Reading - Sapolsky Chapter 9 Flashcards
The basics of Pain Perception
- Receptors in internal organs or the skin
- Respond to tissue damage -> some receptors are specific to painful signals whilst others can be activated by more normal stimulation at an intense level e.g. warmth versus burning sensation
- Inflammation at an injury site causes release of chemicals from cells that make pain receptors more sensitive.
- Pain signals can activate a spinal reflex which causes as an example you to move your hand from the source of pain e.g. a hot stove they can also be sent upwards to the brain.
Sensory Modulation of Pain Perception: types of fibers and types of neurons in the spinal cord
- Different fibers carry information about acute, sharp, sudden pain than slow, diffuse, constant, throbbing pain.
- Two types of neurons in the spinal cord are effected by pain information = a neuron that relays information to the brain, and a local interneuron which inhibits the activity of the ascending neuron.
Sensory ‘path’ for a sharp painful stimulus
○ Information sent from receptor via a fast fibre
○ Both the ascending (X) and interneuron (Y) are activated
○ X sends pain information up to the brain and then Y quickly shuts it off = a sharp burst of pain -> gets you to move fast to avoid the source of the pain
Sensory ‘path’ for dull throbbing pain
○ Information sent on a slow fibre
○ The Slow fiber inhibits the Y neuron from firing meaning the X neuron (which has been stimulated) keeps firing = a slow, prolonged, throbbing pain results -> gets you to hunker down and rest so you can heal
Interaction of the fast and slow pain pathways
These pathways can interact for treatment purposes e.g. stimulate the fast pathway by rubbing, scratching, sending electrical impulses to distract the slow pathway from firing.
Pain that goes on Longer than Normal: name
- You can feel pain long after the noxious stimulus has stopped or the injury has healed -> allodynia/ chronic pain
Pain that goes on Longer than Normal: reasons/ causes
- Could occur at the cellular level e.g. the inflammatory cells that make the neurons responding to pain at a particular site more sensitive could release ‘too much’ resulting in a leaking of the chemicals and subsequent sensitivity to neighbouring areas of healthy issue.
- Additionally neurons in the pain pathway may be injured and contributing to the pain perception. Sometimes growth factors released by inflammatory cells at these sites cause growth and bundling of nerve fibers into neuroma’s which are highly excitable and can lead to excessive pain signalling.
No Brain, No Pain: does the brain’s interpretation of pain always match the degree of sensation?
- The brain’s interpretation of pain can be extremely subjective : a lot of it is about coming up with an emotional response according to the context
- Study in the 1980s proves this : Patients with views of trees from their windows requested significantly less pain medication (after gallbladder surgery) than those who looked out on blank walls.
-The emotional/ interpretative level can be dissociated from the objective amount of pain signal -> study: volunteers did their hands into hot water before and after given a hypnotic suggestion that they feel no pain. Brain imaging carried out during to see which parts of the brain were active. The sensation processing part of the cortex was activated to the same extent in both cases (same amount of receptor activation) however, the emotional parts of the brain activated only in the pre-hypnosis case - they interpreted the pain differently.
- There are factors that can modulate how much the pain system registers e.g. oxytocin will blunt pain responsiveness
Stress-Induced Analgesia Discovery
- Henry Beecher examined injured soldiers as a battlefront medic in world war 2 and compared them to civilians. For similarly bad injuries, approximately 80 percent of civilians requests morphine while only a third of soldiers did.
Stress-induced analgesia: unique to humans?
Stress-induce analgesia happens in animals as well as humans : e.g. the hotplate test -> measure how long it takes for the rat to feel discomfort and move their foot. If do the same thing with a rat that is stressed it takes longer for the rate to notice the heat of the plate.
How does stress-induced analgesia work with example?a
- Mechanism: Opiate drugs bind to receptors in the pain areas of the brain and block pain perception by activating descending pathways and blunting the sensitivity of the X neuron (responsible for ascending pain signals). These exogeneous opiates mimic the action of endogenous opiates falling under three classes (endorphins, dynorphins, enkephalins).
- Stress triggers the release of beta-endorphin from the pituitary gland, enkephalins are also mobilised (endogenous opioids) -> may explain phenomena like ‘runners high’ after 30 minutes. The pain stops due to analgesic effects.
How does acupuncture work? How do we know?
- Acupuncture stimulates the release of large quantities of endogenous opiates for reasons no one really understandings -> when you block opiate receptors e.g. by naloxone acupuncture no longer effectively dulls pain perception.
How do placebo effects work? How do we know?
- Placebo effects can be useful for managing pain e.g. IV infusion of painkillers is more effective if the patient sees the infusion occurring than if it is done on the sly -> work by releasing endogenous opioids and once again if you block opioid receptors via naloxone they no longer work.
Stress-induced hyperalgesia
- Stress-induce hyperalgesia is also a thing though : this doesn’t involve actual pain perception (receptors or the spinal cord). Instead, it involves emotional reactivity to pain. -> interpret the same signal as more painful.
- Shown in brain imaging studies = parts of pain circuitry in the brain become over active during hyperalgesia -> evidence = anti-anxiety drugs have the effect of blocking the hyperalgesia and those individuals who are higher on traits like Neurotism or even rats bred for anxiety tend to get more hyperalgesia.
Fibromyalgia: a form of hyperalgesia
- Fibromyalgia = people have markedly reduced pain tolerance and multiple tender spots throughout the body - often they have paralysing levels of pain but there is no source of that pain -> sufferers have abnormally high activity in the areas of the brain responsible for mediating emotional/ contextual assessments of pain, also glucocorticoid levels are below normal in these people. Still a bit of a mystery but these people are going down the hyperalgesia route as opposed to the analgesia route of pain modulation.
