British Journul of Oral Surgery (1981) 19, 112-115

0 The British Association of Oral Surgeons 0007-117)3/81/00160112$02.00

RELIEF OF CHRONIC FACIAL PAIN BY TRANSCUTANEOUS ELECTRICAL NERVE STIMULATION

RAYMUND O'NEIL, B.D.s., F.D.s., M.R.c.s., L.R.C.P. University College Hospital Medical School, Dental School, Mortimer Market,

London WClE 6JD

Summary. The usefulness of transcutaneous electrical nerve stimulation was compared between 12 cases of trigeminal neuralgia and 12 cases of atypical facial neuralgia. The overall success rate was 58 per cent falling to 42 per cent after six months. There was however a significant difference between the two groups of patients.

Introduction

Opium obtained from the poppy has been used since classical times to relieve pain. The molecular structure of morphine was worked out in 1925 by Gulland and Robin- son. This led to the discovery of the opiate antagonist naloxone. Consequently the question arose does morphine in fact stimulate natural physiological pain inhibitory pathways.

7/-,oqueduc+al

Pituitary- hypothalamic p-endorphin

qinol nucleus of V

MID BRAIN

PONS

MEDULLA

SPINAL CORD

FIG. 1. Diagram illustrating three pain inhibitory systems. These systems are shown operating at both the levels of the spinal cord and the trigeminal nerve (TN).

(Received 28 June 1980; accepted 30 June 1980) 112

TRANSCUTANEOUS ELECTRICAL NERVE STIMULATION 113

The opiate receptors in the brain and spinal cord were demonstrated by several groups in 1973 (Pert & Yaksh, 1974) and the exciting search for the natural ligands resulted in the discovery in 1975 of the opioid peptides, methionine-enkephalin and p-endorphin (Hughes et al., 1975). The discovery of the opioid peptides demonstrated that the body has its own pain-suppression systems, and explained on a physiological basis the known variabilities in the response to painful stimuli usually attributed to an ‘attitude of the mind’.

These pain-suppressing mechanisms are described by David Bowsher (1980) in a recent number of the British Journal of Oral Surgery. It appears that modulation of painful sensory input is carried out at the level of the dorsal horn of the spinal cord by at least three mechanisms. One mechanism is a descending inhibitory pathway from the periaqueductal grey matter in the midbrain, via the raphe nuclei in the brain stem, to the substantia gelatinosa of the dorsal horn of the spinal cord, or its continu- ation in the spinal nucleus of the trigeminal nerve. It is not known whether the enkephalins act as neurotransmitters or whether they modulate the release of neuro- transmitters at these sites.

Imposed on this enkephalinergic and serotoninergic system is a further modulatory influence by ,6-endorphin which is secreted from the anterior pituitary in time of stress. The large precursor molecule from which ACTH is derived, splits into both ACTH and P-endorphin which are released at the same time. The release of the neurohormone /3-endorphin helps to explain why pain may not be felt in time of excitement or stress.

Finally these systems appear to be separate from the phenomenon of segmental gate control by A/? fibre information from overlying skin, which is the reason for the ‘rubbing it better’ effect, by pre-synaptic inhibition of A6 and C fibre nociceptor information from the same region.

If these facts in themselves were not interesting enough it was demonstrated in 1977 by Pomeranz and Chir that acupuncture analgesia also could be reversed by naloxone and is therefore presumably due, in part, to release of opiate peptides in the physiological pain suppression systems, the ascending part of the loop being AS information from skin and muscle nociceptor units.

In 1978 Levine et al. in a classical paper using subjects undergoing third molar surgery, showed that placebo analgesia, occurring in placebo reactors, was reversed by naloxone and thus presumably also involves the release of endogenous opiates to modulate the perception of pain. It is not known, however, what mechanism turns on the placebo response, which of course is a crucial question.

Melzack et al. (1977) have shown a good correlation between acupuncture points and so-called trigger points which are often present in chronic painful conditions. Earlier, Melzak (1975) by using transcutaneous electrical nerve stimulation (TENS) at trigger or acupuncture points, showed an overall success rate of 66 per cent in relieving chronic pain, which was significantly more effective than placebo contri- butions in a control series of patients.

Recently Eriksson and her colleagues in Sweden (1979) demonstrated the use- fulness of transcutaneous nerve stimulation as an alternative to acupuncture, with a success rate of 55 per cent after three months falling to 31 per cent after two years.

Following a suggestion by Professor P. D. Wall of University College I thought it might be helpful to try Eriksson’s stimulator as an adjunct to treatment of patients who attended a facial pain clinic, and this stimulator was used with varying success in a wide selection of cases.

114 BRITISH JOURNAL OF ORAL SURGERY

Materials and method

Due to the difficulty of arranging a controlled clinical trial it was decided to compare the effect of TENS between 12 chronic cases of trigeminal neuralgia and 12 chronic cases of atypical facial neuralgia. The stimulation treatment was used as an adjunct to conventional drug treatment such as carbamazepine or dothiepin hydrochloride. Cefar SIII stimulators were used and treatment administered by nursing staff at a series of visits usually at weekly intervals. Based on the results obtained by Mann- heimer and Carlsson, each patient received 20 minutes treatment, consisting of 10 minutes 100 Hz stimulation followed by 10 mins 4 Hz (interval frequency of 100 Hz) stimulation. The negative electrode was placed in a pre-auricular position overlying the temporomandibular joint and facial nerve. The positive electrode was placed over the infra-orbital foramen or the mental foramen depending on the situation of the pain. The amplitude of the stimulus was increased each minute taking careful notice of the adaptive response of the patient until a suitable plateau of strong but tolerable stimulation was reached.

Graphic rating scales were used (Scott & Huskisson, 1976) in order to assess the effect of stimulation on the patients complaint.

Attempts were made to assess the length of any pain suppression following each treatment and also any change in overall pain between visits. Information was also recorded concerning alteration in drug intake and also any change in social habits, as possible means of assessing any change in the severity of pain.

Results

The results show an overall success rate of 58 per cent falling to 42 per cent after six months and this compares well with Eriksson’s results, although in the present series the conditions treated were strictly limited. There is however a significant dif- ference between the two different groups of patients.

Ten out of the 12 patients with trigeminal neuralgia reported relief of pain for varying periods compared with four out of 12 patients with atypical facial neuralgia. After six months however seven out of 12 patients with trigeminal neuralgia felt they were helped by occasional treatment sessions compared with three out of 12 cases of atypical facial neuralgia.

Discussion

There are several difficulties involved in interpreting these results due to the problem of suitable controls in the clinical situation.

The pain of trigeminal neuralgia is essentially different from the pain of atypical facial neuralgia which is often associated with depression. The stimulation routine used in the series does not distinguish between the effects of 100 Hz and 4 Hz fre- quencies which may conceivably effect different pain suppression systems.

The length of pain relief varied considerably and there was no evidence to show that it bore any marked relationship to the overall progress of the patients’ complaints.

However the treatment sessions appeared to be appreciated by most of the patients and produced results greater than a presumed placebo response.

As most oral surgical clinics have a logistical problem in the diagnosis and treatment of patients with chronic facial pain, supportive treatment with transcutaneous nerve stimulation may be a valuable aid. The techniques are certainly worth further investi- gation.

TRANSCUTANEOUS ELECTRICAL NERVE STIMULATION 115

Acknowledgements

Acknowledgements are made to Mr Derrick Lowe of the Medical Research Council Statistical Unit and to Mr Charles Day of the Photographic Department, University College, London.

References

Bowsher, D. (1980). Central mechanisms of orofacial pain. British Journal of Oral Surgery, 17, 185. Eriksson, M.B.E., Sjolund, B. H. & Nielzen, S. (1979). Long term results of peripheral conditioning

stimulation as an analgesic measure in chronic pain. Pain, 6, 335. Gulland, J. & Robinson, R. (1925). Memoirs and Proceedings of the Manchester Literary and Philoso-

phical Society, 69, 79. Hughes, J., Smith, T. W. & Kosterlitz, H. W. (1975). Identification of two related pentapeptides from

the brain with potent opiate agonist activity. Nature, 258, 577. Levine, J. D., Gordon, N. G. & Fields, H. L. (1978). The role of endorphins in placebo analgesia.

Advances in Pain Research and Therapy, Edited by John J. Bonica et al., Vol. 3. New York: Raven Press.

Mannheimer, C. & Carlsson, C. A. (1979). The analgesic effect of transcutaneous electrical nerve stimulation in patients with rheumatoid arthritis. A comparative study of different pulse patterns. Pain, 6, 329.

Melzack, R. (1975). Prolonged relief of pain by brief intense transcutaneous somatic stimulation. Pain, 1, 357.

Melzack, R., Stillwell, D. M. & Fox, E. J. (1977). Trigger points and acupuncture points for pain: correlation and implications. Pain, 3, 3.

Pert, A. & Yaksh, T. (1974). Sites of morphine induced analgesia in the primate brain. Relation to pain pathways. Brain Research, 136, 523.

Pomeranz, B. & Chir, D. (1976). Naloxone blockade ofacupuncture analgesia. Endorphin implicated. Life Science, 19, 1757.

Scott, J. & Huskisson, E. C. (1976). Graphic representation of pain. Pain, 2, 175.