Transcript Pain Part 2
The Physiology of Pain Pain Receptors bare sensory nerve endings innervate all organs and tissues (except the brain) respond to all types of noxious stimuli Damaged cells release Bradykinin (the most potent pain producing chemical/enzyme known) which binds to pain receptors **** this does not always lead to the perception of pain **** Neural Pathways in Pain impulses travel to the central nervous system through two different fibers 1. Neospinothalamic (lateral) Tract A- delta fibers transmit impulses quickly and end in the motor and sensory areas of the cortex. Believed to mediate localized, sharp, pricking, brief pain mediates the sensory-discriminative dimension via the cerebral cortex mediates the cognitive-evaluative dimension 2. Paleospinothalamic (medial) Tract C – fibers transmit impulses more slowly and end in the lower regions of the forebrain. Believed to mediate dull, burning, aching, prolonged pain. mediates emotional-motivational dimension Reticular Activating Formation involved in aversive drive & similar pain related behavior integrates pain experience with pain behavior blue red Pain is a physical stressor Oxygen from the air we breathe combines with digested food to provide energy. This process generates dangerous byproducts such as free radicals – electronically unstable atoms or molecules capable of stripping electrons from any other molecules they meet in an effort to achieve stability. In their wake they create even more unstable molecules. Retrieved from http://www.drweil.com/drw/u/QAA400537/Stumped-by-Oxidative-Stress.html Putative Mechanisms for Relationship between Stress & Pain Acute Pain Severe tissue damage elevates interleukins (an immune system component) in the blood. These stimulate the pituitary which leads to corticotropin and vasopressin release i.e. initiates the stress response chronic pain Stress releases CRF response = hypersecretion of ACTH and excessive CORT release Result = the negative feedback system (cort-hippo) fails Unimpeded, stress increases … pain increases ANXIETY a common symptom of stress when anxiety increases pain increases when pain/anxiety decreases, so does the other suggests a common mechanism 80% of PTSD (an anxiety disorder) have chronic pain Endocannabinoids and anxiolytics decrease pain and anxiety but you do not have to be anxious to derive the benefits PERSONALITY pain felt more in catastrophizers & hot-reactors pain felt more in people with external locus of control chronic pain felt more in people with low self-esteem i.e. pain felt more in types with poor coping skills for stress FEELINGS OF CONTROL people who feel they have adequate control feel less pain makes sense, controllable stressors are less stressful if stress causes pain, then controllable pain is less painful HYPNOSIS has been used to decrease pain has been used to decrease stress is the decrease in stress responsible for the decrease in pain? do they share a common mechanism? LAUGHTER laughter decreases stress and pain - both through endorphin release PAIN AFTER ALL HEALING “Usually” occurs after a traumatic injury is the chronic pain the result of chronic stress? STRESS INDUCED ANALGESIA Acute stress can decrease pain perception! could this account for some cases of episodic analgesia? MECHANISM FOR STRESS INDUCED ANALGESIA Endogenous opioid and non-opioid mechanisms are implicated, as are the amygdala and the PAG CRF triggers the release of opioid peptides (endorphins) from immune cells in the area of injury Endocannabinoid receptors in the PAG: if blocked, eliminate SIA Contradictory evidence? chronic stress suppresses the immune system therefore, should suppress release of endorphins, pain Memory mechanisms for Stress & Pain Stress can be induced via memories and negative self-talk A memory-like mechanism has been Suggested for pain (e.g. phantom limb pain) Memories may trigger one which Triggers the other, or both are Triggered concurrently