Temporomandibular Joint-Myofascial Pain Dysfunction Syndrome Treatment Apparatus and Methodology

This invention relates to electronic pain suppression apparatus and methodology and, more specifically, to temporomandibular joint-myofascial pain dysfunction syndrome (TMJ-MPDS) treatment apparatus and procedure for treating pain associated with TMJ-MPDS.

It is an object of the present invention to provide improved TMJ-MPDS treatment apparatus and methodology.

More specifically, an object of the present invention is the electronic treatment of TMJ-MPDS in a safe, efficient and rapid manner to alleviate pain associated with the disease.

It is a further object of the present invention to provide electronic transcutaneous electronic nerve stimulating equipment operative at very low, milliampere current levels, which relieves perceived pain, and treats the pain of TMJ-MPDS.

The above and other objects and features of the instant invention are realized in a specific illustrative TMJ-MPDS electronic treatment apparatus and methodology which employs a transcutaneous electronic wave to suppress the perceived pain of TMJ-MPDS. A first positive contact electrode is placed at the pain site, and a second positive contact electrode is placed at contra-lateral temporomandibular joint; the negative contact electrode at the web of the ipsilateral hand. An electronic current wave comprising relatively high frequency pulses with a low frequency modulation is then applied from the first to the second electrodes.

The above and other features and advantages of the instant invention will become more clear from the following detailed description of a specific illustrative embodiment thereof, presented hereinbelow in conjunction with the accompanying drawing, in which:

FIG. 1 is a schematic diagram of electronic TMJ-MPDS treatment apparatus embodying the principles of the present invention; and

FIGS. 2A through 2D are wave forms illustrating the operation of the FIG. 1 apparatus.

The apparatus of the instant invention has been found to suppress pain associated with TMJ-MPDS and produce dramatic results in many patients with a relatively low level current and without chemical intervention.

To illustrate performance of the instant invention in overview, the apparatus of FIG. 1 is utilized to treat the symptoms associated with the TMJ-MPDS. A first positive contact electrode 60 (FIG. 1) is placed at the pain site; a second positive contact electrode 62 (FIG. 1) is placed at the contra-lateral temporomandibular joint. A negative contact electrode 72 (FIG. 1) is placed at the web of the ipsilateral hand. The treatments should be for 15 minutes and may be run concurrently.

An electronic wave (depicted in FIG. 2D) is applied between the positive electrodes 60 and 62, and the electrode 72 which are connected on common. The wave form of FIG. 2D comprises a low level (less than 4 milliamperes) pulse train of relatively high frequency, e.g., between 12 and 20 khz modulated in amplitude by a relatively low frequency wave in the range of 8 to 20 hz. The low frequency wave is preferably non-symmetrical (that shown in FIG. 2D), for example, characterized by a 3:1 duty cycle, being on three quarters of the time and off one quarter of the recurring period. For concreteness only and without limitation, it will hereinafter be assumed that the high frequency pulse occurs at a 15 khz rate and 1-1.5 m.a. level, while being subject to a 15 hz modulation with a 3:1 duty factor.

I have found that the wave of FIG. 2D is effective to block the pain associated with TMJ-MPDS. The particular mechanism causing elimination of the pain of TMJ-MPDS is believed to follow from currents generated by the pain suppressor that achieve a quantitative superiority to nociceptive impulses at the "neurologic gates" that transmit pain to higher centers, which are responsive to the low frequency modulation envelope introduced into the body, with the high frequency wave constituent serving as a transcutaneous carrier for the low frequency modulation, thereby blocking the transmission of the painful impulses. See Melzack R., Wall P.: Pain Mechanisms: A New Theory. Science 1965; 150:971-979.

Alternatively, the Pain Suppressor may induce some neurons to manufacture an endogenous opiate that interacts with pain receptors to produce analgesia similar to that produced by morphine. See Meyer CA, Fields HL: Causalgia treated by selective large fibre stimulation of peripheral nerve. Brain 1972; 95:163-168. R. Dubner, in his article "Neurophysiology Of Pain", Dent Clin North Am 1978; 22:11-30, suggests the effect of the Pain Suppressor on A-beta neurons. The effect of serotonin on pain suppression is discussed in Messing R.: Behavioral Effects Of Serotonin Neurotronics, Annals N.Y. Acad. of Sci., 1978:480-496, the disclosure of which is incorporated by reference. While the precise operative mechanism may be the subject of debate, the fact of the relief of pain is not. The FIG. 1 electronic apparatus 10 for generating and applying the wave form of FIG. 2D will now be specifically considered. A battery 12 is connected to a PNP series pass transistor 18 which, in turn, selectively passes the voltage from battery 12 through a voltage regulator 20 to form the positive direct current voltage supply for the apparatus 10 electronics. The unit is first turned on by momentarily closing a power-on switch 17. This applies a low voltage to the base of PNP transistor 18, turning that device on and effectively coupling the potential of battery 12 to a series pass transistor 21 in the voltage regulator 20. Because the final output of a counter or divider chain 27 is initially low on power turn on, the resulting high output of inverter 35 applies a high potential to the base of transistor 19, turning it on and thereby latching PNP transistor 18 to its conductive condition when switch 17 is released. This maintains the electronic apparatus on for a desired period which is determined by the frequency of an oscillator 25 and the division factor of the divider 27, i.e., the period required for the most significant stage of the counter 27 to reach its high or binary " 1" state. The switched power supply assures that the electronic apparatus is not inadvertently left on to unduly discharge the battery 12.

The regulated output of battery 12 applied through PNP transistor 18 is converted to a lower regulated value by the regulator 20. Regulator 20 is per se well known and includes the series pass NPN transistor 21 having a constant voltage applied to the base thereof by a Zener diode 24 energized by a resistor 22. The constant potential output of regulator 20, which serves as the supply voltage for much of the remaining electronics of FIG. 1, is the characteristic reverse excitation voltage of Zener diode 24 less about 7/10 of a volt for the base-emitter drop of transistor 21.

As above noted, the active power supply interval for circuit 10 of the drawing is fixed and preset to a specific period. The above-discussed time out circuitry is employed to assure that the unit is not inadvertently left on. Many ways of achieving this result will be readily apparent to those skilled in the art. For example, a variable time out may be provided by employing a switch to connect the input of inverter 35 to varying ones of the more significant stage outputs of the pulse counter chain 27. Yet further, separate electronic or electromechanical timer apparatus, fixed or variable, all per se well known, may be employed to supply a positive potential to the base of transistor 19 for the desired "on" period; and to switch off the base drive to transistor 19, thereby turning off series pass transistor 18, when the desired operative period has passed.

A time base oscillator 25 supplies an input to the pulse counter or divider chain 27. The frequency of oscillator 25 is chosen for convenience to be an integral multiple of the pulse frequency (FIG. 2D) desired for delivery to the patient. For the assumed 15 khz desired frequency, a 30 khz oscillation repetition rate may be usefully employed for oscillator 25, such that the 15 khz signal is derived at a divide-by-two tap 28 of divider chain 27. The 15 khz signal is supplied as one input to a NAND gate 34, the output of which corresponds to the ultimately desired wave of FIG. 2D. Outputs 29 and 30 of divider 27 are supplied as inputs to a NAND gate 33, the output of which is supplied as a second input to the NAND gate 34. The output 29 of divider 27 supplies the 30 hz wave of FIG. 2B (pulse division factor 1,000 at tap 29), while the 15 hz wave of FIG. 2A is supplied at a divider output 30 (divider factor: 2,000). Logic gate 33 generates the output wave of FIG. 2C, being at its high or Boolean "1" value when either of the waves of FIGS. 2A or 2B is low (i.e., preceding the time a, during the interval b-e,--and following time f). Correspondingly, during the periods a-b and e-f when the output at divider 27 taps 29 and 30 are both high, the output of gate 33 is low (Boolean "0" value).

The wave form of FIG. 2C is supplied as one input to the gate 34 together with the 15 khz pulse train at the divide-by-two counter 27 output port 28. Accordingly, the output of NAND gate 34 switches between its high and low state during the periods when the FIG. 2C wave is high, i.e., preceding time a, during the interval b-e, following the time f, and so forth for the recurring pattern illustrated by FIGS. 2A-2D.

The voltage wave form of FIG. 2D is converted to a current in the milliampere range for application to the patient by the following circuitry of FIG. 1. As a first matter, a gated constant current generator 36 passes a gated current (either off or of a fixed value) through a potentiometer 38 under control of the output of the NAND gate 34. When the output of NAND gate is low, a transistor 37 in constant current generator 36 is on and a current substantially given by the positive potential output of regulator 20 (applied to the base of transistor 37) less a 7/10 of a volt base emitter drop for the transistor 37, divided by the resistance value of the resistance 39 in the emitter circuit of transistor 37. The voltage at the variable tap of the potentiometer 38 is supplied to the base of a PNP transistor 43 of a constant current pulse generator 40. The output of pulse generator 40 is a current which switches between its off (zero current) state, and a value given by the voltage at the potentiometer 38 tap, less a diode drop for the emitter-base of transistor 43, divided by the resistance value of resistor 42 connected in the emitter circuit of the PNP device 43. This pulsed current output of pulse generator 40 corresponds in wave form to FIG. 2D, and is at a level, determined by the setting of potentiometer 38, in the low milliampere range. It is this current pulse which is ultimately delivered to the patient to provide the requisite relief of symptoms.

In a typical application the patient is provided with the potentiometer 38. The potentiometer is first turned up so that the administered current pulses provide a noticeable tingling sensation on the patient's skin surface. The patient is then instructed to turn down the potentiometer adjustment until the sensation just disappears. This will provide the amount of transcutaneous electronic stimulation to treat the symptoms associated with the patient's disease. The potentiometer setting may be adjusted by the patient as required.

The current pulses from generator 40 pass through a protective, series limiting resistor 50 to an output terminal 51. It there flows via the lead 55 connected to terminal 51 to the electrode 60 adhered to the pain site and the electrode 62 adhered to the contra-lateral temporomandibular joint. The current transcutaneously passes into the patient, flows through the patient, and returns to electronic ground via the electrode pad 72 adhered to the web of the patient's ipsilateral hand. Electrode 72 is connected to electronic system ground via lead 70 and apparatus terminal port 52a.

As above noted, the apparatus and methodology of the instant invention treats the pain associated with TMJ-MPDS. The apparatus and methodology has manifest advantages for alleviating the patient's symptoms.

The above-described arrangement and methodology are merely illustrative of the principles of the present invention. Numerous modifications and adaptations thereof will be readily apparent to those skilled in the art without departing from the spirit and scope of the present invention.

The medical profiles, clinical examinations and radiographic evaluations of 25 TMJ-MPDS patients revealed no evidence of associated systemic or neoplastic disease or of current therapy with such drugs as analgesics, tranquilizers and muscle relaxants.

Palpation of the head and neck as well as masticatory muscles showed muscle spasm most commonly associated with the temporalis and lateral pterygoid muscles. Historic and clinical evidence of clenching or grinding of teeth, varying degrees of occlusal discrepancies, clicking and crepitus, tinnitus and deviation of the mandible were all consistent findings.

Patient response to PAIN SUPPRESSOR, the Minnesota Multiphasic Personality Inventory (MMPI) profiles and the Pain Rating Index are documented in Table 1. The 25 patients accepted for treatment underwent a total of 65 therapeutic sessions during the 12-month experimental period. The average pain rating per patient before the first treatment was 12, and after treatment, 2. The overall pain rating before all therapy was 10, and after therapy, 3. Eighteen (72 percent) of the patients reported long-term relief of pain. These patients were generally those who had an acute problem of recent onset.

Seven patients who received little or no benefit from therapy all related a history of chronic or long-term problems compatible with TMJ-MPDS. Patients 10, 11, 17, 19 and 23 experienced only short-term responses and were still experiencing considerable pain after repeated treatment sessions. Patients 2 and 12 received no benefit from the treatment. A multidisciplinary approach to therapy was intiiated for all seven of these patients. Significant historic and radiographic evidence of anterior condylar displacement, suggestive of capsular laxity resulting from chronic luxation, was diagnosed in two patients (patients 2 and 19). These patients were referred to a surgeon for eminoplasty. Patients 12 and 23 had severe malocclusion and were referred to an orthodontist for treatment. Patients 10, 11 and 17 appeared to suffer from mild to severe somatization reaction and were expected to benefit from relaxation therapy or psychotherapy.

No adverse reactions were reported by any of the patients during therapy.