|Year : 2014 | Volume
| Issue : 1 | Page : 36-41
Transcutaneous electric nerve stimulation in trigeminal neuralgia: A review of literature
Department of Oral and Maxillofacial Surgery, Best Dental Science College, Madurai, Tamil Nadu, India
|Date of Web Publication||19-Mar-2014|
C 72/44, Santanam Road, Tvs Nagar, Madurai - 623 003, Tamil Nadu
Trigeminal neuralgia typically involves nerves supplying teeth, jaws and face of mostly older females around 35 years. A thorough investigation and proper diagnosis is a must prior to treatment for which investigations like computed tomography and magnetic resonance imaging should be done to rule out other systemic pathology. A proper history and multidisciplinary examination is a must for the same. The surgeon should have a thorough knowledge of both odontogenic and non odontogenic cause of pain to confirm the diagnosis and a diagnostic block has been enough in case of no other systemic pathology. Though the etiology is usually obscure, different treatment modalities have been tried for it viz. medicinal treatment, alcohol injection, peripheral neurectomy, rhizotomy and microvascular decompression etc. Transcutaneous electric nerve stimulation (TENS) is a safer, cheaper and promising option for management of neuralgic patients as an adjunct with the drugs used like baclofen or carbamazepine thereby reducing the dose of the drugs taken and minimizing the side-effects of the drugs. The analgesic mechanism of TENS involves gate control theory, physiological block and endogenous pain inhibitory systems. It is a noninvasive and safer adjunct to medical treatment in chronic neuralgic pain, economical and easy for both the doctor and the patient. The reduction of pain can be assessed by patient's verbal response as comparatively objective scale like visual analog scale or McGill's questionnaire could not be clinically applied. TENS cannot be considered as a sole remedy in chronic pain conditions, but as an adjunct whose effectiveness needs a continuous follow-up.
Keywords: Baclofen, carbamazepine, electrical stimulation, fothergill′s disease, McGill′s questionnaire, Tic Douloureux TIC, transcutaneous electric nerve stimulation, trigeminal neuralgia, trigger zones, visual analogue scale
|How to cite this article:|
Usha V. Transcutaneous electric nerve stimulation in trigeminal neuralgia: A review of literature. SRM J Res Dent Sci 2014;5:36-41
|How to cite this URL:|
Usha V. Transcutaneous electric nerve stimulation in trigeminal neuralgia: A review of literature. SRM J Res Dent Sci [serial online] 2014 [cited 2020 May 31];5:36-41. Available from: http://www.srmjrds.in/text.asp?2014/5/1/36/129071
| Introduction|| |
Trigeminal neuralgia, also known as Tic Douloureux, trifacial neuralgia, or fothergill's disease typically involves the nerves supplying teeth, jaws, face and associated structures.
It medical literature historical perspective has been recognized, in fact as early as the first century AD in the writings of Arateus  and later described by Johannes Bausch in 1672. Nicolas Andre in 1756 used the term tic Douloureux (painful spasm). In 1773, Fothergill gave a vivid description. Early treatments included bloodletting and the application of bandages containing arsenic, mercury, cobra, bee venom and other poisons. ,
Trigeminal nerve (V cranial nerve) which is the largest sensory cranial nerve with three divisions viz. ophthalmic, maxillary, mandibular carries information relating to light touch, temperature, pain and proprioception from the face and head to the brain is affected in trigeminal neuralgia. Pain is usually referred to a main division of trigeminal nerve, but in some case more than one division.
| Epidemiology|| |
The disease, typically involves older females aged <35 years and usually involves right half of the face and mostly females. No racial or ethnic risk factors exist. Patients with multiple sclerosis may develop trigeminal neuralgia as a secondary symptom.
| Etiology|| |
The etiology is not fully understood. Many hypotheses being put forth indicate compression of the nerve root commonly by the superior cerebellar artery by tumors and other blood vessels. Furthermore damage to the myelin sheath can cause trigeminal pain; Traumatic accidents, unsuccessful dental work and various infections can damage the trigeminal nerve. The varicella zoster which causes herpes zoster can also cause intense pain in the trigeminal area that is difficult to treat. 
Other proposed etiologies are intrinsic in nature like within the nerve involving proliferative masses of myelin alternating with extreme degeneration or absence of myelin along specific neural segments. About 20% of patients with multiple sclerosis disorder in which plaques of demyelination are traversed by intact axons have trigeminal neuralgia. These plaques have been found in trigeminal neuralgia patient on autopsy. 
| Pathogenesis|| |
Several theories exist but none explain the process completely; may be central or peripheral. Central theory is based on the similarity of trigeminal neuralgia to focal epilepsy and emphasizes the role of deafferentation (secondary to compression of the trigeminal roots or ganglion) state that the genesis of neural hyperactivity. Peripheral theories note that change in peripheral axons and myelin may lead to altered nerve sensitivity to chemical and mechanical stimuli. Calvin concluded that both mechanisms are required to produce trigeminal neuralgia. 
| Clinical Features|| |
It is typically characterized by excruciating paroxysms of pain in the lips, gums, cheeks, or chin and rarely in distribution of ophthalmic division of the fifth cranial (trigeminal) nerve. The pain seldom lasts for a few seconds or a minute, but may be so intense, described as stabbing or lancinating or electric shocks that the patient winces, hence the term "tic". However, the spasmodic contraction of facial muscles is not seen. The paroxysms tend to recur frequently, both during day and night. ,
The pain may be so severe that many sufferers have attempted suicide to put an end to their torment. Another characteristic feature is the trigger zones which precipitate an attack when touched. These are common on vermilion border of lips, alae of nose, cheeks, around the eyes and tongue. Attacks are often triggered by cutaneous stimuli to the face or the oral cavity, which may be such minor activities as talking, chewing, brushing the teeth, or even wind blowing on the face. As a result, facial hygiene as well as a good diet may be neglected. Although 1% of the patients may eventually develop the disorder bilaterally, pain does not cross the midline during any single episode. The clinical course is characterized by exacerbations and remissions, but as the disorder progresses, remissions become shorter and exacerbations more severe. 
No medical test exists to confirm and diagnose the case of trigeminal neuralgia. However in classic cases it is easy to diagnose with a diagnostic block of the involved nerve, which alleviates the pain.
Medical tests should be done to rule out serious medical problems including computed tomography (CT) and magnetic resonance imaging to rule out brain tumor, multiple sclerosis, or associated blood vessel pathology. Very often trigeminal neuralgia is not diagnosed properly and considering as facial pain, many teeth are extracted just to maximize the anxiety of the patient. There is no laboratory or radiological examination that will confirm the diagnosis of trigeminal neuralgia. Lesions should be ruled out and multiple sclerosis to be ruled out in younger patients. All trigeminal neuralgic patients should have a comprehensive oral, maxillofacial and otorhinolaryngologic examination to eliminate organic pathology, CT scan and cryography to rule out vascular anomalies.
As mentioned a positive response to a local anesthetic injection reinforces the clinical impression. A therapeutic response to the first line of medication confirms the diagnosis,
Differential diagnosis is made among various other diseases such as in acute dental diseases where the pain is sharp and continuous and not paroxysmal. When there is gingival recession or dentinal exposure the teeth are sensitive to thermal changes. If the pain is due to unerupted, malposed or supernumerary teeth, removal of the teeth produces a cure. Acute ear diseases can also mimic neuralgic pain but pain here is not paroxysmal but continuous. In traumatic injuries and arthritis, roentgenographic observations show positive findings. Pain from paranasal sinuses is not lancinating but is influenced by posture and other general features of illnesses along with nasal discharge. In facial herpes - presence of vesicles and history of viral illness can be elicited. Pain is not affected by alcohol injection or by resection of the posterior root. In migraine - there is a constant headache whereas trigeminal neuralgia is not associated with headache. Cranial tumors - pain distribution varies in its site. Moreover radiological changes will be seen.
Paroxysmal orofacial pains can cause diagnostic problems, especially when different clinical pictures occur simultaneously. Pain due to pulpitis, for example, may show the same characteristics as pain due to trigeminal neuralgia would. Moreover, the trigger point of trigeminal neuralgia can either be located in a healthy tooth or in the temporomandibular joint (TMJ). Neuralgic pain is distinguished into trigeminal neuralgia, glossopharyngeal neuralgia, Horton's neuralgia, cluster headache and paroxysmal hemicrania. Characteristic pain attacks resembling neuralgic pain result from well understood pathophysiological mechanisms. Consequently, adequate therapy, such as a Janetta procedure (microvascular decompression) and specific pharmacological therapy, could be a cure. 
Neuropathic pain is chronic, diverse in quality, difficult to localize and it occurs in the absence of obvious pathology. To avoid multiple, ineffective dental treatments, general practitioners must be familiar with the signs of nonodontogenic sources of tooth pain. ,
A straightforward diagnosis may not always be possible due to the overlapping clinical signs and symptoms of trigeminal neuralgia and atypical facial pain. ,,,
| Treatment|| |
The diagnosis and treatment of facial pain remains a great challenge for oral and maxillofacial surgeons. The necessity of a multidisciplinary examination is emphasized. Misdiagnosis and multiple failed treatments were common in these patients with chronic orofacial pain. 
Based on patients age, life expectancy, associated medical and psychiatric conditions, compliance with medical therapy and tolerability of adverse effects there are various treatments proposed pharmacologic, surgical and finally non-invasive like transcutaneous electric nerve stimulation (TENS).
Carbamazepine an anticonvulsant being the first and best line of treatment (200 mg bd or tds) had severe side-effects such as drowsiness, fatigue, extreme exhaustion, dizziness, nausea and nystagmus, diplopia and dizziness can be minimized with use of long acting formulation of the drug. Next choice was phenytoin but if no effect has to be discontinued because of its toxicity. Baclofen was also found to be effective. Other drugs tried were oxycarbazine, Lamotrigine, gabapentin, toprimate etc.
Surgery, when indicated, must be based on a specific diagnosis that is amenable to surgical therapy. Neurosurgical treatments may help patients in whom medical therapy is unsuccessful or poorly tolerated.Surgical therapy is indicated who do not respond to medication divided into intra and extra cranial procedures which into percutaneous and open. Intracranial percutaneous techniques are radiofrequency, thermonucleolysis and anhydrous chemoneurolysis. It also included percutaneous ganglion compression. Open intracranial surgery includes sectioning of the nerve root, rhizotomy and microvascular compression. Extra cranial surgery includes percutaneous techniques such as injection of neurotoxic chemicals into the peripheral nerve branch. Extracranial open surgery includes neurectomy, nerve crushing and cryosurgery. ,,
TENS is a non-invasive method that has gained momentum through the success in the treatment of peripheral nerve lesions such as stump pain and phantom limb pain, acute and chronic neuralgias caused by herpes zoster and spinal cord lesions. Combination therapy of drugs with TENS for neuropathic pain produces better outcome and also could be considered safe in geriatric patients. 
| Discussion|| |
Wall and Sweet were pioneers to promote the use of TENS for the treatment of chronic pain. Later on, it was successfully used for the pain of knee osteoarthritis, rib fractures, phantom limb pain and neuropathic pain syndromes etc. 
A study done by Oncel et al. found TENS more effective than non-steroidal anti-inflammatory drugs or placebo in patients with uncomplicated minor rib fractures. 
Fong et al.  advocated that the use of TENS could decrease the use of pethidine for first stage analgesia.
Mechanism of TENS
The analgesic mechanism of TENS involves gate control theory, physiological block and endogenous pain inhibitory systems:
Gate control theory
According to this theory, substantia gelatinosa of spinal cord acts as a gate control system. Activation of large myelinating fibers subserving touch, pressure, vibration is thought to facilitate pre synaptic inhibition of substantia gelatinosa cells in the dorsal horn, thus, reducing pain transmission via small unmyelinated fibers. 
As the frequency of stimulation increases, conduction decreases resulting in physiological block. Basbaum and Field proposed that there is a neural network including midbrain, medulla and spinal cord levels that monitors and modulates the activity of pain transmitting neurons. 
Woolf et al. in their study demonstrated that peripheral electrical stimulation could also excite naloxone dependent anti nociceptive mechanisms, i.e., endogenous opioid systems operating both at spinal and supraspinal levels. 
Kanaka et al. did a study and found that TENS was useful in reducing chronic pain. 
TENS produces electro-analgesia probably by one or of the following mechanisms: Presynaptic inhibition in the dorsal horn of the spinal cord, endogenous pain control (via endorphins, enkephalins and dynorphins), direct inhibition of an abnormally excited nerve and restoration of afferent input.
The intensity and the number of paroxysmal attacks were observed purely from patient's point of view since the objective methods such as visual analog scale (VAS) or McGill's questionnaire could not be clinically applied. VAS has a length of 10 cm the left end representing a pain intensity of '0' no pain in the right end and representing a pain intensity of 10 (unbearable pain) the patient had to choose a point on this scale to describe his intensity of pain. ,
McGill's pain questionnaire consists of 78 adjectives arranged in 20 groups and the patients express their pain. This questionnaire reflects 3 dimensions namely sensory, affective and evaluative. 
Descriptor differential scale applies psychophysical principles to clinical pain assessment. ,
Advantages of TENS
- No Prostaglandins inhibition, since TENS controls pain by gate control mechanism.
- Rapid and timely inhibition of pain at peak progression.
- No adverse effects of drugs
- Short term treatment for 20-40 days when compared with long-term medicinal treatment.
- No need for surgical intervention.
- Doesn't need much expertise.
- Can be used at home with portable machine.
- Equally effective in post neurectomy and post injection alcohol neuralgia.
Transcutaneous electrical nerve stimulator refers to any one of a number of commercially available devices that apply a low voltage electrical impulse to the nerve system via electrodes placed on the skin, one being over painful area and the other elsewhere. A gel like prior to recording to electrocardiogram should be applied prior to the pad placement. The stimulus intensity, frequency and duration are adjusted by the patients to obtain relief from pain, the rationale being that electrical stimulation generated synchronous activity in the large fibers and their collaterals. These neural impulses go to substantia gelatinosa allowing reduction of impulses in smaller nerve fibers. This method can be used in trigeminal area.
| Complication and Contraindication|| |
TENS is remarkably free from side-effects. The only common problem is related to an allergic dermatitis which the patient experience due to the adhesive tape holding the electrodes in patient. A mild erythema occur at the site of stimulation and if insufficient electrolyte gel is used a burning pricking sensation occur.
The only absolute contraindication for using TENS is in patients with pacemakers or other implanted electrical devices, which may be affected by the field generated by the modulator. It is probably best not to use TENS in patients unable to understand the controls such as young children, the mentally retarded, or patients with senile dementia. Since a sudden increase in the amplitude control can produce a highly painful muscle contraction for the same reason it is best for patients working with heavy machinery etc., not to use the stimulator.
| Summary and Conclusions|| |
TENS is used in a variety of different clinical settings to treat a range of different acute and chronic pain conditions and has become popular with both patients and health professionals. 
The management of neuropathic pain is challenging, with medication being the first-line treatment. TENS should be considered as safe, simple and reusable first line of treatment for many pain conditions including trigeminal neuralgia, specially even, in a rural set up where technical expertise for surgical treatment is lacking and in patients in whom there are seen adverse drug reactions or they are not willing to take medicinal treatment, or cannot afford expensive surgical intervention. 
TENS is extremely useful in some dental procedures such as TMJ syndrome and tooth extraction; however, its use is not practical in all situations. The dentist must remember that TENS is an adjunctive form of treatment. ,
Although safe and effective pain control has been achieved using TENS in many fields of medicine, the application of this technique to dentistry remains almost unexplored. A study of the effectiveness of TENS in alleviating pre-existing orofacial pain, in providing analgesia during the primary dental treatment of these patients and as an alternative to conventional local anesthesia during cavity preparation in regular patients was examined. In approximately 80% of patients TENS successfully alleviated pre-existing orofacial pain. Primary dental treatment of these patients, however, was only possible under conventional local anesthesia. Pain induced by cavity preparation was adequately suppressed by TENS in approximately 80% of all cases. 
It is not a panacea for all types of pain, nor should it be used as a last resort. When applied correctly and with care, TENS is useful in the management of pain in the head and face.
Kanaka et al. did a study and proved TENS as a safer adjunct with the anticonvulsant drug used for trigeminal neuralgia. This was useful as the patient could avoid the frequency of drug and thereby drug toxicity was minimal. Further references from the net and journals do prove it is still effective as an adjunct rather than the main line of treatment in chronic neuralgic pain. ,,,,
In short it could be that TENS operated by distorting the functional activity of the nervous system thereby jamming one of its inputs.
TENS is a frequently applied therapy in chronic pain although evidence for effectiveness is inconclusive. Several types of TENS, based on different combinations of frequency, pulse duration and intensity, exist. The precise mechanism of action and the relevance of combinations of stimulus parameters are still unclear and do need further study and evaluation where presently the study done is minimal in practice due to cases being scattered by being referred to neurologist and scattered among the various dentists and not reported or to practitioners who misdiagnose or the patient are only under the anticonvulsant and do not properly follow. If a proper study and evaluation and a proper follow-up done, the patients might be benefitted by this non-invasive safer device for alleviating the incapacitating pain.
| References|| |
|1.||Gintautas Sabalys, Gintaras Juodzbalys, Hom-Lay Wang. Etiology and Pathogenesis of Trigeminal Neuralgia: A Comprehensive Review. JOMR 2012 Oct-Dec; Vol 3 No 4:e2. |
|2.||Loeser D. Cranial neuralgia. In: Loeser JD, Bonica JJ, editors. Bonica′s Management of Pain. 3 rd ed. Philadelphia: Lippincott Williams and Wilkins; 2001. p. 855-61. |
|3.||Siddiqui MN, Siddiqui S, Ranasinghe JS, Furgang FA. Pain management: Trigeminal neuralgia. Hospital physician, 2003. p. 64-70. Available from: http://www.Turner-white.com. |
|4.||Shafer WG, Hine MK, Levy BM. Diseases of the nerves and muscles. In:R Rajendran, B.Sivapathasundaram, editors. A Textbook of Oral Pathology. 6 th ed. Philadelphia: W.B. Saunders Co.; 1983. p. 845-6. |
|5.||Shaber EP, Krol AJ. Trigeminal neuralgia - A new treatment concept. Oral Surg Oral Med Oral Pathol 1980;49:286-93. |
|6.||Calvin WH, Loeser JD, Howe JF. A neurophysiological theory for the pain mechanism of tic douloureux. Pain 1977;3:147-54. |
|7.||Mitchell RG. Pre-trigeminal neuralgia. Br Dent J 1980;149:167-70. |
|8.||Siegfried J. Trigeminal neuralgia and other facial pain - Diagnosis and therapy. Ther Umsch 1997;54:83-6. |
|9.||de Bont LG. Spontaneous pain attacks: Neuralgic pain. Ned Tijdschr Tandheelkd 2006;113:474-7. |
|10.||Law AS, Lilly JP. Trigeminal neuralgia mimicking odontogenic pain. A report of two cases. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1995;80:96-100. |
|11.||Matwychuk MJ. Diagnostic challenges of neuropathic tooth pain. J Can Dent Assoc 2004;70:542-6. |
|12.||Türp JC, Gobetti JP. Trigeminal neuralgia versus atypical facial pain. A review of the literature and case report. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1996;81:424-32. |
|13.||Claeys T, Bremerich A, Cesteleyn L, Kovacs B. Importance of diagnosis in facial pain. Acta Stomatol Belg 1992;89:239-48. |
|14.||Neilson K, Field EA. Trigeminal neuralgia: A cautionary tale. Br Dent J 1994;176:68-70. |
|15.||Krafft RM. Trigeminal neuralgia. Am Fam Physician 2008;77:1291-6. |
|16.||Israel HA, Ward JD, Horrell B, Scrivani SJ. Oral and maxillofacial surgery in patients with chronic orofacial pain. J Oral Maxillofac Surg 2003;61:662-7. |
|17.||Lee KH. Facial pain: Trigeminal neuralgia. Ann Acad Med Singapore 1993;22:193-6. |
|18.||Bremerich A, Krischek-Bremerich P. Treatment for trigeminal neuralgia. An overview. Dtsch Z Mund Kiefer Gesichtschir 1991;15:369-75. |
|19.||Cesteleyn L, Bremerich A, Claeys T, Kovacs B. Treatment concept of facial pain. Acta Stomatol Belg 1992;89:5-14. |
|20.||Bremerich A, Wiegel W, Thein T, Dietze T. Transcutaneous electric nerve stimulation (TENS) in the therapy of chronic facial pain. Preliminary report. J Craniomaxillofac Surg 1988;16:379-81. |
|21.||Wall PD, Sweet WH. Temporary abolition of pain in man. Science 1967;155:108-9. |
|22.||Oncel M, Sencan S, Yildiz H, Kurt N. Transcutaneous electrical nerve stimulation for pain management in patients with uncomplicated minor rib fractures. Eur J Cardiothorac Surg 2002;22:13-7. |
|23.||Fong LH, Irene LY, Grace GY. A pilot study on the use of transcutaneous electric nerve stimulation machine for first-stage analgesia in a teaching hospital. Hongkong Journal of Obstetric and Gynecology 2008;8:9-12. |
|24.||Melzack R, Wall PD. Pain mechanisms: A new theory. Science 1965;150:971-9. |
|25.||Basbaum AI, Fields HL. Endogenous pain control systems: Brainstem spinal pathways and endorphin circuitry. Annu Rev Neurosci 1984;7:309-38. |
|26.||Woolf CJ, Mitchell D, Barrett GD. Antinociceptive effect of peripheral segmental electrical stimulation in the rat. Pain 1980;8:237-52. |
|27.||Kanaka TS, Balasubramaniam V, Sampathkumar M, Renuga S, Avery R. New trends in the management of certain pain syndromes. Institute of Neurology Madras Proceedings. 1980-9. p. 27. |
|28.||Chen HI, Lee YK. The measurement of pain in patients with trigeminal neuralgia. Clinical Neurosurgery. Vol. 57. Ch. 19. 2010.(a publication of the Congress of the Neurological Surgeons, also found in Research Gate) |
|29.||Gracely RH. Measuring pain in the clinic. Anesth Prog 1990;37:88-92. |
|30.||Gracely RH, Kwilosz DM. The descriptor differential scale: Applying psychophysical principles to clinical pain assessment. Pain 1988;35:279-88. |
|31.||Carroll D, Moore RA, McQuay HJ, Fairman F, Tramèr M, Leijon G. Transcutaneous electrical nerve stimulation (TENS) for chronic pain. Cochrane Database Syst Rev 2001;3:CD003222. |
|32.||Holsheimer J. Electrical stimulation of the trigeminal tract in chronic, intractable facial neuralgia. Arch Physiol Biochem 2001;109:304-8. |
|33.||Katch EM. Application of transcutaneous electrical nerve stimulation in dentistry. Anesth Prog 1986;33:156-60. |
|34.||Allgood JP. Transcutaneous electrical neural stimulation (TENS) in dental practice. Compend Contin Educ Dent 1986;7:640, 642-4. |
|35.||Wilder-Smith P, Zimmermann M. Analgesia by transcutaneous electrical nerve stimulation (TENS). Schweiz Monatsschr Zahnmed 1989;99:653-7. |
|36.||Johnson MI, Bjordal JM. Transcutaneous electrical nerve stimulation for the management of painful conditions: Focus on neuropathic pain. Expert Rev Neurother 2011;11:735-53. |
|37.||Murphy GJ. Management of craniofacial pain with transcutaneous electrical nerve stimulation: A clinical protocol. J Pain Symptom Manage 1989;4:41-3. |
|38.||Köke AJ, Schouten JS, Lamerichs-Geelen MJ, Lipsch JS, Waltje EM, van Kleef M, et al. Pain reducing effect of three types of transcutaneous electrical nerve stimulation in patients with chronic pain: A randomized crossover trial. Pain 2004;108:36-42. |
|39.||Yameen F, Shahbaz NN, Hasan Y, Fauz R, Abdullah M. Efficacy of transcutaneous electrical nerve stimulation and its different modes in patients with trigeminal neuralgia. J Pak Med Assoc 2011;61:437-9. |