Introduction to T.E.N.S
Introduction to T.E.N.S.
T.E.N.S. modalities are designated into three distinct categories based on technical parameters and physiologic action. (Mannheimer, J. Clinical Transcutaneous Electrical Nerve Stimulation. F.A. Davis, Philad., 1986).
A T.E.N.S. mode that uses high rate (50 to 100 Hz), asymmetrical biphasic wave (40-75 usec) is referred to as Conventional. High Frequency T.E.N.S. This mode is designed to selectively actuate the large myelinated afferent fibers. Muscle fasciculization is not apparent. Conventional high frequency T.E.N.S. is characterized by fast onset of relief, short therapeutic effect, generally not exceeding length of stimulation. There is little or no endogenous opiate liberation and no reversal by naloxone. The high frequency T.E.N.S. is primarily a local CNS (segmental effect).
A second T.E.N.S. mode is Low Frequency Acupuncture-like T.E.N.S. with a pulse rate of 0.5 Hz to 10.0 Hz using a asymmetrical biphasic wave form of 150-500 usec. It produces muscle contraction, slow onset (20 mm. or more), long therapeutic effect and activates small pain afferent and motor efferent fiber stimulation. There is endogenous opiate liberation, naloxone reversal and long therapeutic effect. The Low Frequency T.E.N.S. allow a period for muscle recovery between pulses with stimulation by surface electrodes in segmentally related myotomes being most efficacious. The Myo-monitor is a low frequency acupuncture-like T.E.N.S.
The third type of T.E.N.S. is a Electrogalvanic Stimulator (E.G.S.) It is characterized by having a monophasic, twin peak wave for each pulse of 10-20 msec utilizing direct current. E.G.S. is designed for local tissue effect, not pain control.
Both low and high frequency T.E.N.S. have ample and specific documentation in the medical literature regarding local histochemical and endorphin effects. The following articles address the mode of action of conventional high frequency T.E.N.S. and low frequency acupuncture-like T.E.N.S.
1. Ersek, R. (1977) Transcutaneous neurostimulation: A new therapeutic – modality for controlling pain. Clinical Orthopedics and Related Research. Vol. 128:314-324.
2. Eriksson, M.D., and Sjolund, B.H. (1978) Pain relief from conventional versus acupuncture-like T.E.N.S. in patients with chronic facial pain. Pain Abstracts. 2nd World Congress on Pain, Montreal: IASP, p 128.
3. Takakora, K., et al. (1979) Pain control by transcutaneous electrical nerve stimulation using irregular pulse of 1 Hz fluctuation. Applied Neurophysiology. 42:314.
4. Murray, W., and Miller, J. (1960) Potency differences of morphine-type agents by radiant heat and „cramping? analgesic assays provide evidence for potentializing substance from the posterior pituitary gland. J. *pharmocologic Exp. Ther. pp 128-380.
5. Goldstein, A., Lowney, L., and Pal, B. (1971) Stereospecific and nonspecific interactions of the morphine narcotic congener leurophanol in subcellular functions of rat brain. Proc. Nat. Acad. Science USA. 68:1742.
6. Moyer, D.J., Price, D.D., and Rafii, A. (1977) Antagonism of acupuncture analgesis in man by the narcotic antagonist nalaxone. Brain Research. pp 121-368.
7. Akil, H., et al. (1978) Encephalin-like material elevated in ventricular cerebrospinal fluid of pain patients after Analgesic facial stimulation. Science. 201:463.
8. Simantor, R., et al. (1976) The regional distribution of a morphine-like encephalin in monkey brain. Brain Research. 106:189.
9. Sjolund, B., and Eriksson, M. (1979) Endorphins and analgesia produced by peripheral conditioning stimulation. Advances in Pain Research And Therapy, vol. 3, Bonica, et al., eds. Raven Press, N.Y.
10. Wall, P.D. (1980) The role of substantia gelatinosa as a gate control. Pain. Research Ed. Bonica, 58:205.
11. Kerr, F.W. (1975) Neuroanatomical substrates of nociception in the spinal cord. Pain. 1:325.
12. Loeser, J.D., et al. (1975) “Relief of pain by transcutaneous stimulation.” J. Neurosurg. 42:308.
13. Arcangeli, P., and Galleti, R. (1974) Endogenous pain producing substances. Recent Advances on Pain: Pathophysiology and Clinical Aspects. Ed. Bonica, p 36.
14. Thorsteinsson, G., et al. (1977) Transcutaneous electrical stimulation: A double-blind trial of its efficacy for pain. Arch. Phys. Med. Rehab. 58:8.
15. Long, D., and Hagfors, N. (1975) Electrical stimulation in the nervous system: The current status of electrical stimulation of the nervous system for relief of pain. Pain. 1:109.
16. Dooley, D.M., and Kasprak, M. (1976) Modification of blood flow to the extremities by electrical stimulation of the nervous system. S. Med. Journal 69: 1309.
17. Abram, S.E. (1976) Increased sympathetic tone associated with transcutaneous electrical stimulation. Anesthesiology. 45:575.
18. Abram, S.E., et al. (1980) Increased skin temperature during transcutaneous electrical stimulation. Anesth. Anaig. 59:22.
19. Rowlingson, J., et al. (1978) The effect of transcutaneous nerve stimulation on blood flow in normal extremities. Pain Abstr. Vol. 1, 2nd World Congress on Pain, mt. Assoc. for Study of Pain, Seattle, p 155.
20. Murphy, T.M., and Bonica, J.J. (1977) Acupuncture analgesia and anesthesia. Arch. Surg. 112:896.
21. Andersson, S.A., and Holmgren, E. (1977) Analgesic effects of peripheral conditioning stimulation parameters. Acupunct. Electro. Res. 2:237.
22. Sjolund, B.H., and Ericksson, M.E. (1976) Electro-acupuncture and endogenous morphines. Lancet. 2:1085.
23. Voll, R. (1975) Twenty years of electroacupuncture therapy using low- frequency current pulses. American J. of Acupuncture. 3:291.
24. Kosterlitz, H.W., and Hughes, J. (1976) Possible physiologic significance of enkephalin on endogenous ligand of opiate receptors. Advances in Pain Research and Therapy. Ed. Bonica, Raven Press, N.Y., p 641.
25. Terenius, L. (1978) Significance of endorphins in endogenous antinociception. Advances in Biochemical Psychoparm. Ed. Costa and Trabucchi. Raven Press, N.Y., p 31.
26. Adams, J.E. (1976) Naloxone reversal of analgesia produced by brain stimulation in the human. Pain. 2:161.
27. Hosobuchi, Y., et al. (1977) Pain relief by electrical stimulation of the central grey matter in humans and its reversal by naloxone. Science. 17:183.
28. Burton, C., and Marrer, D.D. (1974) Pain suppression by transcutaneous electrical stimulation. IEEE Trans. Biomed. Eng. 21:81.
29. Andersson, S.A., et al. (1976) Evaluation of the pain suppression effect of different frequencies of peripheral electrical stimulation in chronic pain conditions. Acta Orthop. Scandia. 47:149.
30. Wolf, C.J., et al. (1980) Antinociceptive effect of peripheral segmental electrical stimulation in the rat. Pain. 8:237.
31. Malow, R.M., and Dougher, M.J. (1979) A Signal detection analysis of the effects of transcutaneous stimulation on pain. Psychosom. Med. 4:101.
32. Ebersold, M.J., Laws, E.R., and Albers, LW. (1977) Measurements of autonomic function before, during and after transcutaneous stimulation in patients with chronic pain and in control subjects. Mayo Clin. Proc. 52:228.
33. Pert, A., and Yaksh, T. (1974) Sites of morphine induced analgesia in the primate brain: Relation to pain pathways. Brain Research. 80:135.
34. Sjolund, B.H., Terenius, L., and Ericksson, M.B, (1977) Increased cerebrospinal fluid levels of endorphin after electro-acupuncture. Acta Physiol. Scand. 100:382.
35. Mayer, D.J., Price, D.D., and Raffii, A. (1977) Antagonism of acupuncture analgesia in man by the narcotic antogonist naloxone. Brain Res. 121:368.
36. Schien, H., and Bentley, G.A. (1980) The possibility that a component of morphine induced analgesia is contributed indirectly via the relase of endogenous opioids. Pain. 9:73.
37. Mao, W., et al. (1980) High versus low intensity acupuncture analgesia for treatment of chronic pain: Effects on platelet serotonin. Pain. 8:331.
38. Cheng, R.S., and Pomeranz, B. (1981) Monoaminergic mechanism of electroacupuncture analgesia. Brain Res. 215:77.
39. Cheng, R.S., and Poneranz, B. (1980) Electroacupuncture is mediated by stereospecific opiate receptors and is reversed by antagonists of type I receptors. Life Science. 26:631.
40. He, L. (1987) Involvement of endogenous opiold peptides in acupuncture alangesia. Pain. 31:99-121.
41. Chen, B.Y., and Pan, X.P. (1984) Correlation of pain threshold and level of beta-endorphin-like immunoreactive substance in human CFS during electroacupuncture analgesia. Acta Physiol. 36:183-187.
42. Chan, C.W., and Tsang, H. (1987) Inhibition of the human flexion reflex by low intensity, high frequency transcutaneous electrical nerve stimulation (TENS) has a gradual
onset and offset. Pain. 28:239-253.
43. Facchinetti, F., et al. (1981) Concomitant increase in nociceptive flexion reflex threshold and plasma opioids following transcutaneous nerve stimulation. Pain. 11:49-63.
44. Hansoon, P., and Ekblom, A. (1983) Transcutaneous electrical nerve stimulation (TENS) as compared to placebo TENS for relief of acute oro-facial pain. Pain. 15:157-165.
The medical literature is clear and unequivocal – low frequency T.E.N.S. (0.5 – 10 Hz) is both safe and efficacious for muscle relaxation and pain control. It is also clear that low frequency T.E.N.S. has a high degree of specificity when utilized for craniofacial pain (Andersson, 1979; Eriksson et al., 1984; Chapman et al., 1979; Andersson et al., 1977; Andersson and Holmgren, 1975; Sjolund et al., 1975; Reichmanis and Becker, 1977; Hansoon and Ekblom, 1983; Tereshalmy et al., 1982; Phero, 1987; Lasagna et al., 1986; Thomas, 1986; Pantaleo et al., 1983; Wessberg and Dinhani, 1977; Konchak et al., 1988).
Choi and Mitani at Osaka Dental University in 1973 applied the Myomonitor to 15 subjects and monitored the evoked response using wire EMG electrodes. The study concluded “The evoked EMG was recorded from the anterior portion of the temporal, the masseter, the anterior ventral of the digastric, and obicularis oris and the buccinator muscles. . . The Myo-monitor pulse stimulates the nerve trunks of the fifth and seventh cranial nerves at the superior mandibular notch percutaneously and it appeared to have afferent and efferent effects.”
Using accepted intensity-duration methodology Jankelson, et al., 1975 demonstrated that the chronaxy values for Myo-monitor generated curves were well below those for direct muscle stimulation. Further verification of neural mediation resulted from the study of Williamson and Marshall, 1986 using succinylcholine. The study concluded “Succinylcholine acts by competing with acetyicholine at the myoneural end plate and, therefore, no neurally stimulated muscle contraction under such conditions is by direct depolarization of the muscle itself. With the Myo-monitor evoking electrical impulses, there was no muscle contraction in either instance. This information would support the conclusion that the Myo-monitor stimulus is transmitted neurally.”
Fujii 1977 at the University of Osaka used multiple site monitoring to distinguish M wave and H wave response. Using multiple anatomically separate recording sites the study concluded “Two kinds of response were obtained with latencies of about 2.0 msec. and about 6.0 msec. respectively. The former was assumed to be a direct potential (M wave) and the latter a monosynaptic reflex potential (H wave).” The use of recording sites anatomically distant from the input stimuli is essential for valid conclusions using this methodology. In a 1988 study of Myo-monitor stimulation, Dao, Feine and Lund for unexplained reasons placed the recording needle proximate to the electrode stimuli site
McMillan et al., 1987 at the University of Hong Kong concluded that “Contraction of muscles of the upper and lower eyelids, the lateral aspect of the nose and the upper lip indicates stimulation of the facial nerve, in particular its zygomatic and buccal branches. The results of our anatomic investigation indicate that this effect is produced by the stimulation of the branches of the upper division of the facial nerve as they pass in a more or less direct anterior course over the preauricular region. These branches will then be directly beneath a surface electrode placed according to the standard protocol. Propagation of the Myo-monitor stimulus along branches from the buccal anastomotic loops of the nerve would ensure contraction of muscles of the upper lip and angles of the mouth. . . This observation supports electromyographic evidence and results of intensity duration tests that indicate muscle contraction resulting from Myomonitor stimulation is neurally mediated.”
Goodgold and Eberstein examined eight individual investigative studies and found that normal distal latency and conduction velocity of peripheral motor nerves ranged from 2.1 to 5.6 msec. and 44.8 to 67.9 msec., respectively. They concluded that the latency to the obicularis oris which is innervated by the facial nerve in response to stimulation at the angle of the jaw, averages 2.5 to 3.0 msec. Basmajian summarized the results of six studies conducted by separate authors on peripheral nerve conduction velocity and found a range of conduction velocity between 37 and 73 meters/sec. Assuming the distance between the stimulation electrode and the wire recording electrode was approximately 2 cm, it should have taken 0.27 to 0.54 msec. for the pulse to travel this distance if the muscles were stimulated directly. This time interval is much less than the 1.80 to 4.4 msec. measured in the Dao study. This suggests the pulse must have traveled a much longer distance. A neurally mediated pulse would have: 1) 0.5 msec. charging the dermal capacitance, 2) neural conduction time of 0.7 msec. assuming a neural conduction pathway of 4 cm and conduction velocity of 55 meters/sec. which is the average of Basmajian?s review, 3) residual latency (delay at the myoneural junction) of 0.6 msec., 4) intermuscular delay of approximately 0.4 msec. depending upon electrode placement. Adding the sum of these phenomena we find the latency of 1.80 to 4.04 msec. as measured by Dao, et al. is well within the range of neurally mediated response, despite their electrode placement.
ARTICLES REVIEWED IN THIS PUBLICATION
SECTION 1: STUDIES THAT DOCUMENT EFFICACY OF LOW FREQUENCY TENS
1. Andersson, S. Pain control by sensory stimulation. Advances in Pain Research and Therapy. Vol. 3, Ed. Bonica et al. Raven Press, N.Y., 1979. p. 569-585.
2. Eriksson, M., Sjolund, B., and Sundbarg, G. Pain relief from peripheral conditioning stimulation in patients with chronic facial pain. J. Neurosurg. 61:149-155, 1984.
3. Chapman, C.R., Chen A.C., and Bonica, J.J. Effects of intrasegmentalelectrical acupuncture on dental pain: evaluation by threshold estimation and sensory decision theory. Pain. Vol. 3, Biomedical Press, pp 213-227, 1977.
4. Sjolund, B., and Eriksson, M. Endorphins and analgesia produced by peripheral conditioning stimulation. Advances in Pain Research and Therapy. Vol. 3, ed. Bonica Raven Press, N.Y. 1979.
5. Chapman R., Wilson, M., and Gehrig, J. Comparative effects of acupuncture and transcutaneous stimulation on the perception of painful dental stimuli. Pain. Vol. 2, p 265-283, Amsterdam 1976.
6. Andersson, S.A., Holmgren, E., and Roos, A. Analgesic effects of peripheral conditioning stimulation – II. importance of certain stimulation parameters. Acupuncture and Electro-Therapeut. Res. mt. J. Vol. 2, No. 3, pp 237-246. Great Britain 1977.
7. Andersson S.A., and Holmgren, E. Analgesic effects of peripheral conditioning stimulation – III. Effect of high frequency stimulation; segmental mechanisms interacting with pain. Acupuncture and ElectroTherapeut. Res. mt. J. Vol. 3, pp 23-36, Great Britain 1978.
8. Andersson, S.A., and Holmgren, E. On acupuncture analgesia and the mechanism of pain. American J. of Chinese Medicine. Vol. 3, No 4, pp 311-344, 1975.
9. Sjolund B., Terenius, L., and Eriksson, M. Increased cerebrospinal fluid levels of endorphins after electro-acupuncture Acta Physiol. Scand. 100: 382-384, Sweden 1977.
10. Cheng, R.S., and Pomeranz, B.H. Electro-acupuncture analgesia is mediated by stereospecific opiate receptors and is reversed by antagonists of type I receptors. Life Sciences. Vol. 26, pp 631 -638, 1980.
11. Reichmanis, M., and Becker, R.O. Relief of experimentally induced pain by stimulation at acupuncture loci: a review. Comparative Medicine East and West. Vol. 5, No 3-4, pp 281-288, 1977.
12. Andersson, S.A., Pain control by sensory stimulation. Advances in Pain Research and Therapy. Vol. 3 Ed. John J. Bonica et al, 1979.
13. Mannheimer, J.S., and Lampe, G.N. Clinical Transcutaneous Electrical Nerve Stimulation. Philadelphia: F.A. Davis, p 341, 1984.
14. Hansson, P., and Ekblom, A. Transcutaneous electrical nerve stimulation (TENS) as compared to placebo TENS for the relief of acute oro-facial pain. Pain. Vol. 15, pp 157-165, 1983.
15. Terezhalmy, G.T., Ross, G.R., and Holmes-Johnson, E. Transcutaneous electrical nerve stimulation treatment of TMJ-MPDS patients. Ear, Nose, and Throat Journal. Vol. 61, pp 22-28, December 1982.
16. Phero, J.C., Raj, P.P., and MacDonald, J.S. Transcutaneous electrical nerve stimulation and myoneural injection therapy for management of chronic myofascial pain. The Dental Clinics of North America. Vol. 31, No. 4, pp 703-722, October 1987.
SECTION 2: STUDIES THAT DOCUMENT NEURAL MEDIATION OF MYOMONITOR STIMULUS
1. Jankelson, B., Sparks, S., and Crane, P., Neural conduction of the Myo-monitor stimulus: A quantitative analysis. J. Prosthetic Dentistry. Vol. 34, No. 3, pp 245-253, September 1975.
2. Fujii, H. Evoked EMG of masseter and temporalis muscles in man. J. of Oral Rehabilitation. Vol. 4 pp 291-303, 1977.
3. Fujii, H., and Mitani, H. Reflex responses of the masseter and temporal muscles in man. J. of Dental Research. Vol. 52, No. 5, pp. 1046-1050, 1973.
4. Choi, B. On the mandibular position regulated by Myo-monitor stimulation. J. Japanese Prosthetic Dentistry. Vol. 17 pp 73-96, 1973.
5. Williamson, E., and Marshall, D. Myomonitor rest position in the presence and absence of stress. Facial Orthopedics and Temporomandibular Arthrography. Ed. Williamson, Vol. 3, No: 2, 1986.
SECTION 3: STUDIES THAT DOCUMENT HISTOCHEMICAL EFFECT OF LOW FREQUENCY TENS
1. Dixon, H.H., and Dickel, H.A. Tension headache. J. Northwest Medicine. Vol. 66, pp. 817-820, Sept. 1967.
2. Dixon, H.H., and O?Hara, M. Fatigue contracture of skeletal muscles. J. Northwest Medicine. Vol 66, pp-8l3-8l6, Sept. 1967.
3. Rodbard, S., and Pragay, E.B. Contraction frequency, blood supply, and muscle pain. J. of Applied Physiology. Vol. 24, No. 2, Feb. 1968.
4. Rasmussen, O.C., Bonde-Peterson, F., Christensen, L.V., and Moller, E. Blood flow in human mandibular elevators at rest and during controlled biting. J. Oral Biology. Vol. 22, pp 539-543, 1977.
5. Lasagna, M., and Orland, C. Modificazione die flussi ematici muscolocutanei indotta dollo stimulazione neurale transcutanea isichemia e dolore nella patologia occlusale. J. Odotostomatologia e Lymplantopratessi. 1986.
6. Thomas, N.R. Spectral analysis in the pre- and post-TENS condition. Presented International College of Cranlo-Mandibular Orthopedics, Oct. 1986.
SECTION 4: STUDIES DOCUMENTING MYO-MONITOR EFFICACY
1. Pantaleo, T., Prayer-Galletti, F., Pini-Prato, G., and Prayer-Galletti, S. An Electromyographic study in patients with myo-facial pain-dysfunction syndrome. Bull. Group. mt. Rech, sc. Stomat. et Odont. Vol 26, pp. 167-179, 1983.
2. Wessberg, G.A., and Dinham, R. The Myo-monitor and the myo-facial pain dysfunction syndrome. J. Hawaii Dental Assoc. Vol. 10, No. 2, pp. 10-13, 1977.
3. Wessberg, G.A., Carroll, W.L., Dinham, R., and Wolford, L.M. Transcutaneous electrical stimulation as an adjunct in the management of myofascial pain dysfunction syndrome. J. of Prosth. Dent. Vol. 45, No. 3, pp. 307-314, 1981.
4. Boschiero, R., Fraccari, F., and Pagnacco, O. Analysis of the results of the use of the myo-monitor in patients with reduced mouth openings. J. Mm. Stomatologica. Vol. 35, pp. 857-864, Sept. 1986.
5. Konchak, P., Thomas, N., Lanigan, D., and Devon, R. Freeway space measurement using mandibular Kinesiograph and EMG before and after TENS. The Angle Orthodontist. Oct. 1988, pp. 343-350.
6. Bazzotti, L. Electromyography tension and frequency spectrum analysis at rest of some masticatory muscles, before and after TENS. Electromyogr Clin Neurophysiol. 1997 Sep; 37(6):365-78.
7. Eble, O.S., Jonas, I.E., and Kappert, H.F. Transcutaneous electrical nerve stimulation (TENS): its short-term and long-term effects on the masticatory muscles. J. Orofac Orthop. 2000; 61(2):100-11.
STUDIES THAT DOCUMENT THE EFFICACY OF LOW FREQUENCY TENS
LOW FREQUENCY (ACUPUNCTURE LIKE) TENS = MYO-MONITOR
LOW FREQUENCY T.E.N.S.
The A.D.A. draft status report on Devices for the Diagnosis and Treatment of Temporomandibular Disorders sites a single study by Block and Laskin as evidence that TENS and a placebo effect elicited similar results. Block and Laskin used a pulse generated stimulator with peak amplitude from 0-76 ma (500 ohm load) and a pulse rate of 12-100 pulses/sec. Block and Clark clearly state that the modality employed in their study is based on the concept of stimulation that increases input into the spinal gate, thereby altering pain awareness by inhibiting pain sensation.
It must be noted that this is an entirely different modality than low frequency, 0.5 Hz-4 Hz, acupuncture-like TENS. The well controlled studies of Chapman, Anderson, Erickson, Sjolund, Bonica, Chang, Holmgren and others clearly support the preference of low frequency TENS for treatment of chronic pain disorders. Low frequency acupuncture-like modalities such as the Myomonitor have ample and specific documentation in the medical literature regarding local histochemical and endorphin effects.
Following are controlled studies from the medical and dental literature supporting the efficacy of low frequency (acupuncture-like) TENS. Low frequency TENS has a 0.5Hz • 10Hz frequency parameter. However, most of the studies utilize 0.5Hz to 9.0Hz in the investigations.
Andersson, S.A. Pain control by sensory stimulation. Advances in Pain Research and Therapy. Vol 3, ed. John J. Bonica et al, Raven Press, N.Y. 1979.
Transcutaneous nerve stimulation (TNS) and acupuncture are the main methods for sensory stimulation used in medical practice.
In contrast to acupuncture, TNS is usually given at high frequency (50 to 100 Hz) and with low intensity which is kept well below that giving pain. The subjective sensation is different from that during acupuncture and is described as tingling or vibration. There are no phasic muscle movements, but a slight tonic contraction may occur in muscles close to the stimulating electrodes (Andersson, S.A. 1979). The afferent nerve fiber discharge consists of a continuous firing in low and high-threshold afferents depending on the intensity.
Another relevant parameter of the sensory stimulation is its frequency. Pain threshold measurements have shown that low frequency (1 to 4 Hz) gives a gradual and slow increase of the threshold which remains elevated during a long-lasting stimulation and returns slowly in the poststimulation period. These effects contrast strongly the transient pain threshold increase observed during stimulation at high frequency (100 Hz). In spite of a continuous stimulation at high intensity, the pain threshold declines to the control level. It should also be noted that the effect is more localized than that at low frequency. Thus low-frequency stimulation of the cheeks increases the threshold of the teeth in both the upper and lower jaws, whereas high-frequency stimulation at the same location and intensity gives a transient effect only in the incisive and canine teeth of the upper jaw.
It should also be noted that the most common type of conditioning stimulation TNS, often has a pronounced effect on chronic pain, but the pain threshold (is) unchanged or increased only transiently at the start of the stimulation. The pain threshold measurements refer to experimental pain mediated via A delta fibers, at least when electrical stimuli are used as tests. Chronic pain may be due to activity in C fibers, and it remains to be determined whether the threshold for C fiber-mediated sensations is increased during high-frequency stimulation.
When the low frequency, high-intensity stimulation is modified into repetitive, high-frequency bursts, the conditioning is less distressing and pain conditions not relieved by high-frequency stimulation can be alleviated. (Eriksson, M. 1976.)
Substances with morphine-like effects, endorphins, appear to be transmitters in the descending control systems, and morphine exerts its analgesic effect partly by activation of such systems (Mayer,D.J. 1976), but it has also a direct action on the spinal cord (Besson, 1973, Fields, 1978, Kitahata, 1974, LeBars, 1976, Zieglgansberger 1976). Administration of naloxone, a specific narcotic antagonist, inhibits the analgesic effect both of electrical stimulation of the brainstem and of morphine. (Fields 1978)
There is evidence that low-frequency stimulation (acupuncture) activates descending control systems. Naloxone decreases or eliminates the analgesia produced by classic needle acupuncture in healthy subjects (Mayer, 1975) Moreover, naloxone inhibits the pain relief elicited by low-frequency electrical stimulation in patients with chronic pain but it does not counteract analgesic effects produced by high-frequency sensory stimulation. (Sjolund 1976) A low concentration of endorphins is often found in the cerebrospinal fluid (CSF) of patients with chronic pain of somatic origin as compared to pain of psychogenic origin (Almay 1978). Low-frequency electrical stimulation producing pain relief increases the CSF concentration of endorphins. (Sjolund 1977). The counteraction by naloxone of the pain relief after acupuncture could thus be due to an effect on the endorphin release by the stimulation.
A pain inhibition center, possibly including the brainstem structure producing analgesia by direct stimulation, receives input from a variety of afferents ranging from large non-pain fibers to pain afferents. Stimulation of these afferents increases the output from the pain inhibition center with blockade of the transmission at different levels of the pain pathway. The pain inhibitory mechanism has endorphins as transmitters in some link. The differences in the characteristic of the pain relief elicited by different types of sensory stimulation appears to reflect at least two different pain inhibitory mechanisms.
Eriksson, M., Sjolund, B. and Sundbarg, G. Pain relief from peripheral conditioning stimulation in patients with chronic facial pain. J. Neurosurg., 61:149-155, 1984.
Departments of Clinical Neurophysiology and Neurosurgery, University Hospital, Lund, Sweden.
In a prospective study, 50 consecutive patients, referred to a pain treatment unit for surgery to alleviate various forms of facial pain, were all given transcutaneous nerve stimulation (TNS) therapy and followed for 2 years. Of the 44 patients remaining at the 2-year follow-up review, 20 (45%) reported satisfactory analgesia from conventional or acupuncture-like TNS. The latter technique markedly improved the overall results. No serious side effects were seen. Atypical facial pain of known etiology responded best to treatment, but satisfactory relief was often produced with tic douloureux. Duration of the pain condition as well as sex of the patient were predictors of treatment results. It is concluded that TNS therapy represents a valid alternative to surgery when pharmacological therapy fails, especially in the elderly and in patients with atypical facial pain.
Patients with chronic so-called intractable facial pain may present management problems. This is true for typical trigeminal neuralgia (tic douloureux) as well as for atypical forms of facial pain. (Anthony, M 1974, Loeser, J.D. 1977, Rasmussen 1965)
A different line of therapy has developed from the hypothesis that trigeminal neuralgia is a result of vascular compression of the trigeminal nerve root. (Dandy, W.E. 1934)
In cases of atypical facial pain, (Gregg, J.M. 1978, Rushton, J.G. 1959) with or without an identifiable organic cause, antiepileptic drugs are generally ineffective. Alcohol injections or surgery, even if giving temporary relief, may later result in a considerable worsening of the condition. (Gregg, J.M. 1975, Rasmussen, P. 1965). Conventional analgesics may be useful when there is an organic cause for the disorder, and tricyclic antidepressant drugs may help when there is not. (Anthony, M. 1974) The available therapeutic methods, however, leave many patients unaided and substantially handicapped by their chronic facial pain.
During the last decade, treatment by conditioning stimulation of peripheral nerves has become increasingly used for patients with acute and chronic pain conditions. (Loeser, J.D. 1975, Long, D.M. 1976, Wall, P.D. 1967) A long-term follow-up study of the effect of two types of transcutaneous electrical nerve stimulation (TNS) showed that, after 2 years, 31% of patients referred to a neurosurgical department still experienced useful analgesia from daily TNS treatment. (Eriksson, M.B.E. 1979) Among these successfully treated patients with chronic pain were several who had previously had intractable facial pain, some of whom had to use a newly developed TNS technique (acupuncture-like TNS)(Eriksson, M.B.E. 1976) to obtain pain relief.
Apart from the need for alternative therapeutic methods among patients with intractable facial pain, it seemed of great interest for the evaluation of the TNS techniques to test and follow a group of patients suffering from chronic pain that was less varied as to type and location than in previous studies. We therefore initiated a prospective long-term follow-up study of 50 patients with intractable facial pain, treated with conventional (Ihalainen, U., 1978, Wall, P.D. 1967) or acupuncture-like (Ericksson, M.B.E. 1976, Eriksson, M.B.E., 1979). The facial pain conditions treated represent two types of pain: namely, acute intermittent (tic douloureux) and chronic continuous (atypical facial pain). The study and the results obtained are the subjects of this report.
The series included 50 consecutive patients with intractable facial pain who were referred to the Department of Neurosurgery at Lund University Hospital for surgery. Twenty-one patients had been classified as having tic douloureux. To comply with the diagnostic criteria, the pain had to be: 1) truly paroxysmal; 2) unilateral; 3) provocable by non-nociceptive facial stimuli; 4) confined to the innervation area of one, two, or three trigeminal branches; and 5) not associated with sensory or other neurological deficit.
Twenty-nine patients did not fulfill the criteria . . . tic douloureux and will be considered here as having “atypical facial pain.” In 18 of these patients the pain resulted from accidental or surgical trauma (11 patients), cerebrovascular disease, (five patients), or herpes zoster oplithalmicus (two patients).
If after the first 2-week trial period, there was no significant pain relief, the patient was instructed how to use the stimulator for acupuncture-like TNS. The positive electrode was then placed in front of the ear and the negative electrode over the forehead, cheek, or chin. The stimulator was set for a train (7 pulses at 100Hz) given at a repetition rate of 1.5 to 2 Hz. (Eriksson, 1976, Eriksson, 1979) and the electrodes adjusted so that visible muscle contractions were produced in the area of pain (Fig. 2). If, after another 2-week trial period at home, there was still no report of significant pain relief, the TNS trial was recorded as a failure. If stimulation treatment was reported to reduce the intensity and frequency of pain paroxysms, or produced useful relief in patients with non-paroxysmal atypical intractable facial pain, the patient was instructed to continue with the treatment and was seen again 2 months later.
After 3 months of treatment, 16 (32%) of the 50 patients experienced successful or moderately successful pain relief with conventional TNS only. (Fig. 3) Of the 34 patients who did not benefit from conventional TNS, acupuncture-like TNS proved to be satisfactory in 13 patients. Thus, in all, 29 (58%) of the 50 patients experienced pain relief from TNS. Twenty patients used stimulation only and were considered a success, and nine patients who added small amounts of adjuvant pharmacotherapy were considered a moderate success.
There was no significant difference in treatment success between patients with tic douloureux (11 of 21 patients) and atypical facial pain (18 of 29 patients). However, significantly (0.025
The success rate of TNS was significantly (0.025
0.05. These findings indicate that the increase in pain threshold that occurred with acupunctural stimulation did, in fact, reflect a decrease in sensory sensitivity to tooth pulp shocks. Response bias played a trivial role in the treatment-induced threshold increase.
In spite of differences in equipment, procedure, site of acupunctural stimulation, and cultural context, we have replicated the dental acupuncture analgesia phenomenon reported by Andersson and Holmgren (Andersson 1973). Intense electrical stimulation at 2-3 Hz over an 😯 min period yielded a gradual increase in dental pain thresholds which reached a relatively stable state after approximately 20 min. An SDT analysis of the discrimination tasks involving high intensity, low intensity, and blank stimuli demonstrated that the pain threshold increase reflected a reduction in sensory sensitivity. There was no significant change in response bias or willingness to call the stimulation experienced painful.
The apparent proclivity of dental structures to respond to acupunctural stimulation when cutaneous tissues do not, may be due to morphological or neurological differences in skin and teeth or to unique properties of the trigeminal system or its projection to the brain stem.
Sjolund, B.H., and Eriksson, M. Endorphins and analgesia produced by peripheral conditioning stimulation. Advances in Pain Research and Therapy. Vol 3, ed. John J. Bonica, et at. Raven Press, New York, 1979.
ACUPUNCTURE – LIKE TNS
Chiang et al. (Chiang 1973) claimed that impulses from deep afferents were necessary to elicit acupuncture analgesia. Andersson and co-workers (Andersson 1973, Andersson 1976, Sjolund, this volume) found that a stimulation strength giving forceful muscle contractions in the facial musculature was necessary for the rise in tooth pain threshold. They also found that the pain threshold increase was induced even more readily with stimulation via surface electrodes than via needles, probably because the surface electrodes allowed more current to be passed (Andersson 1973).
This type of stimulation, acupuncture-like low-frequency TNS, reduced the current necessary to elicit muscle contraction to half or two-thirds of the single shock values and was tried whenever our chronic pain patients did not experience analgesia from conventional high-frequency TNS. The compiled long-term results of stimulation treatment we then improved by about 40% (Eriksson 1976, Eriksson 1979).
INFLUENCE OF NALAXONE
From the present results it thus seems as if the acupuncture-like (lo-) TNS acts through links utilizing endorphins whereas conventional (hi-) TNS produces analgesia via some other mechanism.
When the concentrations of these endorphin fractions were measured in the cerebrospinal fluid of our chronic patients before (Fig. 3, C) and after (Fig. 3, EAP) acupuncture-like TNS, there was a systematic increase of the fraction I concentration in lumbar cerebrospinal fluid of those patients receiving stimulation of lumbar afferents (Sjolund 1977, unpublished; Fig. 3). This confirms the results on naloxone administration and in addition points to a local release and action of the endorphins at the spinal level during acupuncture-like TNS (see Duggan 1976, Yaksh 1976). With conventional TNS, no increase of endorphin concentrations has been seen in pilot experiments (L. Terenius, personal communication).
Chapman, C., Richard, W., Michael, E., and Gehrig, J.D. Comparative effects of acupuncture and transcutaneous stimulation on the perception of painful dental stimuli. Pain, 2:265-283, 1976.
The effects of acupunctural stimulation on the perception of induced dental pain were compared with those of placebo acupuncture and transcutaneous electrical stimulation (TES) at an acupuncture site. Each of 4 groups of 15 subjects received one of the following treatments: acupuncture, placebo acupuncture, TES, or control conditions. Every subject was tested twice, once in a baseline session and on another day in a test session. Four levels of painful dental stimuli were delivered repeatedly and in random order to each subject in each session, who rated the perceived intensity of each stimulus on a pain category scale.
All three treatment groups showed a significant reduction in magnitude of stimulus ratings after treatment. A Sensory Decision Theory analysis of the data was employed to assess the sensory sensitivity of each subject to each of 4 levels of dental stimulation and the willingness of the subject to label the strongest stimulus as painful. Acupuncture and TES groups showed a small but significant sensory analgesic response to treatment and a significant reduction in willingness to identify the strongest stimulus as painful when contrasted to controls, but placebo acupuncture subjects failed to show significant change on either of the response measures. The effects of acupuncture were most pronounced at the lowest level of stimulation, while TES affected the perception of all levels of dental stimuli. The observed effects appeared to be small, reliable, and dependent on the stimulation of a particular anatomical locus.
Four treatment groups were established: acupuncture, transcutaneous electrical stimulation (TES) at an acupuncture site, placebo acupuncture, and control. Subjects in each of these groups were tested twice on two separate days to provide a separate set of baseline and test measurements for each group.
It has been argued convincingly that acupuncture analgesia studies cannot be run double blind (Mark 1973), but is nonetheless desirable to reduce experimenter expectation effects as far as possible. Accordingly, a pseudo-double blind procedure was established in which a visual screen was used to ensure that neither the subject nor the experimenter could see which treatment was being administered to the subject during the test session. Of course, tactile cues were still available to the subject.
While SDT analyses are of intrinsic value, it is of interest to relate them to observable pain behavior. In this study, the perceivable behaviors were the ratings assigned to the dental stimuli, and the analgesic effects evident to an observer were the reductions in the magnitude of rating judgments given to the stimuli. In order to relate changes in d? and C4 to decreases in rating values, multiple regression methods were employed.
Since change scores indicated behavioral changes over sessions, they reflected treatment effects in the acupuncture and TES groups. It was of interest to ask how much of the treatment-induced change in pain ratings could be accounted for on the basis of change in sensory sensitivity and response bias. Multiple regression methods provided a way of estimating this and of evaluating the relative importance of sensory and bias factors.
In brief, this was done by using d? and C4 as predictors in order to create hypothetical estimates of mean rating change values for each subject. The accuracy of such predictions was evaluated by comparing the values predicted on the basis of d? and C4 with the actual mean rating measures. The results obtained indicated that the two SDT measures taken together were meaningful as predictors of the mean rating changes in the treatment groups. This implied that the observable behavioral changes in ratings reflected unobservable changes in sensory abilities and attitude toward reporting the stimuli as painful, in addition to inevitable measurement error.
In order to evaluate whether d? or C4 was most influential in determining the rating behaviors of the subjects, the proportion of variability among the rating change scores which could be accounted for by d? changes measures was estimated, and the same calculation was followed for the C4 values.
The data obtained from the acupuncture subjects have provided a general replication of the sensory hypalgesic effect reported by Chapman et al. (Chapman 1975). However, in the first study the d? analgesic effects appeared to be consistent in magnitude across stimulus levels but this was not replicated here. In Table II it is evident that such changes were greatest at the lowest level of stimulus intensity, and small or negligible at the higher levels. The results of the multiple regression analyses have supported this observation, indicating that acupuncture?s effects were minimal for higher levels of stimulation. As a check, a multiple regression analysis similar to that described above was carried out on the acupuncture data collected by Chapman et al. (Chapman 1975). The essential results, reported in Table V, are highly consistent with those obtained in this study. Thus, while d? scores changed substantially at all levels of stimulus intensity in the earlier study, only the changes at the lower intensity were significantly related to changes in pain ratings. These findings indicate that acupuncture?s analgesic effects were in fact quite similar to those of 33% nitrous oxide.
Interestingly, a similar result was obtained for subjects undergoing TES at an acupuncture site, and this agrees with the report of Andersson et al. (Andersson 1973) who observed a slightly greater increase in pain threshold with TES than with acupuncture. These observations suggest that the analgesic effects reported here were not dependent on the stimulation of deeper structures. Since the placebo acupuncture group showed no positive responses to treatment, it would seem that acupuncturally induced dental hypalgesia requires stimulation of specific loci.
Andersson, S.A., Holmgren, E., and Roos, A. Analgesic effects of peripheral conditioning stimulation – U. Importance of certain stimulation parameters. Acupuncture & Electro-Therapeut. Res. mt. J., Vol 2, No. 3 & 4, pp. 237-246, 1977.
The pain threshold effects in teeth, generally described in a previous paper, are related to certain parameters of the conditioning stimulation. A strong low frequency stimulation (2/see) giving pronounced beating sensations and powerful muscle contractions is needed to produce any significant threshold increase and no changes of the threshold were found at low intensities.
The present results show some important features of the pain threshold effects produced by low frequency conditioning stimulation. Thus, the degree of the threshold increase is mainly related to a relatively segmental location of the stimulating electrodes and to the intensity of the conditioning stimuli. If these parameters are kept constant the effect is also reproducible.
It can, however, be stated that conditioning stimulation of the maxillar branch of the trigeminal nerve influences the pain threshold of the teeth similarly in both the upper and lower jaw, the latter being innervated by the mandibular branch of the trigeminal nerve and thus not strictly segmental to the location of the stimulation electrodes.
The results of the present study give further support to the idea that basic physiological mechanisms are involved in the pain threshold effects of the conditioning stimulation (Andersson et al, 1976). If psychological suggestive components were most important, certain effects on the pain threshold would have been expected already at low intensities of the stimulation (levels A-C). The absence of effects, in spite of the sensations evoked by the electrical pulses, indicates that a suggestive component is not of any significant importance in the present experimental situation. This conclusion is also supported by the reproducibility of the effects at constant stimulation intensities and by the possibility of also producing threshold increases in primarily unresponsive subjects when they have been sufficiently acquainted to the experimental situation to allow an appropriate intensity of the conditioning stimulation.
The above mentioned observations suggest that the activation of large diameter afferent fibres conveying the information from low threshold cutaneous afferents is not sufficient to influence the pain threshold at a low stimulation rate. The pain threshold seems to increase only when the subjective magnitude of the beating and observed muscle contractions exceed a certain level. Apparently the conditioning stimulation must activate not only low threshold afferents but also fibres with higher thresholds. The present finding of a pronounced increase of pain threshold only at intensities giving rise to powerful muscle contractions, suggests that activation of muscle afferents is of importance in obtaining an increase of the pain threshold.
Andersson, S.A., and Holmgren E. Analgesic effects of peripheral conditioning stimulation – IL Effect of high frequency stimulation; Segmental mechanisms interacting with pain. Acupuncture & Electro-Therapeut. Res. mt. J., Vol 3, pp 23-36, 1978.
The effects on the pain threshold of teeth during conditioning stimulation with different frequencies were studied in volunteers. High intensity stimulation of the cheeks at 100/sec produced at onset a transient increase of the pain threshold essentially restricted to teeth of the upper jaw. No increase of the pain threshold was obtained by stimulation at 100/sec of the hands. Conditioning with 10/sec of the cheeks gave a rapid rise of the threshold followed by a gradual increase, but during prolonged conditioning the threshold declined. Stimulation with 2/sec produced a slow gradual increase of the threshold which remained at high level throughout a longlasting period. The after-effect was more pronounced at stimulation with 2/sec as compared to 10/sec. The segmental mechanisms of pain are discussed and it is suggested that the pain afferents should be considered as a subgroup of the flexor reflex afferents and that the segmental connexions of the pain afferents are subject to similar pre- and postsynaptic segmental and supraspinal inhibitory mechanisms as those known to exist with regard to the transmission from the flexor relex afferents to the flexor motoneurones. The effect of low frequency, high intensity conditioning stimulation on the pain threshold and on acute pain is discussed in relation to an increased inhibition at the input stage by feedback systems via the brain stem. High frequency stimulation is suggested to influence the pain threshold and chronic pain mainly due to pre and postsynaptic inhibition elicited by activity in primary afferents at the segmental level.
A method of low frequency (1-3/sec) conditioning stimulation has been developed for Chinese acupuncture. Stimulation can be applied either through manipulation of needles of through low frequency high intensity electrical stimulation via either needles or surface electrodes. Both Chinese (cf. Kaada et al, 1974) and Western reports (Holmdabl, 1973; Mann et al., 1973; Omura, 1973, 1975) argue that this method of stimulation has a relieving effect in acute as well as chronic pain conditions. Electrical stimulation via needles or surface electrodes also produces a marded increase of the pain threshold (Andersson et al., 1977a). In contrast to the almost immediate effect of high frequency stimulation, the onset of the pain relief is gradual, lasting 15-20 min, and the after-effect is longlasting with a slow gradual return of the pain. The pain threshold also showed a gradual increase during low frequency electrical stimulation and a gradual decline in the post-stimulation period (Andersson et al., 1977a). Thus, there is a marked similarity between the time course of the clinical analgesia and the pain threshold increase during low frequency conditioning stimulation. Another similarity between the analgesia and the pain threshold increase is found in the high intensity required to obtain these effects during low frequency stimulation (Anderson et al., 1977c).
A pronounced pain threshold increase is obtained only by an intensity just below that producing pain. The importance of intense stimulation has abs been stressed in reports of surgical analgesia induced by conditioning stimulation (Peking Acupuncture Anaesthesia Co-ordinating Group, 1973; Section of Thoracic Surgery, Peking 1973). Thus pain relief during low frequency stimulation appears to be produced by recruiting another type of afferent fibres as compared with high frequency stimulation which is already effective at a moderate intensity activating low threshold mechano-receptors. The Analgesic effects of high and low frequency conditioning stimulation also differ with regard to their distribution. During low frequency conditioning, non- segmental effects have been stressed, particularly in Chinese reports, and it has been claimed that a generalized analgesia and pain threshold increase can be obtained by manipulation of needles at certain points. This effect contrasts strongly with the closely segmental pain relief found during high frequency stimulation and is also in conflict with the results in a previous report (Andersson et al., 1977c) which showed that the pain threshold increases mainly in regions related to those exposed to conditioning stimulation, i.e. mainly cheek stimulation increased the pain threshold of teeth. Some Chinese reports emphasize, however, the segmental stimulation is of importance to obtain analgesia sufficient for surgery (Hua Shan Hospital of Shanghai, 1973; Shanghai First People?s Hospital, 1973).
Thus, large differences are found in the Analgesic effects of conditioning stimulation with high and low frequencies which suggests that the mechanisms interacting with the sensations of pain are different.
The slowly increasing and longlasting pain threshold changes produced by a conditioning stimulation of 2/sec were completely different from those produced at high frequencies. Stimulation at 100/sec induced an increase of the threshold almost exclusively in teeth into which the sensation of dull pain projected, and the threshold decreased rapidly during the continued conditioning. The threshold effect was obtained only at a high intensity. During continuous stimulation at a constant intensity the test subjects reported a decrease in the sensation of dull pain which approximately paralleled the decrease of the tested pain threshold. Stimulation at 10/sec appeared to produce changes of the threshold with characteristics of the effect from stimulation at 2/sec and at 100/sec. The rapid increase and fall of the threshold at the start and end of the 10/sec conditioning may be related to the transient effect at 100/sec. These threshold changes were followed by a slow increase and decrease respectively at the onset and end of the conditioning which are typical characteristics of the effects of stimulation at 2/sec.
The transmission from the FRA both to flexor motoneurones and to ascending pathways, which may be involved in the transmission of pain, is tonically depressed from supraspinal structures as revealed in acute experiments in decerebrate cats (Holmquist et al., 1960). One such pathway is the dorsal reticulospinal pathway which arises in the brain stem and inhibits the transmission in the FRA pathways at an early stage in the interneuronal chain (Engberg et al., 1968a,b). A similar inhibition appears to be exerted on the FRA pathway by a serontoninergic descending system (Engberg et al., 1968c,d) arising in the dorsal raphe nuclei (Dahlstrom and Fuxe, 1965). It has been shown in behavioural experiments that stimulation of certain brain structures, especially in the mesencephalic central grey and in the dorsal raphe nuclei, induces analgeia without other behavioural changes. This holds true for different species such as rat (Mayer et al., 1971; Balagura and Ralph, 1973) and cat (Oliveras et al., 1974). These Analgesic effects may be due to the above mentioned descending inhibitory influences since the brain stem stimulation inhibits discharges, evoked by stimuli considered to be painful, in spinal neurones of lamina V (Oliveras et al., 1974). Stimulation of the orbital cortex also gives inhibition of these cells, an effect assumed to be mediated via the brain stem (Wyon-Maillar et al, 1972). The dorsal raphe nuclei are known to contain serotoninergic neurones (Dahlstrom and Fuxe, 1965) and further support of their descending Analgesic influence is the fact that analgesia induced by brain stem stimulation is antagonized by the serotonin synthesis inhibitory p-CPA (Akil and Mayer, 1972). A particularly interesting finding is the need for a long induction time (15-20 min) of this brain stem- induced analgesia (Melzack and Melinkoff, 1974). It is not known at present how the activity in these descending control systems varies during different conditions, neither is the functional significance of the input to these systems established. One possibility is that certain descending pathways are parts of a system which controls the level of excitability at an early stage of certain ascending pathways excited from FRA, including the pain afferents. The similarity in the characteristics of the Analgesic effects elicited by electrical stimulation in certain brain stem nuclei (Meizact and Melinkoff, 1974) and by low frequency conditioning stimulation suggests that essentially the same mechanisms are utilized. As a working hypotheses we assume that 2/sec conditioning stimulation induces a slowly increasing activity in descending control systems which inhibit the transmission of impulses both postsynaptically and presynaptically in the pain pathway. A certain topographical arrangement in the descending system is also required to account for the close relation between the regions of conditioning stimulation and the pain threshold although some general increase of the efficiency of the inhibitory effect may be present as suggested by the effect on the pain threshold of teeth due to conditioning stimulation of hands (Andersson et al., 1977c).
Support for the hypothesis that low frequency conditioning stimulation interferes with the transmission of activity in the FRA system has been obtained in animal experiments. After conditioning with 2/sec of forelimb nerves or the infraorbital nerves in awake cats the jaw opening reflex, elicited by electrical stimulation of the tooth pulp and considered as an analogue to the spinal flexion reflex (Sherrington, 1917), is depressed in parallel with reduced aversive reactions (Andersson, 1973; Andersson and Holmgren, in preparation). This observation is consistent with a Chinese report that low frequency (1/sec) electro-acupuncture depresses the jaw opening reflex and reduces the cortical potential evoked by electrical stimulation of teeth (Peking Acupuncture Anaesthesia Co-ordinating Group, 1973). In addition, it has been shown that brain stem stimulation at locations known to induce behavioural analgesia also increases the threshold for the jaw opening reflex (Oliveras et al., 1973)
RELATION TO CLINICAL PAIN
The discussed mechanisms of interaction with the sensation of pain are of interest in relation to clinical pain conditions. It is apparent from clinical reports that low and high frequency conditioning stimulation have different influences on acute and chronic pain. Acute pain seems to be relieved by low frequency conditioning stimulation. The time course of this effect is similar to the observed increase of the pain threshold with a long induction time (15-30 ruin) and longlasting post-stimulation effect. The analgesia is often sufficient to allow surgery. Our findings of an effect on the pain threshold mainly from areas with innervation relatively closely related to that receiving the pain stimulus, are in agreement with a number of recent reports on clinical analgesia during low frequency conditioning. Thus, large similarities seem to exist in the effect on the pain threshold and on clinical pain during conditioning stimulation with low frequencies. It is concluded that the same general pain blocking mechanisms give rise to the pain threshold increase and the clinical analgesia.
Andersson, S.A., and Holmgren, E. On acupuncture analgesia and the mechanism of pain. American Journal of Chinese Medicine. Vol 3, No. 4, pp. 311-334, 1975.
The effect on the experimental tooth pain threshold of conditioning electrical stimulation via needles or surface electrodes applied to the hands and cheeks was studied in 34 dental students. Conditioning stimulation with 2/sec. gave a slowly increasing pain threshold followed by a slow return to the control level in the post-conditioning period. In each individual the amplitude of the threshold increase was reproducible. It was concluded that these effects are not due to motivational but to more basic neurophysiological mechanisms. The pain threshold was increased mainly by segmental conditioning stimulation; segmentally unrelated stimulation gave usually only small effects. Conditioning stimulation with 100/sec. produced only a strict segmental short-lasting effect. Effects with characteristics of both 2/sec. and 100/sec. were obtained by conditioning at 10/sec.
It is suggested that the transmission of impulses from the pain afferents to ascending pathways is controlled at the segmental level by (a) presynaptic inhibition within the group of afferents giving rise to the flexion reflex of which the pain afferents are assumed to be a part; (b) postsynaptic inhibition between alternate pathways excited by flexion reflex afferents; and (c) descending control from supraspinal systems which may utilize similar segmental mechanisms as the primary afferents.
The studies (Andersson, et al, 1975, Andersson, Holmgren and Roos, 1975, Andersson and Holmgren, 1975) summarized in this paper were initiated in order to experimentally elucidate whether a low frequency, electrical peripheral conditioning stimulation can influence the perception of pain. During the initial survey of such effects (Andersson, et al., 1975) using the tooth pulp as a pain test system, it was found that a pain threshold increase could be objectively demonstrated with several characteristics resembling the above mentioned “acupuncture analgesia.”
This paper also includes an extensive discussion regarding possible neurophysiological mechanisms underlying the pain threshold effects reported. These mechanisms are also discussed in relation to clinical pain.
MATERIAL AND METHODS
The present studies were performed on a group of students in the age group of 21-29 years. In order to avoid a biased selection a full class of 42 dental students was requested to participate in this investigation and all but two volunteered. Six students were excluded because of diseases or pregnancy. The remaining 34 students (15 females and 19 males) were all healthy and did not use drugs.
GENERAL PAIN THRESHOLD EFFECTS
The primary question in this study was: Can electrical conditioning stimulation increase the tooth pain threshold? The initial part of the investigation consisted of a standardized test procedure in which 30 students were studied, 18 with needle electrodes and 12 with surface electrodes (Andersson, et al., 1975). Each threshold value represents the mean value of several measurements of one of the six tested teeth. The control threshold was established two times with and interval of 15 to 30 minutes. The needles or surface electrodes were then applied and the stimulator connected to the electrodes but no electrical conditioning stimulation was given. The pain threshold was measured 15 to 20 minutes later. At time zero condition stimulation started with 2 impulses per second to hands and cheeks and the intensity was slowly increased during the following 10 minutes to a level just below that tolerable to the subject. The pain threshold was measured at intervals of 15 minutes. The stimulation was usually discontinued after 75 minutes, and the threshold was measured several times during the post- conditioning period. Since the duration of the conditioning stimulation period varied slightly, the time scale was reset when this stimulation was discontinued.
The transmission from the FRA both to flexor motoneurones and to ascending pathways, which may be involved in the transmission of pain, is tonically depressed from supraspinal structures as revealed in acute experiments in decerebrated cats (Holmquist, Lundberg and Oscarsson 1960). One such pathway is the dorsal reticulospinal system which arises in the brain stem and inhibits the transmission in the FRA pathways at an early stage in the interneuronal chain (Endberg, Lundberg and Ryall 1968a,b). a similar inhibition appears to be exerted on the FRA pathway by a serotoninergic descending system (Endberg ,Lundberg and Ryall 1968c,d) arising in the dorsal raphe nuclei (Dahlstrom and Fuxe 1965). It has been shown in behavioral experiments that stimulation of certain brain structures, especially the mesencephalic central grey and the dorsal rephe nuclei, induces powerful analgesia without other behavioral changes. This holds true for different species such as rat (Mayer et al., 1971; Balagura and Ralph 1973) and cat (Oliveras, et al., 1974). These analgesic effects may very well be due to the above mentioned descending inhibitory influences, since the brain stem stimulation inhibits discharges evoked by stimuli considered to be painful in spinal neurones of lamina V (Oliveras, et al, 1974). Stimulation of the orbital cortex also gives inhibition of these cells, an effect assumed to be mediated via the brain stem (Wyon-Maillard, Conseiller and Besson, 1972). The dorsal raphe nuclei are known to contain serotoninergic neurones (Dalstrom and Fuxe, 1965) and further support for their descending analgesic influences is the fact that analgesia induced by brain stem stimulation is antagonized by the serotonin synthesis inhibitor p-CPA (Akil and Mayer, 1972). A particularly interesting finding is the need for a long induction time (15-20 minutes) of this brain stem induced analgesia (Melzack and Melinkoff, 1974). It is not known at present how the activity in these descending control systems varies during different conditions; neither is the functional significance of the input to these systems established. One possibility is that certain descending pathways are parts of a system which controls the level of excitability at an early stage of certain ascending pathways excited from FRA, including the pain afferents. The similarity in the characteristics of the analgesic effects elicited by electrical stimulation in certain brain stem nuclei (Meizack and Melinkoff, 1974) and by low frequency conditioning stimulation suggests that principally the same mechanisms are utilized. As a working hypothesis we assume that 2/sec. conditioning stimulation induces a slowly increasing activity in the descending control systems which inhibits the transmission of impulses both postsynaptically and presynaptically in the pain pathway. A certain topographical arrangement in the descending systems is also required to account for the close relation between the regions of conditioning stimulation and the Analgesic effect, although some general increase of the efficiency of the inhibitory effect may be present as suggested by the slight influence on the pain threshold of teeth due to conditioning stimulation of hands.
Some further support for the hypothesis that low frequency conditioning stimulation interferes with the transmission of activity in the FRA system has been obtained in experiments in awake cats after conditioning with 2/sec. of forelimb and/or infraorbital nerves. The jaw opening reflex, considered analogous to the spinal flexion reflex (Sherrington, 1917), elicited by electrical stimulation of the tooth pulp was depressed in parallel with reduced aversive reactions (Andersson, 1973; Andersson, 1975). This observation is consistent with a short Chinese note indicating the low frequency elector-acupuncture (1/sec.) simultaneously depresses the jaw opening reflex and reduces the cortical potential evoked by electrical stimulation of teeth (Peking Acupuncture Anaesthesia Co-ordinating Group 1973). Consistent results have also been obtained in experiments on cats where brain stem stimulation, previously known to induce analgesia, increased the threshold to jaw opening elicited by tooth pulp stimulation (Oliveras, Woda, Guilbaud and Besson, 1973).
Sjolund, B., Terenius, L., and Eriksson, M. Increased cerebrospinal fluid levels of endorphins after electro-acupuncture. Acta Physiol. Scand. 100, 382-384, 1977.
In modern Chinese acupuncture, low frequency electrical stimulation of the inserted needles is often used instead of the classical method of manual twirling (Kaada et al. 1974, Bonica 1974). As confirmed in Western investigations (Andersson et al.1973, Chapman et al. 1975) the pain threshold of healthy volunteers is increased with the procedure. Moreover, electro-acupuncture performed via surface electrodes has been found to be more effective than that via needles (Andersson et al. 1973), probably because the amount of current passed can be larger and the seemingly necessary muscle twitches in adjacent regions therefore are stronger (Andersson et al. 1976b). Despite these results, attempts to use acupuncture for the long term relief of chronic pain have been largely unsuccessful (Andersson et al. 1976a, Gaw et at. 1975). However, by modifying the stimulation technique to reinforce muscle contractions, electro-acupuncture via surface electrodes can give satisfactory relief of chronic pain (Eriksson and Sjoluad 1976).
The mechanism behind acupuncture analgesia remains unclear. However, naloxone, a specific opiate antagonist (Martin 1967), counteracts the increase in pain threshold in healthy individuals found after classical needle acupuncture (Mayer et al. 1975) as well as the analgesia from electro-acupuncture in patients with chronic pain (Sjolund and Eriksson 1976). A similar effect has recently been reported with mice receiving electro acupuncture (Pomeranz and Chiu 1976). These results suggest the activation of an inhibitory mechanism releasing endogenous morphinelike substances (endorphins; Hughes et al. 1975, Terenius and Wahlstrom 1975a). Since it is now possible to determine the concentrations of several endorphins in human cerebrospinal fluid (CSF; Terenius and Wahlstrom 1975b), we have investigated whether electro-acupuncture via surface electrodes (Eriksson and Sjolund 1976) changes the endorphin content of the CSF during the period of analhesia experienced by the patients.
The two chromatographic fractions (I and II) account for more that 75% of the total endorphin activity of the human CSF as measured in the receptor binding assay (Wahlstrom et al. 1976). In patients with no pain and apparently healthy, the CSF concentrations of these fractions, express as picomoles of Met-enkephalin/ml are 1.4+/-0.4 (mean +/- S.E.) pmol/ml (I) and 5.2/-+1.8 pmol/ml (II) respectively (Terenius et al. 1976). From the present results it appears that the lumbar CSF content of fraction I is very low in all patients while experiencing pain, confirming earlier observations on patients with trigeminal neuralgia (Terenius and Wahlstrom 1975b). No systematic change is seen with fraction II. During stimulation analgesia a marked rise of endorphin fraction I in lumbar CSF is seen in patients no. 1-4, while this is not the case in the other patients.
Cheng, R.S., and Pomeranz, B.H. Electroacupuncture analgesia is mediated by stereospecific opiate receptors and is reversed by antagonists of type I receptors. Life Sd. Vol 26, pp. 631-638, 1980.
Dextronaloxone, a recently synthesized stereoisomer, which was shown to possess much less opiate receptor affinity than levonaloxone, produces no reversal of electroacupuncture analgesia (EAA) in mice. Since levonaloxone completely reverses EAA, this proves that stereospecific opiate receptors are involved. It has been reported that there are two classes of opiate receptors: Type I and Type II. Type I opiate receptors may be responsible for opiate analgesia. Antagonists of Type I receptors, levonaloxone, naltrexone, cyclazocine and diprenorphine, all block electroacupuncture analgesia at low doses. All together, these results strongly support the hypothesis that electroacupuncture analgesia is mediated by opiate receptors. Possibly Type I receptors are the major components of this system.
Type I opiate receptors are found mostly in the brain areas which mediate analgesia (Pert, C.B., Taylor, D.P. and Pert, A 1979). They are most likely the receptors responsible for exogenous or endogenous opiate analgesia.
However, it is highly unlikely that Type II receptors are involved in EAA since Type I antagonists completely reverse EAA. These results (the stereo- specificity data, and the effects of Type I blockers) strongly support the hypothesis that opiate receptors are involved in electroacupuncture analgesia.
Reichmanis, M., and Becker, R.O. Relief of experimentally-induced pain by stimulation at acupuncture loci: a review. Comparative Medicine East and West. Vol V., No. 3-4 pp. 281-288, 1977.
24 recent studies on acupuncture analgesia for the relief of experimentally- induced pain are reviewed. Negative or equivocal results are reported in 7 of these. The remaining 17(71%) report significant analgesic effects during manual or electrical stimulation (particularly at very low frequencies on the order of 2 Hz) at acupuncture loci. Many investigators note that the full analgesic effect is attained only after about 20 minutes of stimulation. Further investigation of the analgesic effects of stimulation at acupuncture loci, particularly the effect of very low frequency electrical stimulation, is fully warranted by these preliminary findings.
Several studies have been conducted on the effects of stimulation at acupuncture loci for the relief of dental pain, notably by Andersson et al. In a preliminary report, they stated that electrical stimulation at point Li-4 (dorsum of the hand) and other points in the area of the infra-orbital nerve significantly increased pain thresholds in 30 subjects. The analgesic effect reached a maximum about 30 minutes upon cessation (Andersson et al 1973). Surface electrodes were more effective than subcutaneous electrodes, and low frequency constant current stimulation (2 Hz) was more effective than higher frequencies (10 Hz, 100 Hz) in inducing analgesia (Andersson, S.A., and Holmgren E. 1975). Omura (Omura, Y., 1975) has also noted that longer-lasting effects are obtained with very low frequency electrical stimulation. Further tests showed that a fairly strong stimulus was needed for any significant increase in pain threshold (Holmgren, E., 1975).
Andersson, S.A. Pain control by sensory stimulation. Advances in Pain Research and Therapy. Vol. 3 Ed. John J. Bonica et al, 1979.
TNS developed from the hypothesis of pain-controlling gates (Melzack, R., and Wall, P., 1965) according to which an increased activity in large afferent nerve fibers could produce pain relief by blocking of the transmission in the pain pathways.
In contrast to acupuncture, TNS is usually given at high frequency (50 to 100 Hz) and with low intensity which is kept well below that giving pain. The subjective sensation is different from that during acupuncture and is described as tingling or vibration. There are no phasic muscle movements, but a light tonic contraction may occur in muscles close to the stimulating electrodes. The afferent nerve fiber discharge consists of a continuous firing in low-end high- threshold afferents depending on the intensity.
FREQUENCY OF STIMULATION
Another relevant parameter of the sensory stimulation is its frequency. Pain threshold measurements have shown that low frequency (1 to 4 Hz) gives a gradual and slow increase of the threshold which remains elevated during a long- lasting stimulation and returns slowly in. the poststimulation period. These effects contrast strongly the transient pain threshold observed during stimulation at high frequency (100 Hz). In spite of a continuous stimulation at high intensity, the pain threshold declines to the control level. It should also be noted that the effect is more localized than that at low frequency. Thus low-frequency stimulation of the cheeks increases the threshold of the teeth in both the upper and lower jaws, whereas high-frequency stimulation at the same location and intensity gives a transient effect only in the incisive and canine teeth of the upper jaw.
RELATION TO TRADITIONAL ACUPUNCTURE
Activation of high-threshold afferents is a common feature in needle manipulation and in electrical low-frequency stimulation. An obvious difference is, however, that needle stimulation has effects on receptors and afferents only in a limited region at the site of the needling whereas electrical stimulation must activate receptors in a much larger area in order to influence the pain.
Andersson et al. (Andersson, S.A., Block, F., and Holmgren E., 1976) tested low-frequency stimulation applied via surface electrodes. Stimulation a 2 Hz and with an intensity which elicited strong muscle contractions was given at the low back region bilaterally. The pain relief was very good or good in 48% of the women and some analgesia occurred in 37%. The results suggested a relation between high suggestibility and good analgesic effect. However, the study did not indicate that the pain relief was due to the suggestibility only since both suggestion and hypnosis had been used prior to the sensory stimulation without producing paid relief. Probably there are some factors which predispose for both hypnosiblity and analgesic effect during sensory stimulation.
When the low-frequency, high-intensity stimulation is modified into repetitive, high-frequency bursts, the conditioning is less distressing and pain conditions not relieved by high-frequency stimulation can be alleviated (Eriksson, M. and Sjolund, B. 1976).
There is evidence that low-frequency stimulation (acupuncture) activates descending control systems. Naloxone decreases or (?) eliminates the analgesia produced by classic needle acupuncture in healthy subjects. (Mayer, J.D., Price, E.R., Rafii, A., 1975). Moreover, naloxone inhibits the pain relief elicited by low- frequency electrical stimulation in patients with chronic pain but it does not counteract analgesic effects produced by high-frequency sensory stimulation (Sjolund, B., and Eriksson, M.,1977). A low concentration of endorphins is often found in the cerebrospinal fluid (CSF) of patients with chronic pain of somatic origin as compared to pain of psychogenic origin (Almay, B.G. et al., 1978). Low frequency electrical stimulation producing pain relief increases the CSF concentration of endorphins (Sjolund, B., Terenius, L., and Eriksson, M. 1977). The counteraction by naloxone of the pain relief after acupuncture could thus be due to an effect on the endorphin release by the stimulation.
Mannheimer, J.S., and Lampe, G.N. Clinical transcutaneous electrical nerve stimulation. Philadelphia: FA. Davis, p. 341, 1984.
STRONG, LOW -RATE (ACUPUNCTURE – LIKE) T.E.N.S.
Electrical parameters adjusted to provide a low rate 1 to 4 Hz), wide pulse width (150 to 250 usec), and high intensity are know as strong, low-rate (acupuncture-like) T.E.N.S. To be effective, this mode of T.E.N.S. requires an induction period of at least 20 to 30 minutes and must produce strong, visible muscle contractions in segmentally related myotomes. In those experiments comparing the effects of needle or surface stimulation (percutaneous versus transcutaneous), similar results were obtained and in many cases they were somewhat better with surface stimulation.
This mode of stimulation provides a definite prolonged aftereffect of pain relief, which seems to be related to the long onset.
Hansson, P., and Ekblom, A. Transcutaneous electrical nerve stimulation (TENS) as compared to placebo TENS for the relief of acute oro-facial pain. Pain. Vol 15, pp. 157-165, 1983.
The present paper describes the effect of high frequency, low frequency and placebo TENS on acute oro-facial pain in 62 patients, attending to an emergency clinic for dental surgery; they had all suffered pain for 1-4 days. The patients were randomly assigned to one of three groups receiving either high frequency (100 Hz), low frequency (2 Hz) or placebo TENS. In the two groups receiving TENS (42 patients) 16 patients reported a reduction in pain intensity exceeding 50%; out of these 16 patients, 4 patients reported complete relief of pain. In the placebo group (20 patients) 2 patients reported a pain reduction of more than 50%; out of these 2 patients, none reported a complete pain relief
The effect of TENS and placebo TENS was studied in 62 patients aged 19- 54 years (26 males and 36 females) admitted to an emergency clinic for dental surgery for treatment of oro-facial pain. The most common causes for the pain were pulpal inflammation, apical periodontitis (including facial abscesses) and postoperative pain following removal of a tooth. Patients with these diagnoses were represented in equal numbers in the test groups and in the placebo group. All patients suffered from acute pain; most of the patients had experienced pain for 1- 4 days. None of them had taken analgesics within 6 h before submitted for treatment. All of the patients were examined, told the diagnosis and asked if they would take part in the experiments. Those willing to participate were informed about their role in the experiment. Furthermore the subjects were told that they might or might not experience pain relief as well as aggravation of pain during stimulation. Every effort was made to avoid suggestion. The patients were told that they could stop the stimulation at any time and all the patients were informed that they would get a conventional dental treatment after termination of the stimulation.
The patients were assigned randomly to one of the three groups, high frequency, low frequency or placebo TENS. They were asked to rate their pain intensity before they received any stimulation, by using a 5-graded verbal scale.
Previous studies concerning the pain reducing effect of TENS in acute (Augustinsson, et al 1977, Hymes, et al 1974, Rosenberg, et al, 1978, and Van der Ark, et al 1975) and chronic (Ihalainen, et al 1978, Loeser, et al 1975, Long, et al 1975, and Picaza, et al 1975) pain of different origin are consistent in showing temporary alleviation of pain in about 50% of the patients. It must be pointed out, however, that different authors use different criteria in evaluating the pain reduction obtained by TENS, which makes it difficult to compare results in various reports.
The findings in the present study clearly show that TENS of either 100 or 2 Hz may reduce or abolish acute oro-facial pain. On the basis of our results, no significant difference could be observed between the pain relieving effect of high frequency and low frequency TENS. However, it should be noted that most patients found the muscle twitches produced by the low frequency TENS uncomfortable. This was in contrast to high frequency TENS which most often produced a pleasant sensation and a feeling of warmth. Sixteen of the 42 patients treated with TENS experienced a pain relief exceeding 50%, which in the placebo group 2 out of 20 patients reported a similar degree of decrease in pain intensity. The magnitude of the placebo effect in this study, if considering all patients in the placebo group who reported some relief of pain (i.e., 8 out of 20 patients), is similar to that reported in other studies (Thorsteinsson, et al 1978), i.e., a 40% placebo effect. The difference between the pain alleviating effect of TENS as compared to placebo TENS suggests that the reduction of pain obtained in the present study is unlikely to be due to placebo effects.
In studies of any method of treating pain it is important to compare the pain alleviation obtained with that of other modes of treatment. We did compare TENS and placebo TENS to the pain relief obtained from pharmacological substances used by the patients before visiting the clinic. It is interesting to note that only 1 of the 5 patients receiving placebo TENS rated this superior to the analgesic medication used, while 12 out of 23 patients receiving TENS rated the TENS effect higher than analgesics used. All patients rating TENS and placebo – TENS superior to the specific analgesic medication used, experienced a pain relief from TENS or from placebo-TENS exceeding 50%
In conclusion, the observations in the present study suggest that acute oro – facial pain can be effectively reduced by TENS, either at 100 or at 2 Hz. The results of the present study and previous findings (Ottoson, et al 1981) further suggest that vibratory stimulation in some cases is superior to TENS.
Terezhalmy, G.T., Ross, G.R. and Holmes-Johnson, E. Transcutaneous electrical nerve stimulation treatment of TMJ-MPDS patients. Ear, Nose and Throat Journal. Vol 61, pp. 22-28, December 1982.
Correct diagnosis and selection of the most effective therapeutic approach for the management of TMJ – MPDS require not only knowledge of the etiology, physiopathology, symptomatology, and affective qualities of the pain syndrome but also an awareness of the availability of different modes of therapy. The purpose of this study is to examine the effect of transcutaneous electrical nerve stimulation (TENS) on patients with TMJ-MPDS and to analyze factors that might influence patient response to transcutaneous stimulation.
TRANSCUTANEOUS ELECTRICAL NERVE STIMULATION
The Panel on Review of Neurological Devices of the Food and Drug Administration concluded in its 1976 report that (1) TENS is progressing in technical sophistication, (2) a reasonable and acceptable degree of efficacy has been documented in long-term trials, (3) TENS is being accepted by many members of the health care community as a safe and simple therapeutic means of alleviating pain, and (4) TENS provides a meaningful alternative to other types of pain therapy that are known to have a higher degree of risk (FDA Report, 1976)
MATERIALS AND METHODS
Twenty-five patients suffering from pain associated with TMJ-MPDS participated in this study. These patients were selected on the basis of one or more of the following criteria: (1) intrajoint pain associated with muscle tenderness and ear symptoms; (2) muscle spasms related to fatigue and tension due to sudden or chronic stretch; (3) a combination of intrajoint pain and muscle spasms; (4) referred pain from trigger points within a muscle in spasm, and (5) limitation or loss of mandibular function without evidence of systemic or neoplastic disease. Informed consent was obtained from all patients.
A Pain Rating Index was developed on the basis of the McGill Pain Questionnaire?s intensity scale in the sensory temporal, constrictive pressure, dullness, and miscellaneous categories; evaluative category; and two supplementary miscellaneous subclasses. Each subclass has an intensity scale ranging from 1 to 5 in order of increasing intensity. The intensity scores in each subclass were added to determine the Pain Rating Index for each patient
Our study indicates that TENS offers a rapid, noninvasive, and generally predictable means of pain suppression. It can be a valuable alternative to other modes of therapy in the treatment of TMJ-MPDS. If TENS therapy is successful, no other treatment would appear to be necessary. When TENS therapy is less than effective or does not give the desired pain relief, other treatment modalities must be considered. Correction of minor and major dental occlusal discrepancies, pharmacotherapy, and surgery are invasive procedures and are therefore not without risk. As such, we believe that biofeedback techniques and psychological counseling may appropriately take precedence in the treatment of the patient with TMJ – MPDS.
Although comparisons of TENS treatment with a placebo were not done in this study, two separate investigators have shown that the placebo effect with TENS is in the range of 32 to 33 percent (Loeser, et al 1975, Thorsteinsson, et al, 1977). In both of these studies, the placebo effect appeared to be brief and gave little evidence to support the contention that the effect persists for any significant period of time. Our findings of 72 percent long-term responses were considerably greater than the accepted placebo effect.
The McGill Pain Questionnaire appeared to be sufficiently sensitive to provide the clinician with important information concerning patient response to TENS. It has the potential for providing qualitative and quantitative data that can be analyzed, and it should be useful in distinguishing among the effects of different methods of controlling pain
TENS is an effective, noninvasive means for suppressing pain caused by TMJ-MPDS. Patient responses to treatment may be evaluated with the McGill Pain Questionnaire. The MMPI provides important information concerning the patient?s emotional equilibrium and is a valuable prognostic tool. Our data suggests that TMJ-MPDS is multifactorial and that no single discipline or therapeutic approach should necessarily be considered the only method for patient management.
Phero, J.C., Raj, P. P., and McDonald, J.S. Transcutaneous electrical nerve stimulation and myoneural injection therapy for management of chronic myofascial pain. The Dental Clinics of North America. Vol. 31, No. 4, October 1987.
TRANSCUTANEOUS ELECTRICAL NERVE STIMULATION
The present-day use of TENS began after the 1965 publication of Melzack and Wall?s classic paper “Pain Mechanisms: A New Theory” (Meizack, et al 1965). Two years later, it was found that external application of electrical stimulation was effective in relieving pain. This technique was used to determine if a patient was a suitable candidate for the surgical implantation of dorsal column electrodes (Shealy, C. 1972). These researchers laid the foundation for the current utilization of TENS to manage acute and chronic pain.
TENS has been used in a variety of health care settings including pain control centers, emergency rooms, operating rooms, postanesthesia care units, and labor rooms. There is a need for health professionals to develop knowledge and expertise in this noninvasive method of providing patient analgesia. Of key importance is the area of patient education in the use of TENS. With proper training and equipment, the patient can learn to utilize a TENS unit at home with satisfactory results often giving them a significant degree of self-control over their chronic pain.
THEORIES ON MECHANISM OF ACTION
The placebo effect noted with the use of TENS has been a subject of study by many researchers. The placebo effect is believed to be minimal (Long, D. 1974). If it occurs during a trial of TENS it will not be sustained.
INDICATIONS FOR TENS
TENS has been demonstrated to be effective in relieving both acute and chronic pain. TENS therapy alone may be sufficient to modulate pain, but it is most often used in conjunction with other modalities of therapy to maintain relaxation and relief of pain
GOALS OF TENS THERAPY
The goals of TENS therapy as a single modality or in conjunction with other modalities are as follows: a 50 per cent decrease in pain, a 50 per cent increase in function and mobility, and a SO per cent decrease in medication with the elimination of agents with addictive potential. These results have been obtained using TENS on patients experiencing acute pain and chronic pain (Hymes, et al 1974, Long, D. 1977, Shealy, C. 1972, Shealy, C.N. 1974)
MODES OF STIMULATION
ACUPUNCTURE MODE (HIGH WIDTH, LOW RATE)
This setting is often the second mode of choice and is very effective for deep, aching chronic pain. It is useful when previous nerve damage has occurred (3M: TENS, 1983). This mode stimulates the cutaneous, subcutaneous and deep nerve fibers. A low rate,
Over the last several years TENS therapy has become extremely popular to a large extent because it is a noninvasive technique that most patients can be taught to use safely and effectively. An additional advantage to TENS therapy is that it provides many patients with some means of control over their pain, independent of medications and hands-on therapy by health care providers
MYO-MONITOR NEURAL MEDIATION VS. MUSCLE STIMULATION
The following articles are controlled studies supporting the thesis that Myo – monitor induced contraction of muscles is neurally mediated.
Jankelson, B., Spark, S. and Crane, P. Neural conduction of the Myo-monitor stimulus: A quantitative analysis. J. Prosthetic Dentistry. Vol 34 No. 3, pp 245- 253 September 1975.
PURPOSE AND SCOPE OF THE INVESTIGATION
The purpose of this investigation was to examine the response of muscles to external stimulation in order to determine whether the resulting contraction was mediated by direct depolarization of the muscle membrane or whether it resulted from an induced neural action potential which stimulated the muscle via the neuromuscular junction. The scope of this investigation was limited to the specific question of whether contractions that follow transcutaneous stimulation with the Myo-Monitor result from direct muscle fiber stimulation (De Boever, J., and McCall W.D. 1972; Bessette, R.W. and Quinlivan J.T. 1973) or whether the contractions are a response to stimuli transmitted through the motor nerves (Choi, B., and Mitani H., 1973).
METHOD OF INTENSITY-DURATION CURVES
Intensity-duration testing was selected as the core method for the experiments, because it is well established and reliable: “. . . the technique that has proved most satisfactory and is in widest use is the recording of the intensity- duration relationship of applied electrical stimuli. It is a straightforward and reliable investigation. The relationship between the strength of the stimulus and its duration in time for a constant response of an excitable tissue gives an accurate measure of the excitability of that tissue.” (Lenman, J., and Ritchie, A.E. 1973).
This method is based on the observation made in 1883 by Erb (Erb, W. 1883) that has since been firmly established. That is, a long-lasting stimulus will excite both nerve and muscle, whereas a short stimulus will excite only the nerve. Hence, if a stimulus, known to be too short in duration to directly cause muscle depolarization, is applied and muscle contraction results, it can be confidently concluded that the stimulus responsible for the contraction arrived via the motor nerve.
DESCRIPTION OF THE EXPERIMENT
Subjects: The subject sample consisted of six women and four men, ranging from 20 to 60 years of age. One of the subjects was completely edentulous, and none reported clinical symptoms of T.M.J. disorders, occlusal problems, or serious muscle spasm.
Recording curves: The technique of intensity-duration recording requires that one detect the occurrence of a consistent minimal response. While detection of threshold contraction by careful palpation and inspection has been considered adequate and is the means most commonly used in intensity-duration testing, a graphic form of recording has long been sought to lend further objectivity and accuracy to the method.(Lenman, J., and Ritchie A.E., 1973) In these experiments, the mandibular kinesiograph, (Jankelson, B. et al., 1975) an instrument which electronically senses and records mandibular movement, was used to precisely measure and record a consistent amount of mandibular rise (closure). Since the amount of mandibular closure is directly correlated to the degree of muscle contraction, precise graphic recording of the amount of closure assured that a consistent contraction was elicited for each of the various stimulus duration. Throughout the investigation, for each subject and at each stimulus duration being used, the intensity of the stimulus was monitored and adjusted to produce the uniform. 0.2 mm. mandibular closure. Kinesiometric recording of consistent contraction proved to be a useful refinement in intensity-duration testing.
INVESTIGATION TO PROVE APPLICABILITY OF MYO-MONITOR
Following the same protocol as outlined earlier, a subject was sequentially stimulated through the same electrodes with a constant-voltage source, the MyoMonitor, and a constant-current source. In this manner, comparative peak currents could be measured without disturbing the electrode positions, thereby making it possible to assess the relative effect of the Myo-Monitor pulse. The peak current was adjusted for each subject to produce a consistent 0.2 mm. mandibular closure.
Page 100 Myo-monitor – Neural Mediation
A mathematical routine employing a least-squares curve-fitting program was used to match the standard intensity-duration curve to the data. As was done earlier, the data was expressed as a ratio relative to the peak current at 3 msec.
Further examination of the data leads to the conclusion that Myo-Monitor is indeed adequate for use in our investigation. Also, because even the constantcurrent stimulator did not result in a chronaxy of greater than 0.26 msec., these data alone are strong evidence for neural mediation of the current stimulus.
Data on current recordings. Peak current records from the 10 subjects are presented in Table 1. The spread in peak current values for any given pulse duration reflects the variability in anatomic configuration that is to be expected in a population. Fig. 4 expresses these data in terms of the relative stimulus intensity, which is defined as the ratio of the peak current required at a duration of 3.0 msec. (rheobase). Data displayed in this manner tend to normalize the anatomic variability without distorting the critical parameters of the experiment. The mean ratio of the population is plotted in Fig.4.
Chronaxy. The use of transcutaneous stimulation as a diagnostic aid in the determination of muscular innervation hinges on the clear-cut distinction between the excitability curves for nerve and muscle. Among the indices used to quantify intensity-duration curves is the chronaxy, which is defined as the time required for a stimulus of twice the threshold intensity (rheobase) to elicit a consistent response. A mathematical analysis (formula follows) of the data shown in Fig. 4 yields a chronaxy of approximately 0.158 msec. at a relative stimulus intensity of 2.0. Individual chronaxies for the 10 subjects ranged from 0.125 to 0.180 msec. Myo-monitor – Neural Mediation
In all 10 subjects, individual curves followed the same general hyperbolic shape with no significant discontinuities. The data were fitted with a curve of the form:
I = Io 1/(1-e^ -t/k)
where: I = stimulation current (Ma.); Io = rheobase current (Ma.); t = duration of current pulse (msec.); and k = characteristic of data (time constant, msec.).
Chronaxy values for normal muscles of the face being stimulated through their motor nerve range from 0.02 to 0.3 msec., depending primarily on the stimulator impedance. If the muscle fibers were being stimulated directly, without the transmission of the signal across the neuromuscular junction, the chronaxy value would be from 50 to 100 times greater (Fig. 5). (Watkins, A.L. 1968; Harris, R., 1971)
The intensity-duration curves reported for this study support the findings of a previous electromyographic study (Choi, B.B., and Mitani, H., 1973), that is, the muscle contraction resulting from Myo-Monitor stimulation is generated through a neurally mediated sequence. In that investigation of 15 subjects in which tiny wire electrodes were used, it was reported that, “The evoked E.M.G. was recorded from anterior portion of the temporal, the masseter, anterior ventral of the digastric, the obicularis oris and the buccinator muscles….The Myo-monitor pulse stimulates the nerve trunks of the fifth and seventh cranial nerves at the superior mandibular notch percutaneously and it appeared to have afferent and efferent effects. (Choi, B.B., and Mitani, H., 1973).
However, Bessette and Quinlivan, (Bessette, R.W. and Quinlivan, J.T., 1973) in another electromyographic study using surface electrodes, reported that they were unable to record a consistent response from the anterior temporal muscle in five subjects, and in one of the five subjects, a wire electrode inserted into the medial pterygoid muscle failed to detect myographic evidence of contraction. These investigators also measured a single latency and used that measurement to calculate what they incorrectly defined as “conduction velocity.” From that calculation and their inability to record electromyographic signals from the temporal or the medial pterygoid muscles, they concluded that neural conduction was not involved and the contraction was the result of direct stimulation of only the masseter muscle fibers.
When confronted with differing conclusions, one must look to the conditions of the experiment and the analysis of the data.
In the study by Bessette and Quinlivan (Bessette, R.W. and Quinlivan, J.T., 1973) which concluded that neural conduction was not involved, in all five subjects, the single latency was measured as the time from start of the stimulus to peak of the response. This departure from the conventional definition of latency (the time from start of the stimulus to the onset of response) produced a measurement of 3 msec., which then became the basis for their, “conduction- velocity” calculations.
To obtain accurate conduction-velocity measurements, stimulation must be done at two points along the nerve and the latency measured for each response. The distance between the two points of stimulation must then be divided by the difference between the two measurements of latency so that, in calculating the velocity, and allowance is made for the time it takes the impulse to cross the neuromuscular junction, (Watkins, A.L., 1968; Lenman, J., and Ritchie, A.E., 1973; Goodgold, J., and Eberstein, A., 1972; Johnson, E.W., 1971)
Conduction velocity = Distance/(Latency 2 – Latency 1)
A single latency, as used by Bessette and Quinlivan, (Bessette, R.W. and Quinlivan, J.T., 1973) does not give a true indication of conduction velocity along the nerve.
In contrast with peak measurement, the conventional measurement to onset of response would yield a latency of 2 msec. or less (See Bessette and Quinlivan, (Bessette, R.W. and Quinlivan, J.T., 1973) Fig. 2). The neurally mediated pathway would incur (1) a finite delay in charging dermal capacity of about 0.5 msec., (2) neural conduction time (assuming a conduction velocity of 69 M. per second over a distance of cm.) of 0.46 msec., (3) a delay of 0.3 to 1 msec. at the neuromuscular junction, and (4) an intermuscular delay dependent on electrode placement. A latency of 2 msec. (Oester, Y.T. and Light, S., 1971) is well within the expected range of a neurally mediated response.
Neither the methodology nor the analysis of the data of the investigation under discussion (Bessette, R.W. and Quinlivan, J.T., 1973) provided for recognition of neural stimulation that might have occurred. The conclusions that the nerve trunk is anatomically inaccessible to a stimulus and that only muscle fiber stimulation was involved are not warranted either by the method of the data analysis of the experiment.
With the introduction of the Myo-Monitor to dentistry, the question has arisen whether the stimulus is neurally mediated (Choi, B.B. and Mitani, H., 1973) or results from direct depolarization of only the fibers of the masseter muscle. (Bessette, R.W. and Quinlivan, J.T., 1973) Intensity-duration curves recorded for 10 subjects quantified the relationship between stimulus intensity and the duration of the stimulus required to elicit a consistent contraction response to transcutaneous stimulation vie the Myo-Monitor. Individual chronaxies ranged from 0.125 to 0.180 msec., with a mean calculated at 0.158 msec. Stimulating the muscle fibers directly, without transmission of the signal across the neuromuscular junction, would have produced chronaxy values a least 50 to 100 times greater. The distinction is clear-cut. The chronaxy values unequivocally establish transmission of the stimulus across the neuromuscular junction.
In all 10 subjects, contraction of muscles remote from the site of stimulation was evident by inspection and palpation. These data lend support to the conclusion of Choi and Mitani (Choi, B.B. and Mitani, H., 1973) that the MyoMonitor stimulates the fifth and seventh cranial nerves.
The data derived here correlate with those of other investigations and clearly establish that the transmission of the Myo-monitor stimulus is accomplished by transcutaneous neural stimulation.
Fujii, H. Evoked EMG of masseter and temporalis muscles in man. J. of Oral Rehabilitation. Vol 4, pp 291-303, 1977.
Following a percutaneous stimulation on the mandibular notch skin, two kinds of responses were recorded in the ipsilateral masseter and temporal muscles in man. The two responses had their proper stimulating points. The early response appeared with about 2 ms latency and the late one with about a 6 ms latency which was shorter than that of T wave of the same muscle by about 1 ms. No responses were induced in the contralateral masseter and temporal muscles.
Regarding the recovery process of the late response following double stimuli, a testing late response was released about 100% from the effect of conditioning shock at a longer interval that 80 95 ms. it might be safe to consider that the previous assumption, i.e. those two responses seemed to be M and H waves respectively, had been fortified. H response evoked in muscles tested seems to be sensitive enough to show the difference between excitatory states of its reflex arc.
EFFECTS OF STIMULUS ON CONTRALATERAL MUSCLES
After the upper mandibular notch skin was unilaterally stimulated, the EMG of the contralateral masseter, the anterior and posterior portions of the temporal muscles were picked up. In the contralateral muscles, however, it was impossible to record obvious responses (Fig. 5-bd) which were detected in the ipsilateral muscle (Fig. 5-a.), but with about a 10 ms latency a silent period appeared.
LATENCY OF A LATE RESPONSE
A late response and jaw-jerk (zygomatic reflex) response which is known as monosynaptic were recorded under the same condition in order to make a comparison. One example is shown in Fig. 6; fifteen late responses from each muscle tested of the same subject are shown in Table 1 in comparison with the latency of T wave (Paillard, 1955). The average latencies of late responses from the masseter and the anterior and posterior portions of the temporal muscles were 5.97 ± 0.059 ms, 6.06 ± 0.152 ms, and 6.28 ± 0.ll7ms respectively, the corresponding average latencies of T wave being 6.78 ± 0/136 ms, 6.89 ± 0.249 ms, and 6.98 ± 0.084 ms. A significant difference was observed between the latency of a late response and the latency of T wave in each muscle (p<0.001).
DETECTION RATE AND TYPE OF A LATE RESPONSE
From the above results, the early and late responses obtained were likely to be M wave and H wave respectively, in order to clarify the qualities of these responses, a study was carried out on the detection rate and type of the responses picked up from the masseter and temporal muscles.
As a result, it was understood that in the masseter and temporal muscles, the detection rate of H wave was lowered and the threshold of the H wave was mostly higher than that of M wave (high type) under resting conditions. However the H wave was easily detectable and the threshold of H wave mostly lower than that of M wave (low type) under a voluntary contraction.
When an attempt is made to induce H wave by stimulating the nerve fibres innervating the muscle percutaneously, the site where the nerve trunk is adjacent to the skin is generally adopted as a stimulating point. The masseter and temporal muscles are innervated with the masseteric nerve and the deep temporal nerve which are branches of the trigeminal nerve. Both nerve trunks are situated uppermost under the mandibular notch skin and under the anteroinferior wall of the external acoustic meatus (Shapiro, 1954; Ota, 1974). Accordingly, the mandibular notch area seems to be the most favorable position to stimulate the nerve trunks of the masseteric nerve and the deep temporal nerve percutaneously.
Even if the indifferent electrode is removed from the face surface to the brachial area there are induced two responses (Fig. 4), while when the different electrode is move 15mm from the most effective portion the above responses can be no longer recorded (Fig. 3). This obviously shows that the responses actually recorded resulted from the stimulating effects of the different electrode.
Two possibilities are considered regarding the character of the early response recorded in the current experiments; one, M wave due to stimulation of the motor fibres and the other the direct response due to stimulation of muscle fibres. It is reported that the conduction velocity of an action potential in the muscle fibre is about 35 rn/s at 37 C (Buchthal, Guld & Rosenfalck, 1955; Stalberg, 1966; Ganong, 1971), which reaches 4.7 +/- 1.3 rn/s at a voluntary contraction (Midi & Tokizane, 1967). Presently the shortest distance between the stimulating point and the leading electrode is about 4 cm in the masseter muscle and 78 cm in the temporal muscle. Thus, supposing an action potential produced by excitation on the muscle fibres at the stimulating point reaches the recording point with a conduction through these fibres, latency would be 6.67 ms for the masseter muscle and 11.67 ms for the anterior and posterior portions of the temporal muscles. But the latency of an early response which is actually induced from the masseter and the anterior and posterior portions of the temporal muscles was about 2 ms. If it is assumed that the fibres of the masseteric and deep temporal nerves are 12 am(?) in diameter (Carlsoo, 1958), their conduction velocity is about 69 rn/s (Gasser & Grundfest, 1939) and an action potential in motor fibres produced by electric shock is conducted through most of the distance between the stimulating point and leading electrode along the motor fibres, the time required for conduction is 0.58 ms for the masseter muscle and 1.01 ms for the temporal muscle. When these values are added with and end plate delay value which was assumed as 0.31.O ms (Eccles & O?Connor, 1939; Katz & Miledi, 1965; Enomoto et al., 1968) and some intermuscular delay value (McIntyre & Robinson, 1959), about 2 ms is obtained which gives good correspondence with the latency of an early response. Accordingly, this would suggest that an early response is of M wave character. The present result that an early response has a special stimulating point (Figs 3 & 4) strongly supports this likelihood.
Changes in the amplitude of a late response subsequent to an increase of stimulus show a pattern, similar to those of the H wave of the extremity muscles. Furthermore, it has been reported that the late response was free from any effects of superficial sensations around the stimulating electrode (Fujii & Mitani, 1973).
The latency of the jaw jerk known as a stretch reflex of the jaw closing muscles has ranged widely from 6.5 to 9.9 ms, depending upon individual authors (Kugelberg, 1952; McIntyre & Robinson, 1959; Goodwill, 1968; Goldberg, 1971; Munro & Griffin, 1971; Hannam, 1972). This suggests that the latency may be subject to the initial condition of the muscle and to the method of stimulation. Therefore in the current experiments a jaw jerk (Zygomatic reflex) was elicited under the same condition as a late response and recorded as T wave, in an attempt to make a comparison with the latency of a late response. The result showed a T wave with a slightly longer latency that the corresponding late response (Table 1). The T wave is a response elicited through the simplest reflex arc, and since a late response here obtained had a shorter latency than that of T wave, there seem to be two possibilities as to the nature of a late response; on F wave and the other H wave. It is said that the F wave has a higher threshold that the M wave and can be induced by supramaximal stimulus on the M wave, and that it shows a high amplitude during high excitability of the motoneuron and can be recorded from small muscles in the extremities and the Face (Dawson & Merton, 1956; Mayer & Feldman, 1967; Fra & Brignolio, 1968). However, a late response, when viewed from the recovery process of the testing late response, can not be considered to be an F wave (Mayer & Feldman, 1967) which is free from and inhibitory effect of conditioning shock at 220 ms intervals. It shows a recovery process which is similar to that found in the recovery curve of H wave (Tei, 1961) any conditioning shock effect at 8090 ms intervals (Fig. 7, left), being possessed of features of monosynaptic response. Therefore, this late response is assumed to be an H wave and its reflex arc to be composed of the neurons of the mesencephalic and motor nuclei of the trigeminal nerve.
LATENCY OF H WAVE
McIntyre & Robinson (1959) report that the human masseteric nerve is 1012.S cm long; Munro & Griffin (1971) describe the human masseteric nerve and deep temporal nerve as about 8.1 cm and 7.6 cm long, respective. The present author has measure the length between the peripheral end of either the masseteric nerve or the deep temporal nerve and the mesencephalic nucleus of the Vth cranial nerve to be 11 cm in a Japanese cadaver.
As mentioned above, if the conduction velocity of the above nerve fibres is assumed to be about 69 ms, both afferent and efferent conduction times will be about 1.6 ms. In the present study the latency of a late response was obtained as about 6.0 ms. On as assumption that a synaptic delay (Harrison & Corbin 1942; Enomoto et al., 1968) and an end plate delay (Eccles & O?Connor, 1939) are about 1.0 ms and 0.7 ms respectively, the remaining 1.0 ms or so would agree with an intermuscular delay (McIntyre & Robinson, 1959), Therefore, it seems safe to consider that the difference in latency with the T wave represents a receptor delay.
Fujii, H., and Mitani, H. Reflex responses of the masseter and temporal muscles in man. J. of Dental Research. Vol 52, No. 5, pp 1046-1050, 1973.
The H Wave represents a monosynaptic reflex potential of the skeletal muscle that is evoked after selective electric stimulation of the G I a fibers.
COMPARISONS OF LATENCY BETWEEN T WAVE AND A LATE RESPONSE
The latencies of a T wave and late response recorded from the anterior portion of the temporal muscle were about 7.0 and 6.0 msec, respectively (Fig. 4). These latencies were almost the same in the masseter and posterior temporal muscles. Thus, the T wave in all muscles always showed a slightly longer latency.
THE RECOVER CURVE
Double stimuli were given at an intensity at which a control late response showed its highest amplitude (Fig. 5a), and they were subjected to changing intervals. Our results showed 0% amplitude at intervals of less than 10 msec (Fig. 5b), 28% at 20 msec (Fig.5c), 115% at 45 msec (Fig. 5e), and 109% at 60 msec (Fig. 5f), in the masseter muscle.
A recovery curve is shown at the bottom of Figure 5. The anterior and posterior portions of the temporal muscle during medium jaw clenching showed a recovery process similar to that of the masseter muscle.
Investigations (Harrison & Corbin, 1942; Szentagothai, 1948; McIntyre, 1951; Astrom, 1953; Jerge, 1963; Kawamura, 1964) have indicated that the jaw-closing muscles of some animals are governed by monosynaptic innervation, which is the case with upper and lower limbs. At present, few investigators deny that the jaw- closing muscles in man are controlled by proprioceptive innervation monosynaptically. (McIntyre & Robinson, 1959)
Hugelin and Bonvallet, Enomoto et al, and Kawamura, Takata, and Miyoshi recorded action potentials from the masseteric nerve in animals after electric stimulation of the trigeminal mesencephalic tract (nucleus). An impulse resulting from the stimulation was conducted along the G I a fibers antidromically; another impulse descended along the motor fibers by way of a single synapse. The impulses were recorded as a direct response and a monosynaptic reflex response, respectively, in the distal site of the masseteric nerve.
Furthermore, Nakamura, Goldberg and Clemente recorded monosynaptic reflex discharge from the masseteric nerve in a cat after stimulation of the same nerve at a location more proximal that the recording electrode.
Presently, an early response from the masseter and temporal muscles seems to be identified with an M wave (base on latency and response to a gradual increase of stimulus intensity). The M wave represents a direct muscular excitation that originates from the motor nerve stimulation.
A late response, which appears mainly during jaw clenching, is considered to be different in nature from an M wave (based on its response toward a gradual increase of stimulus intensity and double stimuli). The finding that this response did not disappear even while superficial sensation around the stimulated areas was blocked indicated that the response was not a superficial reflex. It also was demonstrated that the T wave always had a longer latency, by 0.5 to 1.0 msec. than a late response. This difference may be considered to be a receptor delay. (McIntyre & Robinson, 1959)
We found that the recovery curve obtained was shifted more to the left than the recovery curve (Magladery, 1955) of the H wave obtained from some lower limb skeletal, muscles of normal individuals, the latter finding seems to be related to a rise in the excitatory state of the motoneuron pool because of a sustained voluntary contraction.
Thus, a late response seems to be reflex in nature, that is an H wave. Impulses evoked by an electric stimulation of the G I a fibers, which supply the related muscle, are transmitted to the trigeminal motor nucleus monosynaptically from the trigeminal mesencephalic nucleus; this results in the development of a reflex response (H wave).
The data in Figure 2 indicate that afferent fibers have a threshold that is lower than or equal to that of efferent fibers. Accordingly at the level of intensity at which efferent fibers are
stimulated, afferent fibers already have been stimulate; some impulses developed in efferent fibers ascend antidromically and abolish orthodromic impulses by was of G I a fibers.
Homma reported that the H wave is recorded easily during voluntary contraction, because the motoneurons already have been stimulated as a result of descending impulses from the upper center. This results in the abolishment of antidromic impulses and leads to an increase of the subliminal fringe in the motoneuron pool and facilitation of the reflex arc. His findings are supported by the present experimental data.
Based on the assumption that the distance from the stimulating site to the center of the nerve was about 11 cm, and that the conducting velocity of the nerve was 69 meters/second, the latency of a late response may be estimated as follows: Afferent and efferent conduction times are each about 1.6 msec; the synaptic delay at the center is about 1.0 msec; the effector delay is about 0.7 msec; the intermuscular delay is about 1.0 msec, which is the remaining period.
After percutaneous electric stimulation of the masseteric and deep temporal nerves, the eletromyographic response of the masseter muscle and of the anterior and posterior portions of the temporal muscle was determined.
Two kinds of response were obtained with latencies of about 2.0 msec. and about 6.0 msec. respectively. The former was assumed to be a direct potential (M wave) and the latter a monosynaptic reflex potential (H wave).
Choi, B. On the mandibular position regulated by Myomonitor stimulation. J. Japanese Prosthetic Dentistry. Vol. 17, pp 73-96, 1973.
In order to clarify the stimulating characteristics and their effects of a Myo-monitor and to investigate the mandibular position, 10 normal and 5 edentulous subjects without stomatognathic symptoms were studied. After examination of the direct output pulse and percutaneous pulse, the Myo-monitor was used according to the instruction manual. The evoke EMG was recorded from anterior portion of the temporal, the masseter, anterior venter of the digastric, the orbicularis oris and the buccinator muscles. Mandibular movement was recorded with pin-pointed miniature lamp luminograph in three dimensions.
Following the investigation of evoked EMG, it was clarified that the Myomonitor pulse stimulates the nerve trunks of the Vth and VIIth cranial nerves at the superior mandibular notch percutaneously and it appeared to have afferent and efferent effects.
The maxillomandibular relationship during the Myo-monitor stimulation (myocentric) in normal subjects coincided with centric occlusion (habitual occlusion) in 7 out of 10 subjects and three showed a slightly posterior position (0.20.4 mm) from centric occlusion, but anterior from centric relation (retruded position or terminal hinge position). In edentulous subjects without upper denture, the vertical movement distance of the mandible was gradually increase following increase stimulating intensity showing individual maximum values between 4.6 mm and 7.2 mm.
The mandibular position during the pause of stimuli, both in normal and edentulous subjects was constantly stable in a range of clinical rest position.
Williamson, E., and Marshall, D. Myo-monitor rest position in the presence and absence of stress. TM Facial Orthopedics and Temporomandibular Arthrography. ed. Williamson, Vol 3, No. 2, 1986.
The exact mechanism by which the Myomonitor affects the resting posture of the muscles is not known. One may hypothesize three mechanisms. The first might be a negating effect on the muscle spindle, inhibiting impulses from causing the muscle of the spindle from contracting and, therefore, taking tension off the nuclear bag. The might occur at either the mesencephalic or motor nuclei.
Secondly, TENS units in some way allow increase production of endorphins and enkephalins – the body?s own opiate type substances. This might decrease the effect of the reticular formation in the hypothalamus. Therefore, fewer impulses would be discharged via the descending tracts to the trigeminal nucleus and subsequently, fewer motor impulses to the muscle of the spindle, which would relieve tension on the nuclear bag.
A third hypothesis might be that the repetitive stimulus of the Myomonitor causes direct contraction of the skeletal muscle, thus causing it to relax. Dixon et al (1967) reported that repetitive electrical stimulation of skeletal muscle at a rate less than 100 times per minute reduced the accumulation of noxious byproducts and improved the physiologic state of the muscle. There have been conflicting reports in the literature regarding the method by which the Myomonitor actually causes the muscle to contract. One report suggests that the muscle contracts by direct muscle depolarization rather than by neural stimulation at the motor end plate (Bessette & Quinlivan, 1973). Therefore, such a contraction would be non- physiologic.
The antithesis to this view was presented by Jankelson in a subsequent paper (1975).
In an attempt to resolve this conflict, two patients undergoing orthgnathic surgery were treated with the Myomonitor prior to being intubated for general anesthesia. At the time of intubation, they were given succinyicholine as a muscle paralyzer. Succinyicholine acts by competing with acetylcholine at the myo-neural end plate, and therefore, no neurally stimulated muscle contraction can occur. The only way a muscle can contract under such conditions is by direct depolarization of the muscle itself. With the Myomonitor evoking electrical impulses, there was no muscle contraction either instance (Williamson and Bays, 1985). This information would support the conclusion that the Myomonitor is transmitted neurally.
LOCAL PHYSIOPATHOLOGY OF MUSCLE AND MYO-MONITOR EFFECT
The physiopatholgy of muscle pain and dysfunction is much better documented in the medical literature than the dental literature. Following are articles related to histo-chemical phenomena involved with Myo-monitor therapy.
Dixon, H. and Dickel, H.A. Tension headache. J. Northwest Medicine. Vol 66, pp. 817-820, Sept. 1967.
The electromyographic check shows a general increase in all muscle output and frequency of firing, but in the muscles served by the motor roots of the cranial nerves, and the first, second and third cervical nerves, there is increased amplitude and increased rate of firing, as one observes in a tense, fatigued muscle. If the patient has sharp pain in the supra-orbital or temporal area the myogram from muscles in these areas will often show the high pitched firing of stretched, fatigued muscle. When the tension headache is occasional, the records show variation in amplitude, but when the headache is constant or long extended, we have the rapid firing seen in the fatigued muscle.
Tension headache is actually one of the symptoms of the anxiety tension state. Rigid tightness of the neck and disturbance of the head, neck, eye reflex system are due to overflow from guarded muscles of the body. The neck muscles tighten most when the individual is alerted by an alarm mechanism. They maintain tightness until the other muscles have been released for some time. Thus muscles in the neck are tense for longer periods than are other muscles. Twenty to 30 percent reduction in the energy of these muscles, as a result of being overly tense, causes a greatly reduced speed in the relaxation phase and, as a consequence, tension fatigue spasm results.
Years ago Ranson outlined the possible connections in the nervous system that would produce these effects. His diagram (Figure 1) was remarkably correct in view of present neuroanatomical findings.
With the existence of generalized muscle guard, inflow from the skeletal muscle causes alteration in hypothalamic control, producing stress symptoms. In head and neck regions all of the muscles served by the motor roots of the cranial nerves show increase in firing that lasts for some time after the tension disappears. This spread includes spinal nerves 1 to 11. Thus the disturbance of head-neck-eye balance. Because of the constancy of overflow into these muscles the disturbances of head, neck and eye balance produce delay in relaxation from fatigue spasm, resulting in the tension-fatigue headache.
In treating the patient we teach him that control should be relaxation not tension and that the fatigued muscle will not stretch. Experimental work with the myograph and chemical analysis indicates that fatigued muscle restores its energy in light, free motion at a rate below 60 contractions per minute. Fatigue spasm can be reduced by electric stimulation. The device used should deliver a fraction of a milliampere, at around 100 volts, in a diphasic wave, at rate of 40 to 60 impulses per minute.
The tension headache can be permanently relieved by teaching tension control and by restoring energy to the muscle that is in fatigue spasm.
Examination of the patient with a severe neck spasm produced by a sudden forward-backward movement of the head, often elicits no evidence of root injury but does reveal muscle trauma.
The strain may leave a fatigue spasm that will continue indefinitely. In 70 percent of the “whiplash” cases we have checked, there has been no root injury. But, due to emotional distress and physical pain, the patient builds up adequate tension to keep the neck and some of the facial muscles in fatigue spasm. We have found that any attempt to reduce this spasm by stretching tends to increase it, but it can be relieved with conditioned relaxation, and light myopulse exercise to restore energy and thus flexibility.
Dixon, H.H., and O’Hara, M. Fatigue contracture of skeletal muscle. J. Northwest Medicine. Vol 66, pp 813-816, Sept. 1967.
Isolated muscle from the frog will develop contracture when directly stimulated at the rate of 40 impulses per minute. It will also develop contracture from chemical change, temperature change, and from trauma. Accompanying contracture, definite chemical alterations occur. In 1928, Dixon, Davenport, and Ranson, measured the phosphate fractions in muscle and showed that a sharp reduction in phosphocreatine always accompanied the change in physical state (Dixon, et al, 1929).
Contracture in mammalian muscle may be produced by rapid stimulation; interruption of cortical inhibitor fibers; chemical agents, such as tetanus toxin; inaction (casting); and trauma. In each case the chemical changes occurring in the phosphate fractions are similar. If the contracture is continued over a period of time it will become a fixed state, either in extension or flexion, defined by Ranson as myostatic contracture (Ranson, et al, 1927 and 1929; Dixon, et al, 1927).
This investigation deals with the comparative evaluation of myography, chemistry, and physical performance of the muscle.
We see this reduction…when there is protracted tension; when there are interferences in muscle function and circulation; and when there is strain or injury. In acute tension the normal cortical inhibition, which would protect the muscle from fatigue, is probably rendered inoperative by the intensity of the interference of somatic emotional function. We find in agitated, depressed people, lowered phosphocreatine, increased inorganic phosphate, and myographic findings characteristic of fatigue (Dixon, et al, 1952). The physical performance shows slowing in the relaxation phase.
In neck spasm due to trauma (whiplash) the physical state shows marked slowing of the relaxation phase, and the myographic recording shows the increased amplitude seen in fatigue spasm or, in extreme cases, in myostatic contracture. In prolonged episodes of rheumatoid arthritis the flexor muscles show the output of fatigue spasm, the extensors, the output of myostatic contracture. Myographic records from several hundred cases of tension headache show increased myographic firing in the upper third of the trapezius, and there is often a similar firing in the temporal, or other muscles served by the motor fibers of the cranial nerves and by the reticulo spinal flow.
Reduction of fatigue spasm or myostatic contracture can be accomplished by the use of compounds which increase the high energy phosphates, and by mild, rhythmic, muscle movement. With recovery of normal physical response myographic tracings are restored to normal. We believe that in conditions where there is extreme reduction of muscular energy (anxiety states- – tension headaches, muscular spasms, rheumatoid disease) the myographic evaluation of muscular energy can contribute to diagnosis, can assist in determining methods of therapy and can aid in the evaluation of therapeutic agents.
Rodbard, S., and Pragay, E.B. Contraction frequency, blood supply, and muscle pain. J. of Applied Physiology. Vol. 24, No. 2, Feb. 1968.
Repetitive contraction of an ischemic skeletal muscle is accompanies by the local development of pain which progresses to such severity that it brings the exercise to a halt (Zak, 1921). Intermittent claudication is a similar syndrome in which walking is hobbled and halted by pain or fatigue (Lewis et al, 1931).
Obstruction of blood flow does not, of itself, produce the pain sensation. The symptoms are probably not due to oxygen depletion since high oxygen concentrations in the breathing mixture to not affect the rate of development of pain (Park et al, 1962). Kissin (Kissin, 1934) suggests that the breathing of hypoxic gas mixtures can induce pain in exercising skeletal muscle. However, Lewis (Lewis, 1942) noted that lack of oxygen was an insufficient factor since arrest of blood flow to the arm for 20 minutes fails in the resting arm to produce or expedite the pain under consideration. Kissin found that pain appeared earlier in generalized hypoxemia than when air was breathed; however, the central effects of hypoxia could not be differentiated from those at the exercising muscle.
Contraction appears to be necessary for the development of pain, apparently due to a metabolite produced in association with the process of shortening. The metabolite is not a breakdown product of glycogen since patients with McArdle?s syndrome, who have a deficiency of the phosphorylase that converts glycogen to lactic acid, develop severe pain during ischemic exercise (McArdle, 1951).
The quantitative nature of the pain response to ischemic exercise offers a means for the analysis of the mechanisms involved. The quantity of the metabolite produced appears to be related to the total mechanical tension developed by the muscle, calculated as a function of the number of contractions, the load, and the duration of each contraction (Horisberger at al, 1961; Park et al, 1962).
Rasmussen, O.C., Bonde-Peterson, F., Christensen, L.V., and Moller, E. Blood flow in human mandibular elevators at rest and during controlled biting. J. Oral Biology. Vol. 22, pp 539-543, 1977.
Blood flow in the anterior temporal and masseter muscles was estimated bilaterally by local clearance of l33Xenon with the mandible at rest, during biting and in a subsequent period of rest. Activity in the same muscles during biting was measured in terms of the mean voltage of their surface electromyograms and of the bite force at first molars in the right side. During biting for 90 s at 22-37 per cent of maximal electrical activity or 45.55 per cent of maximal bite force, blood flow did not differ from that in the previous period of rest; after biting, blood flow increased about 10 fold indicating a marked post-exercise hyperaemia. During biting in the intercuspal position at above 25 per cent of full effort, blood flow was less than 15 per cent of that after contraction. The effect of biting at strengths below 25 per cent of full effort varied from almost total circulatory arrest to flow values similar to those after biting.
Pain and soreness in the muscles of mastication are significant symptoms and signs in patients with functional disorders of the chewing apparatus. Local pain may arise in ischaemic skeletal muscle during contraction (Lewis, 1942, Dorpat, 1952; Rodbard and Pragay, 1968). Both sustained contraction and rhythmic contractions at high rate may also be accompanied by local pain due to obstruction of blood flow caused by the contraction itself (Dorpat, 1952; Rodbard and Pragay, 1968).
In patients with functional disorders of the chewing apparatus, pain in the temporal and masseter muscles is associated with increase of their activity when the mandible is at rest (Lous, Sheikoleslam and Moller, 1970). Pain may arise in these muscles after experimental clenching and grinding of teeth (Christensen, 1967, 1970). Therefore, impaired blood flow due to contraction might be a source of pain in the muscles of mastication. This assumption is not ruled out, because some blood flow may continue during clenching and grinding (Bonde-Petersen and Christensen, 1973) unless the degree of muscle activity is accounted for.
Our purpose was to determine the influence of isometric contraction on blood flow in the elevators.
The right and left anterior temporal muscles and the right and left masseter muscles were studied in pairs during two separate sessions.
The electrical activity in the test muscles was picked up by bipolar surface electrodes, amplified by difference amplifiers (DISA. type 14C10) and recorded simultaneously with the mean voltage (DISA, type 14C20) on an ink-jet recorder (Siemens Mingograph EMT 1600). The degree of activity during contraction was measured as the average level of the mean voltage (Moller, 1966, 1974).
Lasagna, M., and Orland, C. Modificazione die flussi ematici muscolocutanei indotta dollo stimulazioue neurale transcutanea isichemia e dolore nella patologia occlusale. J. Odotostomatologia e Lymplantopratessi, 1986.
In the following research, 12 subjects were examined, of which 5 male and 7 female, of age comprised from 22 to 50 years. That sample of patients has presented subject with serious algic dysfunctional symptomatology in action, and others which did not present a subjective symptomatology worthy of note, also with evident occlusal alteration.
All patients were in good general condition of health and they were not at that moment under any medical therapy which could alter the cutaneous vaso-motorial response by pharmacological way.
The values of cutaneous nutritional flows were measured in correspondence of the anatomic seats of the anterior and the posterior temporalis muscles in conditions of usual rest position and after having subjected the patient to pulsation with the Myo-monitor for times sufficient to induce relaxation controlled through electromyographical evaluation at the level of the masseter and anterior temporalis muscles.
For the measurement of the haematic nutritional capillary flows, it was made use of a laser doppler velocimeter.
The average doppler frequency is linearly correlated to the haematic flow, as confirmed in vivo by studies conducted on human skin by means of the Xenon-133-wash-out technique.
Every recording was preceded by calibration for the zero. The probe was then rested on the portions of the skin under examination. The duration of the gap of measurement for every single portion examined was prolonged until the achievement of a stable recording.
The purpose of our research was to evaluate the effect of TENS stimulation on musculo-cutaneous perfusion. The functional rhythmic contractions, interrupted by gaps of relaxation do not cause pains unless the muscle is not ischemic; the pain which is determined by an ischemic muscle is called angina if it occurs in the cardiac tissue, claudicatio intermittens at the level of lower limbs. For what concern the cranium-mandibular district a similar aetiopathogenetical causal can be indicated in the determination of the painful affections typical of the MPD (myo-facial pain dysfunction). The experimental by Lewis on the muscular pain is one of the classic research of the human physiology. He disposed of a subject which put in motion an ergograph simultaneously to the state of ischemia produced by a pneumatic coupling of sphygmomanometer. The function produced pain in the time of 24-45 seconds which became very high after 60-90 seconds.
Because it seems that the painful stimulus can be accumulated, Lewis and his collaborators concluded that it could be represented by a chemical substance that arise from the process of contraction, event that is inevitably present in the occlusal pathology of disnociceptive origin. This hypothetical metabolite was denominated “P Factor”. It seems to be a normal product of the muscular metabolism, produced either in state of relax and or activity, and it seems to be able to stimulate the pain terminations only when it is accumulated in discreetly abundant quantity. Therefore it appears evident that being this substance produced by muscular contraction, which at his own time induce a reduced haematic blood flow, by the mechanical compression of the muscular blood vessels, it can be difficultly removed from the ischemic circulatory stream.
It will be creased in this way a sort of closed circle contraction – ischemia – pain, very similar and to it superimposable, to that which provocate in the states of contraction a lack of supply of oxygen and then a missed process of phosphorylation ATP-ADP.
Of the many agents which can represent the P Factor (anossia, variation of the pH, lactic acid, potassium, histamine) it can be excluded the lactic acid and the substances intermediate of the Krebs cycle. The potassium, according to Dorpat, is the more probable.
Even further studies have confirmed that the skeletal muscle is relatively poor of algoceptor nervous terminations.
Blood flow values measured after Myo-monitor pulsing in district characterized by a pathological muscular tone, are higher than those measured after pulsing in districts characterized by a physiological muscular tone.
This observation may be compatible with a phenomenon similar to that of post ischemic reactive hyperhemia.
The capillary blood flow, therefore should return in the range of normal values in a relatively short period of time.
To confirm this hypothesis, it would be necessary the blood flow monitoring, during and for several minutes after neural stimulation.
The study of a possible correlation between electromyographic and blood flow values demonstrated that these two parameters are independent under physiological situations, being the nutritional blood flow function of several different variables, like intrinsic vascular tone, muscular activity, and so on.
The chronic pathological muscular hypertone, secondary to an occlusal disease, on the contrary, induces a mechanical relative ischemia, and the blood flow becomes mainly function of the muscular tone. The relief of oro-facial pain is therefore secondary not only to a neurologic mechanism.
We demonstrated, as suggested by Yavelow et al, that mild rhyihmic muscle movement increases the local circulation of blood, which reduces the interstitial edema and accumulation of noxious tissue metabolites.
It has to be mentioned, in addition, the possible beneficial action of TENS in treating chronic pain by stimulating the production of several beta-lipoproteins with analgesic activity.
TENS action decreased EMG values at the level of anterior temporalis muscle from 3.8+1.93 to 1.6+0.43 (P, significancy index, less than 0.001).
This numerical EMG values were obtained by the printer of the Myotronics Bioelectric Processor EM2. We can see in this slide the blood flow tracings before and after Myo-monitor pulsing.
A similar result has been obtained at the level of the masseter muscle. The EMG values for this muscle has been decreased by neural stimulation from 3.6+1.71 to 0.9+0.11 (P less than 0.001).
Muscular relaxation induced a significant increase in musculocutaneous nutritional blood flows at the level of the anatomical sites of temporalis anterior and temporalis posterior muscles.
At the level of the temporalis anterior muscle the capillary blood flow showed an increase by TENS from 3.61+1.24 to 4.79+1.72 arbitrary units (P less than 0.01).
TENS produced also an increase in blood flow at the level of the temporalis posterior muscle from 2.77+1.02 to 3.84+0.94 arbitrary units. (P less than 0.05).
A significant inverse correlation was present between electromyographic and blood flow values (r, correlation index, = -0.6599; P less than 0.05) in the districts characterized by a pathological baseline muscular tone, corresponding to contraction.
In the districts with a normal physiological baseline muscular tone, on the contrary the two variables are independent.
Our study confirmed that the electrical stimulation of the 5th and 7th pair of cranial nerves induce a decrease of the electrical activity in the muscles served by these nerves. In this way a physiological state of muscular electrical activity is obtained, and in consequence, we observed a mandibular spatial repositioning, as well as an improved musculo-cutaneous perfusion. An increase in capillary blood flow in the district under exam was more evident when a base line pathological muscular tone was present.
Thomas, N.R. Spectral analysis in the pre- and post-TENS condition. TM Presented International College of Cranio-Mandibular Orthopedics, Oct. 1986.
Muscle pain is a common symptom of functional disturbances of the masticatory system. Experimentally induced hyperactivity of the masticatory musculature produces similar symptoms (Christensen, 1979; Scott and Lundeen, 1980) supporting the hypothesis that muscle pain is produced by muscle fatigue (Jankelson, 1969, 1975; Laskin, 1969; Derijk Ct al, 1977; Palla and Ash, 1981; Lindstrom and Hellsing, 1983).
Integrated electromyography (IEMG) has commonly been used as a quantitative measure of activity required to maintain a certain level of muscle tension as well as to differentiate between muscle relaxation and fatigue since it has been shown that relaxation is accompanied by minimal I.E.M.G. and fatigue by increasing I.E.M.G. as the time of fatiguing contraction progresses (Viitasalo et al, 1978). Many studies have confirmed the existence of a straight line (or proportional) relationship between muscle force and integrated E.M.G. (Inman et al, 1952; Lippold, 1952; Edwards and Lippold, 1956; Bigland and Lippold, 1954; Milner-Brown and Stein, 1975).
Indeed it has been demonstrated by McKenna and Turker (1978) that the IEMG will reduce as the jaw opens for a fixed muscle tension or constant load (see also Nordstrom and Yemm, 1974). So a decrease in E.M.G. activity is not necessarily a true indicator of elevator muscle relaxation if the jaw is simultaneously opened. Nor is the increase in jaw opening necessarily an indicator of muscle relaxation since this may also occur in muscle fatigue.
Thus without satisfactory evidence to the contrary it may be argued that T.E.N.S., rather than producing relaxation, fatigues the masticatory musculature so that as the load of the mandible opens the jaw there is a reduction in E.M.G. activity as a result of lengthening of the fatigued muscle.
Fortunately there is a simple procedure that can be used to directly test the effect of T.E.N.S. on fatigued masticatory musculature.
In 1912 Piper (Piper, 1912) observed that the peak frequency of the myoelectric signal decreases during fatiguing muscular contractions. Since that time it has been repeatedly shown that fatigued muscle is accompanied by a decrease in the frequency of its EMG activity causing the peak power frequency spectrum to shift to lower frequencies (Chaffin, 1969; Kwatny et al, 1970; and Viitasalso and Komi, 1978). Indeed Palla and Ash (1981) and Lindstrom and Hellsing (1983) demonstrated a similar shift in peak frequency for fatigued masticatory musculature.
It has also been shown by Vrendenbregt and Rau (1968) that a shift in the spectral peak of E.M.G. frequencies during fatigue is only minimally affected by electrode orientation or muscle elongation. Hence it was decided to test the hypothesis that T.E.N.S. does produce muscle relaxation and not muscle fatigue by utilising spectral analysis of elevator E.M.G. on normal and T.M.J. patients pre and post T.E.N,S.
Subjects were seated in a dental chair with the Frankfurt plan kept horizontal. Threshold transcutaneous electroneural stimulation was applied with a pulse duration of 500 u sec., at 1 1/2 sec intervals to the preauricular region overlying the masseteric notch. M.K.G. and E.M.G. instrumentation was applied as defined in the Myo-tronics manual with the addition of gnathodynamometry for force monitoring.
EMG recordings were made prior to TENS stimulation while the subject was at rest for 20 minutes with a measurable freeway space varying between 2.2 and 3.1 mm. The subject was then required to maximally clench (MVC) for 10 sees while EMG magnetic tape recordings were taken using a Sony taperecorder (T.C. Fx600). Finally the subject was asked to maximally clench until fatigue developed. A further ten second tape recording was taken. The subject was then provided with 20 mins of TENS as described above. This procedure was repeated a second time with the exception that 20 minutes rest replaced the TENS treatment.
The I.E.M.G. was seen to increase with the patient?s expression of increasing fatigue. As fatigue developed the spectral peak density gradually shifted from 125 Hz at rest to 75 Hz (Fig. 1). Twenty minutes of TENS like rest restored the spectral peak to 125 Hz for normal control subjects with sharper discrimination (Fig. 2).
However for T.M.J. subjects it was observed that for both the pre and post fatigued condition the frequency spectrum peaked at 75 Hz (Fig. 3). No amount of rest or wearing of a Lucia jig splint could restore the peak to normal relaxed levels (Fig. 4). T.E.N.S. however succeeded in relaxing the musculature of the T.M.J. masticatory system shifting the spectral peak from 75 Hz to 125 Hz.
It is clear that masticatory musculature of T.M.J. subjects as opposed to non-T.M.J. subjects exhibits fatigue. Rest alone does not resolve the masticatory muscular fatigue. It was also found in another set of experiments that rest with a Lucia jig also fails to eliminate the fatigue.
T.E.N.S, however does resolve the fatigue of normal and T.M.J. subjects. The failure of rest to restore normal muscle activity suggests that masticatory muscular fatigue includes a metabolic deficiency such as relative ischemia which cannot be resolved by rest alone (Mortimer et al, 1970; Kovacs, 1942; Stephens and Taylor, 1972; Merton, 1954). T.E.N.S. may act by improving muscle function though removing muscle metabolites and/or reversing muscular ischemia. Further studies are underway to answer this question.
We therefore have in E.M.G. spectral analysis a relatively simple method for assessing the presence or absence of muscle relaxation or fatigue as well as providing a ready procedure for objectively analysing treatment modalities. Certainly T.E.N.S. is effective in resolving masticatory muscle fatigue exhibited in both normal and T.M.J. dysfunction subjects.
MYO – MONITOR EFFICACY
Following are articles supportive of the Myo-monitor (i.e. low frequency TENS) efficacy in treatment of TMD. The controlled studies of Pantaleo and Prayer- Galletti are of particular interest.
Pantaleo, T., Prayer-Galletti, F., Pini-Prato, G. and Prayer-Galletti, S. An electromyographic study in patients with myofacial pain-Dysfunction syndrome. Bull. Group. mt. Rech. Sc. Stomat. et Odont. Vol. 26, pp. 167-179, 1983.
Recently dental research has turned to neuro-muscular system: many dental procedures, in order to be entirely successful, require that the masticatory muscles are relaxed and perfectly balanced. The use of the transcutaneous electrical nerve stimulation (TENS) has been introduced, obtained with adequate stimulators, such as the Myo-monitor (Myo-tronics) (Jankelson 1975, Jankelson 1978, Wessberg 1981): TENS has been able to relieve pain and eliminate the sustained muscle tension of the masticatory muscles of patients with myofacial pain-dysfunction (MPD) syndrome (Laskin 1969), combined with occlusal malrelation, which may be the primary cause of MPD syndrome (Lindblom 1953, Ailing 1977).
Mandibular Kinesiography (MKG) (Jankelson 1975) records the position and the movements of the jaw and studies objectively the occlusal malrelations and their corrections which in many cases are achieved by means of acrylic splints which lead to the orthodontic and/or the prosthetic treatment for a stable resolution of the syndrome (Jankelson 1979).
The mandibular rest position is an important starting point for dental treatment. In normal subjects, in an upright position with the lips slightly in contact but the teeth not together, during the voluntary muscle relaxation, there is virtually no activity in the masticatory muscles investigated (Vitti 1975, Vitti 1977), except for the subjects with occlusal interferences
Therefore, in accordance with Jankelson (Jankelson 1979), the mandibular rest position seems to be determined by passive factors and it is in that balanced state that all the muscles are relaxed at their resting lengths. In the rest position so defined, the normal freeway space recorded with the MKG, is about 1-2 mm; the most favorable situation for the intercuspation is achieved when the jaw moves from the rest position through the interocclusal space for about 1-2 mm on the isotonic relaxed trajectory obtained with the Myo-monitor pulsing (Jankelson 1979). In normal subjects, the voluntary fast closure of the jaws follows this isotonic relaxed trajectory or a trajectory very near to it. If the intercuspation is placed away from the relaxed trajectory, in order to have the same fast movement of closure, it is necessary that the masticatory muscles adjust themselves to avoid excessive variations and corrections.
MKG recordings show that the occlusal position determines that postural adjustment (adaptive holding position) and a different trajectory, too (Jankelson 1979). Such an adaptive holding position could be maintained by neuromuscular spindles which are particularly plentiful in the jaw closing muscles (Voss 1935, Freimann 1954, Cooper 1960) which show stretch reflex responses that are absent in the jaw opening muscles (Hugelin 1956, McIntyre 1957, Hannam 1972, Lamarre 1975, Neilson 1979). Therefore a wrong occlusion appears to program an abnormal muscular activity at rest and abnormal patterns of muscle contraction during the mouth closure with trajectories which are different from the isotonic relaxed one. The prolonged and/or abnormal muscular activity can cause muscular pain (Rodbard 1968, Miller 1979) which in turn provokes motor reflexes so that a vicious circle may be established (Zimmermann 1979): that could be the basis of the MPD syndrome.
The relationship between the electromyographic (EMG) activity of the masticatory muscles and some types of malocclusion has been investigated by earlier researchers (Moyers 1949, Liebman 1960, Moss 1965, Grosfeld 1965, Ahlgren 1966, Ahlgren 1973, Moss 1974, Moss 1975, Pancherz 1980), chiefly regarding temporalis and masseter muscles.
Chaco (Chaco 1973) has reported that the levels of EMG activity of the masseter muscle in patients at rest are higher than the levels in healthy volunteers; there is also evidence that those patients showed an excessive activity of the masseter muscle under stress (Yemm 1969, Thomas 1973)
The present EMG study was undertaken in order to attempt to clear up some aspects of the pathogenesis of the pain and of the muscular dysfunction induced by occlusal malrelations. Preliminary results have been previously presented (Pantaleo 1980).
The subjects studied were 5 healthy volunteers (3 males and 2 females aging from 19 to 38 years) and 11 MPD syndrome patients (6 males and S females ranging in age from 20 to 42 years) who gave their informed consent to the experimental procedures. All the subjects were recorded with Jankelson?s Mandibular Kinesiographs (Model K5R, Myo-tronics). The EMG was recorded from the temporalis and the masseter muscles of the same side of the body with cup surface electrodes (8 mm diameter) filled with electrode jelly and fastened to the skin with adhesive strips
The electrical activity of the muscles was amplified (Tektronix 2A61 AC differential amplifier) and displayed on a double beam oscilloscope (Tektronix 565) and monitored by an audiomonitor (Grass AM4B). Muscle action potentials were full-wave rectified and integrated (IEGM) over time (low-pass filter, time constant 100 ms) in order to provide a one-directional integrated trace describing the time course of EMG events. Furthermore, the IEMG may allow a more quantitative evaluation of muscular activity (arbitrary Units). The integrated activity was fed to the same oscilloscope after amplification (Tektronix 3A74 Amplifier). The photographs were taken with a Kymograph camera Grass C4.
The EMG activity was studied both at rest (with the subjects sitting in an easy and comfortable upright position in an adjustable chair, with their masticatory muscles relaxed, their lips slightly in contact but their teeth not touching and during the maximal biting in the intercuspal position. The EMG study was repeated after the application of TENS in all tested subjects and also after the correction of the occlusal malrelations only in patients with MPD syndrome.
The TENS was applied for periods varying from 10 to 30 minutes in order to achieve muscle relaxation using the Myo-monitor (J3 Model, Myo-tronics).
The correction of the occlusal malrelation was performed with the application of acrylic splints built according to the Myo-monitor procedure (Jankelson 1978, Jankelson 1979) and by checking with the MKG analysis.
Control subjects. In the asymptomatic controls, the Kinesiographic analysis showed a normal vertical dimension (1-2 mm), and a voluntary closure trajectory which corresponded to or was very close to the relaxed trajectory obtained with the Myomonitor. No significant increase in the freeway space was found in control subjects after 20.30 mm of Myo-monitor pulsing.
During the rising of the mandible from rest position only the temporalis muscle presented noticeable EMG activity before the contact of the teeth.
Patients with MPD syndrome; on the MKG analysis they showed the following alterations: 1) difficulty in relaxation; 2) decrease of vertical dimension; 3) abnormal posterior displacement of the jaw during closure; 4) closure trajectory from rest position to centric occlusion different or continually varying from the relaxed trajectory.
The EMG study revealed an involuntary muscular activity at rest in the anterior portion of the temporalis muscle in all tested positions. After a voluntary contraction in the EMG activity came back slowly to the previous levels showing a delay in muscle relaxation. The TENS application for 20-30 mm. produced a remarkable pain relief and caused the disappearance of the involuntary activity at rest; nevertheless a single mouth closure with the teeth in contact was sufficient to cause a resumption of the sustained EMG activity.
The pain and the combined symptomatology of the MPD syndrome also appeared again more slowly in a period varying from only a few to 24 hours.
When the occlusion was corrected with acrylic splints in order to reach normal MKG recordings, the EMG patterns also improved: the involuntary EMG activity greatly decreased and sometimes disappeared after the splint was applied TENS induced a better relaxation even after the occlusal correction. Under these conditions, the closure of the mouth even if repeated several times showed a very little tendency to induce again an abnormal EMG activity at rest.
All MPD patients displayed abnormal EMG patterns during the maximal biting in the intercuspal position, i.e., the EMG activity during the voluntary contraction increased slowly to a low maximum level that was not maintained (progressive decrease of activity).
After the correction of the occlusal malrelations with splints, EMG patterns improved and appeared more similar to those of control subjects: the activity increased more quickly to a higher level than was maintained during the voluntary contractions (plateau).
In the mandibular rest position normal subjects with normal MKG tracings did not show any EMG activity in the masticatory muscles investigated according to previous research (Vitti 1975, Vitti 1977, Voss 1935). This fact confirms the hypothesis that the mandibular rest position is determined by passive factors (Jankelson 1979). The abnormal involuntary activity found in patients with occlusal malrelations together with MPD syndrome, especially in the temporalis muscle which is the most important for posture, confirms previous observations (Funakoshi 1976, Chaco 1973): this activity seems intense enough to cause muscular pain and a vicious circle leading to the MPD syndrome (Miller 1976, Rodbard 1968, Miller 1979, Zimmerman 1979). The TENS performed by the Myomonitor is able to achieve muscular relaxation and pain relief (Jankelson 1978): the MKG and the EMG, as shown by the present results, give evidence of such muscular relaxation.
The TENS effects can be explained by various mechanisms and those in the Central Nervous System (CNS) seem to be the most important (Elzak 1979, Andersson 1979).
The Myo-monitor TENS seems similar in some aspects to the one previously used by other authors in the facial area (Andersson 1979, Andersson 1977, Andersson 1977) which was able to give analgesia especially if intrasegmental and causing muscle contraction (electro – acupuncture).
Nevertheless, the TENS has temporary effects because it does not eliminate the primary cause hypothesized for the MPD syndrome (Lindblom 1953, Ailing 1977); the mouth-closing in MPD patients reestablishes the abnormal EMG activity, suggesting an abnormal involvement of the periodontal and/or muscular afferent activity. Therefore, present EMG observations support Jankelson?s suggestion that the adaptive holding position of the jaw is determined by the occlusal position (Jankelson 1979).
The decrease of the abnormal EMG activity after the correction of the occlusal malrelations with acrylic splints confirms this interpretation and points out that an occlusal discrepancy can be the cause of an abnormal EMG activity and of the consequent MPD syndrome.
These observations agree with the hypothesis that the MPD syndrome pain is due to a muscular hyperactivity (Yemm 1976) and that is possible to obtain the same clinical signs of the MPD syndrome placing the muscles of mastication under stress by fitting healthy volunteers with a complete set of dentures that had faulty occlusion (Brill 1962)
The abnormal EMG patterns during maximal biting in the intercuspal position without the splint correction indicate that the occlusal malrelations induces some alpha motoneurones inhibition; this may originate from dental and periodontal receptors abnormally stimulated in consequence of the occlusal malrelations (Bratzlavsky 1976). Similar observations were previously reported in children with malocclusion (Pancherz 1980).
In conclusion, the EMG study of the masticatory muscles combined with the MKG analysis seem to be a useful tool for studies on the pathophysiology of the stomatognathic apparatus; this approach may be also useful from a diagnostic and therapeutic point of view.
An electromyographic (EMG) study of ipsilateral masseter and temporalis muscles was undertaken in healthy volunteers and in patients with MPD syndrome, with the aim of getting further insight into the pathophysiology of this disease. Unlike controls, patients had abnormal MKG features and displayed involuntary sustained EMG activity at rest, chiefly in the temporalis muscle.
Transcutaneous electrical nerve stimulation (TENS) performed with the Myo-monitor induced relaxation and relief of pain; these effects were however reversed by voluntary mouth closures.
The correction of occlusal position by acrylic splints was able to induce a persistent reduction or a suppression of the abnormal EMG activity at rest and a good relief of pain; moreover, after the correction, higher levels of EMG activity were found during maximal biting in the intercuspal position.
Mechanisms underlying these effects were discussed and in particular it was suggested that abnormal afferent activity from periodontium and jaw muscles may contribute to the establishment of sustained contraction leading to muscular pain, which in turn may cause reflex muscle activity in a vicious circle.
Wessberg, G.A., and Dinham, R. The Myo-monitor and the myofacial pain dysfunction syndrome. Journal of the Hawaii Dental Association. Vol 10, No. 2, Aug. 1977.
The Myofacial Pain Dysfunction Syndrome (MPD, TMJ Syndrome, Craniocervial Syndrome) has plagued dentistry for many years. Therapy for this type of pain has been highly imaginative. A few of the more common modalities mentioned (Ramfjord 1971) are occlusal adjustment, occlusal bite splints, immobilization of the mandible, drug therapy, placebo, diathermy, physical therapy, sclerosing agents, psychotherapy, and surgery. Recent studies of mandibular movement (Jankelson 1976) stress the importance of a “muscularly oriented occlusal position” for the treatment of the MPD Syndrome.
Jankelson (Jankelson 1976) assumes a compromise in these trends of thought actually exists. He describes a relatively precise PRPM at any given stage of development that fluctuates within a minimal range of normal as determined by states of equilibrium within the mandibular musculature.
The postural rest position of the mandible (PRPM) is by definition (Academy of Denture Prosthetists, Glossary of Prosthetic Terms, 1956) the mandibular position assumed when the head is in an upright position and the involved muscles, particularly the elevator and depressor groups, are in equilibrium in tonic contraction, and the condyles are in a neutral, unstrained position.
The Jankelson Myo-monitor was the instrument used to obtain the myocentric position in patients presenting with symptoms associated with the MPD Syndrome. As described in the instruction manual, (Myo-monitor Instruction Manual, 1976), the Myo-monitor delivers a 2 millisecond impulse at 1.5 second intervals to the motor centers of the fifth and seventh cranial nerves. These mild, repetitive impulses are applied via extra-oral surface electrodes to relax the mandibular musculature and result in a highly controllable closure devoid of proprioceptive influences.
Thirty patients ranging in age from 14 to 56 years and in satisfactory physical condition were treated for symptoms associated with the MPD Syndrome. Among the symptoms were complaints of pain in the neck, ears, TMJ, and facial musculature. TMJ crepitus, dental hypersensitivity, and mandibular hypomobility were also present in a few cases. Tomogram radiographs were taken of the TMJ to rule out possible joint trauma or degeneration. Diazepam (Valium) was prescribed for selected patients to alleviate anxiety and facilitate muscle relaxation prior to Myo – monitor therapy.
The treatment results achieved in the Facial Pain Clinic for thirty patients from June 1976 to June 1977 can be seen in Table I. Symptoms were recorded as being present or absent. Treatment was considered complete if Myo-monitor therapy was rendered and occlusal adjustment or splint resulted in a remission of symptoms though the patient didn?t return for definitive follow-up care. The results are termed positive in cases where there was improvement or complete remission of the presenting symptoms. Recalls are termed in a similar manner.
Thirty patients presented symptoms associated with the Myo-facial Pain Dysfunction Syndrome. All of these patients received Myo-monitor oriented therapy and nearly all of them professed some initial relief or total remission of their symptoms during the short time span of this study.
The data presented is based largely on clinical observations and patient response to comparison of their symptoms before and after treatment. Symptoms evaluated were generally related to muscle tenderness and mandibular mobility.
Due to clinical observations and patient response in this investigation, it is concluded that:
1. The centric occlusion position is seldom coincident with the myo-centric position of occlusion in patients who exhibit symptoms associated with Myofacial Pain Dysfunction Syndrome.
2. A Myo-monitor generated occlusal position affords some relief if not complete remission of symptoms in 90% of cases treated.
3. Long-term follow-up studies are necessary to evaluate the success of treatment.
Wessberg, G.A., Carroll, W.L., et al. Transcutaneous electrical stimulation as an adjunct in the management of myofascial pain- dysfunction syndrome. The Journal of Prosthetic Dentistry. Vol 45, No. 3, March 1981.
The beneficial effects of Transcutaneous electrical stimulation may include neurologic, physiologic, psychologic, and pharmacologic mechanisms
Physiologic: Dixon et al. (Dixon 1967) reported on the physiologic aspects of repetitive, electrically induced depolarization of mammalian skeletal muscle. They demonstrated that repetitive depolarizations of skeletal muscle at a rate less than 100/mm in the presence of an adequate supply of high-energy phosphate reduces fatigue contracture. Yavelow et al. (Yavelow 1973) suggests that mild, rhythmic muscle movement increases the local circulation of blood and lymph, which in turn reduces the interstitial edema and accumulation of noxious tissue metabolites. Wessberg et al. (Wessberg, submitted for publication at date of this article) have demonstrated that repetitive, transcutaneous stimuli to the preauricular areas of the face of normal individuals causes a generalized reduction in the resting electromyographic activity of the muscles of mastication. The improved physiologic state of the muscle apparently promotes a reduction in spasm and pain. (Trott 1978, Yavelow 1973).
Pharmacologic: The present study was designed to evaluate the clinical effectiveness of a neuromuscular approach to the management of individuals with MPD syndrome which includes TES to the preauricular areas of the face and the creation of a stable neuromuscular-induced occlusal position.
MATERIAL AND PROCEDURE
Twenty-one patients were selected during a given time period and treated in the Facial Pain Clinic at the Queen?s Medical Center for symptoms of MPD syndrome. Seven men and 14 women, ranging from 16 to 59 years of age, were chosen. All were in generally good health, presented with complete or partially edentulous dentitions, and complained of having had facial pain symptoms for up to 1 year. Seventeen of these patients had been treated by various methods prior to referral. The diagnosis of MPD syndrome was made by clinical and radiographic evaluation.
Radiographs: An orthopantomograph, a dental radiograph unit, and a tomography Unit in the hospital were used to complete a thorough, radio-graphic evaluation to rule out pathologic conditions in the maxilla, mandible, TMJ, and dentition.
TES: The Jankelson Myo-monitor (Model 32) is a solid state electronic unit designed to eliminate occlusal proprioceptive influences in the mandibular musculature via TES. An externally mediated electrical stimulus of 2 msec duration at 1.5-second intervals is directed to the preauricular areas of the face. These stimuli result in a highly repetitive, isotonic mandibular closure devoid of proprioceptive input from the periodontium.
Occlusal splints: Temporary occlusal splints were fabricated when indicated with Myo-Print Sapphire acrylic resin. The technique involved a direct intraoral interocclusal registration with the mandible closing from a relaxed, muscularly determined postural rest position generated by TES
With the patient seated in an upright position, electrodes were placed bilaterally over the sigmoid notch area as directed by the instruction manual. The impulse was balanced. A minimum of 45 minutes of TES at a threshold level was completed.
Following initial examination and consultation, the patient?s clinical symptoms were recorded as shown in Tables I through IV. Treatment sessions were conducted as follows:
First appointment: TES Therapy was performed as described. Alginate impressions were made of dental arches for diagnostic casts, if possible.
Second appointment: TES therapy was followed by direct, intraoral occlusal record as determined by TES at a stimulation level one above threshold. Evaluation of the interocclusal relationship was done to determine if implementation of a temporary occlusal splint or occlusal adjustment was indicated. The goal of adjustment was to provide free entry of the teeth into a stable occlusal position as determined by a relaxed musculature.
Subsequent appointments: TES therapy was repeated at subsequent sessions followed by necessary occlusal adjustments of the splint or dentition until a stable position was achieved. When the patient and clinician were satisfied with the results of therapy, the dental casts were mounted on an articulator and definitive treatment was discussed with the patient. For those patients on whom an occlusal splint was used, observation for a minimum of 1 year was suggested before treatment such as orthodontics, dental reconstruction, or surgical-orthodontic procedures were performed.
Treatment results were grossly subjective, based primarily on the patient?s comparison of the pre-treatment symptoms with their status 1 year after treatment. Objective evaluations by the clinician included a comparison of muscle tenderness, TMJ noises, and mandibular range of motion. Overall treatment was assessed as being either positive (indicating improvement) or negative (indicating no improvement).
Treatments used for these 21 patients included TES for all patients, semipermanent occlusal splints for 16 of the patients, and occlusal adjustment for four of the patients. Immediate post-treatment results showed 20 positive responses and one negative response, a male with severely abraded dentition due to chronic bruxism. This is a 95% success rate.
One-year post-treatment reevaluation of the 21 patients yielded 18 positive and three negative responses. All three negative responses were women. The man with the immediate post-treatment, negative response noted improvement 3 months after insertion of the occlusal splint. This demonstrates an 86% success rate after 1 year. In the case of the three negative responses, all of which were helped initially, lack of success may be due to the fact that two of these patients discontinued the use of the occlusal splint and complained of the high cost of therapy. The third unsuccessful patient received occlusal adjustment only and discontinued therapy. In all three patients, the pain was low-grade in nature and did not significantly limit the patient?s activities.
The results of treatment in Table V show that 10 of the 11 patients treated with semipermanent occlusal splints obtained favorable results
This study evaluates the immediate and long-term results of a muscularly oriented treatment regimen for symptoms of the MPD syndrome. Data obtained from post-treatment evaluation of 21 patients treated with TES demonstrated a success rate of 95% immediately and 86% after 1 year. Our data demonstrated a very high incidence of lateral pterygoid muscle dysfunction (85.7%). This suggests that discrepancies in the transverse and anteroposterior position of the mandible relative to centric occlusion are not well tolerated. Elimination of these discrepancies in maxillomandibular relations via TES and occlusal adjustment or occlusal splint placement appears to promote the long-term relief of muscle symptomology. Attempts should be made to eliminate the splint after the patient becomes asymptomatic for 30 days, as many individuals may function satisfactorily in their existing habitual occlusion once the myospasms subside. Comparison of these results with other reports in the literature is quite favorable. However, few authors present data of long-term follow-up for other treatment modalities.
Boschiero, R., Fraccari, F., and Pagnacco, O. Analysis of the results of the use of the Myo-monitor in patients with reduced mouth opening. MM. Stom. Vol 35, pp 857-864, Sept. 1986.
Fifteen young patients with markedly reduced mouth opening (less than 26 mm) with no severe articular alterations revealed by radiography were subjected to treatment with a Myo-monitor. The mouth opening was measured during stimulation and the data analyses mathematically. The treatment was effective in all cases. In the worst cases the opening was increased by 33.33% and the mean was 87.87%. The mean curve of increase over time showed altering phases of rapid advance and plateaux. The first stage, lasting about 45 minutes constantly produced almost no increase.
Konchak, P., Thomas, N., Lanigan, D., and Devon, R. Freeway space measurement using mandibular kinesiograph and EMG before and after TENS. The Angle Orthodontist October, 1988, pp 343-350.
Lack of knowledge about how physiologic influences bear upon the morphology of persons treated with orthodontics or orthognathic surgery both before and after treatment places clinicians in an unenviable position with respect to sound diagnosis, treatment planning, and prognosis. Although it is well recognized that the morphology of the craniodentofacial complex has functional influences (Schudy 1964, Sassouni 1969, Paolini (1970), the physiologic parameters influenced by morphology are still not well understood. This investigation expands on a previous pilot study (Konchak et al. 1986) concerned with the identification and correlation of certain morphometric and physiologic properties of the cranio facial complex related to mandibular rest position.
Vertical positioning of the maxillary and mandibular dentitions is dependent on the equilibrium between intrusive environmental forces and the eruptive forces of the supporting tissues acting on the teeth. This balance may be affected by a myriad of factors and variables involving bone, teeth, and soft tissues, including therapeutic efforts such as orthodontics and orthognathic surgery.
Orthodontists and maxillofacial surgeons have traditionally approached these relationships using descriptive methods based on clinical examination and cephalometric and/or dental cast analyses. As these emphasize static rather than dynamic factors, the physiology of the stomatognathic system, and in particular the neuromuscular system, often receive little attention.
A patient?s resting vertical dimension, including the freeway space (FWS), is essentially an adaptive physiologic parameter (Mohl 1978, McNamara Ct al. 1978). Rest position has been defined as the neutral rest position attained by the mandible as it is involuntarily suspended by the reciprocal coordination of the elevator and depressor masticatory muscles with the upper and lower teeth separated (Niswonger 1934). McNamara et al. 1978 state that rest position is influenced by the activity of the fusimotor system of the elevator muscles through psychic input, and through stimuli from peripheral receptors such as those located in the temporomandibular joint, periodontal ligament, gingiva, tongue and palate.
Jankelson (1977) has described adaptive and true rest positions of the mandible, and thereby adaptive and true freeway spaces. Adaptive freeway space is defined as the interocclusal space that exists when the patient is instructed to voluntarily allow the jaw to relax. True freeway space is the interocclusal space present after relaxation of the masticatory musculature has been achieved, such as occurs following transcutaneous electrical nerve stimulation (TENS) with a myomonitor.
A relaxed muscle is defined as one that is neither contracted nor stretched (Ganong 1985). At this physiologic resting length the muscle is capable of exerting maximal force and maximal velocity under isometric and isotonic conditions respectively. This capability has been explained by the sliding filament theory of muscle contraction which postulates that the maximal availability of cross-bridge reactive sites is present at a muscle?s physiologic resting length (Huxley 1969).
That masticatory muscle relaxation is achieved following transcutaneous nerve stimulation to the motor division of the trigeminal nerve is confirmed by post-TENS reduction in electromyographic activity, and by an increased muscle response in both force and velocity to electrical stimulation at threshold levels. A spectral analysis of voluntary isometric contraction reveals that fatigue is resolved and not induced by TENS. The power density spectrum frequency maximum shifts from a fatigue level of 75Hz to a relaxed level of 125Hz (Thomas 1987). Comparisons between muscle velocity, force dynamics, and electromyographic spectral analyses confirm that an electrical noise level below 15UV indicates the attainment of physiological resting condition of the masticatory musculature.
After reviewing the results of the pilot study, it was felt that a similar study should be repeated utilizing a larger sample size, and including EMG investigation. The purpose of this research project was to:
1. Determine the percentage of patients who achieved masticatory muscle relaxation following TENS stimulation.
2. Compare adaptive and true freeway spaces.
3. Correlate adaptive and true freeway space values with cephalometric parameters that describe the vertical dimension of the face and facial proportions.
4. Compare freeway space with the Angle classification.
Sixty-two patients seen at the University of Saskatchewan for orthodontic treatment were selected for participation in the study. No criteria for selection were used except that they had to have a natural dentition and be free of symptoms suggestive of temporomandibular joint dysfunction.
Lateral cephalometric radiographs were obtained for each patient with the Frankfort plane horizontal, and with the mandible in the centric occlusion position. From these cephalographs the sellanasion / mandibular plane angle (S N/MP) and percentage nasal height values were measured to represent common descriptive measurements of the patient?s vertical dimension.
Subjects were seated in a chair and transcutaneous electrical nerve stimulation instrumentation applied utilizing the protocol established by (Jankelson 1977, Jankelson and Radke 1978 and Jankelson 1981). This consisted of the myomonitor, mandibular kinesiograph (MKG) (Myotronics Corp. Seattle, Washington). This is illustrated in the pilot study (Konchak et al. 1987). The surface EMG electrodes were applied over the right and left temporalis and masseter muscles in strict accordance with Jankelson?s methodology (1981).
EMG recordings were made prior to TENS stimulation, and the adaptive freeway space was measured from the prepulsed vertical dimension of the occlusion. Subjects were then given a minimum of 40 minutes of TENS immediately prior to recording true freeway space values.
It has previously been established by Thomas (1986) that the masticatory muscles are reliably relaxed at EMG values of 14 UV or less, so this EMG criterion was used to group the patients into relaxed and non-relaxed categories.
Four categories of patient groups were established on the basis of the above criteria:
Type A – relaxed before and after muscle stimulation
Type B – not relaxed before or after muscle stimulation
Type C – not relaxed before, but relaxed after muscle stimulation
Type D – relaxed before, but not after muscle stimulation
The average freeway space value before the muscle stimulation was 2.6mm, and after the stimulation it was 3.4mm. These values in the pilot study were 1.8mm before and 2.9mm after stimulation. S-N/MP averaged 33.4 ÷/- 6.9o, and the percent nasal was 45.4 +/- 2.0%.
It is interesting to note that Group D, albeit a very small sample size, was the only group where the average FWS decreased after TENS. This was the group that demonstrated increased muscle activity after muscle stimulation.
Jankelson (1981) has previously discussed the fact that freeway space has not only a vertical but also an anteroposterior component. He found the A/V (anterior to vertical) ratio to be 1:2, whereby a closing trajectory of the mandible results in a 1mm anterior movement in conjunction with 2mm of vertical movement. This study found an A/V ration of 1:1.8 (r=.72), confirming Jankelson?s findings.
SUMMARY AND CONCLUSIONS
Four categories of relaxation of the masticatory musculature were determined in patients before and after TENS. 58% more patients achieved masticatory muscle relaxation after TENS (50% before, 79% after). The average freeway space measurement increased after TENS. Differences for individual patients in their pre- and post-stimulation freeway space values, however, could be either positive or negative, as some experienced an increase in masticatory muscle activity following TENS stimulation. Clinical and true freeway space values are inversely correlated with the SN/MP angle, but the correlation values are low. Angle classifications were not correlated with freeway space.
S-N/MP angle and percentage nasal height were inversely correlated. No correlation was found between percentage nasal height and FWS. Descriptive factors obtained from cephalometric measurements such as percentage nasal height and S-N/MP angle can be useful in diagnosis and treatment planning, but these values must be correlated with the clinical examination. Previously accepted and unchallenged concepts of freeway space and vertical dimension such as those postulated by Guichet (1970) and Lindegard (1953) were not borne out by our application of kinesiographic technology. In applying FWS values as an aide to orthodontic diagnosis and treatment planning, individual patient values are of greater significance than are group averages. In ongoing studies, individual patient?s freeway space before and after treatment are being investigated to see whether this parameter is important in influencing the ultimate stability of the occlusion.
Bazzotti, L. Electromyography tension and frequency spectrum analysis at rest of some masticatory muscles, before and after TENS. Electromyogr Clin Neurophysiol. 1997 Sep; 37(6):365-78.
On a population of 52 subjects surface electromyographic recordings were performed of 13.5 sec. of duration before and after ULF (Ultra Low Frequency)-TENS relaxing procedure, while they were holding their mandible at rest. For each recording the average of tension (IEMG) and the median of frequency was calculated. To compute the median of frequencies a Fast Fourier Transformer (FFT) was applied. In order to compare modifications induced by the 45′ ULF-TENS relaxing procedure, so that the influence of ULF-TENS could be well isolated from any influence due simply to the time passing between one recording and another, three recordings were performed at different times: the first at time 0′, the second at time 0′ + 20′, and only the third after TENS, time 0′ + 20′ + 45′. The results of the study permit us to draw the following conclusions: 1. it is confirmed that ULF-TENS can decrease muscle IEMG; 2. the study of the IEMG and frequency of the electromyographic signal at rest can be carried out starting from a window whose size and position in the 13.5 sec. of recording is arbitrary; 3. there is no connection between IEMG and frequency: in other words, at rest, there is no necessary correspondence between high or low IEMG and a high or low frequency values; 4. on application of the neurodiagnostic test of ULF-TENS, the IEMG of the electromyographic signal decreases, while the frequency of the signal remains unchanged. These last two observations permit us to hypothesize that the IEMG and the frequency of the electromyographic signal reflect some different and independent characteristics of the electrical activity of the muscle at rest.
Eble, O.S., Jonas, I.E., and Kappert, H.F. Transcutaneous electrical nerve stimulation (TENS): its short-term and long-term effects on the masticatory muscles. J. Orofac Orthop. 2000; 61(2):100-11.
In an electromyographic study on subjects with no functional disturbances of the masticatory muscles, the duration of the post-therapeutic effects of transcutaneous electrical nerve stimulation (= TENS) on the superficial masseter and anterior temporal muscle was analyzed. The myoelectric signals were registered from 20 healthy volunteers in 3 different mandibular positions. The recordings were performed before a 20-minute TENS application with the J-4 Myomonitor and continued with a sequence of follow-up registrations with increasing interval to the initial stimulation. The EMG signals underwent computer-aided analysis and were evaluated by determining the integrated values as a parameter of muscle activity, and after Fourier transformation by 7 describing parameters of the power spectrum (e.g. mean power frequency = MPF). A detailed analysis of variance of all data was used to investigate significant changes of the parameters during the observation period. Muscular response to TENS includes a decrease in muscular activity (= reduction in integrated EMG signals) and a shift in the power spectrum to higher frequencies (increase in MPF). These changes were statistically highly significant for both analyzed muscles and for all different mandibular exercises. As these reactions to TENS are contrary to muscle fatigue, the results can be interpreted as indicating that this type of therapy stimulates a change in the biochemical and physiological muscular conditions, which leads to muscle relaxation.
Electromyographically, the post-therapeutic effect lasted for 2 hours in case of normal masticatory muscle activity but for more than 7 hours in case of low muscular loading. The alterations of the integrated EMG values were more persistent than those of the parameters of the power spectrum.
[Low Frequency TENS Studies cited within the articles reviewed in this publication]
Academy of Denture Prosthetists. Glossary of Prosthetic Terms. J. Pros. Dent., 6:25, 1956.
Akil, H., and Mayer, D.J. Antagonism of stimulation-produced analgesia by p-CPA, a serotonin synthesis inhibitor. Brain Res. 44:692-697, 1972.
Algren, J. Mechanism of mastication. Acta Odontol. Scand., 24: Supp. 44, 1-109, 1966.
Algren, J., Ingervall, B. and Thilander, B. Muscle activity in normal and postnormal occlusion. Am. J. Orthod., 64:445-456, 1973.
Ailing, C.C., and Mahan, P.E. Facial pain. Lea & Febiger, Philadelphia; 1977.
Almay, B.G.L., Johansson, F., von Knorring, L., Terenius, L., and Wahlstrom, A. Endorphins in chronic pain: I. differences in CSF endorphin levels between organic and psychogenic pain syndromes. Pain, 5:153-162, 1978.
Andersson, S.A. Akupunktur for analgesi pa katt. En preliminar rapport. Lakartidningen 70:707-708, 1973.
Andersson, S.A., Erickson, J., Holmgren, E., and Lindquist, G. Electroacupuncture and the pain threshold. Lancet, 2:564, 1973.
Andersson, S.A., Erickson, J., Holmgren, E., and Lindquist, G. Electroacupuncture: Effect on pain threshold measured with electrical stimulation of teeth. Brain Research, 63:393-396, 1973.
Andersson, S.A., and Holmgren, E. On acupuncture analgesia and the mechanism of pain. Amer. J. Chin. Med., 3:311-334, 1975.
Andersson, S.A., Ericson, T., Holmgren, E., and Lindquist, G. Analgesic effects of peripheral conditioning stimulation. I: General pain threshold effects on human teeth and a correlation to psychological
factors. Submitted for publication; 1975a.
Andersson, S.A., Holmgren, E., and Roos, A. Analgesic effects of peripheral conditioning stimulation. II: Importance of certain stimulation parameters. Submitted for publication; 1975b.
Andersson, S.A., and Holmgren, E. Analgesic effects of peripheral conditioning stimulation. III: Effect of high frequency stimulation; segmental mechanisms interacting with pain. Submitted for publication; 1975c.
Andersson, S.A., Block, F., and Holmgren, E. Lagfrekvent transkutan elektrisk stimulering for smartlindring vid forlossning. Lakartidningen 73(26-27); 2421-2423. In Swedish, summary in English;
Andersson, S.A., and Holmgren, E. Pain threshold effects of peripheral conditioning stimulation. Advances in Pain Research and Therapy. ed. J.J. Bonica and D. Albe-Fessard, pp. 761-678, Raven Press, New York 1976.
Andersson, S.A., Hansson, G., Holmgren, E., and Renberg, O. Effects of conditioning electrical stimulation on the perception of pain. Acta ortop. Scand. 47:149-162, 1976a.
Andersson, S.A., Holmgren, E., and Roos, A. Analgesic effects of peripheral conditioning stimulation. Acupunct. Electrother. Res. In Press 1976b.
Andersson, S.A. Ericson, T., Holmgren, E., and Lindquist, G. Analgesic effects of peripheral conditioning stimulation. I: General pain threshold effect on human teeth and correlation to psychological
factors. Acupuncture & Electro-Therapeut. Res. mt. J. 2:307-322, 1977a.
Andersson, S.A., Holmgren, E., and Roos, A. Analgesic effects of peripheral conditioning stimulation. II: Importance of certain stimulation parameters. Acupuncture & Electro-Therapeut. Res. mt. i.
Andersson, S.A. Pain control by sensory stimulation. In: J.J. Bonica et. al. Eds., Advances in pain research and therapy, vol. 3. pp 569-585, New York, Raven Press; 1979,
Andersson, S.A. Augustinsson, L.E., Carlsson, C.A., Holmgren, E., Lund, S., and Roupe G. Afferents involved in the relief of itch and pain during transcutaneous electrical stimulation. In preparation, 1979.
Anthony, M. Relief of facial pain. Drugs 18:122-129, 1974(?).
Apfelbaum, R.I. A comparison of percutaneous radio frequency trigeminal neurolysis and microvascular decompression of the trigeminal nerve for the treatment of tic douloureux. Neurosurgery, 1:16-
Astrom, K.E. On the central course of afferent fibres in the trigeminal, facial, glossopharyngeal, and vagal nerves and their nuclei in the Mouse. Acta Physiol Scan. 29 (suppi 106) pp 209-320; 1953.
Augustinsson, L.E., Bohlin, P., Bundsen, P., Carlsson, C.A., Forssman, L., Sjoberg, P., and Tyreman, N.O. Pain relief during delivery by transcutaneous electrical nerve stimulation. Pain, 4:59-65, 1977.
Azarbal, M. Comparison of myo-monitor centric position to centric relation and centric occlusion. J. Prosthet. Dent. 38:3, 331 -337, 1977.
Balagura, S., and Ralph, T. The analgesic effect of electrical stimulation of the diencephalon and mesencephalon. Brain Res. 60:369-379, 1973.
Basmajian, J.V. Muscle alive. Williams and Wilkins, Baltimore, MD; 1978.
Bazzoti, L. Manuale Pratico di Kinesiologic Centro ricerche scientifiche applicate olotolatrico ed Ortodontico, Milan, Oct. 15, 1983.
Bessette, R.W., and Quinlivan, J.T. Electromyographic evaluation of the Myo-Monitor. J. Prosthet. Dent. 30:19-24, 1973.
Besson, J.M., Wyon-Maillard, M.C., Benoist, J.M., Conseiller, C,.and Hamann, K. Effects of phenoperidine on lamina v cells in the cat dorsal horn. J. Pharmaca (?) Exp. Ther., 187:239-245, 1973.
Biglund, B. and Lippold O.C.J. J. Physiol, 123:214-224, 1954.
Bonde-Petersen, F., and Christensen, L.V. Blood flow in human temporal muscle during tooth grinding and clenching as measured by l33Xenon clearance. Scand. J. Den. Res. 81:272-275, 1973.
Bratzlavsky, M. Human brainstem reflexes. In: M. Shahani Ed., The motor system: neurophysiology and muscle mechanism, Section IV, pp. 135-154, Amsterdam, Oxford, New York, Elsevier Scientific
Publishing Co.; 1976.
Brill, N., Schubeler, S., and Tryde, G. Influence of occlusional patterns on movements of the mandible. J. Prosthet. Dent., 12:255-261, 1962.
Buchthal, F., Guld, C., and Rosenfalck, P. Propagation velocity in electrically activated muscle fibres in man. Acta Physiologica Scand. 34:75, 1955.
Burton, R. The problem of facial pain. J. Am. Dent. Assoc. 79:93, 1969.
Carlsoo, S. Motor units and action potentials in masticatory muscles. Acta Morphologica Neerlando -Scand. 2:13, 1958.
Carlsson, G. Neuromuscular Problems in Orofacial Region. mt. Dent. J., Sept. 30, 1981.
Chaco, J. Electromyography of the masseter muscles in Costen?s syndrome. J. Oral Med., 28:45-46, 1973.
Chaffin, B. J Occup Med 11:109-115, 1969.
Chapman, C.R., Gehrig, J.D., and Wilson, M.E. Acupuncture compared with 33 percent nitrous oxide for dental analgesia. Anesthesiology, 42:532-537, 1975.
Chapman, C.R., Wilson, M.E., and Gehrig, J.D. Comparative effects of acupuncture and transcutaneous stimulation on the perception of painful dental stimuli. Pain, 2:265-283, 1976.
Chiang, C., Chang, C., Chu, H., and Yang, L. Peripheral afferent pathway for acupuncture analgesia. Sci. Sinica., 16:210-217, 1973.
Choi, B.B., and Mitani, H. On the mandibular position regulated by MyoMonitor stimulation. J. Jap. Prosth. Soc. 17:79-96, 1973.
Christensen, L.V. Eksperimentelt provokerede ansigtssmerter fra kaebernes bevaegesystem ved bruxisme. Tandlaegebladet 71:1171-1181, 1967.
Christensen, L.V. Facial pain from experimental tooth clenching: A preliminary report. Tandlaegebladet 74:175-182, 1970.
Christensen, L.V., J. Oral Rehab. 6:119-136, 1979.
Cooper, S. Muscle spindles and other muscle receptors. In: G.H. Bourne Ed., The structure and function of muscle, pp. 381-420, New York, Academic Press, 1960.
Dandy, W.E. Concerning the cause of trigeminal neuralgia. Am. J. Surg., 24:447-455, 1934.
Dahlstrom, A. and Fuxe, K. Evidence for the existence of monamine neurons in the central nervous system. II. Experimentally induced changes in the intraneuronal amine levels of bulbospinal neuron
systems. Acta physial. Scand. 64, Suppl. 247, 1-36, 1965.
Dao, T.T.T., Feine, J.S., and Lund, J.P. Can electrical stimulation be used to establish a physiologic occlusal position? 3 Prosth Dent, 60(4):509-514, 1988.
Dawson, G.D., and Merton, P.A. „Recurrent? discharges from motoneurons. 20th International Congress of Physiology, Brussels, (Abstracts of communication) p 221, 1956.
DeBiasi, S. and Neironi, P. Analisi Kinesiografica ed Elettiomiografica dei muscoli Masticatori nella sindrome di Moebius. Rivista kaliana di Stomalogia 11, 1982.
De Boever, J., and McCall, W.D. Physiological aspects of masticatory muscle stimulation: The Myo-Monitor. Quintessence mt. 3:57-58, 1972.
De Steno, C.V. The pathophysiology of TMJ dysfunction and related pain. Clinical Management of Head, Neck and TMJ Pain Dysfunction, W.B. Saunders Co., Philadelphia, 1977.
Derijk, W.G., Jones, G.L., and Keith, K.D. J. Dent Res, 56, Abs. 193, 1977.
Dinham, R. Treatment of tic douloureux with Jankelson Myo-Monitor. J. Hawaii Dent. Assoc., vol. III, 1970.
Dixon, H.H., O?Hara, M. and Peterson, R.D. Fatigue contracture of skeletal muscle. Northwest Med. 66:813, 1967.
Dixon, H.H., Davenport, H.A., and Ranson, S.W. Chemical studies of muscle contracture. II. The distribution of phosphorus in frog muscle during delayed relaxation. J. Biol. Chem., 82:61-70, (April)
Dixon, H.H. and Ranson, S.W. Elasticity and permanent deformation of muscle when stretched by moderate loads. Anat Rec 35:9-10, (March) 1927.
Dixon, H.H., Peterson, R.D., Dickel, H.A., et al. High energy phosphates in the muscles of depressed and fatigued patients. West 3 Surg 60:327-330, (July) 1952.
Dorpat, T.L. Mechanisms of muscle pain. Thesis University of Washington. Neurophysiology, (Edited: Ruth, T.C., Patton, H.D., Woodbury, J.W. and Towe, A.L.) Saunders, Philadelphia; pp 350-352;
Duggan, A.W., Hall, J.G., and Headly, P.M. Morphine, enkephalin and the substantiagelatinosa. Nature, 264:456-458, 1976.
Eccles, J.C. and O?Connor, W.J. Responses which nerve impulses evoke in mammalian striated muscles. J. of Physiology, 97:44, 1939.
Edwards, R.G. and Lippold, O.C.J. J. Physiol, 132: 677-681, 1956.
Elzack, R., Dennis, S.G. Pain mechanisms: theoretical approaches. In: R.F. Beers, Jr., and E.G. Bassett Eds., Mechanisms of pain and analgesic compounds, pp. 185-193, New York, Raven Press;
Enomoto, T., Fukuoka, K., Imai, Y., Kako, M., Kaneko, Y., Mishimagi, M., Quo, A. and Dubota, K. Masseteric monosynaptic reflex in chronic cat. Japanese J. of Physiology, 18:169, 1968.
Eriksson, M., and Sjolund, B. Acupuncture-like electroanalgesia in TNS resistant chronic pain. Sensory Functions of the Skin, ed. Y. Zotterman, pp 575-581. Oxford University Press, New York, 1976.
Enberg, I., Lundberg, A., and Ryall, R.W. Reticulospinal inhibition of transmission in reflex pathways. J. Physiol., 194:201-223, 1968a.
Enberg, I., Lundberg, A., and Ryall, R.W. Reticulospinal inhibition of interneurones. J. Physiol. 194:225-236, 1968b.
Enberg, I., Lundberg, A., and Ryall, R.W. The effect of Preserpine on transmission in the spinal cord. Acta physiol. Scand. 72:115-122, 1968c.
Enberg, I., Lundberg, A., and Ryall, R.W. Is the tonic decerebrate inhibition of reflex paths mediated by monoaminergic pathways? Acta physiol. Scand. 72:123-133, 1968d.
Enomoto, T., et al. Masseteric monosynaptic reflex in chronic cat. Jap. J. Physiol 18:169-178, 1968.
Eriksson, M. and Sjolund, B. Acupuncture-like electroanalgesia in TNS resistant chronic pain. Sensory Functions of the Skin Ed. Y. Zotterman pp. 575-581, 1976.
Eriksson, M.B.E., Sjolund, B.H., Nielzen, S. Long term results of peripheral conditioning stimulation as an analgesic measure in chronic pain. Pain, 6:335-347, 1979.
Erb, W. Handbook of electrotherapeutic, New York, William Wood, 1883.
Farrar, W.B. The TMJ dilemma. J. Alabama Dent. Assoc., 63:19-26, 1979.
Farrar, W.B., and McCarty, W.L., Jr. Inferior joint space arethrography and characteristics of condylar paths in internal derangements of the TMJ. J. Prosthet. Dent. 41:548, 1979.
Fields, H.L., and Basbaum, A.I. Brainstem control of spinal pain- transmission neurones. Annu. Rev. Physiol., 40:217-248, 1978.
Fra, L. and Brignolio, F. F and H responses elicited from muscle of the lower limb in normal subjects. J. of the Newrological Sciences, 7:251, 1968.
Freimann, R. Untersuchung uber Zahi und Anordnung der Muskeispindein in der Kanmuskein des Menschen. Anat. Anz., 100:258-264, 1954.
Fujii, H., and Mitani, H. Reflex responses of the masseter and temporal muscles in Man. Journal of Dental Research, 52:1046-1050, 1973.
Funakoshi, M., Fujita, N., and Takehana, S. Relations between occlusal interference and jaw muscle activities in response to changes in head position. J. Dent. Res., 55:684-690, 1976.
Ganong, W.F. Review of medical physiology 5th edn. p. 34 Maruzen (Asian edn.) Tokyo. 1971.
Gasser, H.S., and Grundfest, H. Axon diameters in relation to the spike dimensions and the conduction velocity in mammalian A fibres. American J. of Physiology, 127:393, 1939.
Gaw, A.C., Chang, L.W., and Shaw, L.C. Efficacy of acupuncture on osteoarthritic pain. New Engl. J. Med. 293, 375-378, 1975.
Gelb, H. et al. Clinical management of head, neck, and TMJ pain and dysfunction. W.B. Saunders Co., Philadelphia, 1978.
George, J.P., and Boone, M.E. A clinical study of rest position using the Kinesiograph and Myo-Monitor. J. Prosthet. Dent. 41:456, 1979.
Gernet, W. et al. Use of the Myo-monitor in the functionally disturbed system. Deutsche Zahnarztliche Zeitschrift, 35(6), Eng. Abstract, German J., June 1980.
Goodgold, J., and Ritchie, A.E. Clinical electromyography. Philadelphia, J.B. Lippincott Company, pp 7, 42, 56, 62, 65, 1973.
Goodwill, C.J. The normal jaw reflex: Measurement of the action potential in the masseter muscles, Annals of Physical Medicine, 9:183, 1968.
Graber, T.M. Orthodontics, principles and practices. p. 146, Philadelphia; W.B. Saunders; 1961.
Gregg, J.M. Post-traumatic trigeminal neuralgia: response to physiologic, surgical and pharmacologic Therapies. (?) Dent. J., 28:43-51, 1978.
Gregg, J.M., Grady, J.D. Posttraumatic sensory disorders (?) 7th Trigeminal System. J. Dent. Res., 54A:165, 1975 (Abstract).
Grosfeld, O. Changes of muscle activity patterns as a result of orthodontic treatment. Tr. Eur. Orthod. Soc., 41:203-214, 1965.
Hannam, A.G. Effects of voluntary contraction of the masseter and other muscles upon the masseteric reflex in man. Journal of Neurology, Neurosurgery and Psychiatry, 35:66-71, 1972.
Harris, R. Chronaxy. Electrodiagnosis and electromygraphy, ed. 3, New Haven, Conn., Elixabeth Licht, pp. 229, 1971.
Harrison, F., and Corbin, K.B. The central pathway for the jaw-jerk. American Journal of Physiology, 135:439, 1942.
Hodos, W. Nonparametric index of response bias for use in detection and recognition experiments. Psychol. Bull., 74:351-354, 1970.
Holmdahl, M.H.son. Bedovningseffekter av akupunktur. Lakartidningen 70:701-720, 1973.
Holmgren, E. Effects of Conditioning Electrical Stimulation on the Perception of Pain. Doctoral Thesis, Dept. of Physiology, University of Goteborg, Goteborg, Sweden, 1975.
Holmgren, E. Increase of pain threshold as a function of conditioning electrical stimulation. Am. J. Chin. Med. 3:133-142, 1975.
Holmquist, B., Lundberg, A., and Oscarsson, O. Supraspinal inhibitory control of transmission to three ascending spinal pathways influenced by the flexion reflex afferents. Arch. Ital. Biol. 98:60-80, 1960.
Homma, S. On Evoked Electromyogram in Human Body. Medicine of Japan in 1959, 5:399-407 (Japanese); 1959.
Horisberger, B., and Rodbard, S. Relation between pain and fatigue in contracting ischemic muscle. Am. J. Cardiol. 8:481-484, 1961.
Hua Shan Hospital of Shanghai First Medical College, Shanghai. Observations on analgesic effect of needleing chuanliao point in neurosurgery. Report of 619 cases. Chin. Med. J. 2:16, 1973.
Abstract in English.
Hugelin, A., and Bonvallet, M. Etude Electrophysiologique d?un reflexe monosynaptique trigeminal, C R. Soc. Biol (Paris) 150:2067-2071, 1959.
Hughes, J., Smith, T.W., Kosterlitz, H.W., Fothergill, L.A., Morgan, B.A., and Morris, H.R. Identification of two related pentapeptides from the brain with potent opiate agonist activity. Nature 258:577-579 (Lond.) 1975.
Hymes, A., Yonehiro, E.G., Raab, D.E., et al. Electrical surface stimulation for treatment and prevention of ileus and atelectasis. Surg. Forum, 25:222-224, 1974.
Hymes, A.C., Raab, D.E., Yonehiro, E.G., Nelson, G.D. and Printy, A.L. Acute pain control by electrostimulation: A preliminary report. Adv. Neurol., 4:761-767, 1974.
Ihalainen, J., Perkki, K. The effect of Transcutaneous Nerve Stimulation (TNS) on chronic facial pain. Proc. Finn. Dent. Soc., 74:86-90, 1978.
Inman, V.T., Ralston, H.J., Saunders, J.B., and Feinstein, B. EEG Clin Neurophysiol, 4:187-194, 1952.
Jankelson, B. Myo-Monitor. An electronic, extra-oral system delivering unequaled precision in the registration of occlusion. Myo-tronics; 1971.
Jankelson, B. As quoted in Jankelson, J. Prosth Dent, pp 1973; 1969.
Jankelson, B., and Swain, C.W. Physiological aspects of masticatory muscle stimulation: The Myo-Monitor (A Critique of). Quintessence International, 3:12, 57-62, 1972.
Jach, E.T. Miniclinic – The Jankelson Myo-monitor. Chicago Dental Society Review, 1974.
Jankelson, B. Functional positions of occlusion. J. Prosthet. Dent. 30:559, 1973.
Jankelson, B. Neural conduction of the Myomonitor stimulus: A quantitative analysis. J. Prosthet. Dent. 34:3, 1975.
Jankelson, B., Swain, C.W., Crane, P.F., and Radke, J.C. Kinesiometric instrumentation: A new technology. J. Am. Dent. Assoc. 90:834-840, 1975.
Jankelson, B., Sparks, S., and Crane, P.F. Neural conduction of the Myomonitor stimulus: A quantitative analysis. J. Prosthet. Dent. 34:245 – 253, 1975. V
Jankelson, B. Research and diagnostic applications of the mandibular kinesiograph. Unpublished. Myo-tronics Research, Inc., Seattle, 1976.
Jankelson, B., and Radke, J.C. The Myo-monitor: Its use and abuse (I). Quintessence International, 9:35-39, 1978 9:47-52, 1978.
Jankelson, B. Neuromuscular aspects of occlusion. Dent. Clin. North Am. 23:157, 1979.
Jankelson, B. Neuromuscular technology for complete dentures. In Proceedings of the Second International Prosthodontic Congress, St. Louis, The C.V. Mosby Co.; 1979.
Jankelson, B. Research findings and resultant management of craniomandibular (TMJ) symptom cluster syndrome. In Proceedings of the Second International Prosthodontic Congress, St. Louis.;
The C.V. Mosby Co.; 1979.
Jankelson, B. Research findings and resultant management of craniomandibular (TMJ) symptom cluster syndrome. Proceedings of the 2nd International Prosthodontic Congress, W. Lefkowitz Ed., St.
Louis, Toronto, London, C.V. Mosby Co.; 1979.
Jankelson, B. A manual – The Myo-Tronic orthopedic splint. Seattle, WA; Myo – Tronics Research, Inc.; 1980.
Jankelson, B. Measurement accuracy of the Mandibular Kinesiograph: A computerized study. J. Prosthet. Dent. 44:656, 1980.
Jankelson, B. The effect of the Myo-Monitor on relaxation of the craniomandibular musculature. Unpublished manuscript, 1981.
Jankelson, B. Modern diagnosis and management of musculoskeletal dysfunction of the head and neck. Diseases of the Temporomandibular Apparatus, Morgan et al., 2nd ed., C.V. Mosby Co., St. Louis; 1982.
Jannetta, P.J. Neurovascular compression in cranial (nerve?) and systemic disease. Ann. Surg., 192:518-525, 1980.
Jerge, C.R. Organization and function of the trigeminal mesencephalic nucleus. J. Neurophysiol, 26:379-392, 1953.
Johnson, E.W. Electromyographic Examination. Electrodiagnosis and electromyography, ed. 3, New Haven, Conn., Elizabeth Licht., 1971.
Kaada, B. Noel, E., Leseth, K., Nygaard-Ostby, B., Setekleiv, J., and Stovner, J. Acupuncture analgesia in the People?s Republic of China. T. Norske Laegeforen. 94:417-442, 1974.
Katz, B. and Miledi, R. The measurement of synaptic delay, and the time course of acetylcholine release at neuromuscular junction. Proceedings of the Royal Society of London, Series B., V, 161, 483, 1965.
Kawamura, Y. Recent concepts of the physiology of mastication. Advances of Oral Biology, New York, Academic Press. ed. Staple, P.H. pp 77-109; 1964.
Kawamura, Y., Takata, M., and Miyoshi, K. The influence of pyrithioxin on the mandibular reflex system. J. Osaka Univ. Dent. School, 9:139-147, 1969.
Kissin, M. The production of pain in exercising skeletal muscle during induced anoxia. J. Clin. Invest. 13:37-45, 1934.
Kitahata, L.M., Kosaka, Y., Taub, A., Bonikos, K., and Hoffert, M. Lamina specific suppression of dorsal horn unit activity by morphine sulfate. Anesthesiology, 41:39-48, 1974.
Kovacs, R. Electrotherapy and light therapy. 4th ed. chap. 9, p. 185; pub. Lea & Febiger; 1942.
Kwatny, E., Thomas, D.H., and Kwatny, H.G. I.E.E.E. Trans Biomed Engng, 17:303-312, 1970.
Kugelberg, E. Facial reflexes. Brain, 75:385, 1952.
Laskin, D.M. Etiology of the pain-dysfunction syndrome. J. Am Dent Ass., 79: 144, 148-153, 1969.
Lamarre, Y., and Lund, J.P. Load compensation in human masseter muscles. J. Physiol. (Loud.), 253:31 -35, 1975.
LeBars, D., Menetrey, D. and Besson, J.M. Effects of morphine upon the lamina v type cells activity in the dorsal horn of the decerebrate cat. Brain Res., 113:293-310, 1976.
Lenman, J., and Ritchie, A.E. Clinical electromyography. Philadelphia, J. B. Lippincott Company, pp 7, 42, 56, 62, 65, 1973.
Lewis, T. Pain. New York: Macmillan, 1942.
Lewis, T., Pickering, W., and Rothchild, P. Observations upon muscular pain in intermittent claudication. Heart 14:359-383, 1931.
Liebman, F.M. and Cosenza, F. An evaluation of electromyography in the study of the etiology of malocclusions. J. Prosthet. Dent., 10:1065-1077, 1960.
Lindblom, G. Disorders of the temporomandibular joint, causal factors and a value of temporomandibular radiographs in their diagnosis and therapy. Acta Odontol. Scand., 11:61, 1953.
Lindsstrom, I., and Hellsing, G. Archs Oral Biol, 28:297-301, 1983.
Lippold, O.C.J. J. Physiol, 117:492-499, 1952.
Loeser, J.D. The management of tic douloureux. Pain, 3:155-162, 1977.
Loeser, J.D., Black, R.D., and Christman, A. Relief of pain by transcutaneous stimulation. J. Neurosurg., 42:308-314, 1975.
Long, D. Cutaneous afferent stimulation for relief of chronic pain. Congr. Neurol. Surg. 21:257-268, 1974.
Long, D. The comparative efficacy of drugs vs. electrical modulation in the management of chronic pain. LeRoy PL (ed.) Current Concepts in the Management of Chronic Pain. Year Book Medical
Publishers, Chicago, 1977.
Long, D.M. Cutaneous afferent stimulation for the (?) of pain. Prog. Neurol. Surg., 7:35-51, 1976.
Long, D.M. and Hagfors, N. Electrical stimulation in the nervous system: The current status of electrical stimulation of the nervous system for relief of pain. Pain. 1:109-123, 1975.
Lous, I., Sheikoleslam, A., and Moller, E. Postural activity in subjects with functional disorders of the chewing apparatus. Scand. J. Dent. Res. 78:404- 410, 1970.
Lupton, D.E. Psychological aspects of temporomandibular joint dysfunction. J. Am. Dent. Assoc., 79:131, 1969.
Magladert, J.W. Some observations on spinal reflexes in man. Pfluegers Arch., 261:302-321, 1955.
Magora, F., Aladjemoff, L., and Tannenbaum, J., et al. Treatment of pain by Transcutaneous Electrical Stimulation. Acta Anaesth. Scand., 22:589-592, 1978.
Mann, F., Bowsher, D., Lipton, S., Mumford, J., and Miles, J. Treatment of intractable pain by acupuncture. Lancet 2:57-60, 1973.
Mark, L. Double-blind Studies of Acupuncture. J. Amer. Med. Ass., 225:1532, 1973.
Martin, W.R. Oploid antagonists. Pharmacol Rev. 19:262-278, 1967.
Mayer, D.J., Wolfle, T.L, Akil, H., Carder, B., and Liebeskind, J.C. Analgesia from electrical stimulation in the brainstem of the rat. Science 174:1351-1354, 1971.
Mayer, D.J., and Price, D. D. Central nervous system mechanisms of analgesia. Pain, 2:379-404, 1976.
Mayer, J.D., Price, D.D., and Rafii, A. Acupuncture hypalgesia: Evidence for activa…(?)of a central control system as a mechanism of action. 1st World Congress on Pain, Florence abstr. 276, 1975.
Mayer, R.F., and Feldman, R.G. Observations on the nature of F wave in man. Neurology (Minnep), 17:147, 1967.
McArdle, B. Myopathy due to defect in muscle glycogen breakdown. Clin. Sci. 10:13-35, 1951.
McBurney, D.H. Acupuncture, pain and Signal Detection Theory. Science, 189:66, 1975. References Page B-115
McIntyre, A.K. Afferent Limb of the myotatic reflex arc. Nature (Lond.), 168:168-169, 1957.
McIntyre, A.K., and Robinson, R.G. Pathway for the jaw-jerk in man. Brain, 82:468, 1959.
McKenna, B.R., and Truder, K.S. Arch Oral Biol, 23:917-920, 1978.
Meizack, R. and Wall, P. Pain mechanisms: A new theory. Science 150:971, 1965.
Meizack, R., and Melinkoff, D.F. Analgesia produced by stimulation: Evidence of a prolonged onset period. Exp Neurol. 43:369-374, 1974.
Merton, P.A. J Physiol (Lond), 123:553-564, 1954.
Mikhail, M. and Rosen, H. History and etiology of M.P.D. J. Pros. Dent. 44:438, 1969.
Miki I., and Tokizane, T. Kindenzu Nyamom, 3rd edu., p. 19. Nanzando, Tokyo; 1967.
Miller, E. Evidence that the rest position is subject to serv-control. DJ. Anderson and B. Mathews Eds., Mastication, Bristol, Wright and Sons; 1975.
Miller, E., Rasmussen, O.C., and Bonde-Petersen, F. Mechanism of ischemic pin in human muscles of mastication: Intramuscular pressure, EMG, force and blood flow of the temporal and masseter
muscles during biting. In: J.J. Bonica et al. Eds., Advances in pain research and therapy, 3:271-281, New York, Raven Press; 1979.
Milner-Brown, H.S., and Stein R.B. 246: 549-569, 1975.
Moller E. The chewing apparatus. An electromyographic study of the action of the muscles of mastication and its correlation to facial morphology. Acta Physiol. Scand. 69 suppl. 280; 1966.
Moller, E. Action of the muscles of mastication. Physiology of Mastication (Edited by Kawamura, Y) pp. 121-158, Karger, Basel; 1974.
Mortimer, J.T., Magnusson, R., and Petersen, I. Am J Physiol 219:1324-1329; 1970.
Moss, J.P. and Greenfield, B.E. An electromyographic investigation and survey of Class II cases. Tr. Br. Soc. Study Orthod., pp 147-156; 1965.
Moss, J.P. and Chalmers, C.P. An electromyographic investigation of patients with normal jaw relationship and a Class HI jaw relationship. Am. J. Orthod., 66:538-556, 1974.
Moss, J.P. Function-facts or fiction? Am. Orthod., 67:625-646, 1975.
Moyers, R.E. Temporomandibular muscle contraction patterns in Angle Class H, Division 1 malocclusions: An electromyographic analysis. Am. J. Orthod., 35:837-857, 1949.
Munro, R.R., and Griffin, C.I. Electromyograph of the jaw jerk recorded from the masseter and anterior temporalis muscles in man. Archives of Oral Biology, 16:59, 1971.
Myhaug, H. Objektiver nachweis von parafunktionen der inenohrmuskulatur. Parodontologie, 12:107-112, 1971.
Myo-Monitor Instruction Manual Myo-tronics Research, Inc., Seattle, WA; 1971.
Myo-Monitor Instruction Manual Myo-tronics Research, Inc., Seattle, WA; 1974.
Myo-Monitor Instruction Manual Myo-tronics Research, Inc., Seattle, WA; 1976.
Myo-Monitor Instruction Manual Myo-tronics Research, Inc., Seattle, WA; 1977.
Neilson, D.P., Andrews, G., Guitar, B.E., and Quinn, P.T. Tonic stretch reflexes in lip, tongue and jaw muscles. Brain Res., 178:311-327, 1979.
Neilzen, S., Sjolund, B.H., and Eriksson, M.B.E. Psychiatric factors influencing the treatment of pain with peripheral conditioning stimulation. Pain, 13:365-371, 1982.
Nordstrom and Yemm, Archs Oral Biol, 19:353-359, 1974.
Oester, Y.T., and Light, S. Routine electrodiagnosis. Electrodiagnosis and Electromyography ed. 3, New Haven, Conn., Elizabeth Licht, p 206, 1971.
Oliveras, J.L., Besson, J.M., Guilbaud, O., and Liebeskind, J.C. Behavioral and electrophysiological evidence of pain inhibition from midbrain stimulation in the cat. Exp. Brain Res. 20:32-44, 1974.
Oliveras, J.L., Woda, A., Guilbaud, G., and Besson, J.M. Neurophysiologie – Effects analgesiants de la stimulation de la substance grise periaqueducale sur le reflexe d?ouverture de la gueule declenche par stimulation de la pulpe dentaire chex le Chage eveille, libre de ses mouvements. C.R. Acad. Sci Paris, t. 276, 1973.
Omura, Y. The effects of acupuncture on the nervous system: studies on threshold stimulation and conduction velocities of motor and sensory nerve fibers. Abstracts of the Third World Cong. of Acupuncture pp 209-210 Seoul, South Koria, September 25-27, 1973.
Omura, Y. Pathophysiology of acupuncture treatment: effects of acupuncture on cardiovascular and nervous system. Acupuncture & Electro-Therapeut. Res. hit. J. 1:51-141, 1975.
Omura, Y. Electro – Acupuncture: Its electro-physiological basis and criteria for effectiveness and safety – Part I. Acupuncture & Electro-Therapeutics Res. 1:157-181, 1975.
Ota, Y. Personal communication. 1971.
Ott, K., and Winkimair, M. Zur anwendung des Myo-monitor fur die relationsbetimmung. Dtsch. Zahnarztl. Z. 32:594-598, 1977.
Ottoson, D., Ekblom, A., and Hansson, P. Vibratory stimulation for the relief of pain of dental origin. Pain. 10:37-45, 1981.
Palla, S. and Ash, M.M. Archs Oral Biol, 26:547-553, 1981.
Pancherz, H. Activity of the temporal and masseter muscles in Class H, Division I malocclusions. Am. J. Orthod., 77:679-688, 1980.
Pantaleo, T., Prayer-Galletti, F., Pini Prato, G. Physiological mechanism underlying jaw muscles relaxation in the mandibular rest position. 2nd mt. Congress mt. College of Cranio-mandibular
Orthopedics. Florence, Sept 29th-Oct. 1, Abstracts book, p. 25; 1980.
Park, S.R., and Rodbard, S. Effects of load and duration of tension on pain induced by muscular contraction. Am. J. Physiol. 203:735-738, 1962.
Paillard, J. Analysis electrophysiologique et comparaison chez l?Homme du reflexe de Hoffmann et du reflexe myotatique. Pfluegers Archiv fur die Gesamte Physiologic des Menschen und der Tiere. 260, 448; 1955.
Peking Acupuncture Anaesthesia Co-ordinating Group: Preliminary study on the mechanism of acupuncture anaesthesia. Scientia Sins. 16:447-456, 1973.
Pert, C.B., Taylor, D.P., and Pert A. J. of Pharmacol. and Exp. Therap. 154(2), 319-323, 1966.
Picaza, J.A., Cannow, B.W., Hunter, S.E., Boyd, A.S., Guma, J. and Maurer, D. Pain suppression by peripheral nerve stimulation. Surg. Neurol. 4:105-114, 1975.
Piper, H. Elecktrophysiologie Menschlicher Muskein Verlag von Julius Springer, Berlin. 1912.
Pomeranz, B. and Chiu, D. Naloxone blockade of acupuncture analgesia: endorphin implicated. Life Sci. 19:1757-1762, 1976.
Principato, J.J. Prefabricated Diagnostic Occlusal Devices of Temporomandibular Joint Dysfunction. Presentation to Am. Acad. Otolaryngology, New Orleans, Oct. 20, 1982.
Ramfjord, S.P., and Ash, M.M., Jr. Occlusion, ed. 2, Saunders Philadelphia; 1971.
Ranson, S.W. and Dixon, H.H. Contractures caused by tenotomy and by tetanus toxin. Proc Soc Exp Biol Med 24:725 (April) 1927.
Ranson, S.W. and Dixon, H.H. Elasticity and ductility of muscle in myostatic contracture caused by tetanus toxin, Am J. Physiol. 86:312-319 (September) 1929.
Rasmussen, P. Facial pain: A clinical study with special reference to the symptomatology, aetiology and surgical therapy. Copenhagen: Munksgaard, 1965, pp 1-353.
Report on the findings and recommendations on transcutaneous electrical nerve stimulation for pain relief by the panel on review of neurological devices. Food and Drug Administration, 1976.
Research Group of Acupuncture Anesthesia, Peking Medical College. Effect of acupuncture on pain threshold of human skin. Chin. Med. J., 3:151-157, 1973.
Rodbard, S., and Pragay E.B. Contraction frequency, blood supply, and muscle pain. J. appl. Physiol. 24:142-145, 1968.
Rosenbert, M., Curtis, L. and Bourke, D.L. Transcutaneous electrical nerve stimulation for the relief of postoperative pain. Pain. 5:129-133, 1978.
Roth, R.H. Temporomandibular pain dysfunction and occlusal relationships. Angle Orthod. 43:137, 1973.
Rushton, J.G., Gibilisco, J.A., and Goldstein, N.P. Atypical Facial Pain. JAMA, 171:545-548, 1959.
Scott, D.S., and Lundeen, T.F. Pain, 8:207-215, 1980.
Schwartz, L. Pain associated with the temporomandibular joint. J. Am. Dent. Assoc., 51:394, 1955.
Schwartz, L. Disorders of the temporomandibular joint. Philadelphia, W.B. Saunders Co.; 1959.
Schweizer, Hans. Der Myomonitor. Schweiz, Mschr. Zahnheilk, 81:12, 1187- 1194, 1971.
Section of Thoracic Surgery of Peking Acupuncture Anesthesia Coordinating Group: Acupuncture anesthesia in thoracic surgery, clinical analysis of 818 cases. Chin. Med. J. 2:20, 1973, Abstract in English.
Shafer, W.G., Hine, M.K., and Levy, B.M. A textbook of oral pathology. 3rd ed. Philadelphia, W.B. Saunders Co., pp. 26-27; 1974.
Shanghai First People?s Hospital, Shanghai. Acupuncture anesthesia in thyroidectomy. Chin. Med. J. 2:17, 1973, Abstract in English.
Shapiro, H.H. Maxillofacial anatomy with practical applications p. 331. Lippincott, Philadelphia; 1954.
Shealy, C.N. Transcutaneous electroanalgesia. Surg. Forum, 23:419-421, 1972.
Shealy, C.N. Transcutaneous electrical stimulation for control of pain. Clin. Neurosurg., 21:269-277, 1974.
Sherrington, C.S. Reflexes elicitable in the cat from pinna vibrissae and jaws. J. Physiol. 51:404-431, 1917.
Sjolund, B., and Eriksson, M. Electro-acupuncture and endogenous morphines. Lancet, 2:1085, 1976.
Sjolund, B., Terenius, L., and Eriksson, M. Increased cerebrospinal fluid levels of endorphins after electro-acupuncture. Acta Physio. Scand., 100:382-384, 1977.
Sjolund, B.H., and Eriksson, M.B.E. The influence of naloxone on analgesia produced by peripheral conditioning stimulation. Brain Res., 173:295-301, 1979.
Sjolund, B., and Eriksson, M. Endorphins and analgesia produced by peripheral conditioning stimulation. Adv. Pain Res. Ther., 3:587-591, 1979.
Stalberg, E. Propagation velocity in human muscle fibres. Situ. Acta Physiologica Scandinavica., 70, Suppi, 287,1; 1966.
Stephens, LA., and Taylor, A. J. Physiol (Lond), 220:1-18, 1972.
Sutcher, H., et al. Comparison of responses to pharmacological and physical placebo therapy in TMJ disfunction patients. IADR Abstracts. p. 243; 1966.
Szentagothhai, J. Anatomical considerations of monosynaptic reflex arcs. J. Neurophysiol, 11:445-454, 1942.
Tei, K. Evoked EMG potentials as modified by voluntary contraction. Journal of Juzen Medical Society, 67, 65; 1961.
3M:TENS: How it works and when to use it. St. Paul, MN, 3M Corporation, 1963.
Terenius, L, and Wahlstrom, A. Search for an endogenous ligand for the opiate receptor. Acta Phsiol Scand. 94:74-81, 1975a.
Terenius, L and Wahlstrom, A. Morphine-like ligand for opiate receptors in human CSF. Life Sci. 16:1759-1764, 1975b.
Terenius, L, Wahlstrom, A., Lindstrom, L., and Widerlof, E. Increased CSF levels of endorphins in chronic psychosis. Neurosci. Lett. 3:157-162, 1976.
Thomas, L.J., Tiber, N., and Schireson, S. The effects of anxiety and frustration on muscular tensions related to the temporomandibular joint syndrome. Oral. Surg., 36:763-768, 1973.
Thompsan, J.R. Temporomandibular disorders: Diagnosis and treatment. The Temporomandibular Joint, B.G. Sarnat, ed. p. 123, Sprinfield, IL: Charles C. Thomas; 1951.
Thomson, H. Mandibular dysfunction syndrome. Brit. Dent. J. 130-187, 1971.
Thorsteinsson, G., Stonnington, H.H., Stillwell, G.K. and Elveback, L.R. The placebo effect of transcutaneous electrical stimulation. Pain. 5:31- 41, 1978.
Thorsteinsson, G., Stonnington, H.H., Stillwell, G.K., et al. Transcutaneous electrical stimulation: A double-blind trial of its efficacy for pain. Arch. Phys. Med. Rehabil. 58:8-13, 1977.
Travell, J.G., and Simons, D.G. Myofascial pain and dysfunction: The trigger point manual. Baltimore: The Williams and Wilkin Co., pp. 273-281, 1983.
Trott, P.H., and Goss, A.H. Physiotherapy in diagnosis and treatment of the myofacial-pain dysfunction syndrome. mt J. Oral Surg, 7:360, 1978.
Van der Ark, G.D. and McGrath, K.A. transcutaneous electrical stimulation in treatment of postoperative pain. Amer. J. Surg. 130:338-340, 1975.
References – Myo-monitor Efficacy Page 133
Vesanen, E., and Vesanen, R. The Jankelson Myo-monitor and its clinical use. Proc. Finnish Dent. Soc. 69:244-247, 1973.
Viitasalo, J.T., and Komi, P.V. Electromyogr. Clin. Neurophysiol. 18:167-178, 1978,
Vitti, M. and Basmajian, J.V. Muscles of mastication in small children: An electromyographic analysis. Am. J. Orthod., 68:412-419, 1975.
Vitti, M. and Basmajian, J.V. Integrated actions of masticatory muscles: Simultaneous EMG from eight intramuscular electrodes. Anat. Rec., 187:173-189, 1977.
Voss, H. Em besonderes reichliches vorkommen von muskelspindein in der tief en portion des m. masseter des menschen und der anthropoiden. Anat. Anz., 81:290-292, 1935.
Vrendenbregt, J. and Rau, O. New developments in EMG and clinical neurophysiology, 1:607-622, 1973.
Wahlstrom, A., Johansson, L., and Terenius, L. Characterization of endorphins (endogenous morphine-like factors) in human CSF and brain extracts. Opiates and Endogenous Peptides pp. 49-56 Ed.
H.W. Kosterlitz North-Holland, Amsterdam, New York, Oxford, 1976.
Wall, P.D., and Sweet, W.H. Temporary abolition of pain in man. Science, 155:108-109, 1967.
Watkins, A.L. A manual of electrotherapy. Philadelphia, Lea & Febiger, Publishers, pp 141, 166, 1968.
Weiss, M.H. Case report: Successful treatment of Bell?s Palsy. Dent Surv., Aug, 1976.
Wessberg, G. A., Washburn, M.C., and Epker, B.N. An evaluation of mandibular rest positions in subjects with diverse dentofacial morphology. (Submitted for publication).
Wessberg, B.A., Wesley, L.C., Dinham, R., and Wolford, L.M. Transcutaneous electrical stimulation as an adjunt in the management of myofacial pain dysfunction syndrome. J.Prothat. Dent., 45:307-314, 1981.
Williamson, E.H., and Bays, R.A. Unpublished data. Evans, GA: Foundation for Advanced Research and Training, 1985.
Williamson, E.H., and Marshall, D. Myomonitor rest position in the presence and absence of stress. Research Rep. 1:14-16, 1986.
Wood, C.R., Jr. Centrically related cephalometrics. Am. J. Orthod. 71:156, 1977.
Wyon-Maillard, M-C., and Besson, J.M. Effects of orbital cortex stimulation on dorsal horn interneurons in the cat spinal cord. Brain Res. 46:71-83, 1972.
Yaksh, T.L., and Rudy, T.A. Analgesia mediated by a direct spinal action of (narc. .?) Science, 192:1356-1358, 1976.
Yavelow, I., Forster, I., and Wininger, M. Mandibular relearning. Oral Surg. 36:632, 1973.
Yemm, R. Temporomandibular dysfunction and masseter muscles response to experimental stress. Brit. Dent. J., 127:508-510, 1969.
Yemm, R. Neurophysiologic studies of temporomandibular joint dysfunction. Oral Sci. Rev., 7:31-53, 1976.
Zak, E. Uber den Gefasskrampfbei intermittierendem Hinken und uber gewisse kapillomotorische Erschenungen. Wien. Arch. Inn. Med. 2:405, 1921.
Zieglgansberger, W., and Bayerl, H. The mechanisms of inhibition of neuronal activity by opiates in the spinal cord of cat. Brain Res., 115:111-128, 1976.
Zimmermann, M. Peripheral and central nervous mechanisms of nociception, pain, and pain therapy: facts and hypotheses. In: J.J. Bonica e al, Eds., Advances in pain research and therapy, vol. 3, pp. 3-32, New York, Raven Press; 1979.