Pain Flashcards
What is the definition of pain?
- an unpleasant sensory and emotional experience associated with actual or potoential tissue damage.
- pain is a protective mechanism
What is dysethesia?
any abnormal sensation described as unpleasant by the patient
Hyperalgesia
- Exaggerated pain response from a normally painful stimulus
- usually additive of repeated stimulus of constant intensity and aftersensation
hyperesthesia
exaggerated perception of touch stimulus
allodynia
- abnormal perception of pain from a normally non-painful mechanical or thermal stimulus
- usually has elements of delay in perception
hypoalgesia
decreased sensitivity and raised threshold to painful stimuli
anesthesia
reduced perception of all sensation, mainly touch
analgesia
Reduced perception of pain stimulus
*warn pts to expect some pain after surgery, analgesia can only reduce it, not fully eliminate it
paresthesia
- spontaneous abnormal sensation that is not necessarily unpleasant
- usually described as “pins and needles”
- ex. diabetic patients
Causalgia
- burning pain in the distribution of one or more peripheral nerves (wherever the affected nerve(s) innervates)
- ex: shingles
What is the overview of how pain perception works?
- perception depends on the specialized neurons that function as receptors
- neurons detect a stimulus
- stimulus is transduced and conducted to the CNS
- sensation is then felt
Are neurons adaptive?
What are the two types of sensation?
- Neurons are non-adaptive- you never “get used” to pain like you might get used to a noxious smell
- Two types of sensations
- protopathic- noxious
- epicritic- non-noxious
- pressure, light touch, temperature discrimination
What are the two types of pain?
- Fast pain
- myelinated A delta fibers
- felt 0.1 sec after stimulus
- felt on surface of body (sharp, pricking, electric pain)
- easy to localize
- slow pain
- unmyelinated type C pain fibers
- felt 1 sec after stimulus
- felt in deeper tissue and surface tissue (slow burning, aching, throbbing, chronic)
What are the different types of painful stimuli?
- mechanical
- fast and slow pain
- thermal
- fast and slow pain
- chemical- uses bradykinin, Ach, prostaglandins, substance P, and proteolytic enzymes to increase permeability to ions like potassium
- slow pain only
What are the four steps of nociception?
- Transduction- the noxious stimuli is converted to electric activity at the sensory nerve endings
- transmission- propagation of impulses through the sensory nervous system
- Modulation- process of transmission modified by neural influence
- may be up-regulated or down-regulated
- perception- the signal interacts with the psychology of the pt to create what is perceived as pain
What is the transduction process?
list the chemicals (5)
- Mechanical, thermal, and chemical receptors convert to electrical action potential by opening and closing Na and K ion channels
- A noxious stimuli that causes cell damage which release sensitizing chemicals
- prostaglandins
- bradykinin
- serotonin
- substance P
- histamine
What is the route of action potential transmission?
- site of injury to spinal cord
- spinal cord to brainstem and thalamus
- thalamus to cortex for processing
What is the pathway for most pain sensation?
-
First order neuron- from site of problem to spinal cord via dorsal (sensory) root
- may synapse with interneurons, sympathetic neurons, and ventral horn (motor) neurons
-
second order neuron- in gray matter of ipsilateral dorsal horn
- most cross midline and go up the spinothalamic tract to the thalamus, reticuar formation, nucleus raphe magnus, and periaqueductal grey
-
third order neuron- send message from thalamus to somatosensory areas I and II in the parietal cortex and the superior wall of the sulvian fissure
- where pain is localized
Where does the spinothalamic tract lie?
anterolaterally in white matter of the spinal cord
Details about the neospinothalamic tract (fast pain):
Where do first order neurons enter?
Where do second order neurons cross midline?
Where do most travel to?
- First order neurons (via A delta fiber) enter lamina I and V (lamina marginalis) of the dorsal horn of SC.
- Second order neurons cross the midline through the anterior white commissure and pass upwards in the spinothalamic tract
- Few terminate in reticular formation (affecting sleep cycle)
- MOST travel to Ventrobasal Complex of Thalamus
- Third order neurons comminicate to somatosensory cortex
Details of the Paleospinothalamic pathway (slow pain):
Where to first order neurons enter lamina?
Where do second order neurons connect?
Where do the third order neurons terminate?
- First order neurons (C fibers) enter via laminae II and III of the dorsal horns (aka substantia gelatinosa)
- Second order neurons connect in laminae IV-VIII and go up without crossing over
- most join fibers from the fast pathway, crossing to the other side and saking the STT
- 1/10th of fibers stop in thalamus
- the rest terminate in the medulla, pons, and tectum of midbrain mesencephalon periadueductal grey
- B/C these fibers do not go beyond the thalamus to the somatosensory cortex, these sensations are not localized
What three components mediate the analgesia system?
- the periaquaductal grey matter (in the midbrain)
- the nucleus raphe magnus (in the medulla)
- the nociception inhibitory neurons within the dorsal horns of the spinal cord
What is the cellular physiology of acute pain?
Mechanism?
fibers?
- Peripheral mechanism
- Information about noxious stimuli arrives from the periphery along A-delta and C fibers
- Substance P and excitatory amino acids (EAA) i.e. glutamate are released
- Substance P- activates neurokinin-1 (NK-1) receptors
- EEAs activate amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) receptors
What is the cellular physiology of pain in the chronic state?
(not chronic pain, but chronic barrage of signals)
mechanism?
-
Central mechanism- the information is relayed to higher brain areas
- normally the NMDA-linked channels are inoperative b/c they always have the Mg ion “plug”
- the Mg gets bumped off due to intense and prolonged barrages of nociceptive info
- the neurons become sensitized and over respond to subsequent incoming nociceptive signals
- The loss of Mg results in Ca ions influxing in and activating nitric oxide synthase (cNOS), converting L-arginine to nitric oxide
- This NO acts presynaptically to cause exaggerated release of substance P and EAAs
- Postsynaptically NO causes the neurons to become hyperexcitable and releasing Substance P, ACh, etc
What is the current COX concept?
- COX 1- Constitutive
- homeostatic funtions- GI tract, renal, platelet function, macrophage differentiation
- Inhibition undesirable
- COX 2- Induced
- Inflammation
- Inhibition desireable
