Pain Flashcards
what is the definition of pain?
pain is an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of damage
pain duration:
acute: 6 months
what is nociceptive pain?
caused by stimulation of peripheral nerve fibers that respond only to stimuli approaching or exceeding harmful intensity (nociceptors)
what 3 modes of noxious stimulation is nociceptive pain classified by?
1- thermal
2- mechanical
3-chemical
nociceptive pain is divided into what 3 categories?
1-visceral (diffuse, difficult to locate and often referred)
2-deep somatic (dull, aching, poorly localized pain)
3-superficial somatic (sharp, well defined and clearly located)
what is neuropathic pain?
caused by damage or disease affecting any part of the nervous system involved in bodily feelings (somatosensory system)
often described as burning, tingling, electrical, stabbing or pins and needles.
bumping the “funny bone” elicits acute peripheral neuropathic pain
what is phantom pain?
a pain felt in part of the body that has been lost or from which the brain no longer receives signals
it is a type of neuropathic pain
what is psychogenic pain?
pain caused, increased, or prolonged by mental, emotional or behavioral factors
sufferers are often stigmatized because both medical professionals and the general public tend to think that pain from a psychological source is not “real”
mind believes they are in pain, are not faking
what is referred pain?
pain that occurs away from the pain site
nerve- to its area of innervation
dermatomal area
embryologic development
examples:
- heart: upper chest, L shoulder, jaw, arm
- diaphragm: lateral tip of either shoulder
- gallbladder- R shoulder, inferior angle of R scap
- Kerr’s sign: pain on tip of shoulder=ruptured spleen
- L5-S1- lateral leg and foot
what are the 2 types of referred pain?
1- myofascial pain
2- sclerotomic and dermatomic pain
myofascial pain:
trigger points, small hyper-irritable areas within a muscle in which nerve, impulses bombard CNS and are expressed at referred pain
sclerotomic & dermatomic pain:
sclerotome: area of bone/fascia that is supplied by a single nerve root
myotome: muscle supplied by a single nerve root
dermatome: area of skin supplied by a single nerve root
paresthesia=
abnormal spontaneous sensations
such as: burning, tingling, pins and needles
dysesthesia=
any unpleasant sensation produced by a stimulus that is usually painless
anesthesia=
complete loss of sensation
usually discriminative sensation
hypesthesia=
partial loss of touch and pressure sensations
hyperesthesia=
increase sensitivity to touch and pressure sensations
analgesia=
complete loss of pain and temperature sensations
hypalgesia=
partial loss of pain and temp sensations
hyperalgesia=
increase sensitivity to pain sensations
myalgia=
tenderness or pain in the muscles
malaise=
general discomfort; uneasiness
causalsia=
intense burning pain
aka complex regional pain syndrome
when nerve gets inflamed
allodynia=
nonpainful stimuli evokes pain
fast pain:
localized; carried through Adelta axons in skin
more discriminative
- primarily located in marginal nucleus (lamina I)
- projects to more lateral areas via discrete, more direct pathways (lateral thalamus (VPL), post central gyrus of parietal cerebral cortex)
- concerned more w/ perception of sharpness, intensity and location
slow pain:
aching, throbbing, burning
carried by C fibers
primarily located in lamina II & V
produced in response to stim by chem mediators of inflammation
-histamine, protaglandin, substance P, etc
projects more medially via polysynaptic pathways
concerned with the affective component of pain
- anguish, depression, fear, anger
- arousal, attention, motivation
nociceptive neuron transmits pain info to SC via:
unmyelinated C fibers and myelinated Adelta fibers
the smaller C fibers (group IV) carry impulses at a rate of .5-2.0 m/sec
want to avoid- much more uncomfortable
deep pain
the larger Adelta fibers (group III) carry impulses at a rate of 5-30 m/sec
more of awareness/protection
superficial/somatic pain. reflex responses
acute pain:
<6 months
underlying pathology can be identified
usually potential or actual tissue damage
group III fibers primarily
can increase muscle tone, HR, BP, SANS
well localized, esp in skin
proportional to injured area
protective function
chronic pain:
> 6 months
can have no damaging or threatening stimulus present
pain remaining after injury is healed
pain theories:
recent research shows the concept of pain as a sensation produced by injury, inflammation or other tissue pathology is no longer true
pain is a conglomeration of a lot of things
specificity
pattern:
- frequency
- intensity
the neuromatrix outputs produce the multiple dimension of the pain experience and the homeostatic and behavior responses
what does the body self neuromatrix consist of?
sensory
affective
cognitive
more neuropsychology- just need to understand that there are different aspects that affect perception of pain
insular cortex=
feeling that distinguished pain from other homeostatic emotions (itch, nausea)
anterior cingulate cortex=
motivational element
sensory cortex=
distinctly located pain
afferent group III fibers for lamina :
I, IV, V
afferent group IV fibers for lamina:
II
primary afferents synapse on:
tract cells
inhibitory interneurons that regulate ascending flow of nociceptive input
facilitory interneurons that regulate ascending flow of nociceptive input
interneurons that mediate local reflexes
WDR
wide dynamic range cells
multimodal
in lamina IV and V
inflammation and the axon reflex:
The triple response:
stretch skin–> red line, flare, and wheal
the wheal and flare result from the activity of pain receptors that transmit impulses along their axons not only in the normal orthodromic direction towards the CNS but also in the antidromic direction from axon forking nodes into the neighboring skin, where the free nerve endings respond by releasing substance P, resulting in the accumulation of fluid that constitutes the wheal response
what does substance P do?
binds to the artery walls causing them to dilate and to produce the flare response
also binds to mast cells and stimulates them to release histamine. resulting in the accumulation of fluid that constitutes the wheal response
neo thalamic tract
sharp, acute pain
goes medially to brainstem parts concerned with pain, then goes to thalamus
spino thalamic tract
AKA: paleo pain system
dull pain
slower
how do TENs work?
modulation of the dorsal horn
pain goes to projection neuronthat goes to ant/lat system
also projects to interneuron (inhibitory interneuron) and inhibits it (disinhibits); so pain fiber causes excitation of projection neuron or disinhibition of projection neuron; mechanoreceptor goes to lamina 4-5 and facilitate interneurons and excites them, which inhibits the projection cell and inhibits projection neuron; makes pain go away
raphe nucleus produces:
serotonin
lateral tegmental nucleus produces:
norepinephrine
descending modulatory systems:
periaqueductal and raphe nucleus (in midline of reticular formation) and lateral tegmental nucleus
projection cells go up, some to periaqueductal gray
this says “how are we going to react?”
sends descending fibers to the other 2 nuclei
mediator from periaqueductal gray to these 2 sites is endorphins.
fibers from the periaqueductal gray sends signals to the raphe nucleus and lateral tegmental nucleus. raphe releases seratonin, lateral tegmental releases NE on inhibitory interneurons.
tracts come down to dorsolateral fasciculus of dorsal horn, enter dorsolateral tract, produce enkephalin which raises threshold of modulatory interneurons in laminas. –>this makes it harder for projection fibers to fire, causing less pain potentials to be firing off
endogenous opiates modulate pain
hyperactive SANS=
pain
complex regional pain syndrome=
causalia
RSD
shoulder hand syndrome
post-traumatic dystrophy
severe pain out of proportion to injury
hyperesthesia
allodynia
trophic changes (skin- hyperhidrosis, edema, stiffness, sweating, decrease hair grown)
unknown mechanism
theories: excitation of nociceptors (axon reflex), activation of group IV fibers
primary afferent fibers (Abeta, Adelta, and C fibers) transmit impulses from the:
periphery
through the dorsal root ganglion (DRG) and into the dorsal horn of the SC
nociceptive specific cells are mainly found in the :
superficial dorsal horn (laminae I-II)
most WDRs are located:
wide dynamic ranges
deeper than nociceptive cells (lamina V)
