Tuesday, June 14, 2011

Scientific Studies Validating the Low Frequency TENS

There are numerous studies in the scientific literature that support the efficacy of low frequency T.E.N.S. in the diagnosis and treatment of TMJ/TMD.

Three distinct categories for TENS modalities are recognized in this field: 1) Conventional High Frequency TENS - 50-100 Hz asymmetrical biphasic wave (40-75 usec) which is designed to selectively actuate the large myelinated afferent muscle fibers.  Muscle fasiculation is no apparent, there is a fast on set of relief, short therapeutic effect, generally not exceeding length of stimulation with little to no endogenous opiate liberation, no reversal by naloxone and is primarily a local CNS segmental effect, 2) Low Frequency TENS operates at a pulse rate of 0.5 Hz to 10.0 Hz using a asymmetrical biphasic wave form of 150-500 usec.  It produces muscles contract, with slow onset of 20 minutes or more, has a long therapeutic effect, allows a period of muscle recovery between pulse stimulation by surface electrodes in segmentally related myotromes being most efficacious and hasa  acupuncture-like effect and 3) Electrogalvanic Stimulator (EGS) which is characterized by having a monophasic, twin peak wave for each pulse of 10-20 msec utilizing direct current.  EGS is used for local tisseu effect, not pain control.

Both low and high fequency TENS have ample and specific documentation in the medical literature regarding local histochemical and endorphin effects.  The following articles addres the mode of action of conventional hight frequency TENS and low frequency TENS.

  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 Sjolun, 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. Takokora, K., et al. (1979) "Pain control by transcutaneous electrical nerve stimulation using irregular pulse of 1Hz fluctuation." Applied Neurophysology. 42:314.
  4. Muarray, W. and Miller, J. (1960) "Potency differences of mophine-type agents by radiant head and 'crampin'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) Steroespecific and no-specific interactions of the morphine narcotic congener leurophanol in subcellular functions of rat brain." Proc. Nat. Acad. Science USA. 68:1742.
  6. Moyer, J.D., Price, D.D., and Rafii, A. (1977) "Antagonism of acupuncture analgesis in man by the narcotic antagonist naloxone," Brain Reserach. pp. 121-368.
  7. Akil, H., et al. (1978) "Encephalin-like material elevated in ventricular cerebrospinal fluid of pain patients affter analgetic facial stimulation." Science. 201:463.
  8. Simanto, r., et al. (1976) "The regional distribution of a morphine-like encephalin in monkey brian." Brain Research. 106:189.
  9. Sjolund, B. and Eriksoon, 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. Reserach Ed. Bonica, 58:205.
  11. Kerr, F. W. (1975) "Neuroanoatomical substrates of noceception in the spinal cord." Pain 1:325.
  12. Loeser, J.D., et al. (1975) "Relief of pain by transcutanous stimulation." J. Neurosurg. 42:308.
  13. Arcangeli, P. and Galletic, R. (1974) "Endogenous pain producing substances." Recnt 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 Kasparak, M. (1976) "Modification of blood flow to the extremities by electrical stimulation of the nervous system." S. Med. Journal 69:1309.
  17. Abruam, S.E. (1976) "Increased sympathetic tone associated with transcutaneous electrical stimulation." Anesthesiology. 45:575.
  18. Abram, S. E., el al (198) "Increased skin temperature during transcutaneous electrical stimulation." Anesth. Analg. 59:22.
  19. Rowlingson, J., et al. (1978) "The effect of transcutanous nerve stimulation on blood flow in normal extremeties." Pain Abstr. Vol. 1, 2nd World Congress on Pain, Int. Assoc. for Study of Pain, Seattle, p. 155.
  20. Murphy, T. M. and Bonica, J.J. (1977) "Acupuncture analgesia and anestheesia." Arch. Surg. 112:896.
  21. Andersson, S.A. and Holmgren, E. (1977) "Analgesic effects of peripheral conditioning stimulation parameters." Acupunc. 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. M
  25. Terenius, L. (1978) "Significance of endorphins in endogenous antiociception."  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 releif by electrical stimulation of the central grey matter in humans and its reversal by naloxone." Science. 197:183.
  28. Burton, C. and Marrer, d.D. (1974) "Pain suppression by transcutaneous electrical stimulation." IEEE Trans. Bimed. 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." Act 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, .J. (1979) "A Signal detection analysis of the effects of transcutaneous stimulation on pain." Psychosom. Med. 4: 101.
  32. Ebersold, J.J., Laws, E.R. and Albers, J.W. (1977) "Meaasurements of autonomic function before, during and after transcutanous stimulation in patients with chronic pain and in control subjects." May 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 elecro-acupuncture." Acta Physiolo. Scan. 100:382.
  35. Mayer, D. J., Price, D.D. and Raffii,  A. (1977) "Antogonism of acupuncture analgesia in man by the marcotic antogonist naloxone." Brain Res. 121: 368.
  36.  Schlen, H. and Bentlye, G. A. (1980) "The possibility that a component of morphine induced analgesia is contrubted indirectly via the release of endogenous opioids." Pain 9:73.

The medical literature is clear and unequivocal about the use of low frequency TENS (0.5-10 Hz) is both safe and efficacious for muscle relaxation and pain control.  It is also  clear that low frequency TENS has a hgih degree of specificity when utilized for craniofaical pain (Andersson, 1979: Eriksson eta l., 1984; Chapman et al., 1979; Andersson et al., 1977; Andersson and Homgren, 1975; Sjolund et al., 1975; Reichmanis and Becker, 1977; Hansoon and Ekbolom, 1983; Tereshalmy et al., 1982; Phero, 1987; Lasagna et al, 1986; Thomas, 1986; Pantaleo et al., 1983; Wessberg and Dnham, 1977; Kknchak et al., 1988).

Choi and Mitani at Osak Dental University in 1973 applied the Myomonitor 10 15 subjects and monitored the evodked respons using wire EMG electrodes.  The study concluded "The evoked EMG was recorded from the  anterior ortion  of the temporal, the masseter, the anterior ventrl of the digastrics, andobicularis oris and the buccinator muscles.  The Myo-monitor pulse stimulates the nerve trunks of the fifth and seventh cranial neves at the superior mandibular notch percutanously and it appeared to have afferent and efferent effects."
 Using accepted intensity-duraction 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 acetylcholine 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  either instance.  This information would suport the conclusion that the Myomonitor stimulus is transmitted neurally."

Fuji 1977 at the Univestity of Osak used multiple site monitoring to distinguish M wave and H wave response.  Using multiple anatomically separate recording sites and 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 monsynaptic 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 unexplaned reasons place 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 aspects of the nose and the upper lip indictes 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 directedly 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 nervew 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 Myo-monitor stimulation is neurally mediated."

Goodgold and Eberstein examined eight individual investigative studies and found that normal stial 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.  Bamajian summarized the results of six studies conducted by separate authors on peripheral nerve conduction velocity and found an 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 muscle 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 nerla 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 approaximaterly 0.4 msec. depending upon electrode placement.  Adding the sum of these phenomena we find the latency of 1.8 o to 4.04 msec. as measure by Dao, et al. is well within the range of neurally mediated respose, despite their electrode placement.

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