In this article, we will discuss various Theories of Pain. So, let’s get started.
Theories of Pain
Pain theories tried to explain why and how we experience pain from ancient time to modern times. It was previously thought as the work of evil spirits and now understood to be a neurological signal.
1. Intensive Theory (Erb, 1874): Pain resulted from excessive stimulation of the sense of touch.
2. Specificity Theory (Von Frey, 1895): 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).
3. Strong’s Theory (Strong, 1895): Pain was an experience based on both the noxious stimulus and the psychic reaction or displeasure provoked by the sensation.
4. Pattern Theory (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. It suggested that all cutaneous qualities are produced by spatial and temporal patterns of nerve impulses rather than separate, modality specific transmission routes.
5. Central Summation Theory (Livingstone, 1943): Prolonged abnormal activity resulting from the cells transmit the impulses from the spinal cord up nerve and tissue damage bombards cells in the spinal cord, and information is projected to the brain for pain perception
6. The Fourth Theory of Pain (Hardy, Wolff, Goodell, 1940s): Composed of two components: the perception of pain and the reaction one has towards it.
7. Sensory Interaction Theory (Noordenbos, 1959): Fast and slow system. The later presumed to conduct somatic and visceral afferents, whereas the former was considered to inhibit transmission of the small fibres.
8. Gate Control Theory (Melzack and Wall, 1965): Pain stimulation is carried by small, slow fibres that enter the dorsal horn of the spinal cord; then other cells transmit the impulses from the spinal cord up to the brain. The large fibres can prohibit the impulses from the small fibres from ever communicating with the brain. In this way, the large fibres create a hypothetical “gate” that can open or close the system to pain stimulation.