Video: Pain and thermal sensations
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Have you ever wondered why a warm bath feels so soothing but lightly touching a hot stove makes you instantly pull your hand away? Or why a cool breeze on a hot day feels so refreshing but a few ...
Read moreHave you ever wondered why a warm bath feels so soothing but lightly touching a hot stove makes you instantly pull your hand away? Or why a cool breeze on a hot day feels so refreshing but a few minutes out in the cold can be uncomfortable or even painful? It all comes down to a sophisticated network of specialized receptors in your body that are constantly monitoring temperature changes and potentially harmful stimuli to our tissues.
Today, let's dive into the physiology of pain and thermal sensations to see exactly how this system keeps us safe or, at least does its best to.
First let's figure out the difference between nociception and pain because they get mixed up all the time. Nociception is your body's ability to detect potentially harmful stimuli, or more properly, noxious stimuli. These stimuli are detected by specialized receptors called nociceptors, which activate when they exceed a certain threshold and are often perceived as pain by the brain.
The thing is pain is the interpretation of these signals and it's subjective, meaning it varies from person to person. The noxious stimuli are objective and quantifiable but their interpretation isn't. Nociceptors are free nerve endings that are found throughout the body and specialize in detecting different types of noxious stimuli.
Mechanical nociceptors respond to sharp objects or intense pressure like a knife cut or sharp pinch. Thermal nociceptors detect extreme temperatures like touching a hot stove or holding ice in your hand. We have chemical nociceptors which sense corrosive substances or chemicals released during tissue damage like bradykinin, histamine, and serotonin. And lastly, we have polymodal nociceptors which can detect all three.
Importantly, though, not all pain signals are the same. They differ in both speed and character which is based on the type of nerve fiber.
Fast pain is carried by A-delta fibers, which are thin and lightly myelinated, and allows signals to travel at speeds of 6 to 30 meters/second. This kind of pain is sharp and immediate, like when you prick your finger or touch something hot. Slow pain, on the other hand, is carried by C fibers, which are thin and unmyelinated, and send signals more slowly at 0.5 to 2 meters/second. This leads to a dull, aching, or burning sensation like the throbbing feeling after an injury.
Interestingly, both fast and slow pain occurs as a result of mechanical and thermal stimuli, but chemical stimuli usually causes slow pain.
Just as the sensory nerves are entering the spinal cord, there's a quick local reflex causing a motor response to pull away from the stimulus called the withdrawal reflex. This happens alongside the bigger tracts that carry the sensation of pain all the way to the brain. These big tracts are primarily the spinothalamic tracts, which transmit pain signals to the somatosensory cortex via the thalamus for conscious perception.
The lateral spinothalamic tract comprises two main components -- the neospinothalamic tract and the paleospinothalamic tract. The neospinothalamic pathway carries fast pain signals that are sharp and well-localized, meaning you have a good idea of where the problem is. A-delta or fast pain fibers enter the spinal cord and synapse in the posterior horn, specifically, in Rexed lamina I.
The fibers then decussate or cross to the opposite side and ascend to the posterior nuclei and ventroposterior complex of the thalamus which is crucial for processing sensory information. From there, the signals continue to the somatosensory cortex, allowing precise localization and intensity perception of fast pain. Some fibers from this tract also reach the reticular formation of the brainstem which plays an important role in maintaining attention and arousal in response to painful stimuli.
In contrast, the paleospinothalamic pathway carries slow pain signals that are dull and less localized, meaning the location of the problem isn't something you can easily point to. C fibers enter the spinal cord through the posterior horn and usually terminate in Rexed lamina II. Impulses eventually reach lamina V via an interneuron. The fibers then decussate and ascend via multiple ascending tracts including the lateral spinothalamic tract.
This tract goes all the way up to the cortex and along the way, fibers can reach other key areas such as the amygdala, which integrates pain information with emotions like fear and anxiety; the reticular formation of the brainstem, which helps regulate arousal and maintain attention; the intralaminar nuclei of the thalamus, which play a role in the emotional and motivational aspects of pain perception; and the periaqueductal gray, which is involved in pain modulation.
So for example, when the periaqueductal gray, which is located in the midbrain, is activated, it sends signals to the posterior horn of the spinal cord via nuclei in the medulla oblongata. By using neurotransmitters such as enkephalins and serotonin, this pathway can inhibit the incoming pain signals. This descending pain suppression pathway basically intercepts the painful signal before it ascends, reducing the intensity of the pain processed in the brain.
Another clever way to reduce pain intensity is described through the gate control theory which suggests that providing the nervous system with non-painful sensations can close the neuronal gates to noxious stimulus, preventing the signal from making its way to the brain. When you rub a painful area, you activate the fast-conducting, heavily-myelinated neurons that carry touch sensations which can interfere with the pain signals, effectively closing the gate and diminishing the painful sensation.
While neither of these modulation processes completely stops the painful sensation, it's nice to know our body isn't just throwing its hands in the air and giving into the noxious stimuli. The thing is when you stub your toe, get a paper cut, or any number of painful things along those lines, the pain you're feeling is somatic pain -- pain from the surface of the body.
Visceral pain, on the other hand, is pain coming from the internal organs, and unlike somatic pain, visceral pain tends to be more diffuse and challenging to localize. Picture the intense cramping that comes with intestinal issues -- deep, dull, and pressure-like, but also difficult to pinpoint exactly where it's coming from. There are several reasons for this such as fewer sensory receptors in the organs, a lack of specialized nociceptors, and even a convergence of sensory pathways leading to a phenomenon called referred pain.
Referred pain is pain that comes from an internal organ but is felt or perceived as coming from a different part of the body. A classic example is cardiac pain felt in the left arm or with appendicitis, pain that's initially felt near the umbilicus. Essentially when visceral pain becomes intense, it can increase the activity of somatic fibers that synapse in the same spinal region, causing the perception of pain in areas that aren't actually injured.
While referred pain isn't always consistent in its exact location, its general location can be extraordinarily useful for physicians looking to find the cause of specific internal issues.
Let's now explore thermal sensation -- the body's ability to detect temperature changes.
Your body uses specialized thermoreceptors to detect temperature variations which are usually free nerve endings. They detect a range of temperatures with the cold receptors using the lightly myelinated A-delta fibers and the warm receptors using nonmyelinated C fibers. They sense temperatures between 10 and 50 degrees Celsius.
However, under 15 and over 45 degrees Celsius, we're heading into the extreme zones where instead of thermal receptors, nociceptors are activated. These cold and heat pain receptors are why holding an ice cube and touching a hot stove hurts. This overlap in ranges allows for fine discrimination of temperature changes and can trigger protective responses when necessary.
Thermal signals are transmitted to the brain through pathways similar to those for pain signals. They send signals via sensory neurons that enter the spinal cord's posterior horn, synapsing specifically in Rexed laminae I or II, decussate, and then they ascend in the lateral spinothalamic tract. They proceed to the ventrobasal complex of the thalamus and eventually reach the primary somatosensory cortex where temperature is consciously perceived and interpreted.
Some fibers also branch to the reticular areas of the brainstem, affecting arousal which helps explain why extreme temperatures can make us more alert.
The ability to perceive pain and temperature is absolutely crucial for survival as well as comfort. So, next time you enjoy a warm bath or shiver from a cold breeze, try and appreciate the remarkable systems at work within your body.
This is only scratching the surface of pain and thermal sensations. If you're looking for more, be sure to check out our article on the gate theory of pain.
See you next time.