People have acute or dull personal discomfort and avoidance feelings {pain, sense}. Some people cannot feel pain.
physical properties
Painful events include tissue strains and releases of molecules that cause chemical reactions. Molecules vary in size, shape, chemical sites, and vibration states. Chemicals vary in concentration. Painful chemicals chemically bind to tissue chemical receptors.
properties
Pains can be throbbing, burning, dull, or acute/sharp. People perceive pain at body locations and also have overall bad feelings. Lower back pains are the most common. Deviating from chemical and function equilibrium is typically not painful. People in pain can still have humor and laughter.
nature
Perhaps, pain includes dislike or avoidance. Pains are not concepts, observations, or judgments. Pain is not intentional but is only about itself.
brain
Pain uses cerebral cortex and is always conscious. Pain perception uses thalamus and is not conscious. Pain differs in species, because neocortices differ. Squid seem to feel pain.
factors
Prior experience influences pain. Pain anticipation increases pain. Body movement can lessen sharp pain and increase chronic pain. Sensitivity to pain is greatest at 9 PM. Pain sensitivity decreases with age.
senses
Temperature and nociceptive receptor systems interact. Tactile and nociceptive receptor systems interact.
evolution
Humans seem to have higher sensitivity to pain than other mammals. Lower animals have even less pain. Squid seem to feel pain.
development
By 156 days (five months), fetus can have pain. Newborns can have pain. By 4 months, infants have undifferentiated fear reactions to people and animals associated with pain, and so coordinate vision and pain perceptions.
The pain system has skin receptors with ion channels, neurons, fibers, fiber tracts, and brain regions. Pain chemical receptors send to dorsal-horn neurons, which send to cortical regions. Cortex and thalamus control pain {pain, anatomy}.
Skin and body receptors (nociceptor) chemically bind endomorphins, prostaglandins, bradykinin peptides, and protein hormones (such as nerve growth factor), molecules released by inflammation and tissue damage [Woolf and Salter, 2000].
fibers
Body organs and mesentery have pain fibers. Internuncial neurons have pain fibers. Pain fibers are A, C, III, IV, and nociceptive fibers. Large myelinated fibers detect moderate stimulation. Small myelinated fibers detect all stimulations. Myelinated fibers detect sharp localized skin pain. Unmyelinated fibers detect dull deep unlocalized body pain. Itching nerves are separate from pain nerves.
brain
Anterior cingulate gyrus, frontal lobe, Lissauer's tract, locus coeruleus, nociceptive system, protopathic pathway, raphé nuclei, reticular formation, sensory reticular formation, sensory thalamus, spinal cord, spinoreticular tract, and spinothalamic tract affect pain. Throbbing pain, burning pain, and sharp pain use different brain regions. Cingulate cortex receives pain information [Chapman and Nakamura, 1999]. Cortex has pain center connected to sense areas. Reticular formation regulates pain.
brain pathways
Feeling pain and reacting to it involve separate pathways. Spinothalamic tract and central gray-matter path carry pain fibers. Internuncial neurons have pain fibers. Body organs and mesentery have pain fibers. Lemniscal tract has no pain fibers but affects pain. Abdominal pain signals travel in subdiaphragmatic vagus nerve to nucleus tractus solitarius, nucleus raphe magnus, and spinal-cord dorsolateral funiculus [Ritter et al., 1992].
Connective-tissue dendritic cells {nerve-associated lymphoid cells} (NALC) have interleukin-1 binding sites, send to sensory vagus-nerve paraganglia, and are near macrophages, mast cells, and other dendritic cells [Goehler et al., 1999].
Connective-tissue nerve-associated lymphoid cells send to neuron groups {paraganglia} who send along sensory vagus nerve [Goehler et al., 1999].
Nociceptors can have proton ion channels {acid-sensing ion channel} (ASIC).
Nociceptors and other neurons have special calcium-ion channels {N-type calcium channel} {calcium channel, N-type}. Ziconotide (Prialt), modified cone-snail venom, inhibits N-type calcium channels to lessen pain. Gabapentin (Neurontin) anticonvulsant binds to N-type calcium channels.
Outside CNS, nociceptors and other neurons have special sodium-ion channels {TTX-resistant voltage-gated sodium channel}.
Nociceptors and all neurons have sodium-ion channels {voltage-gated sodium channel} {sodium channel, voltage-gated} that open by voltage changes.
Nociceptors can have receptors {bradykinin receptor} for small bradykinin peptides, produced by peripheral inflammation.
Dorsal-horn neurons receive input from nociceptors and have calcitonin peptide receptors {calcitonin receptor} {calcitonin gene-related peptide receptor} (CGRP receptor).
Mouth nociceptors can have pepper-molecule receptors {capsaicin receptor} {VR1 receptor}, which also react to high temperature and protons.
Peripheral pain nerves can add chemical receptors {hormone receptor}. For example, stress hormones can attach to stress-hormone receptors and cause pain [Woolf and Salter, 2000].
Nociceptors can have protein-hormone receptors {nerve growth factor receptor} (NGF receptor).
All neurons that receive input from nociceptors have glutamate receptors {NMDA receptor, pain}. Dorsal-horn neurons have glutamate receptors with a specific subunit {NR2B subunit}.
NTRK1 gene makes receptors {neurotrophin tyrosine kinase receptor type 1} (NTRK1 receptor). NTRK1-gene mutations can cause a rare autosomal recessive disease (CIPA), with pain insensitivity, no sweating, self-mutilation, fever, and mental retardation.
Skin receptors {nociceptor} can detect pain, to warn about skin damage.
Many neurons, including nociceptors, have opium-compound receptors {opioid receptor}.
Nociceptors can have endomorphin receptors {prostaglandin receptor}.
Dorsal-horn neurons receive input from nociceptors and have substance-P receptors {neurokinin-1 receptor} (NK-1 receptor) {substance P receptor}. Substance P can carry saporin toxin into dorsal-horn neurons and kill them.
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.
In undamaged areas, receptors and neurons can have sensitization, so people feel pain from stimuli that are not typically painful {allodynia}.
Intra-uterine devices can cause uterine pain {dysmenorrhoea}.
People can perceive pain {extra-territorial pain} in undamaged tissue near damaged tissue.
Without tissue damage or infection, peripheral pain nerves can increase spontaneous activity and cause pain {false pain}.
People can be sensitive to touch and have low pain threshold {hyperaesthesia, pain}.
Receptor or nerve sensitization can cause greater than normal reaction to pain stimuli {hyperalgesia}.
Tabes dorsalis has shooting pains {lightning pain} [Charcot, 1890].
People can perceive pain {mirror pain}| in undamaged tissue on body side opposite damaged tissue.
Chronic pain {neuropathic pain} can persist after nervous-system injury. Injury can change skin receptors {peripheral neuropathic pain}. Injury can change spinal-cord dorsal horn {central neuropathic pain}.
People that lose limbs often feel like they still have limb or feel sense qualities from former region {phantom limb}| [Melzack, 1992] [Ramachandran and Blakeslee, 1998] [Weir-Mitchell, 1872].
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Date Modified: 2022.0225