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![Page 1: Diagnosis and Management of Craniofacial Pain Richard K. Osenbach, M.D. Director, Neurosurgical Services Cape Fear Valley Medical Center.](https://reader034.fdocuments.us/reader034/viewer/2022051401/56649d895503460f94a6ecd5/html5/thumbnails/1.jpg)
Diagnosis and Management of Craniofacial Pain
Richard K. Osenbach, M.D.
Director, Neurosurgical Services
Cape Fear Valley Medical Center
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Key Points
All facial pain IS NOT trigeminal neuralgia
There are no tests for trigeminal neuralgia or for that matter most causes of facial pain
The wrong diagnosis can lead to the wrong treatment
Despite all the advancements in medicine, it is not possible to cure all pain problems
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Approach to the patient with craniofacial pain
Specific pain syndromes
Pharmacological Management
Surgical Treatments
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Approach to the Patient with Craniofacial Pain
Single most important aspect is to ESTABLISH THE CORRECT DIAGNOSISCareful detailed pain history
LocationDurationTemporal characteristicsQualitySeverityCircumstances of onsetInfluencing factorsNeurological symptomsResponse to medications
The more paroxysmal the pain, the more likely that surgery may be beneficial
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Neuropathic Craniofacial Pain Syndromes
Trigeminal neuralgia
Trigeminal neuropathic
Postherpetic trigeminal pain
Glossopharyngeal neuralgia
Geniculate neuralgia
Occipital neuralgia
Sphenopalatine neuralgia
Vidian neuralgia
Superior laryngeal neuralgia
Carotidynia
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Headache SyndromesClassic migraine
Common migraine
Migraine variants
Chronic daily headache
Cluster headache
Muscle tension headache
Post-traumatic headache
Chronic paroxysmal hemicrania
Headache caused by other disorders
Eg. Brain tumor, hydrocephalus, etc.
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Ocular and Periocular Disorders
Tolosa-Hunt Syndrome
Raeder’s paratrigeminal syndrome
Orbital apex syndrome
Cavernous sinus syndrome
Parasellar syndrome
Corneal pathology
Angle closure glaucoma
Optic neuritis
Orbital cellulits
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Otologic Problems
Otitis externa and interna
Ramsey-Hunt Syndrome
Bullous myringitis
Tumors
Mastoiditis
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Dental and Periodontal Pathology
Periodontal abscess
Bruxism
Burning mouth syndrome
Temporomandibular joint disorders
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What’s The Point?
SUCCESSFUL TREATMENT DEPENDS ON MAKING THE CORRECT DIAGNOSIS
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Classification of Facial PainTrigeminal neuralgia, type 1, (TN1): facial pain of spontaneous onset with greater than 50% limited to the duration of an episode of pain (temporary pain).
Trigeminal neuralgia, type 2, (TN2): facial pain of spontaneous onset with greater than 50% as a constant pain.
Trigeminal neuropathic pain, (TNP): facial pain resulting from unintentional injury to the trigeminal system from facial trauma, oral surgery, ear, nose and throat (ENT) surgery, root injury from posterior fossa or skull base surgery, stroke, etc.
Trigeminal deafferentation pain, (TDP): facial pain in a region of trigeminal numbness resulting from intentional injury to the trigeminal system from neurectomy, gangliolysis, rhizotomy, nucleotomy, tractotomy, or other denervating procedures.
Symptomatic trigeminal neuralgia, (STN): pain resulting from multiple sclerosis.
Postherpetic neuralgia, (PHN): pain resulting from trigeminal Herpes zoster outbreak.
Atypical facial pain, (AFP): pain predominantly having a psychological rather than a physiological origin
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Pharmacological TherapyAnti-epileptics drugs (AEDs)
Antidepressant medications
Opiates
Neuroleptics
Antispasmodics
Miscellaneous drugs
Botox
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General Principles of Pharmacological Management
Rule out surgical lesions (tumor, etc.)
Neuropathic vs. nociceptive?
Develop a strategy
Lay out a plan
Conservative initial dosing to avoid side effects
Monotherapy is preferable if possible
Escalate dose to effect or toxicity
If second drug needed, choose agent in different class
Na+ channel blcoker, GABA agonist, etc.
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Antiepileptic Agents
Tegretol (carbamazepine)
Trileptal (oxcarbazepine)
Neurontin (gabpentin)
Lyrica (pregabalin)
Dilantin (phenytoin)
Depakote (valproic acid)
Topamax (topirimate)
Lamictal
(lamotrigene)
Keppra (levateracitam)
Gabatril
Benzodiazepines
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Antiepileptic Drugs (AEDS)
Similarities in pathophysiology of neuropathic pain and epilepsy
All AEDS ultimately act on ion channels
Efficacy of AEDS most clearly established for neuropathic conditions characterized by episodic lancinating pain
Most clinical studies have focused on DPN and PHN
Use of AEDS in patients with FBSS is nearly entirely empiric
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AEDS Studied in Neuropathic Pain
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Mechanisms of Selected AEDSCarbamazepine (Tegretol)
Modulates voltage-gated Na+ channels
Reduces spontaneous activity in experimental neuromas
Inhibits NE uptake; promotes endogenous descending inhibitory mechanisms
Oxcarbazepine (Trileptal)
Modulates Na+ and Ca+2 channels, incease K+ conductance
Lacks toxicity of epoxide metabolites
Lamotrigine
Blocks voltage-gated Na+ channels
Inhibits glutamate release from pre-synaptic neurons
Gabapentin (Neurontin)
Structural analog of GABA
Binds to voltage-dependent calcium channels
Inhibits EAA release; Interacts with NMDA receptor at glycine site
Pregabalin (Lyrica)
Binds to voltage-gated calcium channels
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Adverse Effects of AEDsAllergic reaction
Up to 7% with CBZ
Some cross-reactivity between CBZ and PHT
Cognitive changes
Sedation
Nystagmus, ataxia, diplopia, dizziness
Nausea, vomiting, headache
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Adverse Effects of 2nd Generation AEDS
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Antidepressant Analgesics
“The results suggest to us that antidepressants may have an analgesic action which is independent of their mood-altering effects”
Merskey & Hester 1972
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Descending Pain ModulationEndorphin link from PAG to pontine raphe nuclei
Serotonergic conection to spinal dorsal horn
Noradrenergic pathway from locus ceruleus to dorsal horn
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Antidepressant AnalgesicsCurrent Evidence
Relieves all components of neuropathic painRCT - clear separation of analgesic and antidepressant effectsAlthough other agents (eg anti-epileptics)) may be regarded as 1st line therapy over antidepressants, there is no good evidence for this practiceMore selective agents are either less effective or not useful (serotonergic, noradrenergic)Because of incomplete efficacy, combination therapy may be neededComparative data regarding other drugs using NNT figures now exists
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Antidepressants in Neuropathic Pain-RCT
Watson et al.: reviewed 29 randomized clinical trials
16 involved PHN or PDNMixed SN agents – 18/21 + effects
Amitriptyline 10/13, Imipramine 5/5,Doxepin 1/1, Venlafexline 2/2
NA – 10/12 + effectsNortriptyline 3/4, desipramine 4/5, maprotiline 2/2, bupropion 1/1
Serotonergic agents – 4/5 + effectsParoxetine 1/2, clomipramine 2/2, citalopram 1/1
86 8380
0
20
40
60
80
100
Mixed NS NA Ser
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Adverse Effect of Antidepressants
Anti-cholinergic autonomic effects (TCAs)Allergic and hypresensitivity reactionsCardiovascular effects
Orthostatic hypotension (avoid imipramine in elderly)Quinidine-like cardiac effects
CNS effectsSedation, tremor, seizures, atropine-like delerium, exacerbation of schizophrenia/mania
Acute overdose may be fatal (>2000mg)Withdrawal reactions
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Guidelines for Use of Antidepressants in Pain Management
Eliminate all other ineffective analgesicsStart low and titrate slowly to effect or toxicityNortriptyline or amitriptyline for initial treatmentMove to agents with more noradrenergic effectsConsider trazadone in patients with poor sleep patternTry more selective agents if mixed agents ineffectiveDo NOT prescribe monoamine oxidase inhibitorsTolerance to anti-muscarinic side effects usually takes weeks to developWithdraw therapy gradually to avoid withdrawal syndrome
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Opioids for Chronic Non-Malignant Pain
Well-established and accepted for acute/cancer pain
Extrapolation of outcomes to non-malignant pain flawed
Information is more anecdotal, contradictory, philosophical, and/or emotional than scientific
Limited number of well-designed RCT with inconclusive results
Reduction in pain scores of around 20% without major benefits on function or psychological outcomes
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Principles of Opioid Therapy in Chronic Non-Malignant Pain
Opioids provide analgesic benefit for a selected subpopulation of patients
Less evidence exists regarding improvement in function
Benefits outweigh risks in well-selected patients
Most benefit in patients with pain from established nociceptive/neuropathic conditions
Identification of other appropriate patients is problematic, and valid diagnostic criteria do not exist
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Implementation of Opioid TherapyPrerequisites
Failure of pain management alternatives; but not a last resortOpioids should only be use as part of a multimodality approachIdentification of realistic goals of treatmentPhysical and psychosocial assessment by multidisciplinary teamConsider history of substance abuse as a relative contraindicationDecision to prescribe by multidisciplinary team or at least two practitionersInformed written consentBest practice – prescribe a trial of opioids and withdraw use if the provision of analgesia does not result in functional improvement
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Implementation of Opioid TherapyTherapeutic Trial Period
Appropriate oral or transdermal drug selection
Defined trial period with regular assessment and review
Opioid dose adjustment or rotation as needed
Decision for long-term treatment predicated upon demonstration of pain relief and/or functional improvement
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Implementation of Opioid TherapyLong-Term Therapy
Opioid contract
Single defined prescriber
Regular assessment and review
Routine urine and serum drug screen
Ongoing effort to improve physical, psychological, and social function as a result of pain relief
Continued multidisciplinary approach to pain
Defined responses to psychosocial or behavioral problems (addiction, diversion, etc)
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Opioid Therapy - RCTPain Type Study Control Results
Nociceptive Arner & Meyerson, 1988 Placebo Pos
Kjaersgaard-Anderson, 1990 Paracetamol Pos***
Neuropathic Arner & Meyerson, 1988 Placebo Neg
Dellemijn & Vanneste, 1997 Placebo/Valium Pos
Kupers, et al., 1991 Placebo Pos
Rowbotham et al., 1991 Placebo Pos
Idiopathic Arner & Meyerson, 1988 Placebo Neg
Kupers, et al., 1991 Placebo Neg
Moulin et al., 1996 Benztropine Pos***
Unspecified Arkinstall et al., 1995 Placebo Pos***
Mays et al., 1987 Placebo/Bupiv Pos
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Opioid Therapy – Prospective Uncontrolled Studies
Pain Type Reference Results
Nociceptive McQuay et al., 1992 Pos
Neuropathic Fenollosa et al., 1992 Pos
McQuay et al., 1992 Mixed
Urban et al., 1986 Pos
Idiopathic McQuay et al., 1992 Neg
Mixed/Unspecified Auld et al. 1985 Pos
Gilmann & Lichtigfeld, 1981 Pos
Penn and Paice, 1987 Pos
Plummer et al., 1991 Mixed
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Adverse Effects of Opioids
Common Occasional Rare
Nausea/vomiting Hallucinations Respiratory dep.
Constipation Myoclonus Seizures
Urinary retention Mood changes Delerium
Sedation Anxiety Hyperalgesia
Cognitive impairment Rigidity Allodynia
Pruritis Dry mouth
Gastric stasis
Bronchoconstriction
Tolerance, Physical Dependence, Addiction
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Miscellaneous AgentsAntiarrhythmics - Mexilitene
Na+ channel blockade Reduce neuronal hyperexcitabilityPossible predictive effect of IV lidocaine challengeMay worsen AV conduction blockMonitor EKG, LFT, renal fxnSignificant incidence of treatment-limiting side effects
Baclofen
GABAB receptor antagonistEfficacious in TNStart 10mg QD and titrate until effect or sedationCannot abruptly withdraw drug!
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Trigeminal Branch Stimulation
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Trigeminal Branch StimulationStimulation of supraorbital, infraorbital nerves
Indications
Trigeminal neuropathic pain
Trigeminal deafferentation pain
Post-herpetic neuralgia
Chronic daily headache
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Peripheral Trigeminal Branch Stimulation for Neuropathic Pain
Johnson M, Burchiel K, Neurosurgery, 2004
0
2
4
6
0 25 50 75 100
0
2
4
6
8
Increase No Change Reduced0
1
2
3
4
5
Slightly Somewhat Mostly Completely
Pain Relief
Medication Use Patient Satisfaction
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Peripheral Trigeminal Branch Stimulation for Neuropathic Pain
Effective for trigeminal neuropathic pain
Less effective for PHN
Simple, low morbidity
Pain relief seems relatively durable
Major problem is erosion of connector
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Motor Cortex Stimulation
Motor cortex stimulation is NOT FDA approved and represents an off-label use of the implanted device
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History of MCS
Developed by Tsubokawa and colleagues during 1980sTreatment of central deafferentation pain
Poststroke painThalamic painBulbar pain
Alternative to other methods of neuromodulation forSCSDBS
Discovered that stimulation of motor rather than sensory cortex produced better pain relief
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Nociceptive Input(Spinothalamic System)
Non-noxious Input(DCML System)
DorsalHorn
SensoryCortex
Thalamus
DCN
Thalamus
SensoryCortex
MotorCortex
InInhibitory
Inhibitory
Inhibitory
Relationship Between Spinothalamic and DCML System - Normal
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Nociceptive Input(Spinothalamic System)
Non-noxious Input(DCML System)
DorsalHorn
SensoryCortex
Thalamus
DCN
Thalamus
SensoryCortex
MotorCortex
InInhibitory
Inhibitory
Facilitation
PNS AA, C-fiber
Thalamic Pain
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Motor Cortex StimulationClinical Indications
Post-stroke pain
Post-herpetic neuralgia
Trigeminal neuropathic pain
Trigeminal deafferentation pain
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Transcranial Magnetic Stimulation
VAPSPre VAPSPost
Sham 7.0 + 0.6 6.5 + 0.6
0.5 Hz TMS 6.4 + 0.7 5.5 + 0.7
10 Hz TMS 7.3 + 0.5 4.8 + 0.8
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Localization of Motor Cortex
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Complications
Stimulation-induced seizures
Pain at stimulation site
Epidural hematoma
CSF leak
Electrode fracture or migration
Infection
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Results of MCSNguyen et. al.: Arch Med Res, 2000
32 patients with central or peripheral neuropathic pain
Mean follow-up 27 months
Substantial pain relief achieved in:
77% (10/13) with central pain
83% (10/12) with neuropathic facial pain
Satisfactory results in 1/3 patient with SCI pain, 1 patient with PHN, 1 patient with plexus avulsion
No patient developed seizures
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Results of MCS
0102030405060708090
100
VAS score
Pre-Op VAS VAS 3 months VAS long-term
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Unanswered Questions
What are the best indications for MCS?What is the value of preoperative pharmacological testing?Is there a predictive value to TMS?What is the optimum electrode location?Is there any value to using multiple electrodes?Are there optimum stimulation parameters?How often should stimulation be applied and for how long?Can long-term reduction in pain be explained by adaptation of the brain to chronic stimulation?
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Deep Brain Stimulation
Deep brain stimulation is NOT FDA approved for pain and represents an off-label use of the implanted device
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Stimulation-Produced Analgesia
Reynolds, 1969: scienceElectrical stimulation of rat midbrain results in profound analgesia without concurrent administration of analgesic drugs
Relationship between SPA and endogenous opioid system
Richardson, 19731st published report of PAG-PVG stimulation in humans
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DBS Pain TargetsPVG AND PAG
Activation of endogenous opiate systemsDescending modulatory pathwaysBest for nociceptive pain
LEMNISCAL SYSTEMVc (VPL,VPm) nucleus, medial lemniscus, ICParesthesia-producing stimulation Best for neuropathic pain
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Results of DBSOverall results variable
30% to 85% excellent/good pain relief
Richardson (Neurosurgery, 1977)
85% effective short-term; 65% at 1 year
Gybels & Kupers (Neurophys Clin, 1990)
initial 61%; 4 years 30%
Plotkin (Appl Neurophys, 1982)
60-65% good results
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Results of Deep Brain Stimulation Gybels and Kupers
Literature review through 1998
1,863 patients (38 reports)
Latest results analyzed
Success defined as:
Pain relief scores of 50% or more
Verbal ratings of “good” or “excellent”
Lack of relief during trial considered failure
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Deep Brain Stimulation Deafferentation Pain
Electrode Site No. Long-Term Success %
PAG-PVG 155 35 23
VPL-VPM 409 228 56
Overall 644 349 54
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Deep Brain Stimulation Nociceptive Pain
Electrode Site No. Long-Term Success %
PAG-PVG 291 247 59
VPL-VPM 51 0 0
Overall 419 172 59
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Pain Type vs. Site of Stimulation
0
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60
Success Rate
Nociceptive pain Deafferentation pain
PAG-PVG VPL-VPM Overall
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Deep Brain StimulationComplications
NeurologicIntracranial hemorrhage 1 - 5%Infection 3 -14%Seizures 3 - 4%
Device-related 2 - 26%Lead fractureLead migration
Stimulation-relatedUsually transient, resolve with adjustments to stimulationHeadache, nausea, diplopia, vertica gaze palsy, nystagmus, uncomfortable paresthesias, unpleasant stimulation side effects
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Cluster Headache
Unilateral headache syndrome
Pain mainly located in orbitotemporal region
Abrupt onset and cessation
Pain last 15 – 3 hours (HIS criteria)
One or multiple attacks per day
Autonomic symptoms
“Cluster periods” lasting weeks to months
Episodic or chronic forms
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Surgical Treatment for Cluster Headache
Microvascular decompression of trigeminal nerve
Ablative trigeminal procedures
RF rhizotomy
Glycerol rhizolysis
Stereotactic radiosurgery
Section of nervus intermedius
Destruction of sphenopalatine ganglion
Deep brain stimulation
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Proposed Eligibilty Criteria for DBS in Patients with Cluster HA
Diagnosis of CH according to HIS criteriaSymptoms present at least 24 monthsCH attacks on daily basis
Symptoms strictly unilateralAll state-of-the-art medications have been tried singly or in combination“Normal psychological profileNo medical/neurological contraindications to DBSNormal neurological exam and imaging studiesPatient agrees to discontinue smoking and/or EtOH consumption
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DBS for Cluster Headache“Stimulation of the Posterior Hypothalamus for Treatment of Chronic Intractable Cluster Headache: First Reported Series” Neurosurgery (2003)
Stim. Parameters: Amp=.7-3V, PW=60, Rate=180 Hz
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Nucleus Caudalis DREZ Procedure
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Indications for Caudalis DREZ
Trigeminal deafferentation pain (following RF lesion)Recurrent refractory trigeminal neuralgiaTrigeminal neuropathic pain (post-traumatic)Post-herpetic neuralgiaCentral pain following brainstem infarctionCluster headacheIntractable migraine headacheAtypical facial painCancer pain
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Anatomical Landmarks
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Caudalis DREZ ResultsVAS Scores
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VAS Score
Pre-op VAS 7.6 9.5 8.7 8.8
Post-op VAS 6.1 6.6 8.4 7.6
AFP PHN TN Overall
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Caudalis DREZ ResultsPercent Improvement
0
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70
Immediate 69 42 14 32
Late 48 41 29 30
AFP PHN TN Overall
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Occipital Neuralgia and Occipital Headache
Syndromes
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Occipital NeuralgiaPain within the distribution of the greater and/or lesser occipital nerves
Neuralgic variant
Sharp, shooting, electric-like pain
Almost always unilateral
Bursts of pain lasting for several seconds to few minutes
Non-neuralgic variant
Dull, aching, throbbing, pounding pain
More constant pain
Often bilateral
Sensory dysfunction in C2 nerve territory
Responds to local blockade of occipital nerve
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Causes of Occipital NeuralgiaIdiopathicPost-traumaticSpinal Disorders
C1 fractureC1-2 instabilityRA with cranial settlingC1-2 arthrosis syndromeHypertrophic facet joint
Inflammatory disorders
Post-OperativeVP shuntRetromastoid craniectomyMastoidectomy
Chiari malformationMetabolic disordersVascular lesionsTumors
Evaluation: Plain X-rays, CT, MRI
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Chiari I Malformation
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Basilar Invagination
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Schwannoma of GON
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Intradural Schwannoma
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Chronic Daily Headache
Chronic migraine subset
Headache present at least 15 days per month
Near daily to continuous pain
Incidence 4% to 5%
Up to 50% unresponsive to medication
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OCCIPITAL NERVE STIMULATION FOR OCCITAL
HEADACHE SYNDROMES
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Indications for ONS
Appropriate clinical condition
Condition refractory to non-operative therapy
Acceptable psychological profile
Positive response to local anesthetic block
Positive response to temporary stimulation trial
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ONS - Technique
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ONS – Electrode Position
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Complications of ONS
Infection
Connector erosion
Electrode migration
Electrode fracture
Motor stimulation
Stimulation tolerance
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130 patients
Average duration of symptoms – 8 years
Unilateral – 88; Bilateral – 42
Mean VAS score – 9.2 (5-10)
Occipital Nerve Stimulation Outcome
Weiner, R
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Results of ONS
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Excellent Good Fair Poor0
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Pre-Op VAS Post-Op VAS
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Chronic Migraine
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Cluster Headache
(May, Bahra, Buchel, Frackowiak & Goadsby, Lancet 1998)