The Physiology of Pain
Pain Receptors
bare sensory nerve endings
innervate all organs and tissues
(except the brain)
respond to all types of noxious stimuli
Damaged cells release Bradykinin (the most potent pain producing
chemical/enzyme known) which binds to pain receptors
**** this does not always lead to the perception of pain ****
Neural Pathways in Pain
impulses travel to the central nervous system through two different fibers
1.
Neospinothalamic (lateral) Tract
A- delta fibers transmit impulses quickly and end in the motor and
sensory areas of the cortex.
Believed to mediate localized, sharp, pricking, brief pain
mediates the sensory-discriminative dimension
via the cerebral cortex mediates the cognitive-evaluative dimension
2.
Paleospinothalamic (medial) Tract
C – fibers transmit impulses more slowly and end in the lower
regions of the forebrain.
Believed to mediate dull, burning, aching, prolonged pain.
mediates emotional-motivational dimension
Reticular Activating Formation
involved in aversive drive & similar pain related behavior
integrates pain experience with pain behavior
blue
red
Pain is a physical stressor
Oxygen from the air
we breathe combines with
digested food to provide energy.
This process generates dangerous
byproducts such as free radicals –
electronically unstable atoms
or molecules capable of stripping
electrons from any other molecules
they meet in an effort to achieve stability.
In their wake they create even more
unstable molecules.
Retrieved from
http://www.drweil.com/drw/u/QAA400537/Stumped-by-Oxidative-Stress.html
Putative Mechanisms for Relationship between Stress & Pain
Acute Pain
Severe tissue damage elevates interleukins (an immune system
component) in the blood.
These stimulate the pituitary which leads to corticotropin and vasopressin
release
i.e. initiates the stress response
chronic pain
Stress releases CRF
response = hypersecretion of ACTH and excessive CORT release
Result = the negative feedback system (cort-hippo) fails
Unimpeded, stress increases … pain increases
ANXIETY
a common symptom of stress
when anxiety increases pain increases
when pain/anxiety decreases, so does the other
suggests a common mechanism
80% of PTSD (an anxiety disorder) have chronic pain
Endocannabinoids and anxiolytics decrease pain and anxiety
but you do not have to be anxious to derive the benefits
PERSONALITY
pain felt more in catastrophizers & hot-reactors
pain felt more in people with external locus of control
chronic pain felt more in people with low self-esteem
i.e. pain felt more in types with poor coping skills for stress
FEELINGS OF CONTROL
people who feel they have adequate control feel less pain
makes sense, controllable stressors are less stressful
if stress causes pain, then controllable pain is less painful
HYPNOSIS
has been used to decrease pain
has been used to decrease stress
is the decrease in stress responsible for the decrease in pain?
do they share a common mechanism?
LAUGHTER
laughter decreases stress and pain - both through endorphin release
PAIN AFTER ALL HEALING
“Usually” occurs after a traumatic injury
is the chronic pain the result of chronic stress?
STRESS INDUCED ANALGESIA
Acute stress can decrease pain perception!
could this account for some cases of episodic analgesia?
MECHANISM FOR STRESS INDUCED ANALGESIA
Endogenous opioid and non-opioid mechanisms are implicated, as are the
amygdala and the PAG
CRF triggers the release of opioid peptides (endorphins) from immune cells
in the area of injury
Endocannabinoid receptors in the PAG: if blocked, eliminate SIA
Contradictory evidence?
chronic stress suppresses the immune system
therefore, should suppress release of endorphins, pain
Memory mechanisms for Stress & Pain
Stress can be induced via memories
and negative self-talk
A memory-like mechanism has been
Suggested for pain (e.g. phantom
limb pain)
Memories may trigger one which
Triggers the other, or both are
Triggered concurrently