Scientists are unraveling the processes within the body that cause the unpleasant feeling of pain. Here’s a straightforward explanation of what happens when you feel one kind of pain.
How Do We Feel Pain?
- You prick your finger on anything sharp. This causes tissue injury, which can be read by nociceptors (microscopic pain receptors) in your skin. Every pain receptor makes one end of a nerve cell (neuron). It’s connected to the opposite end in the spinal cord by a long nerve fiber or axon. After the pain receptor is triggered, it transmits an electrical signal up the nerve fiber.
- The nerve fiber is bundled with many others to make a peripheral nerve. The electrical signal passes up the neurons with the peripheral nerve to reach the spinal cord.
- Within a region of the spinal cord known as the spinal dorsal horn, the electrical signals are sent between neurons through junctions (synapses) via chemical messengers (neurotransmitters). Signals are passed up the spinal cord to the brain.
- In the brain, the signals are sent to the thalamus. This is a sorting channel that relays the signals on to various parts of the brain. Signals are transmitted to the somatosensory cortex (responsible for bodily sensation), the frontal cortex (manage thinking), and the limbic system (linked to feelings ).
The result is that you feel a feel pain in your finger, think ‘Ouch! What was that?’ Or something similar, and respond emotionally to the pain; e.g., you are feeling annoyed or upset.
However, you will have reacted involuntarily before you were consciously aware of the injury. In immediate, intense pain like that caused by cutting your finger, a reflex reaction occurs in the spinal cord.
Motor neurons are stimulated and the tissues of your arm contract, moving your hands away from the sharp thing. This happens in a fraction of a second before the signal has been carried on to the brain, so you will have pulled your arm away before even feeling pain.
How is Pain Modified?
There are many points in the pain pathway, where the signal can be modified, one is the spinal dorsal horn. Within this region, a ‘gate’ process either lets the pain signal through or blocks it.
Gate Control Theory of Pain
The gate control theory of pain was presented by Patrick Wall and Ronald Melzack in 1965. They asserted that there was a ‘gate’ mechanism in the central nervous system that opened to let pain messages through to the brain and closed to prevent them from getting through.
When we feel pain like if we touch a hot cooker, sensory receptors in our skin send a message through nerve fibers (A-delta fibers and C fibers) into the spinal cord and brainstem and then on the brain in which the feeling of pain is registered. The data is processed, and the pain is sensed.
The gate theory describes that as these pain messages come to the central nervous system and the spinal cord (before they get into the brain), they may be turned down, amplified, or even blocked out. There are numerous reports of how individuals injured on the battlefield or in sports games do not feel any pain from injuries until later. This has to do with the mind being busy doing other things and closing the gate until it can focus on the signals.
Large diameter nerve fibers (A-beta fibers) liable for sending signals of touch to the brain can shut the pain gate and so block signals from other smaller diameter nerve fibers that transmit pain.
An example of this could be if a child falls over and her knee hurts. When she rubs her knee, the signal from that feeling of touch temporarily blocks the pain signal going from the injured knee to the brain.
What Influences Your Experience of Pain?
Severe pain gets your attention quickly and normally creates a stronger physical response than moderate feel pain. Your pain’s location may affect how you perceive it. By way of instance, pain coming from the head is more difficult to avoid than pain arising elsewhere in the body.
The location of feel pain does not always show where it is coming from. By way of instance, the pain from a heart attack could be felt in the neck, arms, jaws, or abdomen. This is called referred pain. It happens because signals from various areas of the body converge on the same neurons in the spinal cord.
The Gate Control theory helps describe how the brain affects your experience of pain. It appears that several factors can influence how you interpret pain:
- Emotional and mental condition;
- Memories of previous pain;
- Expectations of and attitudes towards pain;
- Beliefs and values;
- Gender; and
- Cultural and social influences.
Thus the experience of pain differs from person to person.
Kinds of Pain
Doctors classify pain into several types.
Nociceptive pain is induced by any injury to body cells, by way of instance, a cut, burn, or fracture (broken bone). Cancer pain and postoperative pain are other kinds of nociceptive pain. This sort of pain may be sharp, aching, or throbbing. Nociceptive pain can be intermittent or continuous and may be worsened by movement or coughing, depending on its origin.
This is generated by abnormalities in the system which carries and interprets pain — the problem could be in the nerves, spinal cord, or brain.
Neuropathic feel Pain is felt like a burning, tingling, shooting, or electrical sensation. One form of neuropathic pain is related to shingles — a skin condition caused by the varicella-zoster virus. The virus causes inflammation of the nerves. This inflammation may set off a deep burning, tingling, or aching sensation that in some individuals may persist for months after the shingles rash has resolved.
People with neuropathic pain may sense pain from stimuli that aren’t usually painful, such as cold or light touch. They can also be more receptive than usual to painful stimuli. By way of instance, bedclothes touching the affected area could feel unpleasant, and a pinprick could feel excessively sharp.
Neuropathic pain can be due to various processes:
- Physical damage to nerves, causing abnormal signaling.
- Failure of the brain or spinal cord to dampen the pain down.
- ‘Wind-up.’ When the spinal cord is continually bombarded by incoming pain signals from C fibers, it boosts the pain signal that is sent to the brain. This is a little change, lasting only seconds or minutes, but setting the scene for more permanent changes.
- Increased efficacy of signal transmission at the junctions (synapses) between neurons. This is a complicated process that could last up to several months.
This sort of anxiety is caused or worsened by emotional factors. Usually, the pain has a physical cause. However, the degree of disability is out of proportion to what would be experienced by most people with a similar disorder. This does not imply that the pain isn’t real, even if a physical cause can’t be found. Any sort of pain can be complicated by psychological factors.
Doctors Also Differentiate Between Chronic And Acute Pain.
This is temporary to feel pain signaling the body that injury is occurring. It is a symptom of disease or injury at the tissue level and tends to settle as the disease or injury does.
Chronic pain (also called persistent pain) can be brought about by ongoing tissue damage, such as in osteoarthritis. However, no physical cause for the pain can be found, or pain persists long after the injury has healed. In many cases, pain is a disease in itself instead of being the symptom of a disease process.
At the cellular level, several processes can give rise to pain from becoming chronic.
- Pain receptors and neurons along the pain pathway might become too readily activated.
- Connections between the nerves in the pathway could be changed.
- The spinal cord and brain may fail to dampen down the pain signals.
- Pain receptors that are typically silent can become stimulated by inflammation.
- After nerve injury, nerves can regrow but work abnormally.
Chronic pain can continue for months or even years after an initial injury and can be hard to treat. Individuals with chronic pain may experience insomnia, depression, and anxiety, all of which may compound the problem. However, service and support are accessible, often in the form of a multidisciplinary approach, as carried out in pain management practices.
Chronic feel pain is a place that has been researched intensively to alleviate this distressing condition in the future.
Scientists Find A Brain Center That ‘Profoundly’ Closes Down Pain.
A research group of Duke University has noticed a small region of the brain in mice that can thoroughly control the animals’ sensation of pain.
Surprisingly, this brain center turns off the pain, not on. Additionally, it is located in a place where people would never have thought to search for an anti-pain center, the amygdala. This amygdala is regarded as the home of adverse reactions and emotions, such as fight or flight response and general anxiety.
Fan Wang, the senior author, The Morris N. Broad Distinguished Professor of neurobiology at the School of Medicine, stated, “People do believe there’s a central place to alleviate feel pain, that is why placebos work.” “The question is, where is the center in the brain that can turn off the pain.”
“Most of the earlier studies have concentrated on which areas are turned ON by pain,” Wang said. “Although there are a lot of regions processing pain, you would have to turn them off to prevent pain. On the other hand, this one center can turn off the pain alone.”
The work is a follow-up to an earlier study in the laboratory of Wang taking a look at activated neurons rather than suppressed ones, by general anesthetics. In a 2019 study, they discovered that general anesthesia boosts slow-wave sleep by activating the brain’s supraoptic nucleus. But pain and sleep are different, a significant clue that resulted in the new finding that comes online on May 18 in Nature Neuroscience.
The experts found that general anesthesia also activates a special subset of inhibitory neurons in the central amygdala, that they have termed as the CeAga neurons (CeA for central amygdala; ga implies activation by general anesthesia). Mice have a somewhat larger central amygdala than humans. However, Wang said she had no reason to consider we have a different system for managing pain.
Using technologies that Wang’s laboratory has initiated to track the paths of activated neurons in mice, the group discovered the CeAga was connected to a lot of distinct regions of the brain,” that was a surprise,” Wang said.
By providing mice a moderate pain stimulation, the investigators could map each the pain-activated brain areas. They discovered that a minimum of 16 brain centers known to process the psychological or sensory aspects of pain received inhibitory input from the CeAga.
“Pain is a complicated brain reaction,” Wang said. “It involves sensory discrimination, autonomic (involuntary nervous system) responses, and emotion. Treating pain by dampening all these brain processes in several regions is quite tricky to attain. But activating a key node that obviously sends inhibitory signals to those pain-processing areas is more robust.”
Using a technology known as optogenetics, which uses light to activate a small population of cells in the brain, the researchers discovered they could turn off the self-caring behaviors as it feels uncomfortable by triggering the CeAga neurons a mouse exhibits when it feels cramped by stimulating the CeAga neurons. Face-wiping or paw-licking acts were “completely abolished” when the light was turned on to trigger the anti-pain center.
“It’s so severe,” Wang said. “They simply instantaneously stop rubbing and licking.”
When the experts dampened the action of the CeAga neurons, the mice reacted like a temporary insult had become painful or intense again. They discovered that low-dose ketamine, an anesthetic medication that allows sensation but prevents pain, activated the CeAga center and wouldn’t work without it.
Now the Researchers will search for drugs that can activate only these cells to overcome pain as possible future pain killers, Wang said.
“The other thing we are trying to do is to (transcriptome) sequence the hell out of these cells,” she said. The experts are hoping to find the gene for a unique or rare cell surface receptor among these specialized cells that would let a very particular drug to activate these neurons and alleviate pain.