tens in treating chronic pain

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  • TENS in treating

    chronic pain Dennis E McDonnell, MD

    P ain usually serves a useful pur- pose in warning us tha t our bodies are being injured, and it spurs us to take corrective action to pre- vent further injury. We quickly move our hand away from an unexpectedly hot frying pan handle. The absence of pain sensation can lead to severe injury. Decubitus ulcer formation in a n anesthetic-paralyzed patient suffering from a spinal cord injury demonstrates this dramatically.

    Chronic pain and postoperative pain, on the other hand, serve no such protec- tive purpose. Chronic pain is personal, individual, and difficult to measure. Apart from the initiating disease or in- jury, other factors, such as personality type, family conflict, emotional stres- ses, or monetary gain, aggravate and augment the chronicity of pain. Chronic pain can become a disease, and it is dif- ficult to treat successfully.

    Prior to the proposal of the gate theory for pain in 1965, surgical ap- proaches to alleviate pain were destruc- tive, such as cutting nerves and making lesions in the brain (lobotomy) or spinal cord (cordotomy). These procedures can produce relief but at the cost of neuro- logic deficits such as numbness or mus- cle weakness. Often such procedures fail t o give lasting relief.

    For acute postoperative pain, narcot- ics or their synthetic derivatives have often been used. But along with their analgesic effect, these agents bring un- wanted side effects, such as respiratory depression, nausea and vomiting, con-

    Dennis E McDonnell, MD, is associate pro- fessor of neurosurgery, Uniformed Services University of Health Sciences School of Medicine at the Walter Reed Army Medical Center, Washington DC At the time this arti- cle was written, he was associate professor of neurosurgery, University of Iowa Hospitals and Clinics He is a graduate of Creighton Uni- versity School of Medicine, Omaha

    AOR,V Jo l i rnn / . September 1980. Vol 32, N o 3 401

  • stipation, mood alterations and depen- dence.2

    Recently, approaches for pain treat- ment have been more physiologic, ap- plying nondestructive electrical stimu- lation, such as transcutaneous electri- cal nerve stimulation (TENS), to alter or modify pain mechanisms and trans- mission function in the nervous system without damaging it.

    The afferent system of the nervous system, particularly with reference to pain perception, is extremely complex and still incompletely understood. The rationale for using extraneous electri- cal stimulation to relieve pain will be- come clearer with an understanding of pain-signaling mechanisms in t h e peripheral and central nervous sys- tems.

    Peripheral pain receptors, scattered throughout the body, are complex struc- tures with relatively high thresholds to ti mu la ti on.^ These are activated by noxious or painful stimuli. These recep- tors transmit pain impulses via small- diameter, finely myelinated A-delta fibers and unmyelinated C fibers. These fibers conduct slowly and have high thresholds of stimulation. They adapt

    Fig 1. Two-channel transcutaneous stimulator unit showing two pairs of electrodes, regular size 3.75 x 5 cm and large size 5 x 10 em. Powered by three AA size dry cell batteries.

    slowly or not a t all to painful ~ t i m u l i . ~ These fibers transmit pain impulses to the dorsal horn, the posterior column of gray matter in the spinal cord. A-delta fibers evoke sharp, pricking pain, and C fibers evoke deep aching or burning pain.

    Larger, heavily myelinated A fibers transmit other types of sensation such as impulses of touch, vibration, and po- sition. They conduct electrical impulses rapidly. The central input from A fibers tends to balance that from A-delta and C fibers, possibly inhibiting the trans- mission of pain perceptions from these fiber^.^

    All of the impulses coming into the spinal cord are modulated initially by neurons arranged segmentally along the spinal cord in the dorsal horn gray matter, known as the substantia gel- atinosa, before being transmitted to the brain.6 In general, neurons of the substant ia gelatinosa inhibit pain transmission.'

    Transmissions from more specific re- ceptors, such as those from precise touch sensation, travel via the larger, rapidly conducting A fibers to cell bodies in the dorsal root ganglia, which in turn

    402 AORN Journal, September 1980, Vol32, No 3

  • transmit their impulses to the same pool of neurons in the dorsal horn. If the stimulation intensity far exceeds the normal threshold of these specific recep- tors, centrally perceived pain results. Thus, there is no specific system for transmitting pain; rather, the entire peripheral nervous system is involved.8

    It has been proposed that the large A fibers provide major inhibition of pain transmissions in the dorsal horn gray matter, whereas the small A-delta and C fibers excite the neurons and provide relatively little inhibition. Influences from the brain also affect this modula- t i ~ n . ~

    This balanced circuitry of excitation and inhibition has been demonstrated histochemically, with the identification of a pain-receptive neurotransmitter (substance P) and an endogenous anal- gesic transmitter (endorphin).lo

    Fibers transmitting pain impulses take several routes to the brain. Pain transmission involves most sensory f i - bers in the peripheral nerves as well as a dffuse fiber system in the spinal cord. This explains why some destructive procedures such as cordotomy may fail to relieve pain over the long term."

    The clinical importance of these prin- ciples becomes obvious with trans- cutaneous or direct spinal cord stimula- tion. Augmenting the large fiber input by applying extraneous stimulation to the large fibers of peripheral nerves or the dorsal columns of the spinal cord increases the pain inhibition influences on pain perception neurons in the dorsal horn.

    Chronic pain occurs when there is an imbalance, with a dominance of C fiber input tending to block inhibitory action of the substantia gelatinosa cells, open-

    Fig 2. Trial areas of transcutaneous electrical nerve stimulation. Xs mark areas stimulated and 0 s show areas where stirnulation trials failed to relieve the patient's low back and right sciatic pain.

    ing the gate for transmission of pain. By adding an external source of stimula- tion to increase the input of the A fiber system, the inhibitory action of the sub- stantia gelatinosa is augmented, and the gate is closed. External electrical stimulation to peripheral nerves stimu- lates the fast-conducting fibers to close the gate and inhibit pain.'* This theory is particularly attractive because i t suggests that the application of simple, safe electricity through the skin to a peripheral nerve may relieve pain. Electrical stimulation for the treatment of pain is not new and has been used for over 100 years. l3 There was no scientific explanation for the mechanism of its ac- tion, however, until Melzack and Wall's gate theory for pain was published in 1965.14

    This theory was tested initially by stimulating the largest concentration of heavily myelinated fibers in the ner- vous system, the posterior column of the spinal ~ 0 r d . l ~ Results of stimulating the

    AORN Journal, September 1980. Vo132, No 3 403

  • Fig 3-A. A small, compact, two-channel transcutaneous stimulator, light enough to be carried on underclothes for continuous stimulation during normal daily activity.

    spinal cord for pain relief were initially encouraging. TENS developed from a need for a screening device to determine patients who would be candidates for eventual spinal cord stimulation. Transcutaneous stimulation, however, was found to be effective in its own right in relieving pain and therefore sup- planted the need for stimulator im- plants in some cases.16

    Transcutaneous stimulators a r e transistorized electronic devices that generate a pulsating electrical current (Fig 1). The voltage, pulse width, and frequency can be easily adjusted by the patient. They are designed to develop a maximum current of approximately 75 milliamps. The voltage can be regulated from 0 to 100 volts. The electrical wave

    Fig 3-6. Nonreactive adhesive discs secure electrodes with a minimum amount of adhesive contact to the skin, also prevent drying of electrode jelly, and ensure effective electrode contact during normal daily activity.

    form varies with the type of unit and manufacturer. The wave length (pulse duration) can be adjusted from 0.1 to 0.8 milliseconds. Some units have controls with which the patient may adjust wave length, although newer models have the pulse duration pre-fixed." The stimulator unit is powered by dry cell batteries; most newer models have re- chargeable battery packs as a standard power source. The electrodes are car- bonized silicone rubber and have a min- imal area of 4 sq cm.l* Smaller elec- trodes, which are flat and conform com- fortably to the skin surface, are avail- able for special purposes. An aquaphilic gel is used to facilitate current trans- mission from the electrode through skin resistance to the peripheral nerve or

    404 AORN Journal, September 1980. Vol32, No 3

  • painful trigger point. Electrode positioning is critical for

    success. Ideally, the electrodes should be placed proximal to the site of the pain close to the nerve trunk innervating the area of pain. Bipolar electrodes should be positioned from within 2 to 20 cm apart. The electrodes should be posi- tioned as far proximal to the pain as possible. Frequently, however, stimula- tion of points directly over the painful areas is more effective. For postopera- tive pain, sterile electrodes may be posi- tioned immediately after skin closure in the OR. These may be applied to th


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