Download 슬라이드 1 - Brain Facts

PAIN
is critical for our survival
본3
신형철 교수
PAIN:
-definition of pain: an unpleasant sensory or emotional experience
-perception of pain: a product of brain’s abstraction and elaboration of sensory input.
perception of pain varies with individuals and circumstances (soldier injured)
-activation of nociceptors does not necessarily lead to experience of pain (asymbolia for pain;
patient under morphine)
-pain can be perceived without activation of nociceptors (phantom limb pain, thalamic pain
syndrome)
-important for survival, protect from damage: congenital and acquired insensitivity (diabetic
neuropathy, neurosyphilis) to pain can lead to permanent damage
-pain reflexes can be stopped if not appropriate (step on nail near precipice, burn hands while
holding a baby. Pain can be suppressed if not needed for survival (soldier…).
In general 2 clinical states of pain:
Physiological (nociceptive) pain  direct stimulation of nociceptors.
Neuropathic (intractable) pain  result from injury to the peripheral
or central nervous
system that causes permanent changes in circuit sensitivity and CNS connections.
Relationship between injury and pain do not coincide.
A. Injury but No Pain
First, because of nerve damage affecting the part of the body that
is injured.
Second, there are some tissues in our bodies that are relatively
insensitive to injury. most of the brain tissue itself is insensitive
to pain.
Third, there is evidence that people with intact nervous systems can
have injuries but no pain. not clearly understood
Fourth, persons to have injuries and not experience pain because
their minds are involved in something else that is considered
more important at the moment.
B. Pain but No Injury
*phantom limb pain
* thalamic pain syndrome following a stroke.
* imagined pain is every bit as real as pain experienced by persons
with verified physical injuries.
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Individuals who are born without this capacity frequently die at relatively
young ages from injuries that they never felt.
Pain Information processing is distributed across multiple brain regions
and transmitted via parallel pathways. Thus, if any one pathway or
region becomes damaged, other regions and other pathways are still
available to contribute to this experience.
This resiliency of pain processing mechanisms is
clearly in evidence in many cases of chronic pain
- pain which persists long after healing has
occurred.
Many forms of chronic pain, particularly those
arising from damage to nerves, fail to respond to
conventional treatments and cause an
incalculable degree of both emotional and
economic hardship.
The market for all pain therapies was US$17 billion in 2000, and is
expected to grow to $25 billion, $33 billion and $41 billion by 2001, 2005
and 2010 of which an increasing proportion will be for chronic pain
conditions.
Events that can cause pain
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*
*
*
*
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excessive stimulation of a sensory organ
external pressure on a nerve - pinched nerve
nerve damage - generally not repairable
exceeding thresholds of cold, heat, pressure
swelling of an internal organ
extended contraction of a muscle
muscle spasms
low blood flow to an organ
Components of Pain
1. Sensory discriminative: when started and ended, where, how long
2. Affective (emotional): unpleasant
3. Autonomic: blood pressure, heart rate, respiration, visceral pain
4. Motor: escape of protection reflex
5. Cognitive: evaluation of pain, past experience
Many Systems are simultaneously or separately involved
Variability of pain sensation depends on situation, education, society etc.
PAIN LOCATION
A. Somatic
1) Superficial
(initial & delayed)
2) Deep
e.g., chronic, acute joint pain
B. Visceral
PAIN Duration
1. Acute Pain: e.g., burning, where, how
long: Signal & warning function
2. Chronic Pain: e.g., back pain, tumor,
migrane headache : No Physiological
Function
: Real damage---not equal to the
degree of pain sensation
: Location ...... separate syndrome
: psychogenic pain
Chronic Pain Syndrome
Refers to the collection of additional problems which frequently accompany
chronic pain conditions. They may include any combination of the following:
•Interference with work and leisure-time activities
* Decreased income, increased financial pressures
* Activity intolerance
•* Reduced social activities, social withdrawal
* Feelings of depression & discouragement, anger & irritability, tension
* Decreased interest in previously enjoyed activities combined with
increased preoccupation with pain
•* Interference with concentration and memory
* Decreased self-confidence and self-esteem
* Negative attitudes regarding self, others, and life in general
•* Misuse of pain medications or alcohol
* Development of secondary physical problems and complaints
* Sleep difficulties
•* Decreased sexual interest and/or problems with sexual performance
* Conflicts with medical providers and disability compensation systems
Not everyone with chronic pain possesses all features of the chronic pain
syndrome.
Nociceptors
Mechanical nociceptors
activated by strong stimuli such as pinch, and sharp objects that penetrate,
squeeze, pinch the skin.  sharp or pricking pain, via A-delta fibers.
Thermal nociceptors
activated by noxious heat (temp. above 45°C), noxious cold
(temp. below 5°C), and strong mechanical stimuli.  via A-delta fibers.
Polymodal nociceptors
activated by noxious mechanical stimuli, noxious heat, noxious cold,
irritant chemicals.
 slow dull burning pain or aching pain, via non-myelinated C fibers.
Persists long after the stimulus is removed.
A-delta
Mylenated
2-5 um, 6-30 m/sec
A-Fiber Mechano-Heat nociceptors
"First Pain": Early, Brief, Sharp, and Pricking
Excitatory amino acids (glutamate, aspartate, or ATP)
Light Pressure, Heavy Pressure, Heat (45+ deg. Cent.),
Chemicals, Cooling
C-Fiber
Unmylenated
0.3-3.0 um, 1-2.5 m/sec
C-PolyModal Nociceptor
"Second Pain": Slow, Dull, and Burning
Glutamate, Substance P (however, there are C-nociceptors
without Substance P), Neurokinins A&B, Cholycstokinin,
CGRP, Vasointestinal peptide
Light Pressure, Heavy Pressure, Heat (45+ deg. Cent.),
Chemicals, Warmth
Nociceptors
1. The nociceptors (pain sensitive) sensory endings associated with C fibers are
polymodal. They respond to a number of stimuli including: heat, mechanical stimuli
and chemicals. C fibers are non-myelinated and conduct slowly at 0.5 - 2 m/sec.
2. The nociceptor sensory endings associated with A-delta fibers respond to
thermal or mechanical stimuli. A-delta fibers are myelinated and conduct at 5-30
m/sec.
3. The end of nociceptor neurons are not specialized as with other sensory neurons
but are bare (free) nerve endings.
Pain Sensory Receptors
1.
Heat sensitive receptors
Above a threshold of 43oC these heat activated channels will open, allow cations (Na+ in
particular) to flow into the cell thus causing a depolarization.
The greater the stimulus temperature above threshold the greater the frequency of action
potential firing. (These neurons are distinct from the heat sensitive sensory neurons which will
respond to increasing temperatures that are non-painful. The two types of sensory neurons
are active in different temperature ranges).
2.
pH-gated channels
Acid sensing channel, responds to pHs below 6.5 (stimulated by tissue damage or
anoxic/overactive cells). Some of these receptors have recently been shown to be the same
as the capsaicin receptor (Tominaga et al., 1999)
3.
ATP gated channels
ATP is released from damaged cells. ATP-gated ion channels found in nociceptors.
4.
Bradykinin
Damaged cells release proteolytic enzymes which result in the break down of a preprotein
into a nine amino acid peptide called bradykinin. Bradykinin binds to its B2 receptor which
belongs to the metabotropic class of receptors i.e. 7 transmembrane receptor linked to a G
protein. Activation of the B2 receptor triggers a second messanger that activates a transient
inward current (Na+ channel) to depolarize the sensory neuron.
5.
K+
K+ ions will be released after damage to surrounding cells. This will increase the extracellular
concentration of K+ around the pain sensory neuron ending and result in a depolarzation of
the neuron.
Mechanisms associated with
peripheral sensitization to
pain
Agents that Activate or Sensitize Nociceptors:
Cell injury  arachidonic acid  prostaglandins   vasc. permeability
(cyclo-oxygenase)
 sensitizes nociceptor
Cell injury  arachidonic acid  leukotrienes   vasc. permeability
(lipoxygenase)
 sensitizes nociceptor
Cell injury   tissue acidity   kallikrein   bradykinin   vasc. permeability
 activates nociceptors
  synthesis & release of prostaglandins
Substance P (released by free nerve endings)  sensitize nociceptors
  vasc. perm., plasma extravasation
(neurogenic inflammation)
 releases histamine (from mast cells)
Calcitonin gene related peptide (free nerve endings)  dilation of peripheral capillaries
Serotonin (released from platelets & damaged endothelial cells)  activates nociceptors
Cell injury  potassium  activates nociceptors
Peripheral
sensitization
to pain:
Some definitions:
Hyperalgesia increased
sensitivity to an already painful stimulus
Allodynia normally non painful
stimuli are felt as painful (i.e .light touch of a
sun-burned skin)
Allodynia
Root of the Term : "allo" meaning "other" + "odyne"
meaning pain
Definition: Pain due to a stimulus that does not
normally provoke pain.
Characteristics: non-noxious tactile, thermal
stimuli--->painful shift (change) of sensory
modality
Difference from Hyperalgesia?
Analgesics and Anesthetics
Analgesia - reduction of sensibility to pain, production of loss of pain
sensation without loss of consciousness or other vital functions in response
to stimuli that would normally be painful.
Anesthesia - absence of all sensory modality and loss of consciousness
without loss of vital functions
Peripheral sensitization to pain:
CGRP
CGRP
Serotonin, bradykinin, histamine, prostaglandins, substance P (sP) , and
various ions (ie, H+ or K+)--the biochemical mediators released as a
result of tissue injury--have been implicated in nociceptive activation
and sensitization (hyperalgesia).
Hyperalgesia results in enhancement of spontaneous pain via
1) a reduction in pain threshold
2) and a lengthening in duration of nociceptor response to stimuli.
PGE1, PGE2, and PGF2a, are the most potent prostaglandins to
produce these sensitization effects.
Substance P, synthesized by cells of the spinal ganglia, has been
identified at the peripheral terminal of unmyelinated primary afferent
fibers.
suggested that this putative neurotransmitter may play a role in the
propagation of visceral nociceptive pain from the gastrointestinal (GI)
tract, ureters, and urinary bladder. In addition, to SP, other potential
nociceptive transmitters include glutamate, aspartate, somatostatin,
cholecystokinin (CCK), and vasoactive intestinal polypeptide (VIP).
To summarize peripheral sensitization to pain
-Sensitization results from the release of various chemicals by the
damaged cells and tissues (bradykinin, prostaglandins, leukotrienes…).
These chemicals (algogenic substances) alter the type and number of
membrane receptors on free nerve endings, lowering the threshold for
nociceptive stimuli.
-The depolarized nociceptive sensory endings release substance P and
CGRP along their branches (axon reflex), thus contributing to the spread
of edema by producing vasodilation, increase in vascular permeability
and plasma transvasation, and the spread of hyperalgesia by leading to
the release of histamine from mast cells.
-Aspirin and NSAID (nonsteroidal anti-inflammatory drug) block the
formation of prostaglandins by inhibiting the enzyme cyclooxygenase.
-Local anesthetic preferentially blocks C-fiber conduction, cold
decreases firing of C-fibers, ischemia blocks first the large myelinated
fibers.
Pathophysiology of Transduction
Injury to somatic (skin, muscle, or bone) or to
visceral tissues is known as nociceptive pain.
Pressure from a mass that encircles and
constricts neural tissue (e.g., nerve plexus,
nerve root, spinal cord) and that is sufficient
to injure the tissue, produces pain known as
neuropathic pain.
Burns are obvious examples of tissue damage
from thermal stimuli. Superficial burns injure
somatic tissue and result in nociceptive pain.
Massive burns, however, are likely to injure
peripheral nerve fibers as well as somatic
tissues. Therefore, extensive burns may result
in both neuropathic and nociceptive types of
pain.
Neuropathic (intractable)
pain:
Pain following peripheral
nerve injury. Greater loss of
small fibers than large diameter
fibers. Axons of surviving Abeta fibers sprout new branches
and make connection to neurons
vacated by the lost C fibers .
Non-painful stimuli become
painful. Change from innocuous
to noxious sensation is called
allodynia.
Thalamic pain syndrome:
usually following stroke in the
ventral basal thalamus.
Rearrangement of local circuit
leads to excruciating pain.
Phantom limb pain:
A-beta
Pain
Signaling
neurons
C fibers
N
Afferents to Spinal Dorsal Horn
layer I (marginal zone): A-delta,
high density of projection neurons
layer II (substantia gelatinosa): C-fibers,
output layer III
layer III: from layer II (C input)
layer IV: A-alpha & A-beta, from layer V (Adelta)
layer V: A-delta, output to layer IV
Pain input to the spinal cord:
-Projecting neurons in lamina I receive A-delta and C fibers info.
-Neurons in lamina II receive input from C fibers and relay it to other laminae.
-Projecting neurons in lamina V (wide-dynamic range neurons) receive A-delta, C and A-beta
(low threshold mechanoceptors) fibers information.
How is pain info sent to the brain: hypotheses  pain is signaled by lamina I and V
neurons acting together. If lamina I cells are not active, the info about type and
location of a stimulus provided by lamina V neurons is interpreted as innocuous. If
lamina I cells are active then it is pain.
Thus: lamina V cells details about the
stimulus, and lamina I cells whether it
is painful or not
-A-delta and C fibers release glutamate
and peptides on dorsal horn neurons.
-Substance P (SP) is co-released with
glutamate and enhances and prolongs the
actions of glutamate.
-Glutamate action is confined to nearby
neurons but SP can diffuse and affect
other populations of neurons because
there is no specific reuptake.
types of neurons:
Projection N.: relay incoming sensory information to higher ctrs.
Local excitatory N.: relay sensory input to projection neurons.
Inhibitory N.: regulate the flow of nociceptive information
Two Major Nocicpetive Cell Types:
Noceceptive specific N. (NS, HT): layer I
excited soley by nociceptors
Wide Dynamic Range N. (WDR): layer I, V & VI
excited by nociceptors & by low-threshold mechanoreceptors
Neurotransmitters: Glutamate, Substance P, Enkephalin 등등
:small electron-translucent synaptic vesicles: excitatory amino acids
A-delta fiber에 다, evokes fast synaptic potentials
:large dense-core vesicles: neuropeptides
C-fiber에 다, elicit slow excitatory PSP
Ascending Pathways:
->localization, intensity,
type of pain stimulus
->arousal, emotion; involves limbic system,
amygdala, insula, cingulate cortex, hypothalamus.
Mediate descending control of pain (feedback loop)
Centrally mediated hyperalgesia:
Under conditions of persistent injury, C fibers fire repetitively and the response of
dorsal horn neurons increase progressively (“wind-up” phenomenon). This is due to
activation of the N-methyl-D-aspartate (NMDA)-type glutamate receptor and diffusion
of substance P that sensitizes adjacent neurons. Blocking NMDA receptors can block
the wind-up.
Noxious stimulation can produce these long-term changes in dorsal neurons
excitability (central sensitization) which constitute a memory of the C fiber input. Can
lead to spontaneous pain and decreases in the threshold for the production of pain.
Carpal tunnel syndrome: median nerve frequently injured at the flexor retinaculum.
Pain ends up affecting the entire arm. (rat model  partial ligature of sciatic nerve or
nerve wrapped with irritant solution)
Mechanisms of early-onset
central sensitization:
Winduphomosynaptic activity-dependent
plasticity characterized by a progressive
increase in firing from dorsal horn neurons
during a train of repeated low-frequency Cfiber or nociceptor stimulation.
During stimulation, glutamate + substance P
+ CGRP elicit slow synaptic potentials
lasting several-hundred milliseconds.
Windup results from the summation of these
slow synaptic potentials. This produces a
cumulative depolarization that leads to
removal of the voltage-dependent Mg2+
channel blockade in NMDA receptors and
entry of Ca2+. Increasing glutamate action
progressively increases the firing-response
to each individual stimulus (behavioral
correlate: repeated mechanical or noxious
heat are perceived as more and more painful
even if the stimulus intensity does not
change.
Both the thalamus (lower activation focus) and the primary
somatosensory cortex (upper activation focus) are activated
by acute pain produced by injection of capsaicin (chile
pepper extract) into the skin.
Regional activations are determined by statistical analysis of
positron emission tomography (PET) scans from 14 subjects.
Itch: Anatomy & Physiology
Peripheral Stimuli
Histamine
Onset: Delay of 30 to 60 seconds
Duration: 10 minutes
Itch axons are mechanically insensitive
Mustard oil: Stimulates distinct axons conveying dysesthesias associated with itch
Primary itch afferents
C-fibers
Physiology
Transcutaneous electrical threshhold: High
Conduction velocity: Low
Mechanical stimuli: Unresponsive
Histamine sensitive
Secondary itch afferents
Location of cell bodies: Lamina I of spinal dorsal grey
Projection pathway
Spinothalamic tract
Conduction velocity of axons: Slow
Termination: Thalamic nuclei
Ventral posterior inferior (VPI)
Periphery of Ventral posterior lateral (vVPL)
Inhibited by painful stimuli
Neural Mechanisms of Itch Sensation
What are the signs and symptoms of the condition?
What are the causes and risks of the condition?
What can be done to prevent the condition?
How is the condition diagnosed?
What are the treatments for the condition?
Causes of Visceral pain
1. Extreme expansion of gut, bladder
2. ischemia-->Strong contraction or severe stretching of muscular wall
3. Mechanical or chemical (acid, base) stimulation of mucosal layer
Unmyelinated Vagus nerve (mechano, chemoreceptor: gastric motility, secretion)
Referred Pain:
stomach problems may refer to the spine between the shoulder blades.
Visceral pain and its Management
New pathway for visceral pain:
selective lesion of fibers in the ventral
part of the fasciculus gracilis reduces
dramatically the perception of pain from
the viscera.
General problems with surgery:
Rhizotomy (cutting dorsal root)
Anterolateral cordotomy (cutting ALS)
In both cases, pain come back,
excruciating.
Thalamus: lesion VPL, VPM 
thalamic syndrome. Intralaminar nuclei
 (arousal + limbic)
Cortex: S1 cortex  localization,
quality and intensity of pain stimuli.
Lesion of cingulate gyrus and insular
cortex  asymbolia for pain
Gate Control Hypothesis
Wall & Melzack 1965
Hypothesized interneurons
activated by A-beta fibers act as a
gate, controlling primarily the
transmission of pain stimuli
conveyed by C fibers to higher
centers.
i.e. rubbing the skin near the site of
injury to feel better.
i.e. Transcutaneous electrical nerve
stimulation (TENS).
i.e. dorsal column stim.
i.e. Acupuncture
Gate Control Theory of Pain:
Therapeutic implications of the gate control theory
1. stimulation of tactile fibers of the skin inhibits the transmission of pain signals
from the same area of the body.
e.g., rubbing, stroking, massage, vibration, application of liniments and other
ointments.
2. electrical stimulation of the skin's sensory nerve fibers (transcutaneous electrical
nerve stimulators [TENS]) inhibits pain.
3. morphine and other opioid drugs inhibit or block SG activity and, thus, pain.
4. normal and excessive environmental stimuli can close the pain gate.
5. the pain gate can be closed by inhibitory signals from the cerebral cortex and
thalamus.
e.g., decreasing anxiety, fear, teaching the client
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F%2Fvideo.yahoo.com%2Fvideo%2Fsearch%3Fei%3DUTF-8%26p%3Dchronic%2Bpain%26b%3D21
http://www.metacafe.com/watch/227740/no_more_pain/
HYPNOSIS MIGHT ALLEVIATE pain by
decreasing the activity of brain areas
involved in the experience of suffering.
Positron emission tomography (PET) scans
of horizontal (top) and vertical (bottom) brain
sections were taken while the hands of
hypnotized volunteers were sunk into
painfully hot water.
The activity of the somatosensory cortex,
which processes physical stimuli, did not
differ whether a subject was given the
hypnotic suggestion that the sensation
would be painfully hot (left) or that it would
be minimally unpleasant (right).
In contrast, a part of the brain known to be
involved in the suffering aspect of pain, the
anterior cingulate cortex, was much less
active when subjects were told that the pain
would be minimally unpleasant (bottom).
1. proopiomelanocortin (POMC) gene
2. proenkephalin gene
3. prodynorphin gene
three peptides are distributed differently in the CNS
two inhibitory mechanisms
1. postsynaptic inhibition produced partly by increasing K+ conductance
2. by presynaptic inhibition
Descending pathways regulating the
transmission of pain information:
intensity of pain varies among individuals
and depends on circumstances (i.e. soldier
wounded, athlete injured, during stress).
Stimulation of PAG causes analgesia so
profound that surgery can be performed.
PAG stimulation can ameliorate intractable
pain. PAG receives pain information via the
spinomesencephalic tract and inputs from
cortex and hypothalamus related to
behavioral states and to whether to activate
the pain control system. PAG acts on raphe &
locus ceruleus to inhibit dorsal horn neurons
via interneurons and morphine receptors.
Application: Intrathecal morphine pumps
Three classes of opioid receptors
mu, d-delta and kappa
genes cloned and found to be members of the G protein receptors.
•Types
om Receptor
•Agonists: Morphine; [D-Ala2,N-Me-Phe4,Gly-ol5]-enkephalin (DAMGO)
•Antagonist: H-D-Phe-Cys-Tyr-D-Trp-Arg-Thr-Pen-Thr-NH2 (CTAP)
•System stimulation: Reduces acute pain & hyperalgesia in most models
od Receptor
•Agonist: 4-[(aR)-a-((2S,5R)-4-allyl-2,5-dimethyl-1-piperazinyl)-3methoxybenzyl]-N,N-diethylbenzamide (SNC80)
•Antagonist: Naltrindole
•System stimulation: Reduces acute pain & hyperalgesia in inflammatory
pain models
•May have fewer side effects (Constipation, respiratory depression,
physical dependence) than m-agonists
ok Receptor
•Agonist: (1S-trans)-3,4-dichloro-N-methyl-N-[2-(1pyrrolidinyl)cylcohexyl]-benzeneacetamide hydrochloride (U50,488)
•System stimulation: No effect on chronic muscle pain
•Locations: PAGM, Ventral medulla, Dorsal horn
Factors that influence the production of enkephalins, endorphins,
dynomorphins
1.
2.
3.
4.
prolonged strenuous activity
TENS
acupuncture
placebo effect
Following are some situations and conditions which are thought to
stimulate endorphin production.
1) Emergency situations requiring the person to perform physical
actions despite pain and injury.
2) Intense physical activity. Moderate physical activity over an extended
period of time can also increase the supply of endorphin.
3) Positive beliefs and expectations (e.g., the "placebo effect").
4) Positive emotional states such as happiness, joy, laughter, and love.
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3Fp%3Dchronic%2Bpain%26toggle%3D1%26cop%3Dmss%26ei%3DUTF-8%26b%3D31
Analgesics:
1)
May act at the site of injury and decrease the pain associated with an inflammatory reaction
(e.g. non-steroidal anti-inflammatory drugs (NSAID) such as: aspirin, ibuprofen, diclofenac).
Believed to act through inhibition of cyclo-oxygenase (COX). COX-2 is induced at sites of
inflammation. Inhibition of COX-1 causes the unwanted effects of NSAID, i.e.
gastrointestinal bleeding and nephrotoxicity. Selective COX-2 inhibitor are now used.
2)
May alter nerve conduction (e.g. local anesthetics): block action potentials by blocking Na
channels. Used for surface anesthesia, infiltration, spinal or epidural anesthesia. Used in
combination to steroid to reduce local swelling (injection near nerve root). Local anesthetic
preferentially blocks C fiber conduction, cold decreases firing of C fibers, ischemia blocks
first the large myelinated fibers.
3)
May modify transmission in the dorsal horn (e.g. opioids: endorphin, enkephalin,
dynorphin…). Opioids act on G-protein coupled receptors: Mu, Delta and Kappa. Opioid
agonists reduce neuronal excitability (by increasing potassium conductance) and inhibit
neurotransmitter release (by decreasing presynaptic calcium influx)
4)
May affect the central component and the emotional aspects of pain (e.g. opioids,
antidepressant). Problems of tolerance and dependence
Pathophysiologic Consequences of Unrelieved Pain
Physically and psychologically dangerous.
Immune system: decreasing natural killer cell number, function and activity. Can lead to death.
Pulmonary system: causing reflex muscle spasm leads to splinting which decreases pulmonary vital
capacity, functional residual capacity.
Cardiovascular system: causing sympathetic over activity.
Gastrointestinal system: causing increased sympathetic activity, which increases GI secretions and
smooth muscle sphincter tone decreases intestinal motility. Leads to gastric stasis and paralytic ileus.
Musculoskeletal system: Unrelieved pain causes segmental and supra segmental reflexes with
increased muscle spasm leads to impaired muscle metabolism and to muscle atrophy.
Neuronal plasticity: Unrelieved pain causes primary and secondary hyperalgesia.
Psychologic consequences of unrelieved pain include anxiety, fear, depression, distress, and
suffering, hopelessness, helplessness and a decreased will to live (wish for assisted suicide or
euthanasia).
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Dchronic%2Bpain%26ei%3DUTF-8%26b%3D21
http://www.nature.com/cgi-taf/DynaPage.taf?file=/nature/journal/v421/n6921/full/421328a_fs.html
http://www.acupuncturedoc.com/national.htm
http://www.westons.com/comtensj.htm
Phantom limb pain
Phantom limb pain occurs among between 50 and 80
percent of amputees.
Phantom pain can occur anytime, from just after an
amputation to years later. Its occurrence is not related
to psychological factors, age, sex, location of the
amputation, or reason for the amputation (e.g. trauma
vs. disease).
What causes Phantom Pain ?
1. Prior experience with pain prior to amputation.
2. Incorrect surgical procedure.
3. Climatic conditions - changes in air pressure and temperature.
4. Stress.
5. Inactivity - Remaining in a relatively same position for long periods of time.
6. Periodic illness - Colds, flu, strep throat, infections, viruses can increase
the level of phantom sensation.
REMEMBER - Increased blood flow to the amputated area will (in many cases) reduce
the amount of pain.
REMEMBER - The easiest and worst way to combat phantom pain to fill yourself full of
medication.
Phantom limb pain:
during amputation under general
anesthesia the spinal cord can
still “experience” the insult
produced by the surgical
procedure and central
sensitization occurs. To try to
prevent it, local infiltration of
anesthetics in the site of surgery.
But studies show also
rearrangement of cortical circuits
(cortical region of the missing
limb receives afferents from
other site of the skin)
Phantom Pain intensity
as a function of Cortical
Reorganization.
Projected Pain:
e.g., nerve 자극: 그 nerve가 innervate한 지역의 pain으로 느낌
compression of spinal nerve
Neuralgia:
continuous irritation of a nerve or a dorsal root
(chronic nerve damage)---> spontaneous pain
Deafferentation pain:
motor cycle injury
: dorsal root가 pulled away from the spinal cord (brachial plexus avulsion)
: burning or electric pain in the dermatomes corresponding to the denervated area.
: because of the hyperactivity of dorsal horn neurons in the deafferented region of the
spinal cord
: 치료: surgical ablation of the superficial dorsal horn
Causalgia: (reflex sympathetic dystrophy syndrome)
: activity of efferent fibers of the sympathetic nervous system following peripheral nerve
injury
---> activation of damaged nociceptive afferents