Dr tarek pain controle

PAINManaging Pain

Dr TAREK NASRALLAH

RHEUMATOLOGY

AL AZHAR

What is Pain?

• “An unpleasant sensory & emotional experience associated with actual or potential tissue damage, or described in terms of such damage” –

The International Association for the Study of Pain

• Subjective sensation• Pain Perceptions – based on expectations, past

experience, anxiety, suggestions– Affective – one’s emotional factors that can

affect pain experience– Behavioral – how one expresses or controls

pain– Cognitive – one’s beliefs (attitudes) about pain

What is Pain

• Physiological response produced by activation of specific types of nerve fibers

• Experienced because of nociceptors being sensitive to extreme mechanical, thermal, & chemical energy.

• Composed of a variety of discomforts • One of the body’s defense mechanism

(warns the brain that tissues may be in jeopardy)

• Acute vs. Chronic – – The total person must be considered. It

may be worse at night when the person is alone. They are more aware of the pain because of no external diversions.

Where Does Pain Come From?

• Cutaneous Pain – sharp, bright, burning; can have a fast or slow onset

• Deep Somatic Pain – stems from tendons, muscles, joints, periosteum, & b. vessels

• Visceral Pain – originates from internal organs; diffused @ 1st & later may be localized (i.e. appendicitis)

• Psychogenic Pain – individual feels pain but cause is emotional rather than physical

Pain Sources• Fast vs. Slow Pain –

– Fast – localized; carried through A-delta axons in skin

– Slow – aching, throbbing, burning; carried by C fibers

– Nociceptive neuron transmits pain information to spinal cord via unmyelinated C fibers & myelinated A-delta fibers.• The smaller C fibers carry impulses : rate 0.5

to 2.0 m/sec.• The larger A-delta fibers carry impulses : of 5

to 30 m/sec.

Acute pain: lasts less than 6 months, subsides

once the healing process is accomplished.

• Chronic pain:

• Complex processes & pathology. Usually altered anatomy & neural pathways.

• Constant & prolonged, > 6 months,

sometimes for life.

• “Lasting longer than expected time frame”

Altered Neuronal StructureChronic pain accompanied by

cortical reorganization Chronic back pain is accompanied

by brain atrophy

Most Common Chronic Pain Syndromes

• Low Back• Headaches• Neck• Facial• Arthritides• Fibromyalgia• Cancer

What is Referred Pain?• Occurs away from pain site

• Examples: McBurney’s point

• Types of referred pain:– Myofascial Pain – trigger points, small

hyperirritable areas within a m. in which n. impulses bombard CNS & are expressed at referred pain

– Sclerotomic & Dermatomic Pain – deep pain; may originate from sclerotomic, myotomic, or dermatomic n. irritation/injury• Sclerotome: area of bone/fascia that is supplied by

a single n. root• Myotome: m. supplied by a single n. rootDermatome: area of skin supplied by a single n. root

Terminology• Noxious – harmful, injurious

– Noxious stimuli – stimuli that activate nociceptors (pressure, cold/heat extremes, chemicals)

• Nociceptor – nerve receptors that transmits pain impulses

• Pain Threshold – level of noxious stimulus required to alert an individual of a potential threat to tissue

• Pain Tolerance – amount of pain a person is willing or able to tolerate

• Accommodation phenomenon – adaptation by the sensory receptors to various stimuli over an extended period of time (e.g. superficial hot & cold agents). Less sensitive to stimuli.

• Hyperesthesia – abnormal acuteness of sensitivity to touch, pain, or other sensory stimuli

• Paresthesia – abnormal sensation, such as burning, pricking, tingling

• Inhibition – depression or arrest of a function– Inhibitor – an agent that

restrains/retards physiologic, chemical, or enzymatic action

• Analgesic – a neurologic or pharmacologic state in which painful stimuli are no longer painful

• Dysesthesia – An unpleasant abnormal sensation, whether spontaneous or evoked.

• Allodynia – Pain due to a stimulus which does not normally provoke pain, such as pain caused by light touch to the skin

• Hyperalgesia – An increased response to a stimulus which is normally painful

• Hyperesthesia - Increased sensitivity to stimulation, excluding the special senses. Hyperesthesia includes both allodynia and hyperalgesia, but the more specific terms should be used wherever they are applicable.

Nerve Endings• “A nerve ending is the termination of a nerve

fiber in a peripheral structure.” (Prentice, p. 37)

• Nerve endings may be sensory (receptor) or motor (effector).

• Nerve endings may be: – Respond to phasic activity - produce an impulse

when the stimulus is or , but not during sustained stimulus; adapt to a constant stimulus (Meissner’s corpuscles & Pacinian corpuscles)

– Respond to tonic receptors produce impulses as long as the stimulus is present. (muscle spindles, free n. endings, Krause’s end bulbs)

– Superficial – Merkel’s corpuscles/disks, Meissner’s corpuscles

– Deep – Pacinian corpuscles,

Nerve Endings• Merkel’s

corpuscles/disks - – Sensitive to touch &

vibration– Slow adapting– Superficial location – Most sensitive

• Meissner’s corpuscles – – Sensitive to light touch &

vibrations– Rapid adapting– Superficial location

• Pacinian corpuscles -– Sensitive to deep pressure

& vibrations– Rapid adapting– Deep subcutaneous tissue

location

• Krause’s end bulbs – – Thermoreceptor

• Ruffini corpuscles/endings– Thermoreceptor– Sensitive to touch &

tension– Slow adapting

• Free nerve endings -– Afferent – Detects pain, touch,

temperature, mechanical stimuli

Types of Nerves

• Afferent (Ascending) – transmit impulses from the periphery to the brain– First Order neuron– Second Order neuron– Third Order neuron

• Efferent (Descending) – transmit impulses from the brain to the periphery

Peripheral and Central Pathways for Pain

Ascending TractsAscending Tracts Descending TractsDescending Tracts

Cortex

Midbrain

Medulla

Spinal Cord

Thalamus

Pons

First Order Neurons• Stimulated by sensory receptors• End in the dorsal horn of the spinal cord• Types

– A-alpha – non-pain impulses– A-beta – non-pain impulses

• Large, myelinated• Low threshold mechanoreceptor; respond to light touch &

low-intensity mechanical info– A-delta – pain impulses due to mechanical pressure

• Large diameter, thinly myelinated• Short duration, sharp, fast, bright, localized sensation

(prickling, stinging, burning)– C – pain impulses due to chemicals or mechanical

• Small diameter, unmyelinated• Delayed onset, diffuse nagging sensation (aching,

throbbing)

Second Order Neurons• Receive impulses from the FON in the dorsal horn

– Lamina II, Substantia Gelatinosa (SG) - determines the input sent to T cells from peripheral nerve• T Cells (transmission cells): transmission cell that connects

sensory n. to CNS; neurons that organize stimulus input & transmit stimulus to the brain

– Travel along the spinothalmic tract – Pass through Reticular Formation

• Types– Wide range specific

• Receive impulses from A-beta, A-delta, & C

– Nociceptive specific• Receive impulses from A-delta & C

• Ends in thalamus

Third Order Neurons• Begins in thalamus• Ends in specific brain centers

(cerebral cortex)– Perceive location, quality,

intensity– Allows to feel pain, integrate past

experiences & emotions and determine reaction to stimulus

Descending Neurons• Descending Pain Modulation (Descending Pain

Control Mechanism)• Transmit impulses from the brain (corticospinal

tract in the cortex) to the spinal cord (lamina)– Periaquaductal Gray Area (PGA) – release

enkephalins– Nucleus Raphe Magnus (NRM) – release serotonin– The release of these neurotransmitters inhibit

ascending neurons• Stimulation of the PGA in the midbrain & NRM

in the pons & medulla causes analgesia.• Endogenous opioid peptides - endorphins &

enkephalins

Pain Process

The neural mechanisms by which pain is perceived involves a process that has four major steps:

–Transduction

–Transmission

–Modulation

–Perception

Facilitating Transduction

• Biochemical mediators: “Chemical Soup”

ProstaglandinsBradykininsSerotonin

HistaminesCytokines

LeukotrienesSubstance P

Norepinephrine

Peripheral Excitatory MediatorsPeripheral Excitatory Mediators(Pain)(Pain)

SubstancSubstancee

ReceptorReceptor MechanismMechanism

Substance PSubstance P

(SP)(SP)NKNK11 neuronal excitability, edemaneuronal excitability, edema

ProstaglandinProstaglandin

(PG)(PG)?? Sensitize nociceptors, Sensitize nociceptors,

inflammation, edemainflammation, edema

BradykininBradykinin BB22 (normal) (normal)

BB11 (inflammation)(inflammation)

Sensitize nociceptorsSensitize nociceptors

PG productionPG production

HistamineHistamine HH11 C-fiber activation, edema,C-fiber activation, edema,

VasodilatationVasodilatation

SerotoninSerotonin 5-HT5-HT33 C-fiber activation, release SPC-fiber activation, release SP

NorepinephrineNorepinephrine

(NE)(NE)11 Sensitize nociceptorsSensitize nociceptors

Activate nociceptorsActivate nociceptors

• NSAIDs ( local & systemic )• Antihistaminic drugs

Acetaminophen (paramol)

• Analgesic, antipyretic

• Inhibits prostaglandin synthetase in the CNS, weak peripheral anti-inflammatory activity

• Serotonergic effect at descending pathway

• Used to treat osteoarthritis

Acetaminophen (Tylenol)

• American Pain Society: Maximum dose 4,000 mg/day,

• American Liver Foundation: 3,000 mg/day

• Risk of hepatotoxicity with higher doses

• Antidote – acetylcysteine (Mucomyst, Acetadote)

Major Categories of Pain

Classified by inferred pathophysiology:

1. Nociceptive pain (stimuli from somatic and visceral structures)

2. Neuropathic pain (stimuli abnormally processed by the nervous system)

Mixed TypeCaused by a

combination of both primary injury or secondary effects

Nociceptive vs Neuropathic Pain

NociceptivePain

Caused by activity in neural pathways in

response to potentially tissue-damaging stimuli

Neuropathic Pain

Initiated or caused by primary lesion or dysfunction in the nervous system

Postoperativepain

Mechanicallow back pain

Sickle cellcrisis

Arthritis

Postherpeticneuralgia

Neuropathic low back pain

CRPS*

Sports/exerciseinjuries

*Complex regional pain syndrome

Central post-stroke pain

Trigeminalneuralgia

Distalpolyneuropathy (eg, diabetic, HIV)

COMPONENT DESCRIPTORS EXAMPLESSteady, Dysesthetic

• Burning, Tingling

• Constant, Aching

• Squeezing, Itching

• Allodynia

• Hypersthesia

• Diabetic neuropathy

• Post-herpetic neuropathy

Paroxysmal, Neuralgic

• Stabbing

• Shock-like, electric

• Shooting

• Lancinating

• trigeminal neuralgia

• may be a component of any neuropathic pain

FEATURES OF NEUROPATHIC PAIN

Local Anesthetic Agents

•Patch (topical)•Eml gel: Lidocaine (topical)•Oint. 4% lidocaine (topical)

Local Anesthetics

Blocks conduction of nerve impulses by decreasing or preventing an increase in the permeability of excitable membranes to Na+.

Inhibits depolarization of nerve

Blocks neuronal firing

Lidoderm 5% Patch

Mentholatum

Menthol generates analgesic

activity through:• Ca2+ channel blocking

activity• Binding to kappa opioid

receptors

Methyl Salicylate Toxicity

• Salicylic acid derivative

• Lipid solubility increases toxicity

–More toxic than aspirin

–1 teaspoon (5ml) wintergreen oil contains 4,000 mg salicylate

–30ml wintergreen oil is a fatal dose in adults

• Risk of toxicity reduced with use for acute pain, limited to a small area of dermal application

Anticonvulsants

1)Inhibit sustained high-frequency neuronal firing by blocking Na+ channels after an action potential, reducing excitability in sensitized C-nociceptors.

2)Blockade of Na+ channels and increase in synthesis and activity of GABA, in inhibitory neurotransmitter, in the brain.

3)Modulates Ca+ channel current and increases synthesis of GABA.

Antiepileptic Agents• Broad clinical

actions in the CNS:– Reduce seizures– Neuropathic pain– Bipolar disorder– Anxiety– Schizophrenia– Agitation

• Impulse dyscontrol

• Dementia• Delirium

• Three proposed mechanisms of action:

– Blockade of voltage gated sodium channels ( glutamate release)

– Blockade of voltage gated calcium channels – alpha 2 delta subunits (reduces excessive neurotransmitter release)

– Enhancement of GABA actions

Lyrica PregabalinSchedule V

Transmission of pain

Defined as: Projection of pain into the

Central Nervous System

Transmission

A synapse contains three elements:

the presynaptic terminal

the synaptic cleft

the receptive membrane

Transmission

• The presynaptic terminal is the axon terminal of the presynaptic neuron

• Here that the presynaptic neuron releases neurotransmitters which are found in vesicles

Neurotransmitters

Chemical substances that allow nerve impulses to move from one neuron to another Found in synapses– Substance P - thought to be responsible for the

transmission of pain-producing impulses– Acetylcholine – responsible for transmitting motor

nerve impulses– Enkephalins – reduces pain perception by bonding

to pain receptor sites– Norepinephrine – causes vasoconstriction– Endorphins - morphine-like neurohormone; thought

to pain threshold by binding to receptor sites – Serotonin - substance that causes local

vasodilation & permeability of capillaries

Capsaicin• Hot peppers• May deplete & prevent

re-accumulation of substance P in primary afferent neurons responsible for transmitting painful impulses from peripheral sites to the CNS.

• Absorption, distribution, metabolism & excretion, half life – unknown

• May produce transient burning with application, usually disappears in 2-4 days, but may persist for several weeks.

Transmission• The synaptic cleft is the narrow

intercellular space between neurons. • Neurotransmitters cross the synaptic

cleft and bind to specific receptors on the postsynaptic neurons

• This will excite or inhibit the postsynaptic neurons.

Questions to Ask about Pain

• P-Q-R-S-T format• Provocation – How the injury occurred & what

activities the pain• Quality - characteristics of pain – Aching

(impingement), Burning (n. irritation), Sharp (acute injury), Radiating within dermatome (pressure on n.)?

• Referral/Radiation – – Referred – site distant to damaged tissue that

does not follow the course of a peripheral n.– Radiating – follows peripheral n.; diffuse

• Severity – How bad is it? Pain scale• Timing – When does it occur? p.m., a.m., before,

during, after activity, all the time

Pattern: onset & durationArea: locationIntensity: levelNature: description

Pain Assessment Scales

• McGill pain questionnaire– Evaluate sensory,

evaluative, & affective components of pain

– 20 subcategories, 78 words

Assessment of Pain Intensity

No Mild Moderate Severe Very Worstpain pain pain pain severe possible

pain pain

Verbal Pain Intensity Scale

No

pain

Visual Analog Scale

Faces Scale

0 1 2 3 4 5

0–10 Numeric Pain Intensity Scale

No Moderate Worstpain pain possible pain

0 1 2 3 4 5 6 7 8 9 10

Worstpossible

pain

21

Smiling Faces

Patients seldom remember how good a clinician your are. But they do remember how much they hurt when you were treating them.

• Questions