likely be thought of as effects, rather than causes of symptoms. In the Upton and McComas study of 115 patients, using comprehensive electromyographic evaluations of carpal tunnel syndromes or ulnar nerve entrapments at the elbow, there were 81 cases with associated lesions of the neck. The functional association was thought to be a constraint of axoplasmic flow in the nerve fibers due to axonal narrowing. This could result in increased susceptibility to injury, distally.
Upton and McComas suggested that there are often two sites of neurologic trauma, one of which is frequently undiagnosed. There have been few reports22-23 that pursued the theory that distal loss might cause proximal faulting to occur, although one other author wrote of possible occurrence of "double crush" in his report of 19 cases.24
Recently, laboratory findings have clarified the issue somewhat, when Nemoto, et al.,25 experimented with the "double crush" concept using clamps on the sciatic of dogs. The Nemoto study showed that a single nerve lesion clamping caused axoplasmic flow to be reduced to 43% initially, but in three weeks axoplasmic flow improved to 38%, followed by a recovery to 65% of normal in six weeks after clamp removal. A principal point made by Nemoto, et al., was that even after clamp removal there was not restoration to the beginning level of axoplasmic flow. When an additional clamp was applied distally, the axoplasmic flow reduced to 14% throughout the, nerve. Significantly, if both clamps were removed, there was restoration in about 70% of the original diameter of the nerve fibers. Velocity of flow in the group with two clamps was reduced, but when the clamps were removed there was approximately 65% of neural recovery. Nemoto proposed the term double lesion neuropathy.
lt must be considered that the insult of the surgery and damping would lessen full recovery; however, the question remains as to whether a nerve can be restored to full function in humans after a crush lesion. If so, to what degree?
The demonstration of sensory nerve loss of thermography has been abundantly documented in the literature26-34 but little attention has been given to quantification of residual losses, if they exist; nor has there been any thermographic research on double lesion neuropathy. It is often concluded that therapy was efficacious to the sensory nerve, when subjective examination was used as the determinant.
Furthermore, when thermography is the determinant of sensory loss there have been few if any publications to note if there is residual thermal asymmetry after therapeutic application. The case symptoms are often lessened, and thereby it is assumed that recovery has been accomplished, without further documentation. Since thermography is a relatively simple, non-invasive and objective technique, the lack of follow-up documentation is unjustified. The Nemoto study does answer some questions for the thermographic clinician, and thermography is an excellent tool for answers for many of the remaining problems. In our experience we have noted residuals to occur in that the warming or cooling of the dermatome remained somewhat abnormal when compared to the opposite side even after therapy. It was considered that, perhaps, the spinal adjustment was lacking in its therapeutic capacity or in its application. If the adjustment did have value then why would not the dermatome return to normal thermal symmetry? There frequently remained a small but measurable loss that usually displayed at the most distal portion of the dermatome. After a period of time had elapsed, which might vary considerably, the case would report in again and the same dermatome would display on the thermogram as previously noted. Rarely would the thermal loss be of the same degee as initially seen, but customarily it was along the same neural path.
It is generally accepted that if trauma to an area of the neural path has occurred recently, the dermatome will appear heated, whereas slow overgrowth of osteophytes and other chronic neural impairments seems to cause a loss of temperature. In cases of osteophytic overgrowth it was felt that a double lesion neuropathy may present with a painful, yet cool, dermatome. In cases with double lesion neuropathy, without trauma in an acute phase, but with a chronic condition represented by a weakening of a nerve or neuromuscular component, trying to understand the varying presentation of heated or cooled dermatomes is difficult at best. Surely more work must be done to delineate the actual cellular mechanisms responsible for dermatomal microvascular responses.
Case Study
ACK is a 37-year-old female with no surgeries or fractures. Initial complaint was of night-time left shoulder, arm, hand and chest pain that alleviated through the day. Occupation was not contributory. Trauma was denied.
Findings: Cervical films showed no osseous pathology evident but there was mild retrolisthesis. Tinels sign was negative, Phalens was also negative. Abductor pollicus brevis was weak on the left. The thermographic scan showed loss of temperature along the left 6th cervical dermatome with the greatest loss midway on the radial forearm of 1.25"C as compared to the right. Portions of the dermatome on a thermographic scan noted loss varying from .3"C to .75"C. Treatment to the cervical spine produced considerable relief; however, after several adjustments a specific elbow pain was noted on the same side. An elbow brace was fitted and afforded relief; In two weeks the patient was asymptomatic, the brace was removed, and a rescan was performed. The follow-up scan noted only one area of thermal loss; the left index finger was .3"C less than the right. After ten months she returned again with a complaint of stiffness of the neck. The thermographic scan showed a left C6 dermatome to exist with the greatest loss .75"C at the left wrist.
Discussion
The above case is representative of hundreds we have seen in which functional and incomplete recovery was accompanied by comparable and consistent residual findings on thermographic scans. A high percentage of cases do not fully recover from the thermal deficit, which until recently left one to consider that inadequate therapy had been applied.
However, the "double crush" model of Upton and McComas now provides a possible explanation for the functional and thermal loss. The distal injury possibly preexisted the cervical trauma and may not have resulted in functional loss. However, the cervical trauma and symptoms both aggregated and masked the distal nerve injury. Once the cervical injury was alleviated, the distal nerve trauma became apparent and, in fact, reaffirmed the cervical syndrome. Both areas of neurologic deficit must be recognized and treated.
Future investigation is called for to delineate the exact nature of the loss.
References
1. American Chiropractic Association, Policy Statement on Thermography, March, 1988.
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33. Wexler, C.E., Small, R.B.; Thermographic Demonstration of a Sensory Nerve Deficit, Journal of Neurological & Orthopedic Surgery, Vo1.3, No. 1, Apr1982, pp73-74.
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ACA Journal of Chiropractic/May 1989