Pain and how you sense it
Scientists are gradually unravelling the processes within the body that lead to the unpleasant sensation of pain. Here’s a simple explanation of what happens when you feel one type of pain.
- You prick your finger on something sharp. This causes tissue damage, which is registered by microscopic pain receptors (nociceptors) in your skin. Each pain receptor forms one end of a nerve cell (neurone). It is connected to the other end in the spinal cord by a long nerve fibre or axon. When the pain receptor is activated, it sends an electrical signal up the nerve fibre.
- The nerve fibre is bundled with many others to form a peripheral nerve. The electrical signal passes up the neurone within the peripheral nerve to reach the spinal cord in the neck.
- Within an area of the spinal cord called the dorsal horn, the electrical signals are transmitted from one neurone to another across junctions (synapses) by means of chemical messengers (neurotransmitters). Signals are then passed up the spinal cord to the brain.
- In the brain, the signals pass to the thalamus. This is a sorting station that relays the signals on to different parts of the brain. Signals are sent to the somatosensory cortex (responsible for physical sensation), the frontal cortex (in charge of thinking), and the limbic system (linked to emotions).
The end result is that you feel a sensation of pain in your finger, think ‘Ouch! What was that?’ or something similar, and react emotionally to the pain; e.g. you feel annoyed or irritated.
However, you will probably have reacted involuntarily even before you were consciously aware of the injury. In sudden strong pain like that generated by pricking your finger, a reflex response occurs within the spinal cord. Motor neurones are activated and the muscles of your arm contract, moving your hand away from the sharp object. This occurs in a fraction of a second — before the signal has been relayed on to the brain — so you will have pulled your arm away before even becoming conscious of the pain.
Types of nerve fibre
Different sensations are carried by different types of nerve fibre, as shown in the table below.
|Features of different types of nerve fibre|
|Speed of signal conduction
Sharp, pricking pain is carried by A-delta fibres while dull throbbing pain travels via C fibres. A-delta fibres conduct signals faster than C fibres as they are larger and are coated in myelin, which acts an electrical insulator. This explains why, on pricking your finger, the first type of pain you feel is a sharp sensation (‘fast pain’, carried by the A-delta fibres), followed by a slower spreading ache (‘slow pain’, carried by the slower C fibres).
How is pain modified?
There are several points in the pain pathway where the signal can be modified. One is the dorsal horn of the spinal cord. In this area, a ‘gate’ mechanism either lets the pain signal through or blocks it from going any further. This is the basis of the gate control theory of pain described below.
|Gate control theory of pain|
The gate control theory of pain was put forward by Ronald Melzack and Patrick Wall in 1965. They proposed that there was a ‘gate’ mechanism in the central nervous system that opened to allow pain messages through to the brain and closed to prevent them getting through.
When we feel pain, such as when we touch a hot stove, sensory receptors in our skin send a message via nerve fibres (A-delta fibres and C fibres) to the spinal cord and brainstem and then onto the brain where the sensation of pain is registered, the information is processed and the pain is perceived.
The gate theory says that as these pain messages come into the spinal cord and the central nervous system (before they even get to the brain), they can be amplified, turned down or even blocked out. There are many accounts of how people injured on the battlefield or in sports games don’t feel any pain from their injuries until afterwards. This has to do with the brain being busy doing other things and shutting the gate until it can pay attention to the messages.
Large diameter nerve fibres (A-beta fibres) responsible for transmitting signals of touch to the brain have the ability to close the pain gate and so block signals from other smaller diameter nerve fibres which transmit pain.
An example of this would be when a child falls over and hurts her knee — if she rubs her knee, the signal from that sensation of touch temporarily blocks the pain signal travelling from the injured knee to the brain.
What affects your experience of pain?
Severe pain quickly gets your attention and usually produces a stronger physical response than mild pain. The location of your pain can also affect how you perceive it. For example, pain coming from the head is harder to ignore than pain originating elsewhere in the body.
The location of pain in your body does not always indicate where it is coming from. For example, the pain from a heart attack can be felt in the neck, jaws, arms or abdomen. This is known as referred pain and occurs because signals from different parts of the body often converge on the same neurones in the spinal cord.
The gate control theory helps explain how the brain influences your experience of pain. It seems that several factors can affect how you interpret pain:
- emotional and psychological state;
- memories of previous pain;
- expectations of and attitudes towards pain;
- beliefs and values;
- sex; and
- social and cultural influences.
Hence the experience of pain differs from person to person.
Types of pain
Doctors classify pain into several types.
This is the type of pain illustrated in the first diagram. Nociceptive pain is caused by any injury to body tissues, for example, a cut, burn or fracture (broken bone). Postoperative pain and cancer pain are other forms of nociceptive pain. This type of pain can be aching, sharp or throbbing. Nociceptive pain can be constant or intermittent and may be worsened by movement or by coughing, depending on the area it originates from.
This is caused by abnormalities in the system that carries and interprets pain — the problem may be in the nerves, spinal cord or brain.
Neuropathic pain is felt as a burning, tingling, shooting or electric sensation. One form of neuropathic pain is associated with shingles — a skin condition caused by varicella zoster virus. The virus triggers inflammation of the nerves and this inflammation can set off a constant deep aching, tingling or burning sensation that in some people can persist for months after the shingles rash has resolved.
People with neuropathic pain may feel pain from stimuli that are not normally painful, such as light touch or cold. They can also be more sensitive than normal to stimuli that are usually painful. For example, bedclothes touching the affected area could feel painful, and a pin prick could feel excessively sharp.
Neuropathic pain can be caused by various processes.
- Physical damage to nerves, causing abnormal signalling.
- Failure of the spinal cord or brain to dampen down the pain.
- ‘Wind-up’. When the spinal cord is constantly bombarded by incoming pain messages from C fibres, it amplifies the pain signal that it sends to the brain. So you feel more intense pain. This is a brief change, lasting only seconds or minutes, but it may set the scene for more permanent changes.
- Increased efficiency of signal transmission at the junctions (synapses) between neurones. This is a complex process that can last up to several months.
This type of pain is caused or worsened by psychological factors. Often the pain has a physical cause, but the degree of pain and disability are out of proportion to what would be experienced by most people with a similar disorder. This does not mean that the pain is not real, even if a physical cause cannot be found. Any kind of pain can be complicated by psychological factors.
Doctors also distinguish between acute and chronic pain.
This is short-lived pain warning the body that damage is occurring. It is a symptom of injury or disease at the tissue level, and tends to resolve as the injury or disease does.
Chronic pain (also called persistent pain) can be caused by ongoing tissue damage, such as in osteoarthritis. However, in some cases no physical cause for the pain can be found or pain persists long after the injury has healed. In many cases chronic pain is a disorder in itself rather than being the symptom of a disease process.
At the cellular level, several processes can contribute to pain becoming chronic.
- Pain receptors and neurones along the pain pathway may become too easily activated.
- Connections between the neurons in the pathway can be altered.
- The brain and spinal cord may fail to dampen down the pain signals.
- Pain receptors that are normally silent (dormant) can become activated by inflammation.
- After nerve injury, nerves may regrow but function abnormally.
Chronic pain can persist for months or even years after an initial injury and can be difficult to treat. People with chronic pain may experience sleeplessness, anxiety and depression, all of which can compound the problem. However, support and help are available, often in the form of a multidisciplinary approach, as carried out in pain management clinics.
Chronic pain is an area that is being researched intensively, with the hope of relieving this distressing condition in the future.
Last Reviewed: 29/02/2012
1. Merck Manual Home Health Handbook. Overview of pain (updated Aug 2007). http://www.merckmanuals.com/home/brain_spinal_cord_and_nerve_disorders/pain/overview_of_pain.html (accessed Mar 2012). 2. Merck Manual Home Health Handbook. Types of pain (updated Aug 2007). http://www.merckmanuals.com/home/brain_spinal_cord_and_nerve_disorders/pain/types_of_pain.html (accessed Mar 2012). 3. Physiology and pathophysiology of pain (revised September 2007). In: eTG complete. Melbourne: Therapeutic Guidelines Limited; 2011 Nov. http://online.tg.org.au/complete/ (accessed Mar 2012). 4. Types of pain (revised February 2010). In: eTG complete. Melbourne: Therapeutic Guidelines Limited; 2011 Nov. http://online.tg.org.au/complete/ (accessed Mar 2012).
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