pathophysiology of pain painpain “…is whatever a person says it is and exists whenever the...

Pathophysiology of PainPathophysiology of Pain

PAINPAINPAINPAIN

“…is whatever a person says it is and exists whenever the person says it does.”

(McCaffery)

PainPainPainPain

5th Vital Sign

Should be recorded along with temperature, pulse, respiration, & blood pressure

(American Pain Society)

Multidimensional Experience

Physical– Medical-Surgical conditions

(special standards for acute post-operative pain)

Social– Support system & societal response

Psychological– Coping abilities, internal locus of control vs. external

locus of control

Cultural– Emotionally expressive, introverted, stoic

Why it is necessary to study pain

• Pain is the primary symptom that motivates people to seek medical treatment

• Pain is subjective and therefore can only be measured indirectly

The Economic Cost of Pain in AmericaThe Economic Cost of Pain in America

$100 billion/year related to chronic pain

* includes healthcare expenses * compensation * litigation

Pain accounts for approximately:

* 25% all sick days taken in US * 21% of emergency room visits (NIH, 2002)

Physiological Componentsof Pain

Physiological Componentsof Pain

TransductionTransduction

Noxious substance changes to an electrical stimulus by activating nociceptors

(afferent nerve fibers that initiate the pain experience).

Pain Receptors and Periferal Afferent Pathways

Pain Receptors and Periferal Afferent Pathways

Stimulus impulse Information about possible tissue damage.

Specific theory (von Frey):– Distinctive end organs on the skin, each stimulus has

specific end organ

Intensity theory:– Pattern or Summation Theory (Goldscheider):

• Any sensory stimulus is sufficiently intense could produce pain.

Afferent fibers:– C fiber (0.4-1.1 mm)

– A-delta fiber (1-5 mm)

Types of NociceptorsTypes of Nociceptors

C-nociceptors– Polymodal nociceptors (C-MH, mechano-heat sensors)

• Loc.: skin 50-70%

• Stim.: >50 oC, mechanical (biting, twinging), endogen substances (bradikinin, serotonin, acidic pH), exogen substances (capsaicin etc.)

• Function: inflamatory pain and heat sensing. PGE2 and PGI2 potentiate the effect of bradikinin COX inhibitors

• Signal transduction: VR-1 cation (Na+/Ca2+ chanell) capsaicin and heat

• Mediators: Substance P, CGRP and somatostatin

• Substance P: neurogenic inflammation extravasation, leukocytosis, Ig secretion of B lymphocytes, TNF production of hystiocytes

• CGRP: enhance microcirculation, potentiate neurogenic inflamation

• Somatostatin: possible inhibits the inflammatory reactions

Types of NociceptorsTypes of Nociceptors

C-nociceptors– Heat receptors

• Loc: skin 4%, (pig 30%)

• Stim: heat, capsaicin and chemicals but mechanical stimuli not!

– Chemoreceptors• Stim: electrical but heat and mechanical not. However they

respond to repeated stimuli. (sleeping or silent receptors)

– Others• High-Treshhold-Mechanociceptors (C-HTM): heat, capsaicin

• C-Mechano-Cold (C-MC): Cold sensitive HTM receptors

Types of NociceptorsTypes of NociceptorsTypes of NociceptorsTypes of Nociceptors

A-delta Nociceptors– A-delta Mechano-Nociceptors

• Loc: basal part of the epidermis and between of collagen fibers of joints

• Stim: Hight-Treshhold-Mechanoreceptors sensing the pricking, cutting. Heat, capsaicin and irritants do not stimulate

– A-delta Polynodal Nociceptors (AHH)• Loc: palm and hairless areas (Type I.)

Hairy areas (Type II.)• Stim: mechanical• Function: Sensing of the first pain

– Visceral Receptors

TransmissionTransmission

Passage of electrical impulse from the site of injury through the dorsal horn of spinal nerves & up the spinalthalmic tract to the brain.

Figure 10-9: Sensory pathways cross the body’s midline

Substances That Stimulate Nociceptors:Substances That Stimulate Nociceptors:

Bradykinin: a powerful vasodilator that increases capillary permeability and constricts smooth muscle. Plays a role in chemistry of pain at site of injury.

Postaglandins: hormone-like substances that send additional pain stimuli to CNS

Substance P: believed to act as a stimulant at pain receptor sites and may influence inflammatory response

Neuromodulators:Neuromodulators:

EndorphinsEnkephalinsDynorphin

Theories of pain

• Specificity model

• Patterning theory

• Gate control theory

• Multidimensional model

Hereditary Sensory and Autonomic Neuropathy (HSAN)

5 Types

HSAN4 neurotroph tirozin-kináz receptor1 (NTRK1) mutation

Autosomal reseccive

Patterning Theory

• Multiple neural pathways cause pain

• Nociceptors plus other receptors

• Cannot fully account for subjective nature pain

If you hurt yourself, you often rub the affected area to make it

feel better. Why does this work?

Counter Irritant TheoryCounter Irritant Theory

Gate Control Theory– Gate Cells

– Tract Cells

Touch Input– Ab Fibers

Local Inhibition– GABA and Enkephalin

Gate Control Theory(Melzack & Wall 1960’s)

Gating Mechanism

Transmission cells

Spinal cord

From pain fibres

From other peripheral fibres

Modulation of pain information by a gate mechanism

Cingulate Cortex Periaqueductal Gray

– Opiod Receptors– Projects to Raphe Nuclei

Raphe Nuclei– Project down to dorsal horn and Spinal

5 Nucleus– Serotonin (5-HT)– Inhibits Ascending Systems

• Substance P release by Primary Afferents

Locus Coeruleus– Norepinephrine

Hormonal Analgesia

Descending Pain ControlDescending Pain Control

Gate Control Theory

• Accounts for high pain perception with

Low damage (e.g. back ache)

• Accounts for low pain perception with high damage (e.g. sport, bed of nails)

• Does not fully account for reinforcement/ learning and environmental influences

Multidimensional model

This model is consistent with Gate Control

Theory and distinguishes four dimensions of

pain: • Nociception - neural detection

• Sensation - experience of pain (e.g. intensity)

• Emotion - emotional response (e.g. anxiety)

• Behaviour - e.g. withdrawal

Multidimensional model

Physiological

Sensation

Behavioural response

e.g limping

Emotional response

e.g. tension

Learning Environment

??

Psychosocial Determinants of Pain

• Emotional response

• Cognition

• Conditioning

• Cultural/social context

Emotional response

• Stress/Anxiety: Associated with pain

• Motivation reduces pain, e.g sport. Possible opioid mechanism.

• Depression: associated with increased pain.

Cognitive response

• Appraisal e.g. pain is perceived as greater when it is life threatening

• Higher self-efficacy = less pain

• Expectations e.g. anxious dental patients expect more pain and therefore experience more pain

Conditioning

• Reinforcement e.g. children with eczema who receive more attention in response to their pain behaviour are likely to increase their pain behaviour

Culture

• e.g Bedouin women report less pain during child birth than in other cultures because it is not culturally acceptable to report pain

Types of PainTypes of PainTypes of PainTypes of Pain

Somatic– Smooth muscle walls,

receptors in abdominal cavity, cranium, & thorax

Visceral– Arises from ligaments,

tendons, bones

Referred– Pain experienced from a site

distant from injury

Phantom– Sensations of burning, tingling

felt in absent limb

Neuropathic– Pain signal from injury to

higher centers of brain

Acute Pain Acute Pain vs.vs. Chronic Pain Chronic Pain Acute Pain Acute Pain vs.vs. Chronic Pain Chronic Pain

Usually sudden, self-limiting < 6 months

Precipitating event Resolves with treatment Restless, anxious, crying

May be sudden or gradual with periods of remission & exacerbation > 6 mo.

May not be associated with injury

Difficult to treatment Depressed, withdrawn

Classification of AnalgesicsClassification of AnalgesicsClassification of AnalgesicsClassification of Analgesics

Non-opiod (non-narcotic)– Acetaminophen

- NSAIDS:

ASA, Advil, Motrin, Naprosyn, Feldene

Toradol (Ketorolac)

Cox – 2 Inhibitors (Vioxx & Celebrex)

- Side Effects:

Gastric erosion, GI bleeding, fluid retention, Platelet dysfunction, & renal insufficiencies

Classification of AnalgesicsClassification of AnalgesicsClassification of AnalgesicsClassification of Analgesics

Opiod Analgesics: Synthetic NarcoticsCommonly Used:

- Morphine Sulfate, Oxycontin- Dilaudid (hydromorphone)- Oxycodone (Percodan, Percocet, Oxycontin SR- Demerol (Meperidine)- Fentanyl- Codeine Plain

- Tylenol 300 mg - # 2 (15 mg), # 3, (30 mg) # 4 (60mg)- Vicodin (Hydrocodone 5/500, 7.5/750, 10/660

Non-pharmacological InterventionsNon-pharmacological InterventionsNon-pharmacological InterventionsNon-pharmacological Interventions

Heat & cold Progressive relaxation Massage Meditation, Guided Imagery Music Biofeedback Transcutaneous Electric Nerve Stimulation Therapeutic Touch Yoga

Invasive Pain ManagementInvasive Pain ManagementInvasive Pain ManagementInvasive Pain Management

Epidural Intrathecal Nerve Blocks