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Diagnosis and Management of Craniofacial Pain

Diagnosis and Management of Craniofacial Pain

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Diagnosis and Management of Craniofacial Pain

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  1. Diagnosis and Management of Craniofacial Pain Richard K. Osenbach, M.D. Director, Neurosurgical Services Cape Fear Valley Medical Center

  2. 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

  3. Approach to the patient with craniofacial pain • Specific pain syndromes • Pharmacological Management • Surgical Treatments

  4. Approach to the Patient with Craniofacial Pain • Single most important aspect is to ESTABLISH THE CORRECT DIAGNOSIS • Careful detailed pain history • Location • Duration • Temporal characteristics • Quality • Severity • Circumstances of onset • Influencing factors • Neurological symptoms • Response to medications • The more paroxysmal the pain, the more likely that surgery may be beneficial

  5. Trigeminal neuralgia Trigeminal neuropathic Postherpetic trigeminal pain Glossopharyngeal neuralgia Geniculate neuralgia Occipital neuralgia Sphenopalatine neuralgia Vidian neuralgia Superior laryngeal neuralgia Carotidynia Neuropathic Craniofacial Pain Syndromes

  6. Headache Syndromes • Classic 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.

  7. 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

  8. Otologic Problems • Otitis externa and interna • Ramsey-Hunt Syndrome • Bullous myringitis • Tumors • Mastoiditis

  9. Dental and Periodontal Pathology • Periodontal abscess • Bruxism • Burning mouth syndrome • Temporomandibular joint disorders


  11. Classification of Facial Pain • Trigeminal 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

  12. Pharmacological Therapy • Anti-epileptics drugs (AEDs) • Antidepressant medications • Opiates • Neuroleptics • Antispasmodics • Miscellaneous drugs • Botox

  13. 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.

  14. Tegretol (carbamazepine) Trileptal (oxcarbazepine) Neurontin (gabpentin) Lyrica (pregabalin) Dilantin (phenytoin) Depakote (valproic acid) Topamax (topirimate) Lamictal (lamotrigene) Keppra (levateracitam) Gabatril Benzodiazepines Antiepileptic Agents

  15. 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

  16. AEDS Studied in Neuropathic Pain

  17. Mechanisms of Selected AEDS • Carbamazepine (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

  18. Adverse Effects of AEDs • Allergic reaction • Up to 7% with CBZ • Some cross-reactivity between CBZ and PHT • Cognitive changes • Sedation • Nystagmus, ataxia, diplopia, dizziness • Nausea, vomiting, headache

  19. Adverse Effects of 2nd Generation AEDS

  20. 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

  21. Descending Pain Modulation • Endorphin link from PAG to pontine raphe nuclei • Serotonergic conection to spinal dorsal horn • Noradrenergic pathway from locus ceruleus to dorsal horn

  22. Antidepressant AnalgesicsCurrent Evidence • Relieves all components of neuropathic pain • RCT - clear separation of analgesic and antidepressant effects • Although other agents (eg anti-epileptics)) may be regarded as 1st line therapy over antidepressants, there is no good evidence for this practice • More selective agents are either less effective or not useful (serotonergic, noradrenergic) • Because of incomplete efficacy, combination therapy may be needed • Comparative data regarding other drugs using NNT figures now exists

  23. Antidepressants in Neuropathic Pain-RCT • Watson et al.: reviewed 29 randomized clinical trials • 16 involved PHN or PDN • Mixed SN agents – 18/21 + effects • Amitriptyline 10/13, Imipramine 5/5,Doxepin 1/1, Venlafexline 2/2 • NA – 10/12 + effects • Nortriptyline 3/4, desipramine 4/5, maprotiline 2/2, bupropion 1/1 • Serotonergic agents – 4/5 + effects • Paroxetine 1/2, clomipramine 2/2, citalopram 1/1

  24. Adverse Effect of Antidepressants • Anti-cholinergic autonomic effects (TCAs) • Allergic and hypresensitivity reactions • Cardiovascular effects • Orthostatic hypotension (avoid imipramine in elderly) • Quinidine-like cardiac effects • CNS effects • Sedation, tremor, seizures, atropine-like delerium, exacerbation of schizophrenia/mania • Acute overdose may be fatal (>2000mg) • Withdrawal reactions

  25. Guidelines for Use of Antidepressants in Pain Management • Eliminate all other ineffective analgesics • Start low and titrate slowly to effect or toxicity • Nortriptyline or amitriptyline for initial treatment • Move to agents with more noradrenergic effects • Consider trazadone in patients with poor sleep pattern • Try more selective agents if mixed agents ineffective • Do NOT prescribe monoamine oxidase inhibitors • Tolerance to anti-muscarinic side effects usually takes weeks to develop • Withdraw therapy gradually to avoid withdrawal syndrome

  26. 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

  27. 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

  28. Implementation of Opioid TherapyPrerequisites • Failure of pain management alternatives; but not a last resort • Opioids should only be use as part of a multimodality approach • Identification of realistic goals of treatment • Physical and psychosocial assessment by multidisciplinary team • Consider history of substance abuse as a relative contraindication • Decision to prescribe by multidisciplinary team or at least two practitioners • Informed written consent • Best practice – prescribe a trial of opioids and withdraw use if the provision of analgesia does not result in functional improvement

  29. 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 reliefand/or functional improvement

  30. 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)

  31. Opioid Therapy - RCT

  32. Opioid Therapy – Prospective Uncontrolled Studies

  33. 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

  34. Miscellaneous Agents • Antiarrhythmics - Mexilitene • Na+ channel blockade • Reduce neuronal hyperexcitability • Possible predictive effect of IV lidocaine challenge • May worsen AV conduction block • Monitor EKG, LFT, renal fxn • Significant incidence of treatment-limiting side effects • Baclofen • GABAB receptor antagonist • Efficacious in TN • Start 10mg QD and titrate until effect or sedation • Cannot abruptly withdraw drug!

  35. Trigeminal Branch Stimulation

  36. Trigeminal Branch Stimulation • Stimulation of supraorbital, infraorbital nerves • Indications • Trigeminal neuropathic pain • Trigeminal deafferentation pain • Post-herpetic neuralgia • Chronic daily headache

  37. Peripheral Trigeminal Branch Stimulation for Neuropathic PainJohnson M, Burchiel K, Neurosurgery, 2004 Pain Relief Medication Use Patient Satisfaction

  38. 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

  39. Motor Cortex Stimulation Motor cortex stimulation is NOT FDA approved and represents an off-label use of the implanted device

  40. History of MCS • Developed by Tsubokawa and colleagues during 1980s • Treatment of central deafferentation pain • Poststroke pain • Thalamic pain • Bulbar pain • Alternative to other methods of neuromodulation for • SCS • DBS • Discovered that stimulation of motor rather than sensory cortex produced better pain relief

  41. Sensory Cortex Sensory Cortex Motor Cortex Inhibitory Thalamus Thalamus Inhibitory DCN Dorsal Horn InInhibitory Nociceptive Input (Spinothalamic System) Non-noxious Input (DCML System) Relationship Between Spinothalamic and DCML System - Normal

  42. Thalamic Pain A, C-fiber A PNS

  43. Motor Cortex StimulationClinical Indications • Post-stroke pain • Post-herpetic neuralgia • Trigeminal neuropathic pain • Trigeminal deafferentation pain

  44. Transcranial Magnetic Stimulation

  45. Localization of Motor Cortex

  46. Complications • Stimulation-induced seizures • Pain at stimulation site • Epidural hematoma • CSF leak • Electrode fracture or migration • Infection

  47. 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

  48. Results of MCS

  49. 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?

  50. Deep Brain Stimulation Deep brain stimulation is NOT FDA approved for pain and represents an off-label use of the implanted device