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From Wikipedia, the free encyclopedia

Pain stimulus

Pain stimulus is a technique used by medical personnel for assessing the consciousness level of a person who is not responding to normal interaction, voice commands or gentle physical stimuli (such as shaking of the shoulders).[1] It forms one part of a number of neurological assessments, including the first aid based AVPU scale and the more medically based Glasgow Coma Scale.

The objective of pain stimulus is to assess the level of consciousness of the patient by inducing vocalisation in an acceptable, consistent and replicable manner, and to this end, there are a limited number of techniques which are normally considered acceptable.

The pain stimulus can be applied centrally and/or peripherally, and there are benefits and drawbacks to each type of stimulus, depending on the type of patient and the response being assessed.

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  • How does your brain respond to pain? - Karen D. Davis
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Transcription

Let's say that it would take you ten minutes to solve this puzzle. How long would it take if you received constant electric shocks to your hands? Longer, right? Because the pain would distract you from the task. Well, maybe not; it depends on how you handle pain. Some people are distracted by pain. It takes them longer to complete a task, and they do it less well. Other people use tasks to distract themselves from pain, and those people actually do the task faster and better when they're in pain than when they're not. Some people can just send their mind wandering to distract themselves from pain. How can different people be subjected to the exact same painful stimulus and yet experience the pain so differently? And why does this matter? First of all, what is pain? Pain is an unpleasant sensory and emotional experience, associated with actual or potential tissue damage. Pain is something we experience, so it's best measured by what you say it is. Pain has an intensity; you can describe it on a scale from zero, no pain, to ten, the most pain imaginable. But pain also has a character, like sharp, dull, burning, or aching. What exactly creates these perceptions of pain? Well, when you get hurt, special tissue damage-sensing nerve cells, called nociceptors, fire and send signals to the spinal cord and then up to the brain. Processing work gets done by cells called neurons and glial. This is your grey matter. And brain superhighways carry information as electrical impulses from one area to another. This is your white matter. The superhighway that carries pain information from the spinal cord to the brain is our sensing pathway that ends in the cortex, a part of the brain that decides what to do with the pain signal. Another system of interconnected brain cells called the salience network decides what to pay attention to. Since pain can have serious consequences, the pain signal immediately activates the salience network. Now, you're paying attention. The brain also responds to the pain and has to cope with these pain signals. So, motor pathways are activated to take your hand off a hot stove, for example. But modulation networks are also activated that deliver endorphins and enkephalins, chemicals released when you're in pain or during extreme exercise, creating the runner's high. These chemical systems help regulate and reduce pain. All these networks and pathways work together to create your pain experience, to prevent further tissue damage, and help you to cope with pain. This system is similar for everyone, but the sensitivity and efficacy of these brain circuits determines how much you feel and cope with pain. This is why some people have greater pain than others and why some develop chronic pain that does not respond to treatment, while others respond well. Variability in pain sensitivities is not so different than all kinds of variability in responses to other stimuli. Like how some people love roller coasters, but other people suffer from terrible motion sickness. Why does it matter that there is variability in our pain brain circuits? Well, there are many treatments for pain, targeting different systems. For mild pain, non-prescription medications can act on cells where the pain signals start. Other stronger pain medicines and anesthetics work by reducing the activity in pain-sensing circuits or boosting our coping system, or endoprhins. Some people can cope with pain using methods that involve distraction, relaxation, meditation, yoga, or strategies that can be taught, like cognitive behavioral therapy. For some people who suffer from severe chronic pain, that is pain that doesn't go away months after their injury should've healed, none of the regular treatments work. Traditionally, medical science has been about testing treatments on large groups to determine what would help a majority of patients. But this has usually left out some who didn't benefit from the treatment or experienced side effects. Now, new treatments that directly stimulate or block certain pain-sensing attention or modulation networks are being developed, along with ways to tailor them to individual patients, using tools like magnetic resonance imaging to map brain pathways. Figuring out how your brain responds to pain is the key to finding the best treatment for you. That's true personalized medicine.

Central stimuli

U.S. Army soldiers demonstrating a sternal rub

A central stimulus is one which can only be successfully found if the brain is involved in the response to the pain (as opposed to peripheral stimuli, which can induce a result as a result of reflex. The four commonly used central pain stimuli are:

  • the trapezius squeeze - which involves gripping and twisting a portion of the trapezius muscle in the patient's shoulder[1]
  • mandibular pressure - this is the manual stimulation of the mandibular nerve, located within the angle of the jaw
  • supraorbital pressure - this is the manual stimulation of the supraorbital nerve by pressing a thumb into the indentation above the eye, near the nose.[2]
  • sternal rub - this involves creating a turning pressure (akin to a grinding motion with a pestle and mortar) on the patient's sternum[1]

Central stimuli should always be used when attempting to assess if the patient is localising to pain (i.e. moving their arms to the site where the pain is being applied),[3] however it has been suggested that central stimuli are less suitable for the assessment of eye opening, compared to peripheral stimuli, as they can cause grimacing.[4] There is also a statistical reason behind central pain stimuli being inaccurate, especially regarding the GCS, which depending on the patient's eye response, the total score, and thus severity of patients' condition, can be altered with varying prognostic accuracy.[5]

If the patient reacts to the central pain stimulus normally, then a peripheral stimulus is unlikely to be required, unless there is suspicion of localised paresthesia or paralysis in a particular limb.[1]

Central stimuli are likely to have to be applied for at least 15 and potentially up to 30 seconds in order for the clinician to accurately assess their efficacy.[1][3]

The various acceptable central stimuli have been criticised or deemed suboptimal for various reasons. For instance, the sternal rub may leave bruising (especially on fair skinned patients)[1] and for this reason is discouraged by some.[6]

It has been claimed that supraorbital pressure and trapezius squeeze are more effective than the sternal rub or peripheral stimulation, but sternal rub remains the most common.[7][8]

Supraorbital and mandibular pressure may not be suitable for patients with head injuries, or those with periorbital swelling.[9]

Peripheral stimuli

Peripheral stimuli are generally applied to the limbs, and a common technique is squeezing the lunula area of the finger or toe nail, often with an adjunct such as a pen.[1] Like the sternal rub, though, this can cause bruising, and is recommended against, in favour of squeezing the side of the finger.

References

  1. ^ a b c d e f g Lower, Judith (2002). "Facing neuro assessment fearlessly" (PDF). Nursing. 32 (2): 58–65. doi:10.1097/00152193-200202000-00054. PMID 11924168. Archived from the original (PDF) on 2014-08-19.
  2. ^ Rank, Wendi (March–April 2010). "Simplifying neurologic assessment". Nursing Made Incredibly Easy!. 8 (2): 15–19. doi:10.1097/01.NME.0000368746.06677.7c. S2CID 76248224.
  3. ^ a b Mistovich, Joseph; Krost, William (2006-07-01). "Beyond the basics: Patient assessment". EMS World. Archived from the original on 2017-03-20. Retrieved 2012-11-13.
  4. ^ Iankova, Andriana (2006). "The Glasgow Coma Scale: clinical application in Emergency Departments". Emergency Nurse. 14 (8): 30–5. doi:10.7748/en2006.12.14.8.30.c4221. PMID 17212177. S2CID 9654886.
  5. ^ Green, Steven (2011). "Cheerio, Laddie! Bidding Farewell to the Glasgow Coma Scale" (PDF). Ann Emerg Med. 58 (5): 427–430. doi:10.1016/j.annemergmed.2011.06.009. PMID 21803447.
  6. ^ Middleton, Paul (2012). "Practical use of the Glasgow Coma Scale: a comprehensive narrative review of GCS methodology". Australasian Emergency Nursing Journal. 15 (3): 170–83. doi:10.1016/j.aenj.2012.06.002. hdl:10654/45077. PMID 22947690.
  7. ^ Young, G Bryan; Aminoff, Michael; Hockberger, Robert (2009). "Stupor and coma in adults" (PDF). UpToDate.
  8. ^ Waterhouse, Catheryne (2008). "An audit of nurses' conduct and recording of observations using the Glasgow Coma Scale". British Journal of Neuroscience Nursing. 4 (10): 492–499. doi:10.12968/bjnn.2008.4.10.31343.
  9. ^ Jeyaretna, Deva; Whitfield, Peter (2009). "4 Clinical assessment of the head-injured patient: an anatomical approach" (PDF). Head Injury: A multidisciplinary approach. Cambridge Medicine. p. 44.

External links

This page was last edited on 4 March 2024, at 11:15
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