Pain control is at first synapse, near spinal cord {pain, physiology}. Prostaglandins block glycine receptors and so excite dorsal-horn neurons. More and wider brain activation indicates more pain [Chapman and Nakamura, 1999]. Drugs can make pain feel pleasurable. The fundamental pain characteristic is repulsion or withdrawal, and the fundamental pleasure characteristic is attraction or advance [Duncker, 1941].
Tissue damage, inflammation, and high-intensity stimuli release chemicals that excite nociceptors. Pain detects and measures relative concentrations of pain-causing chemicals released by body inelastic strains or tissue damage. People can distinguish strength and type of pain.
High pressure, high temperature, harsh sound, intense light, and sharp smells and tastes cause neuron changes {pain, causes}. Inflammation or acute-pain aftereffects can cause pain.
Pain involves too much small-nerve-fiber activity, uninhibited by large neurons. Blows to body release histamines, bradykinin, and prostaglandins, which excite neurons. Gut distension causes pain, but gut squeezing, cutting, and burning do not. Infection can amplify pain. Tissue damage can amplify pain. Damaged tissue activates immune cells, which release molecules that excite nerves and glia. Arginine vasopressin, encephalin, endorphin, and substance P can affect pain.
Randomly placed brainstem electrodes produce pain 5% of time. Direct cerebral-cortex stimulation can cause other sense qualities but never causes pain. Cortex stimulation does not decrease pain.
Pain causes people to push painful object farther away or to move farther from pain source {pain, effects}. Sharp pain causes withdrawal reflexes, writhing, jumping away, and wincing as people try to alleviate pain. Writhing escapes stimulus or pushes away stimulus. Painful skin stimuli cause flexion reflexes. Muscle contractions inhibit blood flow and squeeze out poisons. To avoid reinjury and allow body to rebuild rather than use, dull and chronic pain reduces overall activity. People can have no reaction to pain.
Pain causes attention to object. People cannot ignore pain caused by high-intensity stimulus. Pain makes other goals seem unimportant. To allow recovery from tissue damage, pain causes attention to damage, such as wounds. To avoid future pain causes, pain triggers learning about possibly painful situations. People also learn pain responses.
Pain can cause anxiety, increase breathing rate, increase blood pressure, dilate pupils, increase sweat, and make time appear to flow more slowly.
Spinal-cord dorsal-horn substantia-gelatinosa neural circuits receive signals from brain and inhibit nerve-impulse flow from spinal cord to brain {gate control theory of pain}|. Large-fiber inputs, such as from gentle rubbing {counterstimulation}, stimulate substantia-gelatinosa neurons to inhibit signal flow, closing the gate. Small-fiber inputs, such as from pinching {diffuse noxious inhibitory control} {counterirritation}, inhibit substantia-gelatinosa neurons to release signal flow, opening the gate. Direct brain signals also inhibit flow and close the gate [Melzack, 1973] [Melzack, 1996].
Pain-activated microglia (immune cells) release pro-inflammatory cytokines, which activate glia {glial activation} and cause pain, but other glia types do not release cytokines in response to pain. Spinal glial activation affects nociceptive neurons at NMDA receptors.
Blocking glial activation with drugs blocks pathological pain. Blocking neuron pro-inflammatory-cytokine receptors with drugs does not affect normal pain responses but does decrease exaggerated pain responses. Intrathecal drugs {fluorocitrate} can inhibit glial metabolism. Acids {kynurenic acid} {2-amino-5-phosphonovaleric acid} (AP-5) can prevent such inhibition. Amines {6,7-dinitroquinoxaline-2,3-dione} (DNQX) {picrotoxin} and strychnine do not prevent such inhibition [Ma and Zhao, 2002] [Watkins et al., 2001].
Chemicals, biofeedback, distraction, and imagery can lessen pain {pain relief}. Hypnosis can relieve pain.
Endorphin and dynorphin inhibit pain pathways. Flight-or-fight responses use endorphin neurotransmitters to suppress pain. Aspirin and nitrous oxide alleviate pain. Opiate drugs, such as morphine, are similar to endorphin and suppress pain. Ziconotide (Prialt), modified cone-snail venom, inhibits N-type calcium channels to lessen pain.
Adaptation, distraction, or drugs can decrease pain {analgesia, pain}|.
Drugs can make pain be felt but not remembered {hyoscine sleep}|. Twilight-sleep drug, from thorn apples, binds to acetylcholine receptors and affects long-term memory recall.
Inserting large needles at skin locations {acupuncture}| can reduce pain. Acupuncture-needle stimulation activates brain area that makes endorphin and dynorphin to inhibit pain pathways. Traditional acupuncture-needle insertion sites correspond to myofascial-nerve locations. Traditionally, acupuncture makes energy {qi} travel along body meridians.
Massaging with ice {ice massage} reduces pain.
Stimulating brain area that makes endorphin and dynorphin {transcutaneous electrical nerve stimulation} (TENS) inhibits pain pathways.
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Date Modified: 2022.0225