Pain can cause emotional disorders and vice versa
-Difficult to determine which came first (Chicken or the EGG)
-Important to treat BOTH the pain and the emotional stress
Diagnostic tests for pain
- examples (and uses for each)
EMG & nerve conduction studies are useful for dx of
Diagnostic neural blockade: uses LA to specify a pain mechanism
What are the different classifications of pain?
Transient Acute Pain
Of skin, SC tissue, bone, muscle
Of internal organs,
Perceived as occurring in an area other than the stimulus
Acute pain (aka)
- its biologic fcn is..
- duration can be up to..
- what type of transmission is involved?
- major NT of acute pain?
- psych s/sx are..
Acute pain has a protective biological fcn (eg p/o pain)
- short term lasting up to 6 mo
Acute pain is r/t Nociceptive transmission (somatic/visceral)
- major NT is Glutamate
assoc/psych s/sx are minimal
Nociceptive pain originates via..
- and it is transmitted via
- it can be either ____ or _____
consists of what 4 processes?
Transmitted via normal pathways Originating by stimulation of nociceptors
Transmitted via Ad (first pain) or C fibers (second
Either somatic or visceral
Pain consists of four processes:
Nociception (depolarization at the peripheral nociceptors)
Transmission (along primary afferent nociceptive axons to the SC --> to the brain)
Perception (intellectually recognized by the brain as pain)
Modulation (augmentation or inhibition at multiple levels)
Chronic pain is phase ___ pain
- biological fcn
- lasts for..
- unlike acute pain, chronic pain is more ____ than the amount expected for the stimulus
- chronic pain can be either ____ or ______
- major NT in chronic pain
Phase II Pain
Serves no protective biological function
Persist beyond expectations (>3-6 months)
More intense than stimulus warrants (sensitization)
Can be either nociceptive or neuropathic
The major neurotransmitter of chronic pain is Substance P (also glutamate and aspartate)
chronic pain is rarely treated effectively
What is repetitively bombarded in chronic pain?
- what will adjust/change because of this? --> sequence
The dorsal horn has been bombarded by severe pain for a long period of time
-The interneuron adjusts by adding fast pain receptors to amplify pain signal--> to the ascending tract --> brain recognizes severe intractible pain --> modifier pathways attempt to inhibit pain but fails
What is inflammatory pain precipitated by?
- what endogenous substances sensitize the nocicpetors?
Precipitated by an insult to the integrity of tissues at a cellular level.
Endogenous susbstances can sensitize nociceptors: the inflammatory "soup"
Mast cells release histamines and 5HT
Macrophages activate fibroblasts, which in turn release IL and TNF
Cyclooxygenase activates prostaglandin and leukotrienes
The hyperemia associated with inflammation delivers NO and bradykinin
Inflammatory mediators can directly affect nociceptors or may sensitize them to touch or movement, even some distance from the inflammatory field
In chronic pain, what normally dormant nerve fibers transmit pain?
if this increased pain lasts, it can cause..
A-Beta nerve fibers
- these nerve fibers pass through the highly sensitized cells in the dorsal horn--> SC --> transmitted as pain
If this increased pain lasts it can cause wind up pain in the cell bodies of the dorsal horn interneurons and further induce wide dynamic range neurons to stimulate sympathetic coupling
Phase III pain is... aka
- occurs d/t..
Neuropathic pain, phase III pain PATHOGENIC
Produced by pathologic changes or damage to
Can result from
-Partial of complete nerve transection
describe the pain response in neuropathic pain?
- what is the character/type of pain?
- what are the hallamarks of neuropathic pain?
Pain response is exaggerated and can be
-Evoked by innocuous stimuli
The hallmarks of neuropathic pain are
what is the primary cause of neuropathic pain?
- what are the mechanisms underlying:
Phantom limb pain
...connections connections between sensory and sympathetic fibers, and such cross–connections may play a role in the pathogenesis of sympathetically mediated pain
Central neuropathic pain-
sensitization of neurons can occur where?
- after peripheral injury, these large afferents..
sensitization of neurons can occur within the dorsal horn
After peripheral nerve injury, these large afferents gain access to spinal regions involved in transmitting high intensity, noxious signals, instead of merely encoding low threshold information
repeated episodes of windup can precipitate...
- how long does this last?
- relation to chronic pain?
what NT receptors are formed when the dorsal horn is bombarded with pain?
- this also triggers a cascade of events leading to..
- what can block this cascade of events?
long–term potentiation (LTP), which involves a long lasting increase in the efficacy of synaptic transmission.
Where "wind–up" is thought to last only minutes, LTP lasts at least one hour and maybe even months. Both "wind–up" and LTP are believed to be part of the sensitization process involved in many chronic
NMDA-type glutamate receptors are formed when the dorsal
horn is bombarded with pain for an extended period of time.
activation triggers a cascade of events leading to sensitization of dorsal horn
wide dynamic range neurons
The NMDA receptor
antagonists ketamine and dextromethorphan can block this cascade of events
which contribute to sensitization
Central pain, aka..
there is damage to where?
meaning "other pain", is an exaggerated painful response to normally non-noxious non-painful stimuli
Pain from light touch/pressure applied to the skin in the
area of the damaged nerve
Pain from normally mild skin temperatures in the affected
the associated nerve damage results in decreased firing thresholds of nociceptive fibers
peripheral nerve injury could induce collateral sprouting of non-nociceptive primary afferent neurons, such as A-beta low threshold mechanoreceptors, into the superficial (nociceptive) lamina in the dorsal horn of the spinal cord