As long as humans have experienced pain, they have given explanations for its existence and sought soothing agents to dull or cease the painful sensation.^[1]Several theoretical frameworks have been proposed to explain the physiological basis of pain, although none yet completely accounts for all aspects of pain perception. A number of theories have been postulated to describe mechanisms underlying pain perception. These theories date back several centuries and even millennia (Kenins 1988; Perl 2007; Rey 1995) ^[2]

 

1. Intensive Theory (Erb, 1874)

An Intensive (or Summation) Theory of Pain (now referred to as the Intensity Theory) has been postulated at several different times throughout history. First, conceptualized in the fourth century BCE by Plato in his oeuvre Timaeus (Plato 1998), the theory defines pain, not as a unique sensory experience but rather, as an emotion that occurs when a stimulus is stronger than usual^[3]. This theory is based on Aristotle’s concept that pain resulted from excessive stimulation of the sense of touch. Both stimulus intensity and central summation are critical determinants of pain. It was implied that the summation occurred in the dorsal horn cells.Arthur Goldscheider further advanced the Intensity Theory, based on an experiment performed by Bernhard Naunyn in 1859 [cited in Dallenbach (1939)].^[3] These experiments showed that repeated tactile stimulation (below the threshold for tactile perception) produced pain in patients with syphilis who had degenerating dorsal columns. When this stimulus was presented to patients 60–600 times/s, they rapidly developed what they described as unbearable pain. Naunyn reproduced these results in a series of experiments with different types of stimuli, including electrical stimuli. It was concluded that there must be some form of summation that occurs for the subthreshold stimuli to become unbearably painful.

2. Specificity Theory (Von Frey, 1895)

Specificity theory is one of the first modern theories for pain. It holds that specific pain receptors transmit signals to a "pain center" in the brain that produces the perception of pain^[4]Von Frey (1895) argued that the body has a separate sensory system for perceiving pain—just as it does for hearing and vision. This theory considers pain as an independent sensation with specialised peripheral sensory receptors [nociceptors], which respond to damage and send signals through pathways (along nerve fibres) in the nervous system to target centres in the brain. These brain centres process the signals to produce the experience of pain. Thus, it is based on the assumption that the free nerve endings are pain receptors and that the other three types of receptors are also specific to a sensory experience.

3. Strong's Theory (Strong, 1895)  

This theory states that pain was an experience based on both the noxious stimulus and the psychic reaction or displeasure provoked by the sensation.

4. Pattern Theory

In an attempt to overhaul theories of somaesthesis (including pain), J. P. Nafe postulated a “quantitative theory of feeling” (1929). This theory ignored findings of specialized nerve endings and many of the observations supporting the specificity and/or intensive theories of pain. The theory stated that any somaesthetic sensation occurred by a specific and particular pattern of neural firing and that the spatial and temporal profile of firing of the peripheral nerves encoded the stimulus type and intensity^[5].Goldschneider (1920) proposed that there is no separate system for perceiving pain, and the receptors for pain are shared with other senses, such as of touch. This theory considers that peripheral sensory receptors, responding to touch, warmth and other non-damaging as well as to damaging stimuli, give rise to non-painful or painful experiences as a result of differences in the patterns [in time] of the signals sent through the nervous system. Thus, according to this view, people feel pain when certain patterns of neural activity occur, such as when appropriate types of activity reach excessively high levels in the brain. These patterns occur only with intense stimulation. Because strong and mild stimuli of the same sense modality produce different patterns of neural activity, being hit hard feels painful, but being caressed does not. It suggested that all cutaneous qualities are produced by spatial and temporal patterns of nerve impulses rather than by separate, modality specific transmission routes.

5. Central Summation Theory (Livingstone, 1943)

It proposed that the intense stimulation resulting from the nerve and tissue damage activates fibers that project to internuncial neuron pools within the spinal cord creating abnormal reverberating circuits with self-activating neurons. Prolonged abnormal activity bombards cells in the spinal cord, and information is projected to the brain for pain perception.

6. The Fourth Theory of Pain (Hardy, Wolff, and Goodell, 1940s)

It stated that pain was composed of two components: the perception of pain and the reaction one has towards it. The reaction was described as a complex physiopsychological process involving cognition, past experience, culture and various psychological factors which influence pain perception.

7. Sensory Interaction Theory (Noordenbos, 1959)

It describes two systems involving transmission of pain: fast and slow system. The later presumed to conduct somatic and visceral afferents whereas the former was considered to inhibit transmission of the small fibers.

8. Gate Control Theory (Melzack and Wall, 1965)

Melzack has proposed a theory of pain that has stimulated considerable interest and debate and has certainly been a vasy improvement on the early theories of pain. According to his theory, pain stimulation is carried by small, slow fibers that enter the dorsal horn of the spinal cord; then other cells transmit the impulses from the spinal cord up to the brain. These fibers are called T-cells. The T-cells can be located in a specific area of the spinal cord, known as the substantial gelatinosa. These fibers can have an impact on the smaller fibers that carry the pain stimulation. In some cases they can inhibit the communication of stimulation, while in other cases they can allow stimulation to be communicated into the central nervous system. For example, large fibers can prohibit the impulses from the small fibers from ever communicating with the brain. In this way, the large fibers create a hypothetical "gate" that can open or close the system to pain stimulation. According to the theory, the gate can sometimes be overwhelmed by a large number of small activated fibers. In other words, the greater the level of pain stimulation, the less adequate the gate in blocking the communication of this information.

There are 3 factors which influence the 'opening and closing' of the gate^[6]:

• The amount of activity in the pain fibers. Activity in these fibers tends to open the gate. The stronger the noxious stimulation, the more active the pain fibers.
• The amount of activity in other peripheral fibers—that is, those fibers that carry information about harmless stimuli or mild irritation, such as touching, rubbing, or lightly scratching the skin. These are large-diameter fibers called A-beta fibers.Activity in A-beta fibers tends to close the gate, inhibiting the perception of pain when noxious stimulation exists. This would explain why gently massaging or applying heat to sore muscles decreases the pain.
• Messages that descend from the brain. Neurons in the brainstem and cortex have efferent pathways to the spinal cord, and the impulses they send can open or close the gate. The effects of some brain processes, such as those in anxiety or excitement, probably have a general impact, opening or closing the gate for all inputs from any areas of the body. But the impact of other brain processes may be very specific, applying to only some inputs from certain parts of the body. The idea that brain impulses influence the gating mechanism helps to explain why peopie who are hypnotized or distracted by competing environmental stimuli may not notice the pain of an injury.

The beauty of theory is that it provides a physiological basis for the complex phenomenon of pain. It does this by investigating the complex structure of the nervous system, which is comprised of the following two major divisions:^[7]

Central nervous system (the spinal cord and the brain)
Peripheral nervous system (nerves outside of the brain and spinal cord, including branching nerves in the torso and extremities, as well as nerves in the lumbar spine region)

 

                                   

9. Biopsychosocial Model of Pain

It states that pain is not simply a neurophysiological phenomenon, but also involves social and psychological factors. It says that factors like culture, family, nociceptive stimuli and environment influence pain perception and thus ultimately affect a person’s emotions, behaviors and cognition.

 

Recent Related Research (from Pubmed)

Reference