Study of Gate Control: Theory and Pain

I thought I knew what pain meant until I got asked to define it. That is when I realised my ignorance and surprisingly, I was not alone. People frequently find it hard to describe commonly used words despite the fact that they are very much part of our lives.

In my search for an official definition of human pain I came upon the one provided by the International Association for the Study of Pain which is: “an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage” (IASP 1979).

Undoubtedly, being able to feel pain upon external harmful stimulation or internal damage is a vital survival mechanism. In the words of the psychologist and poet Asenath Petrie: “There is nothing in human experience more central than our capacity to feel, and no aspect of this so crucial as our capacity to suffer, perhaps more particularly to suffer from extremes of physical pain.”

Nonetheless, those fortunate enough to be able to experience pain have one thing in common; they all want it to stop. Thus pain has increasingly been considered a significant cause of suffering and reduced quality of life.

Gate Control Theory:

Going back to the 17th Century, the prominent explanation of pain had been proposed by the French philosopher and scientist, René Descartes. Termed the Specificity Theory of pain his conceptualization hypothesized that pain was transmitted from the periphery along specific pain fibres, up the spinal cord to finally arrive to the brain and activate a region associated with pain perception. Thus, Descartes described pain in terms of an alarm bell ringing in a bell tower, where pain impulses travelled directly to the brain.

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Despite the prevalence of Descartes’ ideas, his theory was clearly flawed and allowed little space for psychological factors in the experience of pain. Had it been correct, the feeling of pain would be directly proportional to the extent of physical damage caused.

In 1965, the collaboration between Canadian psychologist Ronald Melzack and British physiologist Patrick Wall put forward a concept that was to have a major impact on our understanding of pain. Their paper, ”Pain Mechanisms: A New Theory,” has previously been described as ”the most influential ever written in the field of pain”.

The Gate Control Theory, as it was termed, provides a multi-dimensional understanding of the complex phenomenon of pain and its multiple influences. It emphasises the mechanisms in the central nervous system that control the perception of a noxious stimulus, and thus integrates afferent, upstream processes with downstream modulation from the brain.

Melzack and Wall simply stated, in an elegant and concise way, a pattern-based theory about mechanisms underlying pain, postulating the operation of a neural gate in the dorsal horn of the spinal cord to control activation of ascending projections; thus, the pain perception can be increased or decreased depending on influences on the gating system.

Absence of specific pain receptors and a lack of dedicated central pathways was core to this proposal. It was emphasized that despite many years of study, few primary afferent fibres or CNS cells were reported to be selectively activated by pain-causing stimuli. This was buttressed by reports of the absence of complaints of pain by soldiers at the time of grievous injury and the occurrence of pain in CNS disorders, such as thalamic syndrome, in which noxious stimuli were not involved.

According to the theory excitations and inhibitions are independently controlled. The degree to which the gate increases or decreases sensory transmission can be influenced by two proposed means.

First, descending inhibitory impulses from neurons in the brainstem and cortex can interfere with the ascending pain signal from the tissue damage. These signals from the brain might include cognitive or emotional factors, such as thoughts, beliefs, emotions, mood, prior experience, expectations, memories, attention, and cultural attitudes. For example, memories of a prior negative experience or anxiety might heighten pain experience, whereas a positive mood or pleasant distraction might decrease the pain.

The second mechanism influences pain perception through ascending signals from the peripheral nerves, which function as competing sensory information. They proposed that primary nociceptive cells synapse with a T cell which carries the impulse onward to higher centres. There are two types of nerve fibres that carry the majority of pain signals to the spinal cord: small diameter myelinated and unmyelinated (α-δ and C) fibres and large diameter myelinated (α-β) fibres.

Physical stimulation such as rubbing, massage, and vibration cause excitation in the α-β nerve fibres, which conduct the signal more quickly than the α-δ fibres, where pain due to tissue injury is transmitted. If a pain signal is travelling to the brain via the α-δ fibres and a simultaneous physical stimulation signal is sent via α-β fibre, the physical stimulation signal will reach the brain first because it is moving at a greater speed than the pain signal. According to the Gate Control Theory, the pain perception will be diminished via interference by the other physical stimulation. Given this complex theory of pain, assessment of pain typically involves a comprehensive sequence.

Crucial to this theory was the presence of an inhibitory interneuron in the substantia gelatinosa (laminae II and III), which prevented activation of the T cell (Figure 1). The theory proposed that pain would be ‘gated-out’ by stimulating the α-β fibres in the painful area but opened when the slow conducting C ”pain” fibres transmitted a high volume and intensity of sensory signals. The gate could be closed again if these signals were countered by renewed stimulation of the large fibres.

Figure 1 The Gate Control Theory. The inhibitory interneuron can be activated by the α-β fibres and inhibited by the α-δ and C fibres that close in response to normal stimulation of the fast conducting α-β ”touch” nerve fibres.

In summary, the Gate Theory proposed that small fibres activated excitatory systems that excited output cells – these latter cells had their activity controlled by the balance of large-fibre mediated inhibitions and were under the control of descending systems. Incoming pain signals are therefore subjected to the modulating influence of the neural gate before it evokes pain perception and response.

Despite the fact that it was a theory, vigorous debate and a great deal of research were generated to disprove or support it. As historians of science have pointed out, good theories are instrumental in producing facts that eventually require a new theory to incorporate them. And this is what happened.

Wall went on to add to and refine the theory to include changes in afferents, prolonged central excitability, and changes in these systems after nerve damage. The concepts of convergence and modulation espoused by the gate control theory reduced the emphasis on destruction of pathways and led to the idea that pain could be controlled by modulation – reduce excitation or increase inhibition.

Although not entirely new or correct in its details, it nevertheless stood the test of time. The gate control theory’s most important contribution to our understanding of pain was its emphasis on central nervous system (CNS) mechanisms. Never again could anyone try to explain pain exclusively in terms of peripheral factors. The theory forced the medical and biological sciences to accept the brain as an active system that filters, selects and modulates inputs. The dorsal horns, too, were not merely passive transmission stations but sites at which dynamic activities – inhibition, excitation and modulation – occurred. The theory highlighted the CNS as an essential component in pain processes.

Placebo analgesia:

The emphasis of the theory on the modulation of inputs in the spinal dorsal horns and the dynamic role of the brain in pain processes had a clinical as well as a scientific impact. Psychological factors, which were previously dismissed as reactions to pain, were now seen to be an integral part of pain processing, and new avenues for pain control were opened.

The Gate Theory of pain has made us think about changeable transmission. This plasticity, the capacity of pain signalling and modulating systems to alter in different circumstances, has changed our ways of thinking about pain control. Signalling events are not fixed, and are not the same in all situations but are subject to alteration.

Placebo analgesia is a clinical example of the cognitive modulation of pain. It represents a complex psychobiological phenomenon that can be attributed to different mechanisms including expectation of clinical improvement, Pavlovian conditioning and reduction of anxiety.

Any medical treatment is surrounded by a psychosocial context that affects the therapeutic outcome. If we want to study this psychosocial context, we need to eliminate the specific action of a therapy and to simulate a context that is similar in all respects to that of a real treatment. To do this, a sham treatment (the placebo) is given, but the patient believes it is effective and expects a clinical improvement.

Belief in the healing power of positive expectations has existed since the beginning of recorded history. The power of expectation to make people feel better has been exploited by physicians and charlatans-sometimes to promote healing and other times for less altruistic reasons. The healing potential of expectations has formally been recognized in scientific literature as the ”placebo effect,” a term that generally refers to beneficial effects of a treatment that cannot be ascribed to the physical action of the treatment itself. A patient in pain, for example, may report feeling less pain after an injection of saline (i.e., a placebo injection), if the patient believes that a painkiller was administered.

Endogenous opioids, which are naturally produced by the brain in small amounts and play a key role in the relief of pain and anxiety, have been implicated in placebo analgesia. Brain imaging studies have shown that placebo analgesia stimulates release of endogenous opioids from higher brain regions associated with pain modulation and is associated with a decrease in signals from pain-sensitive areas.

The pioneering PET study on placebo analgesia, revealed a shared neural network of rostral anterior cingulate cortex (rACC) and periaqueductal grey matter (PAG) underlying both opioid and systemic placebo analgesia (intravenous saline), with the aim of disentangling the neural mechanisms producing placebo analgesia in humans.

It has been hypothesized that placebo analgesia also recruits the opioidergic descending pain control system, which inhibits pain processing in the spinal cord and, therefore, subsequently reduces pain-related responses in the brain, leading to a decreased pain experience.

In a recent study, Eippert and colleagues employed sophisticated brain imaging techniques to examine both higher cortical and lower brainstem responses in two groups of subjects: one receiving a drug called naloxone, which blocks opioid signaling opioid antagonist, and one group with a natural opioid state.

Expectations of pain relief were induced in both groups by applying a supposedly analgesic cream on one hand (somatotopically localized placebo analgesia).

Naloxone reduced behavioural placebo effects as well as placebo-induced responses in pain-modulatory cortical structures, such as the rACC. Most importantly, they also observed that, under placebo, cortical areas interacted with brainstem structures implicated in pain control and that these interactions were dependent on endogenous opioids and were related to the strength of experienced placebo effects.

Taken together, the findings show that opioid signaling in pain-modulating areas and the projections to downstream effectors of the descending pain control system are crucially important for placebo analgesia. It will be interesting to see whether opioid-dependent activation of the descending pain control system is a common feature of different forms of pain modulation, such as hypnosis and attentional distraction, which share some common neuroanatomical features.

Conclusion:

If a patient succeeds in seeing his pain in terms of a significance and if his doctor and friends succeed in caring, then the pain experience can be said to have passed beyond the meaning of the Latin original poena, namely punishment, to the meaning of the Sanscrit root pu, namely purification. At a broader level, future research must lay the foundations for bridges between psychological and neurobiological descriptions of placebo and other regulatory processes. The stronger these bridges, the more we will have objective biological measures for processes such as expectation, emotion, and pain that were previously knowable only through self-report.