SUPP

• Pain is caused by a noxious stimulus and it is a protective mechanism
• Nociceptors refers to pain receptors that respond to thermal, chemical and mechanical stimuli
• Gate control theory refers to when "gates" in the spinal nerve that open to allow for pain stimulus or close to block them
• Nociception are the physiological mechanisms involved in pain sensation
• Nociception is divided into 4 stages: Transduction, Transmission, Perception and Modulation
• Transduction: is the conversion of painful stimuli to neuronal action potentials at sensory receptors
• Transmission is the movement of action potentials from peripheral receptor to spinal cord and then brain
• Perception is the stage in which the brain interprets the signals as painful
• Modulation is the alteration of synaptic transmission of pain signals
• Transmission involves A Delta fibers and C fibers
• A delta fibers are larger and faster; they're responsible to acute and sharp pain. They're sensitive to thermal and mechanical stimuli
• C fibers are smaller and slower. They're responsible for chronic pain. Gates in gate theory are opened by C fiber stimulation. Distracted or guided imagery may close these gates
• Pain transmission flow: A delta and C fibers synapse with the dorsal horns of the spinal cord, either stimulates a withdrawal reflex(transmission ends) or A delta and C fibers cross over in the spinal cord. After that they ascend the spinothalamic tracts to terminate in the thalamus or reticular formation. From the RF, neurons can send the messages up to the cerebral cortex somatic sensory areas
• 75-90% of pain fibers terminate in the medulla and pons area prior to being sent up so general pain is still felt even if higher pathways are destroyed(TBIs)
• Many C fiber pathways terminate in the RF and activate the RAS; this arouses the body
• C fibers cause a dull, sickening and a poorly localized pain
• Chemotactic substances such as prostaglandins, bradykinins and histamines can also stimulate nociceptors
• Substance P can be released by some neurons after injury to stimulate pain response
• Neurologic pain follows a dermatomal distribution pattern which is called radiculopathy
• The brain has the power to control intensity of pain signals and this is done thru transmitters such as enkephalins and serotonins. This occurs in the spinal cord and pons
• Serotonin acts on neurons that secrete encephalin
• Enkephalins inhibit the release of substance P
• Pain tolerance is a variable period of pain endurance before a pain response is initiated. Influenced by a lot of factors
• Pain threshold is the point at which noxious stimuli is perceived as pain
• Acute pain increases risk of hypoxia and increases glycogenolysis
• There are 6 types of pain: cutaneous, visceral, referred, headache, phantom limb and hyperplagesia
• Cutaneous pain is direct and acute; localized from the skin and each layer has a different type. The epidermis will itch and burn, the dermis will be superficial and the subcutaneous tissue will be aching and throbbing
• Visceral pain is diffuse and poorly localized and its decribed as dull/gnawing/burning. Some of it is referred in nature
• Referred pain is located away from the original site and often occurs bcuz of reflex muscle spasm. Ischemia, chemical stimuli and overdistention can also cause it. Often perceived as sharp and excruciating pain. It occurs when C fibers over onto Delta A fibers
• Esophageal, gastric and gallbladder pain may be confused with cardiac due to the nerve tracts they share
• Headache pain results from internal/external stimuli
• Internal headaches occur usually from vascular stretching, meningeal trauma and low ICP. Stimulation of nociceptors above the tentorium cause frontal headaches while beneath cause occipital headaches.
• External headaches are: nasal sinus, tension, ocular changes and TMJ(temporomandibular joint disorder)
• Phantom limb pain a tingling/burning/intolerable pain in an amputated extremity. It could last weeks to years and its the stimulation of nerve endings
• Hyperplasgesia is the hyperactivity of pain pathways. Is AKA neuralgia and due to very sensitive nociceptors. Have severe pain with normal light and stimulation