The Gate Control Theory of Pain

Pages: 39-41
Year: 2001
Dr. Ida Rolf Institute

Structural Integration – The Journal of the Ida Rolf Institute – Spring 2001 – Vol 29 – Nº 02

Volume: 29

The unfortunate inability of surgeons to consistently abolish pain by making lesions in the supposed pain transmission systems, at every level of neural organization, is notable. This led one investigator, nearly fifty years ago, to question some of the hypotheses of the traditional view.’ In some cases, he reported, pain is increased by surgical lesions; the effects are apparently unpredictable and seem almost arbitrary. In the traditional view (here referred to as the Specificity Theory), there are neurons that specialize in transmitting pain, and it is afferent activity in them that is felt as pain. It follows from this theory that a surgeon ought to be able to simply cut the right neurons in his patient to relieve him of chronic pain, if the researcher could only tell him which ones to cut; and that a chiropractor ought to be able to simply free the right pinched nerve to relieve the pain in his patient.

Livingston2, Melzack3, and Melzack and Wall’ note that there are a number of psychological factors in the subjective sensation of pain. Livingston finds that his “dolorimeter” is only effective within certain clinical limits in measuring perceived pain. Many athletes know of picking up scrapes or shocks which are only sensible after the contest is over. Melzack and Wa115 cite Pavlov, who was able to train dogs to anticipate food rewards when stimulated by shocks, without the usual signs of pain, while shocks of the same intensity couldff; elicit pain when applied to other areas of the skin.


There are two general classes of peripheral fibers: the myelinated (“A”) and the unmyelinated (“C”). The larger fibers have higher conduction rates, generally speest C fibers. The destinations of the largest A fibers are synapses on cells of the dorsal column system as well as synapses on cells of the dorsal horn. All other fibers project only to the dorsal horns .6 Perl found C and A-delta (i.e., small A) fibers with such high thresholds that they responded exclusively to damaging cutaneous stimuli. He concluded that the specific responses of such specialized reception pathways were the only signals evoking the experience of pain. This would seem to be the simplest explanation; but there are a number of problems with it.

Firstly, it does not necessarily follow that receptor fibers which do not respond to noxious stimuli exclusively do not contribute positively to pain sensation; there is in fact a continuum across the levels of receptor fiber thresholds, and some receptors fire at increasing rates in response to increasing stimulation. While the small diameter fibers that have been called “nociceptors” respond exclusively to noxious stimuli, stimuli also activate the large A-beta fibers; and indeed it is true that a noxious stimulus evokes activity across the entire range of diameters and thresholds.

The larger fibers in general have low thresholds, so that minimal stimulation evokes discharges in a relatively high proportion of A fibers, measurable as a continuous negative dorsal root potential.’ As stimulation increases, the higher-threshold fibers join in the total activity of receptor fibers, resulting in a relative increase in the ratio of small to large fibers. Furthermore, if stimulation is prolonged, the ratio increases further, because fibers with higher conduction rates within a class of receptor group show a tendency to adapt more quickly than fibers with lower conduction rates’; Melzack and Wall’s theory’ proposes that the relative amount of large and small (i.e., generally fast- and slow-conducting, respectively) fiber discharges is an important king, and the largest A fibers are larger than the large factor in pain.

Secondly, Hunt and McIntyre10 have found that a large number of receptor fiber units respond, with different temporal firing patterns, to both of two of the classic modalities, for instance to both temperature and pressure. One might well ask if the traditional view, in which there are four modalities subserved by specific receptor sites, is tenable in the face of such evidence.

Thirdly, we assume that the mechanisms of pain are included in the homeostatic systems of the body; but this assumption may t well be incompatible with a specificity I model of nerve energies. One is tempted to t suggest that pain is the homeostatic system par excellence, especially since the degree of 1 aversive reaction and avoidance behavior l in a clinical setting seems to be correlated ‘ closely to the intensity of the noxious stimulus. But precisely for this reason it is essential to consider pain in the context of the organism as a whole; it may well be that suppression of the sensation of pain in some instances is essential to the integrity of the ‘ organism, and the advantage of a hierarchical nervous system that is evaluative at t various levels to screen out or minimize some stimuli in favor of others is evident.

And evaluation from a physiological point of view means summation; excitation and inhibition are effected on a neuron from higher levels of system organization and by different cells of the same and lower orders; while it is clearly advantageous to receive detailed information, as Perl, for one, recognizes11, the details must occur in the overall context of ongoing activity. Hence, we would expect the degree of attention paid to lower-order information to be subject to considerable variation, and evaluation to be consistently effected at as low a level as possible – this so that nervous activity that is most important for the organism as a whole is given preferential attention.

From the point of view of homeostasis, pain is an evaluation; Perl begs the question by calling pain a “sensory system.”12

Fourthly, it is not a simple matter to characterize pain; it may falsify it to pigeonhole it as a sensory experience. Although it is difficult to conceive of pain without a sensory dimension, there is evidence that the sensory dimension of what in normal subjects would be painful stimuli exists also in persons who are congenitally insensitive to pain, but who are nevertheless quite capable of perceiving that the intensity of a stimulus is increasing; nevertheless an affective dimension of the experience is lacking that is present in normal subjects.” This observation led to Melzack’sl” development of the McGill Pain Questionnaire, which consists of three classes of word descriptors: sensory, affective, and evaluative.

Of course, in the face of these considerations, it is still conceivable that some specific fibers transmit information that is always interpreted as pain.

Firstly, it is quite clear that certain receptor fibers are fairly characterized as nociceptors, since noxious stimuli are indeed what they transmit. One must ask if pain can be evoked in the absence of highintensity stimulation of nociceptors; even if other receptor fibers play a role in pain transmission, it is conceivable that pain perception can only be elicited in the presence of nociceptor stimulation.

Secondly, although a receptor fiber fires in response to two or more kinds of stimuli, it can still be classified according to the specific energies it emits. It may be that its discrete response patterns are still recognized as specific signals.

Thirdly, there is no guarantee that always and everywhere the best homeostatic system has developed for an organism.

There are several interesting studies, however, that provide concrete evidence against the specificity theory of reception. Melzack and Schecter15 did experiments in which the influence of vibration on itch was assessed by taping an irritant to a subject’s arm and measuring the subjective report of itch intensity during and following vibration (it is commonly assumed that C fibers are responsible for transmitting the sensation of itch). The level of experienced itch was observed subjectively to decrease, suggesting that the low-intensity stimulation of the vibration was involved in some way with the inhibition of the pain mechanism. Melzack and Wall16 cite the even more curious finding that vibration intensifies high levels of pain. In Melzack and Schecter’s study,17 distraction of attention was ruled out as an alternate explanation.

Vibration effects on pain are strongly suggestive that the specificity theory is inadequate; the experiments suggest that there is a patterned monitoring of sensory inputs rather than a fixed reception of specific information.


The dorsal horns are two systems on either side of the spinal cord that extend its length. The six zones which make it up are designated Laminae I through VI, situated dosal to ventral; they each serve apparently different functions, although much remains to be discovered about their anatomy and physiology. A region within these six zones has been designated the Substantia Gelatinosa, comprised of Laminae II and III. This region has been proposed by Melzack and Wall as being the location of- the gate control mechanism in their theory.

Lamina I cells play a role in pain, since they receive projections from nociceptive peripheral fibers and project themselves in turn to higher levels of the cord18.

Lamina II and Lamina III cells (the Substantia Gelatinosa) receive inputs from both large and small afferents; the anatomy of the region is particularly interesting with regard to these19. The small-diameter fibers enter the Substantia Gelatinosa dorsally while the large-diameters enter ventrally. Wall20 calls this fact suggestive, noting that “in the accessory olive … afferents from one cochlear nucleus end on one end of the cell and excite, while afferents from the other side end on the other end and inhibit.” In other words, there is a precedent in vertebrate neural anatomy for the sort of summation-structure that would exercise gate control.

Substantia Gelatinosa cells are small and they do not project outside the Laminae, but they enclose dendrites from the more ventral Lamina IV. They connect with one another, however, via short fibers and at a distance via the Lissauer Tract, which rune along the Substantia Gelatinosa 21

Unfortunately, it is extremely difficult to study individual cells of the Substantiz Gelatinosa because they are so sma1122 However, Wall has made some intriguing discoveries about afferent spinal processes: that suggest that these cells play an important part in pain.

First, there is the evidence that the membrane potential of cutaneous afferent terminals is controlled by Substantia Gelatinosz cells. Stimuli were evoked in one dorsa: root, and in another one that exerted an inhibitory effect on the reflex that usually fol. lowed stimulation of the first root

Isopotential maps were then made of the potentials of cord cells during the “tail” of the dorsal root potential and pre-synaptic inhibition; it is the Substantia Gelatinosa that exhibits the only important region of activity.

In a second experirnent23 – it is necessary to quote at length -, “The dorsal columns and Substantia Gelatinosa had been completely sectioned between L6 and L7 [a cat has seven lumbar vertebrae], but Lissauer’s tract and other white matter was intact. An afferent volley was fired into the intact segment 10 msec, 20 msec and 30 msec before the current distribution was analyzed in the deafferented segment 16. 10 msec after the stimulus, a dense group of current sinks were located along the border of the lateral white matter and in the region of Lissauer’s tract. After 20 and 30 msec the more ventral activity fades, while the sinks in the region of the Lissauer tract extend medially into the region of the Substantia Gelatinosa. The height of the dorsal root potential is reached after 30 msec…section of the Lissauer tract between L6 and L7 abolishes the dorsal root potential and the activity of the Substantia Gelatinosa…”

In a third experiment24, the activity of the large fibers of a peripheral nerve was arrested. In this situation the small fibers alone are active; the result of an afferent volley in these is a positive dorsal root potential, as opposed to the negative one elicited by low-threshold fibers alone. Wall finds that “[the] opposing direction of terminal arborizations together with the opposing effect of their volleys on the dorsal root potential is suggestive.”25

The outcomes of these experiments are interpreted by Melzack and Wa1126 as suggesting that the Substantia Gelatinosa functions as a gate control mechanism.

The cells of Lamina IV, like the cells of Lamina V, are large, as contrasted with the cells of the Substantia Gelatinosa. The Lamina IV cells, as noted above, receive inputs from Substantia Gelatinosa cells; they respond to electrical stimulation of the large afferent fibers, which terminate on the Lamina IV side of the Substantia Gelatinosa. They have small receptive fields, as contrasted with Lamina V cells, and respond to low-intensity stimulation, but have not been shown to exhibit any special changes during noxious stimulation. This is not to claim, of course, that they do not function at all in pain processes.

The interpolation of Lamina I V between the Substantia Gelatinosa and Lamina V, together with the fact that Lamina IV receive inputs from Substantia Gelatinosa cells an( is affected by large-afferent impulses, an( the probability that Lamina V cells receive inputs from Lamina IV cells and are indirectly affected by large-afferent cells, have led Hillman and Wall27 to theorize that Lamina IV cells transmit the impulses from large afferents to Lamina V.

Melzack28 has proposed that the cells o Lamina V are the central transmission cell: in the Gate Control mode129. The evidence shows that they at least play a role in pair processes and that their functioning is consistent with the mode130.

Hillman and Wall31 did experiments it which it was found that a typical Lamina cell has a receptive field of three concentric geographical areas on the skin. In the central area all stimuli that affected the cell, a; determined by alterations of the ongoing activity rate, had excitatory effects, from mild touch to hard pinch. The intensity o: the excitatory stimulus increased with the firing rate of the cell. The cells initially exhibited a high frequency of firing rate following the onset of continuously appliec stimulus, followed by adaptation to a lower frequency that persisted as long as the stimulus continued. The temporal firing patterns were quite interesting; in an experiment in which electrical stimulation of cutaneous receptive fields was effectedthrough hypodermic needles, it was found that the temporal response of an excited cell had a characteristically different pattern from the ongoing activity – the total number of impulses was higher, but they spiked in bunches followed by periods of silence.

Stimulation in the second concentric skin area produced results on the same Lamina V cell different from stimulation in the first area. Mild stimulation by electrodes resulted in inhibition, measured as a lower firing rate than at rest, whereas after a point increasingly higher intensities produced excitation. Low-level stimulation of the second region inhibited the Lamina V cell during simultaneous first-region stimulation as compared with simple first-region stimulation.

Stimulation of any intensity in the third concentric circle resulted only in inhibition, which leveled out, however, above a certain intensity of cutaneous stimulation.

The similarity of these findings to that of the Melzack and Schecter32 study of vibration is apparent, and leads us naturally to ask if a correlation exists between input fiber diameter and Lamina V activity. What is probably happening in the second concentric zone is that the low-threshold fibers, which include all the larger fibers, inhibit in some way the output of the Lamina V cell, while the high-threshold ones excite it.

Since the low-threshold fibers respond to gentle stimulation (by definition), it must be they that are exciting the Lamina V cell in the first concentric region to fire in response to low intensities, while it must also be they in the second concentric region who inhibit the same cell. Adequately intense stimulation of the second concentric region activates excitatory high-threshold fibers; the resultant effect, that the Lamina V cell is excited above a certain intensity, is consistent with the second-zone results.

Furthermore, the effect of large afferents on Lamina V cells was found to be characteristically different from that of small afferents. Small afferents produced what is known as the “wind-up” effect – increasing potentiation of the target cell followed repeated stimulation. However, low-threshold, large-diameter afferents produced a burst of activity followed by silence .33 This inhibitory effect following excitation is evidence supporting the fundamental assumptions of the Melzack and Wall Gate Control Theory.

The characteristic firing pattern of the Lamina V cell during first region stimulation indicates that excitation is being modulated by inhibition, like the escapement mechanism of a clock. Only low-threshold fibers can be responsible for this, since the effect is demonstrated at all intensities above minimum. The indication is that low threshold fibers have an excitatory and inhibitory effect on Lamina V cells. This suggests that a negative-feedback mechanism is operative.

Hillman and Wall’s34 analysis of their findings, that Lamina V cell activity is the product of the interaction between the activity of large and small fibers, is supported by this and by another part of Hillman and Wall’s study34 They stimulated the dorsal columns, since low-threshold cutaneous afferents send axons up it;35 these same afferents also branch into the dorsal horns. The response of Lamina V cells was similar but more pronounced than that to stimulation of the second concentric receptive region, namely, that bursts were followed by relatively long periods of silence; the bursts were shorter and the silences longer than during low-level second-region stimulation.

These results are important for this reason: they demonstrate that pain is a function of central analysis of patterns of information, by showing that large fibers play a role that complements the role of small fibers. It will be noted that this summation of inputs by the complementary effects of different classes of afferents contradicts Perl’s36 and others’ assertion of the specificity of cutaneous reception analysis.


The proposed gate control mechanism is located in the Substantia Gelatinosa. It is proposed that it selectively transmits afferent impulses to central transmitter cells in the. dorsal horn. These transmitter cells, it is proposed 31 are the Lamina V cells. The unmodified afferent impulses influence brain processes via dorsal column fibers directly, providing the possibility for higher-level control .38

Impulses in large peripheral fibers have an initial effect on central transmitter cells, but continued stimulation is mitigated by a negative feedback mechanism. The proposal is that these cells have an excitatory effect on transmitter cells, but also excite cells in the Substantia Gelatinosa, which in turn exercise an effect of inhibition on the excitation of transmitter cells by large fibers. Impulses in small peripheral fibers, on the other hand, act with positive feedback effects. Feedback of both kinds is effected in the Substantia Gelatinosa.39 Melzack and Wall’s conclusion is that the intensity of pain felt is dependent not only on the absolute intensity of the stimulus and the ongoing activity of the central cells but also on the differential firing rates of large and small fibers.

An account of a pain sensation in this model would begin with a noxious stimulus, at First increasing the relative number of large peripheral fibers that fire. This would tend 😮 inhibit the stimulus of the central transmission cells that trigger the system that leads to pain experience. The transmission :ell firing rate increases slowly at first, since :he large and small fibers are both stimulating the transmission cells, as well as can-ceiling each other’s feedback effects. The more-adaptable large fibers exert a progressively diminishing effect of inhibition, sc the transmission cell firing rate increases It is the volume of impulses from the transmitter cells that effects the action patterr that leads to pain experience.


1. Livingston, WK. “What is Pain?,” Sci. Amer., vol. 196 (March), p. 59.

2. Ibid.

3. Melzack, R. “The Perception of Pain,” Sci. Amer., vol. 204 (February), p. 41.

4. Melzack, R., and Wall, RD. “Pain Mechanisms: A New Theory,” Science, vol. 150, p. 971.

5. Ibid.

6. Wall, P.D. “Two Transmission Systems for Skin Sensations,” in W.A. Rosenblith (ed.), Sensory Communication. Wiley 1961.

7. Perl, E.R. “Is Pain a Specific Sensation ?, ” J. Psychiat. Res., vol. 8, p. 273.

8. Burgess, P.R., Petit, D., and Warren, R.M. (1968). “Receptor Types in Cat Having skin Supplied by Myelinated Fibres,” J. Neurophysiol., vol. 31, p. 833.

9. See note 4.

10. Hunt, C.C., and McIntyre, A.K. (1960). “Properties of Cutaneous Touch Receptors in Cat,” J. Physiol., vol. 153, p. 88.

11. See note 7.

12. Ibid.

13. Sternbach, R.A. Pain: A Psychophysiological Analysis. Academic Press 1968.

14. Melzack, R. “The McGill Pain Questionnaire: Major Properties and Scoring Methods,” Pain, vol. 1, pp. 27799.

15. Melzack, R., and Schecter, B. “Itch and Vibration,” Science, vol. 147, p. 1047.

16. See note 4.

17. See note 15.

18. See note 7.

19. Szentagothai, J. “Neuronal and Synaptic Arrangement in the Substantia Gelatinosa Rolandi,” J. Comp. Neurol., vol. 122, p. 219.

20. Wall, P.D. “Presynaptic Control of Impulses at the First Central Synapse in the Cutaneous Pathway,” Progr. Brain Res., vol. 12, p. 92.

21. See notes 19 and 20.

22. See note 20.

23. Ibid.

24. Ibid.

25. Ibid.

26. See note 4.

27. Hillman, P., and Wall, P.D. (1969). “Inhibitory and Excitatory Factors Influencing the Receptive Fields of Lamina 5 Spinal Cord Cells,” Exper. Brain Res., vol. 9, p. 284.

28. Ibid.

29. Cf. note 4.

30. See note 27.

31. Ibid.

32. See note 15.

33. Mendell, L.M. and Wall, P.D. “Presynaptic Hyperpolarization: A Role for Fine Afferent Fibres,” J. Physiol., vol. 172, p. 274. And see note 27.

34. See note 27.

35. Ibid.

36. Ibid.

37. See note 7.

38. See note 27.

39. Ibid.

See also:

Dimond, E.G. (1971). “Acupuncture Anaesthesia,” J.A.M.A. vol. 218, p. 1558.

Levine, J.D., Gormley, J. and Fields, H.L. (1976). “Observations on the Analgesic Effects of Needle Puncture (Acupuncture),” Pain, vol. 2, pp. 149-59.

Melzack, R. “Akupunktur and Schmerzbeeinflussung,” Anaesthesist, vol. 25, pp. 204-7.

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