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