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Pain control.

There is a variety of different approaches including;


NSAID’s - By blocking the synthesis of prostaglandins (esp. Prostaglandin E2 ) by
inhibition of cyclo oxygenase enzymes they prevent the direct stimulation of pain
receptors. Also this will have the effect of decreasing the vascular effects and reduce
the edema which could cause pain
Acetaminophen/Tylenol - May work in a similar way by blocking a Cox-3 pathway
( not yet clearly demonstrated. It does act as an analgesic and an antipyretic but doesn’t
show much anti-inflammatory effect.
Opioid drugs - such as morphine, codeine and a wide variety of other products such as
oxycodon. Basically they work by being chemically similar to naturally occurring
chemicals in our body called Endorphins and enkephalins. These chemicals are found
in the central nervous system and act as an internal reward system that lead to an
enhanced feeling of well being and reduced pain in response to things like satisfying
food intake, sex and exercise. They work by binding to receptors ( called opioid
receptors) on CNS neurons leading to modification of impulses ( ie.
neuromodulation)such as by blocking the release of pain neurotransmitters such as
substance P. Opiate drugs were first discovered in opium poppies (Papaver
somnifierum) where they act as plant defense chemicals against herbivores. Opium,
heroin, morphine and codeine are derived from these chemicals and work by binding to
the opiate receptors in the CNS. These drugs are powerful analgesics and create an
enhanced sense of well being but they also can lead to dependence ( need the drug
present to feel normal) and tolerance ( need increasing doses to get the same effects)
and if given in excess doses can lead to respiratory depression. These issues do not
normally present as serious problems with normal use to treat pain but can inhibit
practitioners from using adequate doses to accomplish the right level of pain control.
Some antidepressants: especially those tricyclics that are seratonin re-uptake
inhibitors that can significantly reduce the perception of chronic pain.Some anti-seizure
medications also seem to reduce neurogenic pain
Anti-inflammatories : Corticosteroids or even the application of cold packs etc. can
reduce inflammation and more specifically edema and in doing so reduce the level of
edema induced pain
Sensory stimulation / The Gate Control Theory: This may involve sensory input
travelling along larger myelinated sensory fibres reaching the spinal cord before the
slower pain impulses and then essentially blocking pain impulses from transmission up
interneurons of the ascending tracts. This may be the case for methods such as
massage or T.E.N.S. ( transcutaneous electrical nerve stimulation) in which a device
with a battery pack and electrodes to the skin preiodically send a mild electrical current
to the skin of the painful region. This may also partly account for acupuncture effects.
Anesthetics : can block neural function and lead to the loss of touch sensation as well
as pain. They can be applied locally to the skin ( eg. lidocaine) or regionally such as the
case with an epidural ( around the spinal cord) or as a general anesthetic to reduce the
level of cerebral cortex activity.
Altering conscious perception : Pain is perceived in the brain in a complex
interaction of several regions of the brain. It is possible to alter the individuals response
to, or perception of pain by a variety of techniques including distraction (eg.
concentrating on regulation of breathing during childbirth , imagery and placebo effects.
surgical intervention : as a last resort with persistent pain that resists other treatments
it is possible to destroy specific pain nerves from the affected region.

Types of Pain. Previously we have discussed acute and chronic pain but there are
some other ways to describe some specific forms of pain including;
Visceral pain: Paint that arises from deep body organs. These organs typically have
fewer pain receptors and so the pain is poorly localized in the brain and felt as more
diffuse or referred to the skin. Often the stimuli that provoke visceral pain are a little
different and can include ischemia, strong contractions or distention of the organ.
Referred Pain: This is pain that is perceived as arising from somewhere other than the
site of origin. Visceral pain is often referred pain because the relatively few pain fibres
from organs enter the spinal cord bundled with pain and touch fibres arising from the
skin of that region ( dermatomes) and ascend to the brain where they are perceived
together. A good example of this is when the pain of an MI (myocardial infarction or
heart attack) is felt as pain in the left chest, neck, shoulder and arm region. It can be
difficult with referred pain to determine the actual point of origin.
Phantom Limb Pain : is felt as if it arises from part of a limb that has been amputated.
Loss of a limb often does not lead to the death of the sensory neurons for touch or pain
because their cell bodies are located in the dorsal root ganglia of spinal nerves. Also the
area of the somatosensory cortex for the amputated limb is still intact and if it receives
impulses they are interpreted initially as arising from that structure. Often damaged
nerve axons will regrow to formed branched endings on the limb stump area and so if it
is irritated ) eg. by clothing or a prosthesis) it will generate impulses that go to the brain
and stimulate a perception of pain from the missing limb. Eventually this effect often
wears off since it is contradictory to other evidence ( eg. visual) and the brain adapts.
Neurogenic or Neuropathic Pain: arises from damaged nerves either in the
peripheral or central nervous system and is the result of damage to the neurons rather
than stimulation of pain receptors. Loss of neurons that secret the neurotransmitter
GABA ( Gamma aminobutyric acid) can lead to pain because this neurotransmitter
functions to inhibit transmission of impulses such as pain impulses. Examples of this
can include Post-herpetic Herpes zoster or shingles that occurs subsequent to a
chicken pox ( varicella) infection often years to decades later as a result of the virus
remaining latent in the nerves. Neurogenic pain can also be associated with damage
resulting from a stroke (CVA) or trigeminal neuralgia or diabetic neuropathy.

Pain threshold refers to the amount of noxious stimulus at a nociceptor required to


stimulate the generation of a pain impulse. The threshold level is about the same for all
individuals.
Pain tolerance refers to the maximum duration or intensity of pain that an individual will
endure before seeking treatment or some way of dealing with the pain. This varies
widely between individuals based on many factors including age, history of pain, level of
knowledge about that pain, cultural background, general mental attitude and state of
health and many other factors. It is difficult to judge the level of another individuals pain
because of the way all these factors affect perception. We are all a little bit different
from one another

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