How Pain Works
Descartes described pain as animal spirits traveling up hollow tubes to the brain.
Although there remain many questions in science about pain, the basic mechanics are well understood. I find that a lot of my patients have little if any understanding of how pain works. The relationship people have with pain is also complicated. We may dread the sting of a needle but embrace the pain felt from a good workout. The same low-back condition in two different patients can cripple one and barely affect the other. How can this be? As we will see, pain is always coupled with a psychological response. Understanding the biological circuitry of the pain system gives us these clues. Here, I wanted to give an accessible outline of the pain system and explain how this knowledge is important for its treatment. Understanding pain is critical for spine patients who suffer disproportionately from severe pain. Even a basic understand of how pain works can help the patient not only comprehend what is happening but how it may be reduced.
René Descartes was the first philosopher to describe pain. In his theory, published as The Treatise on Man in 1662, he described how the hollow tubes of nerves convey sensory function by sending “animal spirits” to the brain. Since that time our understanding of the basic neural structure responsible for the sensation of pain has advanced, but as you will see, the overall concept is essentially the same as that described by Descartes.
Pain is defined as “an unpleasant sensory and emotional experience associated with actual or potential tissue damage” (1). The perception of pain is triggered by a cascade of neurobiological events starting in the peripheral nervous system and ascending into the brain. The sensation of pain in the brain results in a behavioral response that can either be a motor reflex (quickly withdrawing your hand from a sharp needle) or psychological (fearing the needle after having been stuck once, and thus avoiding the doctor’s office). Patients tend to think of pain as purely bad, but pain is a defensive signal that helps the body avoid injury. As such, the skin, our outermost organ system, is the most sensitive to pain.
To understand pain, one must understand the nervous system. The nervous system consists of a peripheral component (the nerves) and a central component (the brain and spinal cord). Both the central and peripheral nervous systems are composed of the basic unit, the neuron. The neuron is a long fiber-type cell capable of transmitting a chemical signal from one end to the other, similar to how a wire transmits an electrical signal. Neurons have three main components: a sensing end (the dendrites), a transmission component (the axon), and an action end (the synapse). Pain is sensed by certain receptors throughout the body that respond to tissue damage or chemicals, and send this signal through the nerve to other nerves. In this way, tissue damage is converted to a signal that is transmitted through the peripheral nervous system, up the spinal cord, and into the brain.
The basic architecture of the somatic pain-sensing system (pain from the skin) is that tissue damage or perturbation causes receptor activation at specialized pain nerves (A-delta and C-fibers) that transmit this signal to the spinal cord. A-delta nerve fibers transmit sharp pain quickly. C nerve fibers transmit slow, burning pain. Nerve fibers terminate in the spinal cord where the signals are relayed to the neospinothalamic tract, a nerve information super highway that ascends on the opposite side of the spinal cord to a brain region known as the. From the thalamus, the signal is processed and related to the seat of consciousness in the brain, the somatosensory portion of cortex.
A second nerve tract, called the paleospinalthalamic tract, ascends up the spinal column (opposite the neospinalthalamic tract) and interacts with the rostral ventral medulla, the hippocampus and the limbic system (amygdala, cingulate, and insula)—areas of the brain involved in emotional processing of pain and memory. These areas of the brain can suppress or amplify pain signals depending on the context. The interpretation of pain by the brain is thus very complex and not localized to one area.
These two systems form the primary and secondary pain matrices. The primary matrix is involved in localizing the pain (i.e. this pain is coming from my finger). The secondary matrix is involved in our attention to the pain (“this is a big deal; I need to see a doctor or go the emergency room” vs. “it’s just a small stab; I’ll go get a Band-Aid”). This neural architecture highlights the fact that pain is a dynamic sense, constantly surveying the body to create a perception in the mind to protect the patient.
There are several theories that have been postulated to further describe how pain is interpreted by the body on a cellular level.
The specificity theory is the most basic theory describing pain, put forth by the anatomist Charles Bell in 1811. In the specificity theory, one receptor type detects one type of pain stimulus (hot, cold, sharp, dull, etc.) and transmits this via one fiber to the brain. The nerves and brain are in this way heterogenous and bundled together for transmission purposes only. This is a simplistic and analog description of the pain system but helps explain how when you get poked by something sharp—it translates to pain. One problem with this theory is that it does not describe how chronic pain can occur when the noxious stimulus has been removed or how two people may respond differently to the same pain. Overall, this view of pain helps us understand how it can work but is ultimately overly simplistic because it suggests that pain would be experienced similarly by all individuals.
A second theory, the pattern theory of pain, proposed by J. P. Nafe in 1929, theorized that it was not the fiber specifically but rather the firing pattern of the nerve fiber that encoded the stimulus and intensity. This theory suggests that a given stimulus is encoded as a signal to the brain based on the pattern of neural activation, rather than the activation of specialty nerve fibers. In this theory, any nerve can cause pain if active in the correct fashion. This was eventually disproven with the discovery of specific touch and pain fibers. However, aspects of the theory are correct in that there is modulation between fibers in the spinal cord.
Finally, in 1965, Ronald Melzack and Charles Patrick developed the gate control theory of pain, which connected the pattern and specificity theories. This theory addresses shortcomings of both previous theories. In this theory, nociceptors (pain fibers) and touch fibers synapse in two different regions of the dorsal horn of the spinal cord—the substantia gelatinosa and the transmission cells. The gate is the substantia gelatinosa, which modulates the signal going to the transmission cells. Large pain fibers close the pain gate; small sensory fibers open the gate. Although the gate control theory of pain is one of the most widely accepted theories describing pain, it has been found to not totally match what is found in the nervous system architecture. However, it is still very useful to help describe the behaviors patients have surrounding pain perception.
Our behaviors surrounding pain can be deduced from this neural architecture. For example, when we stick our finger with something sharp, activation of the primary matrix causes us to localize the pain to the finger and retract it to avoid further damage. We are able to modulate this pain when we know it’s for a purpose, such as sticking our finger for a glucose test or getting a blood draw, which are seen as good for us. The effects of a placebo can also be explained through this system, where pain can be down regulated by the higher-order areas of the neural matrix, relieving pain. The mental state of a person can influence pain. It also explains how memory and the emotional centers of the brain regulate pain. If you think “this is a big deal and I need to pay attention to this pain” it is likely to be memorable, more intense and alter future behaviors to avoid further contact with the pain source.
This is just a basic introduction to how pain works. In future blog posts, I hope to describe how pain can get out of control and go from what is called acute pain to chronic pain. Acute pain is easily understood and treated by patients and physicians. However, those with chronic pain tend to be stigmatized. It’s important for physicians and patients alike to learn how to unpackage chronic pain and thus treat it.
1. Moayedi M, Davis KD. Theories of pain: from specificity to gate control. Journal of Neurophysiology. 2013 Jan 1;109(1):5–12.