dr. mansoor aqil b.sc., m.b.b.s., f.c.p.s associate professor, king saud university & consultant...

DR. MANSOOR AQIL B.Sc., M.B.B.S., F.C.P.S

ASSOCIATE PROFESSOR, KING SAUD UNIVERSITY &CONSULTANT KING KHALID UNIVERSITY HOSPITAL,RIYADH.

PAIN PATHOPHYSIOLOGY

& MANAGEMENT

DR. MANSOOR AQIL B.Sc., M.B.B.S., F.C.P.S

ASSOCIATE PROFESSOR, KING SAUD UNIVERSITY &CONSULTANT KING KHALID UNIVERSITY HOSPITAL,

RIYADH.

PAINPAIN

Word pain is derived from

Latin word “Poena”, meaning penalty, suffering or punishment

PAIN

PAIPAINN

An unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage.(International association of study of pain)

CLASSIFICATION OF PAIN

S U P E R F IC IA L D E E P

S O M A TIC

TR U E V IS C E R A L TR U E P A R IE TA L R E F E R E D V IS C E R A L R E F E R E D P A R IE TA L

V IS C E R A L

A C U TE

D E A F F E R E N TA TIO NP A IN

S Y M P A TH E TIC A L L YM E D IA TE D P A IN

C H R O N IC

P A IN

TYPES OF PAINTYPES OF PAINAccording to durationAccording to duration

Acute

Chronic

TYPES OF PAINTYPES OF PAINAccording to According to

EtiologyEtiology

Postoperative

OR Cancer pain

TYPES OF PAINTYPES OF PAINAccording to Type of the organ According to Type of the organ

affectedaffected

ToothacheEaracheHeadacheLow backache

TYPES OF TYPES OF PAINPAIN

(According to Pathophysiology)(According to Pathophysiology)

Nociceptive; Due to activation or sensitization of peripheral

nociceptors.

Neuropathic: Due to injury or acquired abnormalities of

peripheral or CNS.

ACUTE ACUTE PAINPAIN

Caused by noxious stimulation due to injury, a disease process or abnormal function of muscle or viscera

It is nearly always nociceptive Nociceptive pain serves to detect, localize and limit the

tissue damage.

PHYSIOLOGICAL PROCESSES PHYSIOLOGICAL PROCESSES IN NOCICEPTIONIN NOCICEPTION

TransductionTransmissio

nModulationPerception

400 years ago Reneé Descartes described pain transmission: The flame that burns the hand is transmitted along the nervous system to the brain as a stimulus, where it torments man as a small flame

Mechanisms in Nociception

1 Noxious stimulus

2 Activate nociceptors

3 Transmit to Brain

4 Perception of Pain

Ouch!

If it were only that simple…..

Noxiousstimulus

Transduction Conduction Modulation Perception

primary sensory neuron central neuron

Modulation

Nociception

“Ouch” Pain

TYPES OF ACUTE PAINTYPES OF ACUTE PAIN

Somatic OR

Visceral

SOMATIC SOMATIC PAINPAIN

SuperficialOR

Deep

SUBTYPES OF SUBTYPES OF VISCERAL VISCERAL

PAINPAIN

Localized visceral pain

Referred Visceral pain

True Localized parietal pain

Referred parietal pain

TRUE VISCERAL TRUE VISCERAL PAINPAIN

Dull, diffuse and in Midline

Frequently associated with sympathetic or parasympathetic activity – Nausea – Vomiting– Sweating – Changes in HR and BP.

PARIETAL PARIETAL PAINPAIN

Sharp (stabbing sensation) either localized or referred to a distant site.

Phenomenon of visceral pain or parietal pain referred to cutaneous area results from embryologic development and migration.

PATTERNS OF REFERRED PAINPATTERNS OF REFERRED PAIN

Lungs T2 – T6

Heart T1 –T4

Aorta T1 –L2

Esophagus T3 – T8

Pancreas & Spleen T5 –T10

Stomach, liver and gall bladder T6 –T9

Adrenals T6 – L1

Small intestine T6 – T9

Colon T10 – L1

Ureters T10 – T12

Uterus T11 – T12

Bladder and prostate S2 – S4

Urethra & Rectum S2 – S4

Kidneys, Ovaries & Testis T10 – L1

REFERRED PAINREFERRED PAIN

PAIN PATHWAY

FIRST ORDER FIRST ORDER NEURONNEURON

Reach the spinal cord through dorsal spinal root.– Some through ventral root

– Trigeminal N Gasserian ganglion

– Facial N Geniculate ganglia

– Glossopharyngeal N Superior and Petrosal ganglia

– Vagus Ganglion Nodosum and Jugular ganglia

Nociceptive pathways: peripheral sensory nerves

Dorsal Root Ganglion

Blood vessels

Skeletal muscle

Muscle and skin receptors

Tendon bundle

Peripheral nerve Sympathetic ganglion

Viscera

Spinothalamic tract

Dorsal horn of spinal cord

Nociceptive terminals

C and A fibres

Nociceptive sensory fibres are C-fibres and A fibresC-fibres umyelinatedA myelinatedSlow conduction velocitySignal variety of noxious stimuli - polymodal

SPINOTHELAMIC TRACTSPINOTHELAMIC TRACT

Axons of the second order neurons cross the midline form spinothalamic tract Thalamus, Reticular formation, Nucleus Raphe Magnus and Periaquaductal gray matter.

1. Medial tract Medial Thalamus

2. Lateral tract: Ventral Posterolateral Nucleus of Thalamus

THALAMIC THALAMIC NUCLEINUCLEI

ALTERNATE ALTERNATE PATHWAYSPATHWAYS

1. Spinomesencephalic

2. Spinoreticular

3. Spinohypothalamic

4. Spinotelencephalic

5. Spinocervical

6. In the dorsal column

THIRD ORDER THIRD ORDER NEURONNEURON

Located in Thalamus. Send projections to sensory area 1 &II and

Superior wall of Sylvian fissure.

Interlaminar and medial nuclei Anterior Cingulate Gyrus.

PAIN PAIN CENTRECENTRE

Post Central Gyrus

CINGULATE CINGULATE GYRUSGYRUS

Receptors ---Free nerve endings

Receptors ---Free nerve endingsReceptors ---Free nerve endings

Mechanoreceptors: Pinch and Pinprick

Silent Nociceptors: Inflammation

Polymodal mechanoheat nociceptors: Excessive pressure, Extremes of Temperature and Alogens like Bradykinin, Serotonin, Histamine, H, K, Prostaglandins and ATP.

Types of Peripheral Fibers

A. B.C.

Pain Fibers and C

Classification & Function of Peripheral Nerve Fibers

A. Myelinated A- Fibers: : Motor , Proprioception (afferent) Motor, Touch (afferent) Muscle spindles (efferent) Pain, Temperature (afferent)

B. Myelinated B-Fibers: Pre-ganglionic Sympathetic Fibers

C. Non-Myelinated C- Fibers: Pain, Temperature.

PHYSIOLOGY OF PHYSIOLOGY OF NOCICEPTIONNOCICEPTION

Fast pain (First pain)

Slow pain (Second pain)

Peripheral Terminal Activation in Acute pain: Phase 1

Second pain - dull, burning, aching, not localised, diffuse

C-fibres umyelinated slow conduction (0.5 - 2 m/s

First pain - sharp, pricking, localisingA fibres myelinated (12-30 m/s)

Time

Pai

n In

tens

ity

MODULATION

MODULATION OF MODULATION OF PAINPAIN

Peripheral Modulation

Central modulation

PERIPHRAL PERIPHRAL MODULATIONMODULATION

Primary Hyperalgesia

Secondary Hyperalgesia

1.    Decrease threshold

2.     Increase in frequency of response

3. Spontaneous discharge

PRIMARY PRIMARY HYPERALGESIAHYPERALGESIA

Low intensity stimulation High intensity (noxious) stimulation

Innocuous sensation

State of normosensitivity

PAIN

State of Normosensitivity Response proportional to stimulus

Noxious stimulus

Pain neuron

DRG

Response

Peripheral tissue Central nervoussystem

ALOGENS

DAMAGED TISSUE

MAST CELLSBASOPHILLSPLATELETS

HISTAMINE

MAST CELLSPLEATELETS

SEROTONIN

ACTIVATEDFACTOR XII

BRADY-KIANIN

PRIMARY HYPRALGESIASTIMULATION OF C- FIBERS

SENSITIZARIONSENSITIZARION((STIMULATION)STIMULATION)

RECEPTOR

G-RPOTEIN PLC PIP2 DAG

PKCIP3

RELEASEINTRACELLULAR

CALCIUM

PC

ARACHADONICACID

COX LIPOXY-GENASE

PROSTAG-LANDINS

LEUKOTRINESTHROM-BOXANE

Innocuous/Noxiousstimulus

Reduced Transduction Threshold

primary sensory neuron central neuron

Peripheral Sensitization

Primary hyperalgesia

Inflammation

There are prostanoid and non-prostanoid sensitizers

Peripheral SensitizationPeripheral Sensitization

PKC

PKA

(SNS/SNS2)

VR1

Ca2+

PG

EP/IP

AACox-2PGS

Primary sensory neuronperipheral terminal

Tissue Tissue damagedamage

MacrophageMacrophage

Mast Mast cellcell

IL1, IL6TNF

H+ COX-2Sensitive

SECONDRY SECONDRY HYPERALGESIAHYPERALGESIA

“Triple response”

(Neurogenic Inflammation)sP and CGRP from collateral axons.

sP degranulates Histamine and 5HT, vasodilates causing tissue edema and induces formation of Leukotrines.

SECONDRYSECONDRY HYPERALGESIAHYPERALGESIA

ANTI- DROMIC CONDUCTION“TRIPPLE RESPONSE”

To spinal cord activation of nociceptors

SP SP SP CGRP?

Histamine, Serotonin, Oedema

VASODILATION

BLOOD VESSEL

INJURY

STIMULATION

INHIBITION

CENTRAL MODULATIONCENTRAL MODULATION

CENTRAL SENSITIZARIONCENTRAL SENSITIZARION((STIMULATION)STIMULATION)

Wind up & Sensitization

Receptor Field Expansion

Hyperexcitabality of flexion reflexes

CENTRAL SENSITIZARIONCENTRAL SENSITIZARION((STIMULATION)STIMULATION)

Chemical mediators: sP, CGRP, VIP, Angiotensin Cholecystokinin L- Aspartate & L- glutamate Galanin Substance Y

Wind up phenomenon

C-Fibre

C-Fibre

Mild painstimulus

Mild painstimulus

Increased nociceptor drive leads to central sensitisation

Mild pain

Severepain

C fibre activation will stimulate mild pain

NORMAL

Weak synapseinnocuous

stimulusnon-painful sensation

innocuous stimulus

painful sensation

Increased synaptic strength

AA fibre mechanoreceptor fibre mechanoreceptor

Central Sensitization Central Sensitization Receptor field expansionReceptor field expansion

Receptor field expansion ACQUISITION BY A- FIBRES OF C-FIBRE-PHENOTYPE

A beta fibre

nociceptor

Substance P, BDNF

Central sensitisation

noxiousstimulus

innocuousstimulus

Post-inflammation & after nerve damage, (2) Phenotype switch, (3) NGF dependent (4) NK1 & NMDA receptors involved (5) GABA inhibition (6) induction sensitive to MO

SENSITIZARIONSENSITIZARION((STIMULATION)STIMULATION)

RECEPTOR

G-RPOTEIN PLC PIP2 DAG

PKCIP3

RELEASEINTRACELLULAR

CALCIUM

PC

ARACHADONICACID

COX LIPOXY-GENASE

PROSTAG-LANDINS

LEUKOTRINESTHROM-BOXANE

Central Terminal

Glutamate

Sub P

PKC

Activity

PKA

NK1

mGluR

NMDA TyrS/T

S/T

IP3

Ca2+

AMPAAMPA

pERKsrc

Central Sensitization - Acute PhaseCentral Sensitization - Acute Phase

Glut

Mg2+

NMDA receptors contribute to spinal cord sensitisation

Glut

Na+

Brief Depolarisation

EXCITATION

AMPAEAA receptors: NMDA mGluR

Na+

Sustained Depolarisation

EXCITATION

+

Na+

Ca2+

iCa2+

PKC, NOS

NMDA Receptor Antagonists

Ketamine Amantadine Dextromethorphan Methadone Dextropropoxephene

INHIBITIONINHIBITION

    Segmental inhibition (Gate theory)

Superaspinal Inhibition

CENTRAL SENSITIZATION(INHIBITION)

GATE CONTROL OF PAINGATE CONTROL OF PAIN

Stimulation of A fibers segmental inhibition of small primary pain afferents and reduce response to painful stimuli in dorsal horn secondary afferents

MECHANISM OF ACTION Exact mechanisms of actions are as yet unknown and certainly

unproven 1965- Melzack and Wall proposed the Gate Theory of Pain

– Nociceptive A delta/C fibres project in SC to second-order projection neuron but also send fibres to inhibit an inhibitory interneuron

– Large myelinated A alpha neurons in DC send collaterals to activate these same interneurons thereby inhibiting (closing the gate) the pain sensory action potentials

GATE THEORY OF PAIN

Glycine and GABA are inhibitory transmitters. GABA A and GABAB Muscimol and Beclofen.

  GABAB increases K conductance GABAA increases Cl conductance Glycine also increases Cl conductance Strychnine and Tetanus toxide are Glycine receptor antagonists Glycine is facilitatory on NMDA receptors

Adenosine has two types of receptors A1 and A2 A1 inhibits adenyl cyclase and A2 stimulates adenylcyclase. A1 mediate antinociceptive action.

TRANSCUTANEOUS TRANSCUTANEOUS NERVE STIMULATION (TENS)NERVE STIMULATION (TENS)

Asymmetric biphasic waveform of

12-20mA at 50-100Hz via 1000 ohms resistance has proved successful for post operative analgesia

TRANSCUTANEOUS ELECTRICAL TRANSCUTANEOUS ELECTRICAL NERVENERVE STIMULATION (Tens)STIMULATION (Tens)

Effective

Over all analgesic effect is modest

Absolutely safe for the fetus

Usually causes electrical interference with fetal heart rate when used

concurrently with internal fetal scalp electrode

TENS AdvantagesTENS Advantages

NoninvasivePatient controlledNo side effectsNon-addictiveDecreased analgesic needs

SUPRASPINAL INHIBITIONSUPRASPINAL INHIBITION

Originate from

Cerebral cortex Thalamus Reticular formation of brain stem (Ventro-median

Medulla VMM). Neurotransmitter is Serotonin.

NMR & Locus Ceruleu Nor Adrenaline containing fibers from

SUPRASPINAL INHIBITIONSUPRASPINAL INHIBITION

Afferent Central Terminal

Glutamate

Sub P

Activity

NK1

mGluR

NMDA

AMPAAMPA

VGCCGABAAdensosineOpiateDopamineNor-Ephinephrine

Dorsal Horn Neuron

Supraspinal Supraspinal /Modulation/Modulation

Modulation - InhibitoryModulation - Inhibitory

Supraspinal – Endorphins,

– Enkephalins,

– Dynorphins,

– Norepinephrine (alpha 2),

– GABA,

– Somatostatin (5HT1),

– Neurotensin

Ascending Ascending vv Descending FibresDescending Fibres

GABA

PERIPHERY

P.A.G.(Midbrain)

LIMBICSY STEM

THALAMUS

SubstantiaGelatinosa

(LAMINA I I)

-

SOMATOSENSORY CORTEX

+

+

N.M.R.(ReticularFormation)

+

+

-

ENK EPHALINS5-HT

DorsalHorn

GlutamateSubstance P

+

ENDORPHINS

DescendingAnalgesic

Fibres

Ascending pathway

Adapted from Rang & DaleInhibitory interneurons

-

PAIN PAIN NEUROTRANSMITTERSNEUROTRANSMITTERS

InhibitoryGlycine

InhibitoryA, B-Aminobutyric Acid

GABA

Inhibitory5-HT, (5HT3)Serotonin

InhibitoryA1Adenosine

InhibitoryNorepinephrine

Inhibitory -Endorphin

InhibitoryEnkephalins

InhibitoryMuscarinicAcetylcholine

inhibitorySomatostatin

ExcitatoryP1, P2ATP

ExcitatoryNMDA, AMPA,

Kinate, quisqualate

Aspartate

ExcitatoryNMDA, AMPA,

Kinate, quisqualate

Glutamate

ExcitatoryCGRP

ExcitatoryNK-1Substance P

EFFECT ON NOCICEPTIONRECEPTORNEUROTRANSMITTER

PRE EMPTIVE ANALGESIA

PRE EMPTIVE ANALGESIAPRE EMPTIVE ANALGESIA

“Administration of local anesthetics/

analgesics may reduce the post operative

requirement of analgesics due to reduction

in pain intensity.”

PRE EMPTIVE ANALGESIAPRE EMPTIVE ANALGESIA

Pain after surgery is possibly amplified by noxious events induced by surgical incision (sensitization).

Idea by Crile and later on by Wall.

PRE EMPTIVE ANALGESIAPRE EMPTIVE ANALGESIA

• Promising results from experimental studies

• Prospective studies in humans show conflicting results

• No ultimate understanding of the nature of pre-emptive measures needed

SYSTEMIC RESPONCES TO SYSTEMIC RESPONCES TO ACUTE PAINACUTE PAIN

Cardiovascular effectsCardiovascular effects

        Tachycardia

        Hypertension

        Increased SVR

RESPIRATORY RESPIRATORY SYSTEMSYSTEM

O2 demand and consumption M .V Splinting and Guarding and decreased

chest excursion Atelactasis, increased shunting,

hypoxemia V.C, retention of secretions and chest

infection

GASTROINTESTINAL AND GASTROINTESTINAL AND URINARY EFFECTSURINARY EFFECTS

Sympathetic tone Motility, ileus and urinary retention

Secretion of stomach Chance of aspiration Abdominal distension leads to decreased

chest excursion

ENDOCRINE ENDOCRINE EFFECTSEFFECTS

Catecholamine, Cartisol and Glucagon Insulin and Testosterone Increased Aldosterone Increased ADH Increased Angiotensin

HEMATOLOGICAL HEMATOLOGICAL EFFECTSEFFECTS

Platelet adhesiveness• Fibrinolysis leading to

Hypercoagulatability

IMMUNE IMMUNE EFFECTSEFFECTS

Leukocytosis

Lymphopenia

Reduce T killer cell cytotoxicity

Depression of Reticuloendothetial system

GENERAL SENSE OF GENERAL SENSE OF WELL-BEINGWELL-BEING

AnxietySleep disturbancesDepression

PAlN MEASUREMENTPAlN MEASUREMENT

Descriptive scales such as – Mild. – Moderate. – Severe

Generally unsatisfactory.

Numerical scaleNumerical scaleVAS (Visual Analogue scale) VAS (Visual Analogue scale)

0 corresponds to No pain

10 designates Worst possible pain.

0 1 2 3 4 5 6 7 8 9 10

Wong Baker faces rating scaleWong Baker faces rating scale

Wong Baker faces rating scale

POSTOPERATIVE PAlNPOSTOPERATIVE PAlN

OUTPATIENTS

1 : Oral Analgesics

Cyclooxygenase Inhibitors Opioids

2. Infiltration of Local Anesthetic

POSTOPERATIVE PAlNPOSTOPERATIVE PAlN

INPATIENTS

1. Opioids

Subcutaneous & Intramuscular Injections

Patient-Controlled Analgesia

2. Peripheral Nerve Blocks

HYPNOSISSEDATION

ANALGESIA

PAIN

TIME

I/M orI/V

INJECTIONS

POSTOPERATIVE PAlNPOSTOPERATIVE PAlN

INPATIENTS

3. Central Neuraxial Blockade & Intraspinal drugs

Local Anesthetics

Opioids

Local Anesthetic & Opioid Mixtures

HYPNOSISSEDATION

DESIRED ANALGESIA

PAIN

TIME

PCA PCA (patient controlled analgesia)(patient controlled analgesia)

PCA analgesia has been used successfully in patients ranging in age from 7-90 years of age.

PCA PCA (patient controlled analgesia)(patient controlled analgesia)

PCA IV, Epidural, Transdermal patch

HYPNOSISSEDATION

ANALGESIA

PAIN

TIME

HYPNOSISSEDATION

ANALGESIA

PAIN

TIME

PCA IV, Epidural, spinalTransdermal patch

OverdoseNaloxone

Anesthesia

Potential Benefits of Epidural AnalgesiaPotential Benefits of Epidural Analgesia

Superior “dynamic” pain relief (while coughing, deep breathing

and ambulating)

Decreased pulmonary complications

Decreased cardiovascular complications

Attenuated neuroendocrine/metabolic response to surgical stress

Lower incidence of DVT and vascular graft occlusion

Earlier return of bowel function

Decreased time on ventilator

Shorter postoperative stay in ICU

Decreased length of hospitalization

Decreased cost of health care

Chronic pain

PATHOPHYSIOLOGY OF CHRONIC PAINPATHOPHYSIOLOGY OF CHRONIC PAIN

Chronic pain may be caused by a combination of

1. Peripheral, 2. Central, 3. Or psychological mechanisms.

Sensitization of nociceptors plays a major role

EVALUATING THE PATIENTEVALUATING THE PATIENTWITH PAlNWITH PAlN

Why?

EVALUATING THE PATIENTEVALUATING THE PATIENTWITH PAlNWITH PAlN

Acute pain is primarily therapeutic

Chronic pain additionally involves investigative measures.

EVALUATING THE PATIENTEVALUATING THE PATIENTWITH PAlNWITH PAlN

A written questionnaire– Nature of the pain, – Onset – Duration, – Previous medication and treatments.

Diagrams can be useful in defining patterns of radiation.

Investigations Investigations

Plain radiographs, Computed tomography (CT), Magnetic resonance imaging (MRI),Bone scans.

MRI is particularly useful for soft tissue analysis and can show nerve compression.

ELECTROMYOGRAPHY & NERVE CONDUCTION STUDIES

For confirming the diagnosis of entrapment syndromes, radicular syndromes, neural trauma, and polyneuropathies

Can often distinguish between neurogenic and myogenic disorders

DIAGNOSTIC DIAGNOSTIC & & THERAPEUTICTHERAPEUTICNEURAL BLOCKADENEURAL BLOCKADE

Can be useful in delineating pain mechanisms, but, more importantly, it plays a major role in the management of patients with acute or chronic pain.

SOMATIC BLOCKS– Trigeminal Nerve Blocks– Facial Nerve Block– Glossopharyngeal Block– Cervical Paravertebral Nerve Block

SYMPATHETIC BLOCKS

– Cervicothoracic (Stellate) Block A. INDICATIONS - This block is often used in patients with head, neck,

arm, and upper chest pain.

– Intravenous Regional Sympathetic Blockade A Bier block utilizing guanethidine (20-40 mg) can selectively interrupt sympathetic

innervation to an extremity.

Cervicothoracic (Stellate) Cervicothoracic (Stellate) BlockBlock

DIFFERENTIAL NEURAL BLOCKADEDIFFERENTIAL NEURAL BLOCKADE

Pharmacological or anatomic differential neural blockade has been advocated as a method of distinguishing somatic, sympathetic, and psychogenic pain mechanisms.

The pharmacological approach relies on the differential sensitivity of nerve fibers to local anesthetics

Preganglionic sympathetic (B) fibers are reported to be most sensitive, closely followed by pain somatosensory C and A delta fibers and finally motor fibers (Aa).

By using different concentrations of local anesthetic, it may be possible to selectively block certain types of fibers while preserving the function of others.

PHARMACOLOGICALPHARMACOLOGICALINTERVENTIONSINTERVENTIONS

Pharmacological interventions in pain management include – COX inhibitors, – Opioids, – Antidepressants, – Neuroleptic agents, – Anticonvulsants, – Corticosteroids, – Systemic administration of local anesthetics – Alpha 2 agonists– Botulinum toxin

THERAPEUTIC ADJUNCTSTHERAPEUTIC ADJUNCTS

PSYCHOLOGICAL INTERVENTIONS

PHYSICAL THERAPY

Heat and cold

ACUPUNCTURE

THERAPEUTIC ADJUNCTSTHERAPEUTIC ADJUNCTS

ELECTRICAL STIMULATION

– Transcutaneous Stimulation

– Spinal Cord Stimulation (SCS) Proposed mechanisms include activation of descending modulating systems and inhibition of sympathetic outflow

– lntracerebral Stimulation Deep brain stimulation may be used for intractable cancer pain (periaqueductal and periventricular gray areas for nociceptive pain)

Permanent Implantable IPGPermanent Implantable IPG

CANCER PAINCANCER PAIN

ORAL OPlOlD THERAPY

TRANSDERMAL OPlOlDS

PARENTERAL THERAPY

INTRASPINAL OPlOlDS

NEUROLYTIC TECHNIQUES

Transdermal patchTransdermal patchFentanyl 50 mic/hrFentanyl 50 mic/hr

ALCOHOL ALCOHOL & & PHENOLPHENOLNEUROLYTIC BLOCKSNEUROLYTIC BLOCKS

Neurolytic blocks are indicated for patients with severe intractable cancer pain

RADIOFREQUENCY ABLATION RADIOFREQUENCY ABLATION && CRYONEUROLYSIS CRYONEUROLYSIS

Percutaneous radio-frequency ablation relies on the heat produced by current flow from an active electrode that is incorporated at the tip of a special needle. The needle is positioned under fluoroscopy.

Electrical stimulation A z (2'Hz for motor responses and 50 Hz for sensory responses) via the electrode and impedance measurement prior to ablation also help confirm correct positioning.

Radiofrequency Neurotomy

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