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PAIN – SOME FACTS
Dr. S. Parthasarathy MD., DA., DNB, MD (Acu), Dip. Diab. DCA, Dip. Software statistics
DEFINITION An unpleasant sensory and
emotional experience associated with actual or potential tissue damage, or described in terms of such damage.
ISSP definition
SOME SAY AS An unpleasant sensation, occurring in
varying degrees of severity as a consequence of injury, disease, or emotional disorder.
pain always has a subjective component
MARGO MCCAFFREY
Whatever the patient says hurts.
WHAT IS NOCICEPTION ?? Nociception is the activation of a
nociceptor by a potentially tissue-damaging (noxious) stimulus. It is the first step in the pain pathway
WHAT IS A NOCICEPTOR ?? nociceptor is a specialized, neurologic
receptor that is capable of differentiating between innocuous and noxious stimuli
Terminals of A delta and C fibres
ANALGESIA Patient has no pain
But the noxious stimulus is there
Anaesthesia – all sensory modalities gone
While analgesia – only pain
PARAESTHESIA Abnormal sensation
Spontaneous or evoked
Painful or painless Painful paraesthesia is dysaesthesia Formication is a form of paresthesia in
which the patient feels as though bugs are crawling
ANAESTHESIA DOLOROSA pain is felt in an area that is otherwise
numb ordesensitized Trigeminal neuralgia Trigeminal nerve is ablated no sensation but suddenly shooting pain comes
HYPERPATHIA hyperpathia refers to an abnormally
intense pain response to repetitive stimuli.
Usually hyperpathic area of skin is not sensitive to a simple stimulus but over responds to multiple stimuli
Pin prick
ALGOGENS Histamines, substance P, potassium,
and prostaglandins, bradykinin, 5 HT are
examples of algogenic substances
Produced or injected – nociception
HYPERALGESIA- SHIFT OF THE STIMULUS PAIN RESPONSE CURVE TO THE LEFT
Primary Pain to a non noxious
stimulus in the area of injury
Pharyngitis – swallowing – painful
Secondary Pain to a non noxious
stimulus in the area by the side or encircling the injury
stimulus
PAIn
PRIMARY SECONDARY Starts within
minutes Area of injury Sensitive to heat
and mechanical Peripheral
sensitization
Delayed onset Wider area Only thermal Central role
PRIMARY HYPERALGESIA – MECHANISMS Expansion of receptive field of
nociceptor Sensitization of nociceptor Loss of central inhibition
Increased CAMP levels Activation of protein kinase C
SECONDARY HYPERALGESIA Antidromic release of algogens Dorsal horn neurons – sensitive WDR neurons – plastic changes
Sometimes irreversible Post op pain - !!!
SENSITIZATION shift of the
stimulus - nerve fibre response curve to the left
stimulus
FIBres
SENSITIZATIONSensitization is a state in which a
peripheral receptor or a central neuron either responds to
stimuli in a more intense fashion than it would under baseline conditions or responds to a stimulus to which it is normally insensitive.
Sensitization occurs both at the level of the
nociceptor in the periphery and at the level of the second-order neuron in the spinal cord
CLASSIFY PAIN
TYPES OF PAIN Nociceptive Somatic Visceral
Nonnociceptive Peripheral Central Psychogenic
NOCICEPTIVE – SOMATIC Dull or sharp Localized Increased with movement
Eg. Tooth ache
SKIN, MUSCLE, BONE, JOINT ETC….
VISCERAL NOCICEPTION
autonomic sensationsincluding nausea, vomiting, and diaphoresis. There are often cutaneous referral sites
NEUROPATHIC burning, electrical, and numbing
Intervening normal
Sudden Post herpetic, trigeminal,
glossopharyngeal
CENTRAL PAIN Central pain syndrome is a neurological
condition caused by damage or malfunction in the Central Nervous System (CNS) which causes a sensitization of the pain system. Trauma, tumors, stroke, Multiple Sclerosis, Parkinson's disease, or epilepsy .
Pain can either be relegated to a specific part of the body or affect the body as a whole.
DEJERINE ROUSSY SYNDROME severe, persistent, paroxysmal, often
intolerable, pains on the hemiplegic side, not yielding to any analgesic treatment
THEORIES HAVE BEEN PROPOSED- NEUROPATHIC PAIN
that state there are specific cellular and molecular changes that affect membrane excitability and induce new gene expression after nerve injury, thereby allowing for enhanced responses to future stimulation.
the ectopic impulses of neuroma, changes of sodium and calcium channels in injured nerves, sympathetic activation, and deficient central inhibitory pathway contribute to the mechanisms of neuropathic pain
PSYCHOGENIC PAIN Psychogenic pain, also called psychalgia, is
pain that is caused by increased, or prolonged by mental, emotional, or behavioural factors
Headache, back pain, or stomach pain are some of the most common types of psychogenic pain.
It accompanies or induced by social rejection, broken heart, grief, love sickness, or other such emotional events.
PSYCHOGENIC PAIN No nociception No neuropathic mechanism
But some evidence of psychologic symptoms to meet criteria for somatoform pain disorder, depression,
Usually chronic
WHY DO WE NEED TO CLASSIFY PAIN ??
Origin of pain
Treatment modalities
Prognosis
TEMPORAL CLASSIFICATION Acute Acute pain is temporally related to
injury and resolves during the appropriate healing period
Chronic pain that persists for more than 3
months or that outlasts theusual healing process.
Recurrent Duodenal ulcer
OTHER CLASSIFICATIONS
Etiology Arthritic Cancer Site Appendix Mastitits
HISTORY AND THEORY Aristotle believed that pain was due to evil
spirits entering the body through injury, Hippocrates believed that it was due to an
imbalance in vital fluids. it was thought that pain originated outside the
body, perhaps as a punishment from God In 1644, René Descartes theorized that pain
was a disturbance that passed down along nerve fibers until the disturbance reached the brain
THEORIES OF PAIN - SPECIFICITY THEORY
body has a separate sensory system for perceiving pain just as it does for hearing and vision— Von Frey (1895)
and this system contains its own special receptors for detecting pain stimuli, its own peripheral nerves and pathway to the brain, and its own area of the brain for processing pain signals
SPECIFICITY THEORY when someone pulls
the rope to ring the bell, the bell rings in the tower.
Proved not correct
PATTERN THEORY- GOLDSCHNEIDER (1920)
there is no separate system for perceiving pain,
receptors for pain are shared with other senses, such as of touch.
people feel pain when certain patterns of neural activity occur.
OTHER THEORIES Wilhelm Erb's (1874) "intensive"
theory, that a pain signal can be generated by intense enough stimulation of any sensory receptor, has been soundly disproved
Central processing theory Inputs – same but the central
processing differs to produce pain
MELZACK WALL GATE CONTROL THEORY pain stimulation is carried by small,
slow fibers that enter the dorsal horn of the spinal cordWall highlighted that pain messages are carried by the specific nerve fibresthat can be blocked before reaching the brain by the actions of other nerves andpsychological factors
THE GATE OPENS AND CLOSES
THE GATE CONTROL THEORY The gate control theory states that non
painful stimulus such as distraction competes with the painful impulse to reach the brain.
This rivlary limits the number of impulses that can be transmitted in the brain by creating the hypothetical gate
Distraction – mechanical , endorphins, psychological
Only theory – multifaceted pain approach
THE IDEA IS
if the large fibers remain un stimulated, the pain signal will be propagated, but if they are activated, they act as an electrical gate, blocking the transmission of pain up the C fiber.
How is pain perceived ??
TYPES OF FIBRES MYELIN – DIA MM VELOCITY MM/S
Aα Proprio, somatic Motor yes 12–20 70–120 Aβ Touch, pressure yes 5–12 30–70Aγ Motor muscle spindle Yes 3–6 15–30Aδ Pain, cold, touch Yes 2–5 12–
30B Preganglionic autonomic Yes 3 3–15C Pain, temperature,No 0.4–1.2 0.5–
2
PAIN STARTS Pain receptors (nociceptors) The sensation of pain then travels from
the periphery to the spinal cord along A-delta and C fibers
Lissauer’s tract synapse on second order neurons in
substantia gelatinosa in dorsal horn (second order neuron)
Spino thalamic tract (Neo and paleo) crossing via the anterior white commissure
before ascending contralaterally. Before reaching the brain, the
spinothalamic tract splits into lateral neospinothalamic tract and medial paleospinothalamic tract
Neo - posterolateral nucleus of the thalamus
Paleo spinothalamic neurons carry information from C fibers and terminate throughout the brain stem, a tenth of them in the thalamus and the rest in the medulla, pons and periaqueductal grey matter
OTHER SECOND ORDER NEURONS Spino mesencephalic Midbrain – behavioural responses
to pain
Spino reticular Alerting and arousal motivational
aspects -pain Pontine and medullary reticular
formation
Third order neurons from thalamus to cortex
anterior cingulate cortex (emotional aspect )
Somatosensory cortex
SIMPLE NEUROANATOMY OF PAIN
DESCENDING INFLUENCE
DESCENDING INFLUENCE In 1858 Bernard found that spinal
afferents can be modified by supraspinally organized systems.
Three and three
Brain ,thalamus and brainstem PAG, LC, NRM Serotonin , noradrenaline and opioids
Additional GABA , glutamate and acetyl choline
COX ET AL Medial forebrain Lateral hypothalamus
Electrical stimulation attenuated foot pain
ESSENTIAL NUCLEI Periaqueductal grey PAG – extensive connections
Opioids
NUCLEUS LOCUS CERULEUS Pons Projection to hippocampus ,spinal cord
and cortex Noradrenergic system
NUCLEUS RAPHE MAGNUS Medulla Serotonin – originally
But now multiple , glutamate and opioids
PAIN FACTS – SUMMARY DEFINITION CLASSIFICATION THEORIES PATHWAYS DESCENDING CONTROL
OH !! PAINFUL LECTURE ENDS ??
Thank you all