1. Although the world is full of suffering, it is also full of
the overcoming of it. Helen Keller
2. PAIN The sensation of marked discomfort that is either sharp
and well localised or dull & diffuse. or An unpleasant sensory
and emotional experience assocaited with actual or potential tissue
damage.
3. The Nervous System and Pain Somatosensory System Brain
Somatosensory Cortex Thalamus Spinal Cord Dorsal Horn Ventral Root
PNS Afferent Neuron Efferent Neuron A-delta Fibers C-Fibers
4. The Brain Thalamus : The sensory switchboard of the brain ,
Located in the middle of the brain. Somatosensory cortex : Area of
cerebral cortex located in the parietal lobe right behind the
frontal lobe . Receives all info on touch and pain.
5. Spinal Cord Spinal Layers Spinal grey matters divided into
10 layers Substantia Gelatinosa Composed of a layer of cell bodies
running up and down the dorsal horns of the spinal cord Receive
input from A and C-fibers Activity in SG inhibits pain
transmission
6. PNS Nerve Fiber Types Afferent Sensory Neurons Three Types
Are Important to Understand Pain A-delta fibers smaller, fast
transmitting, myelinated fibers that transmit sharp pain
Mechanoreceptors Triggered by strong mechanical pressure and
intense temperature C-fibers smallest, slow transmitting
unmyelinated nerve fibers that transmit dull or aching pain.
Mechanoreceptors Mechanical & Thermal Chemoreceptors Triggered
by chemicals released during inflammation A-beta fibers large
diameter, fast transmitting, myelinated sensory fibers Efferent
Motor neurons
7. Pain Pathways Going Up Pain information travels up the
spinal cord through the spino-thalamic track (2 parts) PSTT
Immediate warning of the presence, location, and intensity of an
injury ASTT Slow, aching reminder that tissue damage has
occurred
8. Pain Pathways Going Down Descending pain pathway responsible
for pain inhibition.
9. The Neurochemicals of Pain Pain Initiators Glutamate -
Central Substance P - Central Brandykinin - Peripheral
Prostaglandins - Peripheral Pain Inhibitors Serotonin Endorphins
Enkephalins Dynorphin
10. NOCICEPTIVE PAIN Nociceptive pain typically is classified
as either somatic (arising from skin, bone, joint, muscle, or
connective tissue) or visceral (arising from internal organs such
as the large intestine or pancreas). Whereas somatic pain most
often presents as throbbing and well localized, visceral pain can
manifest as pain feeling as if it is coming from other structures
(referred) or as a well-localized phenomenon
11. PP OF NOCICEPTIVE STUMILATION TRANSMISSON PERCEPTION
MODULATION INFLAMMATION
12. STUMILATION The first step leading to the sensation of pain
is stimulation of free nerve endings known as nociceptors. They
distinguish between noxious and innocuous stimuli, and they are
activated and sensitized by mechanical, thermal, and chemical
impulses. Release of chemicals Receptor activation leads to action
potentials that are transmitted along afferent nerve fibers to the
spinal cord.
13. Transmission These afferent, nociceptive pain fibers
synapse in various layers of the spinal cords dorsal horn,15
releasing a variety of neurotransmitters,including glutamate,
substance P, and calcitonin generelated peptide. The complex array
of events that influence pain can be explained in part by the
interactions between neuroreceptors and neurotransmitters that take
place in this synapse. These pain-initiated processes reach the
brain through a complex array of at least five ascending spinal
cord pathways, which include the spinothalamic tract.
14. Pain Perception At this point in transmission, pain is
thought to become a conscious experience that takes place in higher
cortical structures. The brain may accommodate only a limited
number of pain signals, and cognitive and behavioral functions can
modify pain. Relaxation, distraction, meditation, and guided mental
imagery may decrease pain by limiting the number of processed pain
signals.
15. MODULATION 3 theories The body modulates pain through a
number of complex processes. One, known as the endogenous opiate
system, consists of neurotransmitters and receptors (e.g., , , and
) that are found throughout the central nervous system. Like
exogenous opioids, endogenous opioids bind to opioid receptor sites
and modulate the transmission of pain impulses.
16. DESCENDING INHIBITORY OF CNS The CNS also contains a highly
organized descending system for control of pain transmission. This
system can inhibit synaptic pain transmission at the dorsal horn
and originates in the brain. Important neurotransmitters here
include endogenous opioids, serotonin, norepinephrine,
-aminobutyric acid (GABA), and neurotensin.
17. Gate-Control Theory Ronald Melzack (1960s) Described
physiological mechanism by which psychological factors can affect
the experience of pain. Neural gate can open and close thereby
modulating pain. Gate is located in the spinal cord. It is the
SG
18. Opening and Closing the Gate When the gate is closed
signals from small diameter pain fibres do not excite the dorsal
horn transmission neurons. When the gate is open pain signals
excite dorsal horn transmission cells.
19. Three Factors Involved in Opening and Closing the Gate i.
The amount of activity in the pain fibers. ii. The amount of
activity in other peripheral fibers. iii. Messages that descend
from the brain.
20. Conditions that Open the Gate Physical conditions Extent of
injury Inappropriate activity level Emotional conditions Anxiety or
worry Tension Depression Mental Conditions Focusing on pain
Boredom
21. Conditions That Close the Gate Physical conditions
Medications Counter stimulation (e.g., heat, massage) Emotional
conditions Positive emotions Relaxation, Rest Mental conditions
Intense concentration or distraction Involvement and interest in
life activities
22. Adaptive Inflammation Inflammatory pain can be thought of
as the bodys shifting from preventing tissue damage to the
promotion of healing. As a result of the inflammatory process, the
pain threshold is reduced and the injured area becomes more
sensitive to pain. When this course of action outlives its
functionality or when it is caused by diseases such as arthritis,
it can move from an acute to a chronic problem (maladaptive
inflammation).
23. NEUROPATHIC PAIN/FUNCTIONAL PAIN Chronic pain Neuropathic
pain is a result of nerve damage, whereas functional pain can be
thought of as abnormal operation of the nervous system. A number of
neuropathic pain syndromes (e.g., postherpetic neuralgia,
diabeticneuropathy) and functional pain syndromes (e.g.,
fibromyalgia, irritablebowel syndrome, sympathetic induced pain,
tension-type headaches,and some noncardiac chest pain)12
exist.
24. The mechanism responsible for neuropathic and functional
pain may be the nervous systems endogenous dynamic nature. Nerve
damage or certain disease states may evoke changes seen in
inflammatory pain, ectopic excitability, enhanced sensory
transmission, nerve structure reorganization, and loss of
modulatory pain inhibition. Anatomical & biochemical changes .
This produces spontaneous nerve stimulation autonomic neuronal pain
stimulation, and a progressive increase in the discharge of dorsal
horn neurons.
25. CLASSIFICATION OF PAIN ACUTE CHRONIC CANCER
26. SIGNS & SYMPTOMS ACUTE PAIN CHRONIC Often obvious
distress (e.g., trauma) Can be described as sharp, dull,
shock-like, tingling, shooting,radiating, fluctuating in intensity,
and varying in location. Hypertension, tachycardia, diaphoresis,
mydriasis, and pallor, but these signs are not diagnostic In some
cases there are no obvious signs Comorbid conditions usually not
present Outcome of treatment generally predictable Can appear to
have no noticeable suffering Over time, the pain stimulus may cause
symptoms that completely change. Hypertension, tachycardia,
diaphoresis, mydriasis, and pallor are seldom present In most cases
there are NO obvious signs Comorbid conditions often present (e.g.,
sleep problems,depression, relationship problems) Outcome of
treatment often unpredictable
27. TREATMENT
28. Nonopioid Agents MOA: These drugs prevent formation of
prostaglandins produced in response to noxious stimuli, thereby
decreasing the number of pain impulses received by the CNS. CLASS
G.N DOSE (mg) Salicylates Aspirin 3251,000 every 46 h Propionic
acid Ibuprofen, naproxen 200400 every 46 h Fenamate Mephenamic acid
Initial 500 Enolic acid piroxicam 20 bd Acetic acid Kerotolac
,indomethacin 1530 every 6 h 25-30 BD Cyclooxygenase-2 inhibitors
Celecoxib Initial 400 followed by another 200 on first day, then
200 twice daily para-Aminophenol Acetaminophen 3251,000
29. OPIOID S Act centrally via endogenous opiate system
Short-acting Long-acting Problems Tolerance Dependence
30. Medical Treatments for Pain Skin Stimulation Massage Great
as an adjunct TENS(Transcutaneous electrical nerve stimulation)
Mixed results Acupuncture Effective for a number of types of pain
Reduces the need for meds
