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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