Trigeminal Neuralgia (TN) has been called the Suicide Disease. The medical community typically considers carbamazepine and oxcarbazepine as First Line Treatment. I suggest that for many patients Sphenopalatine Ganglion Blocks are a far safer and offer a far more effective first line approach to addressing Trigeminal Neuralgia (TN) without a multitude of medication side effects. Side effects of Carbamazepine (Tegretol) and oxcarbazepine (Trileptal) include:
- dizziness, lightheadedness or fainting
- dry mouth,
- swollen tongue,
- loss of balance or coordination.
- Mental Slowness
- Trouble Concentrating and/or memory problems.
- Trouble Sleeping
- Trouble Walking
- Changes in Vision
- Uncontrolled muscle movements
- Chest Pain
- Bleeding or Bruising
- Stomach Pain
- Changes in vision
- Bloody Stool
- Dark urine or change in volume of urine
Trigeminal neuralgia is probably the most painful chronic pain known and it affects the trigeminal nerve, which carries sensation from your face to your brain. Trigeminal neuralgia, even slight touch or wind on your face or activities like brushing your teeth or putting on makeup can trigger a jolt of excruciating pain.
TN sufferers may experience short, mild attacks initially but it can progress causing longer and more-frequent bouts of searing, shooting or burning pain. TN affects women more often than men, and it occurs more frequently in people who are older than 50.
Because of the variety of treatment options available, having trigeminal neuralgia doesn’t necessarily mean you’re doomed to a life of pain. Doctors usually can effectively manage trigeminal neuralgia with medications, injections or surgery.
There are a wide variety of treatments for Trigeminal Neuralgia. One of the least invasive and frequently successful alternatives treatments is Sphenopalatine Ganglion Blocks (SPG Blocks) also called Pterygopalatine Ganglion Blocks or Nasal Ganglion Blocks.
The best method of delivering SPG Blocks is with a cotton tipped nasal catheter, and I will explain further after discussing more common methods. Trigeminal Neuralgia patients especially seem to respond well to the use of cotton tipped nasal catheters.
SPG Blocks can be administered in multiple ways. There are multiple methods of Injection both intraoral and extraoral. They can be done with or without fluoroscopy though it is rarely needed can offer, The Suprazygomatic injection is the most reliable in my practice.
There are also multiple means of delivering Sphenopalatine Ganglion Blocks with nasal Catheters. There are three commercial brands of nasal catheters specifically designed for SPG Blocks.
The Sphenocath nasal is what I utilize in my office for a patients who are not good candidates for the cotton tipped nasal catheter. The Allevio is similar to the Sphenocath as well. The third type is the TX360. It is the device utilized for the MiRX protocol. All three devices are basically squirt guns that shoot anesthetic over the mucosa covering the Shenopalatine Ganglion.
I feel that the cotton tipped nasal catheters are by far the best delivery method for multiple reasons.
1. The supply a continuous capillary feed of anesthetic to the mucosa over the ganglion. Even if an exact location is missed the continuous feed guarantees that the anesthetic flows to the proper area.
2. They are relatively easy for patients to self administer. Frequency of doing the Block is key to the highest success. I generally have patients due the blocks twice a day initially until the pain is well controlled.
3. Convenience of a self administered block avoids trips to the physician or ER, travel, wait times etc.
4. Cost is a major factor. All other methods are very expensive running from $700 to thousands of dollars per application. Self-administered after initial appointment is approximately$1.00 per bilateral application.
5. Highest Success due to more frequent use secondary to low cost and convenience
Side effects of SPG Blocks:
- most common is slight nasal irritation
- reduction of high blood pressure
- reduced sympathetic activity
- reduced anxiety
- self of well being or calm
- Beneficial body effects of lidocaine
SPG Blocks: Patient Stories and Testimonials:
Neuromuscular Dntistry also has been shown to calm down the Trigeminal Nervous system. The ULF TENS or Myomonitor is a safe and effective stimulator of the Sphenopalatine Ganglion that is primarily designed to relax masticatory muscles. Reduction of excessive input to the trigeminal system with the myomonitor also decreases irritability of trigeminal nerves.
I advise that no one considers the following Neurolytic Agent treatments unless they first try regular administration of twice daily self-administered SPG Blocks.
Neurolytic agents may provide a longer duration of pain relief by causing destruction of nerve fibers and wallerian degeneration of axonal fibers and Schwann cells. The neurons regenerate in 3-5 months. 1-2 weeks may be required before complete pain relief is experienced.
Neurolytic agents used in trigeminal nerve blocks:
Glycerol (100%) – This agent is frequently utilized for treating trigeminal neuralgia; it is a mild neurolytic agent, but it can cause perineural damage.
Alcohol (50-70%) –This has a high rate of complications; it can seep into surrounding tissues and cause necrosis and permanentcellular injury, and it can also cause vasospasm. I do not Recomend it’s use.
Phenol (4-10%) – This agent is also commonly used; it can cause warmth and numbness on injection. It can cause convulsions and cardiovascular collapse if inadvertently injected intravascularly (into blood vessels)
Curr Pain Headache Rep. 2017 Jun;21(6):27. doi: 10.1007/s11916-017-0626-8.
Sphenopalatine Ganglion Block in the Management of Chronic Headaches.
PURPOSE OF REVIEW:
Sphenopalatine ganglion (SPG) block has been used by clinicians in the treatment of a variety of headache disorders, facial pain syndromes, and other facial neuralgias. The sensory and autonomic fibers that travel through the SPG provided the scientific rationale for symptoms associated with these head and neck syndromes. Yet, despite the elucidation of this pathogenic target, the optimal method to block its pain-producing properties has not been determined. Clinicians have developed various invasive and non-invasive techniques, each of which has shown variable rates of success. We examined the available studies of sphenopalatine ganglion blockade and its efficacy in the treatment of cluster headaches, migraines, and other trigeminal autonomic cephalalgias.
Studies have demonstrated that SPG blockade and neurostimulation can provide pain relief in patients with cluster headaches, migraines, and other trigeminal autonomic cephalalgias. Patients with these conditions showed varying levels and duration of pain relief from SPG blockade. The efficacy of SPG blockade could be related to the different techniques targeting the SPG and choice of therapeutic agents. Based on current studies, SPG blockade is a safe and effective treatment for chronic headaches such as cluster headaches, migraines, and other trigeminal autonomic cephalalgias. Future studies are warranted to define the optimal image-guided technique and choice of pharmacologic agents for SPG blockade as an effective treatment for chronic headaches related to activation of the sphenopalatine ganglion.
Cluster headache; Hemicrania continua; Migraine headache; Paroxysmal hemicrania; Sphenopalatine ganglion block; Trigeminal autonomic cephalalgias
Sphenopalatine ganglion block: a safe and easy method for the management of orofacial pain.
The sphenopalatine ganglion (SPG) block is a safe, easy method for the control of acute or chronic pain in any pain management office. It takes only a few moments to implement, and the patient can be safely taught to effectively perform this pain control procedure at home with good expectations and results. Indications for the SPG blocks include pain of musculoskeletal origin, vascular origin and neurogenic origin. It has been used effectively in the management of temporomandibular joint (TMJ) pain, cluster headaches, tic douloureux, dysmenorrhea, trigeminal neuralgia, bronchospasm and chronic hiccup.
The pterygopalatine ganglion and its role in various pain syndromes: from anatomy to clinical practice.
- Pain Pract. 2012 Nov;12(8):673.
The postsynaptic fibers of the pterygopalatine or sphenopalatine ganglion (PPG or SPG) supply the lacrimal and nasal glands. The PPG appears to play an important role in various pain syndromes including headaches, trigeminal and sphenopalatine neuralgia, atypical facial pain, muscle pain, vasomotor rhinitis, eye disorders, and herpes infection. Clinical trials have shown that these pain disorders can be managed effectively with sphenopalatine ganglion blockade (SPGB). In addition, regional anesthesia of the distribution area of the SPGsensory fibers for nasal and dental surgery can be provided by SPGB via a transnasal, transoral, or lateral infratemporal approach. To arouse the interest of the modern-day clinicians in the use of the SPGB, the advantages, disadvantages, and modifications of the available methods for blockade are discussed.▪
© 2011 The Authors. Pain Practice © 2011 World Institute of Pain.
A novel revision to the classical transnasal topical sphenopalatine ganglion block for the treatment of headache and facial pain.
The sphenopalatine ganglion (SPG) is located with some degree of variability near the tail or posterior aspect of the middle nasal turbinate. The SPG has been implicated as a strategic target in the treatment of various headache and facial pain conditions, some of which are featured in this manuscript. Interventions for blocking the SPG range from minimally to highly invasive procedures often associated with great cost and unfavorable risk profiles.
The purpose of this pilot study was to present a novel, FDA-cleared medication delivery device, the Tx360® nasal applicator, incorporating a transnasal needleless topical approach for SPG blocks. This study features the technical aspects of this new device and presents some limited clinical experience observed in a small series of head and face pain cases.
Pain management center, part of teaching-community hospital, major metropolitan city, United States.
After Institutional Review Board (IRB) approval, the technical aspects of this technique were examined on 3 patients presenting with various head and face pain conditions including trigeminal neuralgia (TN), chronic migraine headache (CM), and post-herpetic neuralgia (PHN). The subsequent response to treatment and quality of life was quantified using the following tools: the 11-point Numeric Rating Scale (NRS), Modified Brief Pain Inventory – short form (MBPI-sf), Patient Global Impression of Change (PGIC), and patient satisfaction surveys. The Tx360® nasal applicator was used to deliver 0.5 mL of ropivacaine 0.5% and 2 mg of dexamethasone for SPG block. Post-procedural assessments were repeated at 15 and 30 minutes, and on days one, 7, 14, and 21 with a final assessment at 28 days post-treatment. All patients were followed for one year. Individual patients received up to 10 SPG blocks, as clinically indicated, after the initial 28 days.
Three women, ages 43, 18, and 15, presented with a variety of headache and face pain disorders including TN, CM, and PHN. All patients reported significant pain relief within the first 15 minutes post-treatment. A high degree of pain relief was sustained throughout the 28 day follow-up period for 2 of the 3 study participants. All 3 patients reported a high degree of satisfaction with this procedure. One patient developed minimal bleeding from the nose immediately post-treatment which resolved spontaneously in less than 5 minutes. Longer term follow-up (up to one year) demonstrated that additional SPG blocks over time provided a higher degree and longer lasting pain relief.
Controlled double blind studies with a higher number of patients are needed to prove efficacy of this minimally invasive technique for SPG block.
SPG block with the Tx360® is a rapid, safe, easy, and reliable technique to accurately deliver topical transnasal analgesics to the area of mucosa associated with the SPG. This intervention can be delivered in as little as 10 seconds with the novice provider developing proficiency very quickly. Further investigation is certainly warranted related to technique efficacy, especially studies comparing efficacy of Tx360 and standard cotton swab techniques.
Additional References that may be of interest:
|1.||The International Classification of Headache Disorders. 2nd edition. Cephalalgia 2004; 24 (Suppl) 1: 9-160. Google Scholar|
|2.||Magis D, Jensen R, Schoenen J. Neurostimulation therapies for primary headache disorders: Present and future. Curr Opin Neurol 2012; 25: 269–276. Google Scholar Crossref, Medline|
|3.||Barbanti P, Fabbrini G, Pesare M, . Unilateral cranial autonomic symptoms in migraine. Cephalalgia 2002; 22: 256–259. Google Scholar Link|
|4.||Lai TH, Fuh JL, Wang SJ. Cranial autonomic symptoms in migraine: Characteristics and comparison with cluster headache. J Neurol Neurosurg Psychiatry 2009; 80: 1116–1119. Google Scholar Crossref, Medline|
|5.||Gupta R, Bhatia MS. A report of cranial autonomic symptoms in migraineurs. Cephalalgia 2007; 27: 22–28. Google Scholar Link|
|6.||Obermann M, Yoon MS, Dommes P, . Prevalence of trigeminal autonomic symptoms in migraine: A population-based study. Cephalalgia 2007; 27: 504–509. Google Scholar Link|
|7.||Gelfand AA, Reider AC, Goadsby PJ. Cranial autonomic symptoms in pediatric migraine are the rule, not the exception. Neurology 2013; 81: 431–436. Google Scholar Crossref, Medline|
|8.||Goadsby PJ, Lipton RB. A review of paroxysmal hemicranias, SUNCT syndrome and other short-lasting headaches with autonomic feature, including new cases. Brain 1997; 120 (Pt 1: 193–209. Google ScholarCrossref, Medline|
|9.||Sluder G. The role of the sphenopalatine (or Meckel’s) ganglion in nasal headaches. N Y State J Med 1908; 27: 8–13. Google Scholar|
|10.||Lad SP, Lipani JD, Gibbs IC, . Cyberknife targeting the pterygopalatine ganglion for the treatment of chronic cluster headaches. Neurosurgery 2007; 60: E580–E581; discussion E1. Google Scholar Crossref, Medline|
|11.||Maizels M, Geiger AM. Intranasal lidocaine for migraine: A randomized trial and open-label follow-up. Headache 1999; 39: 543–551. Google Scholar Crossref, Medline|
|12.||Narouze S, Kapural L, Casanova J, . Sphenopalatine ganglion radiofrequency ablation for the management of chronic cluster headache. Headache 2009; 49: 571–577. Google Scholar Crossref, Medline|
|13.||Meyer JS, Binns PM, Ericsson AD, . Sphenopalatine gangionectomy for cluster headache. Arch Otolaryngol 1970; 92: 475–484. Google Scholar Crossref, Medline|
|14.||Uddman R, Hara H, Edvinsson L. Neuronal pathways to the rat middle meningeal artery revealed by retrograde tracing and immunocytochemistry. J Auton Nerv Syst 1989; 26: 69–75. Google Scholar Crossref, Medline|
|15.||Walters BB, Gillespie SA, Moskowitz MA. Cerebrovascular projections from the sphenopalatine and otic ganglia to the middle cerebral artery of the cat. Stroke 1986; 17: 488–494. Google Scholar Crossref, Medline|
|16.||Hara H, Zhang QJ, Kuroyanagi T, . Parasympathetic cerebrovascular innervation: An anterograde tracing from the sphenopalatine ganglion in the rat. Neurosurgery 1993; 32: 822–827; discussion 7. Google Scholar Crossref, Medline|
|17.||van der Werf F, Baljet B, Prins M, . Innervation of the lacrimal gland in the cynomolgous monkey: A retrograde tracing study. J Anat 1996; 188 (Pt 3: 591–601. Google Scholar Medline|
|18.||Sibony PA, Walcott B, McKeon C, . Vasoactive intestinal polypeptide and the innervation of the human lacrimal gland. Arch Ophthalmol 1988; 106: 1085–1088. Google Scholar Crossref, Medline|
|19.||Lundberg JM, Anggård A, Emson P, . Vasoactive intestinal polypeptide and cholinergic mechanisms in cat nasal mucosa: Studies on choline acetyltransferase and release of vasoactive intestinal polypeptide. Proc Natl Acad Sci U S A 1981; 78: 5255–5259. Google Scholar Crossref, Medline|
|20.||Ten Tusscher MP, Klooster J, Baljet B, . Pre- and post-ganglionic nerve fibres of the pterygopalatine ganglion and their allocation to the eyeball of rats. Brain Res 1990; 517: 315–323. Google Scholar Crossref, Medline|
|21.||van der Werf F, Baljet B, Prins M, . Innervation of the superior tarsal (Müller’s) muscle in the cynomolgus monkey: A retrograde tracing study. Invest Ophthalmol Vis Sci 1993; 34: 2333–2340. Google Scholar Medline|
|22.||Moore KL, Dalley AF. Clinically oriented anatomy 20065th edn. Baltimore, USA: Lippincott Williams & Wilkins. Google Scholar|
|23.||Moskowitz MA, Macfarlane R. Neurovascular and molecular mechanisms in migraine headaches. Cerebrovasc Brain Metab Rev 1993; 5: 159–177. Google Scholar Medline|
|24.||Moskowitz MA. The neurobiology of vascular head pain. Ann Neurol 1984; 16: 157–168. Google Scholar Crossref, Medline|
|25.||Iversen HK, Nielsen TH, Olesen J, . Arterial responses during migraine headache. Lancet 1990; 336: 837–839. Google Scholar Crossref, Medline|
|26.||Friberg L, Olesen J, Iversen HK, . Migraine pain associated with middle cerebral artery dilatation: Reversal by sumatriptan. Lancet 1991; 338: 13–17. Google Scholar Crossref, Medline|
|27.||Asghar MS, Hansen AE, Amin FM, . Evidence for a vascular factor in migraine. Ann Neurol 2011; 69: 635–645. Google Scholar Crossref, Medline|
|28.||Goadsby PJ. Sphenopalatine ganglion stimulation increases regional cerebral blood flow independent of glucose utilization in the cat. Brain research 1990; 506: 145–148. Google Scholar Crossref, Medline|
|29.||Delépine L, Aubineau P. Plasma protein extravasation induced in the rat dura mater by stimulation of the parasympathetic sphenopalatine ganglion. Exp Neurol 1997; 147: 389–400. Google Scholar Crossref, Medline|
|30.||Yarnitsky D, Lorian A, Shalev A, . Reversal of cerebral vasospasm by sphenopalatine ganglion stimulation in a dog model of subarachnoid hemorrhage. Surg Neurol 2005; 64: 5–11; discussion 11. Google ScholarCrossref, Medline|
|31.||Bar-Shir A, Shemesh N, Nossin-Manor R, . Late stimulation of the sphenopalatine-ganglion in ischemic rats: Improvement in N-acetyl-aspartate levels and diffusion weighted imaging characteristics as seen by MR. J Magn Reson Imaging 2010; 31: 1355–1363. Google Scholar Crossref, Medline|
|32.||Takahashi M, Zhang ZD, Macdonald RL. Sphenopalatine ganglion stimulation for vasospasm after experimental subarachnoid hemorrhage. J Neurosurg 2011; 114: 1104–1109. Google Scholar Crossref, Medline|
|33.||Levi H, Schoknecht K, Prager O, . Stimulation of the sphenopalatine ganglion induces reperfusion and blood-brain barrier protection in the photothrombotic stroke model. PloS One 2012; 7: e39636–e39636. Google Scholar Crossref, Medline|
|34.||May A, Goadsby PJ. The trigeminovascular system in humans: Pathophysiologic implications for primary headache syndromes of the neural influences on the cerebral circulation. J Cereb Blood Flow Metab 1999; 19: 115–127. Google Scholar Link|
|35.||Goadsby PJ, Lipton RB, Ferrari MD. Migraine—current understanding and treatment. N Engl J Med 2002; 346: 257–270. Google Scholar Crossref, Medline|
|36.||Gonzalez G, Onofrio BM, Kerr FW. Vasodilator system for the face. J Neurosurg 1975; 42: 696–703. Google Scholar Crossref, Medline|
|37.||Goadsby PJ, Lambert GA, Lance JW. The peripheral pathway for extracranial vasodilatation in the cat. J Auton Nerv Syst 1984; 10: 145–155. Google Scholar Crossref, Medline|
|38.||Drummond PD. The mechanism of facial sweating and cutaneous vascular responses to painful stimulation of the eye. Brain 1992; 115 (Pt 5: 1417–1428. Google Scholar Crossref, Medline|
|39.||Goadsby PJ, Duckworth JW. Effect of stimulation of trigeminal ganglion on regional cerebral blood flow in cats. Am J Physiol 1987; 253 (2 Pt 2): R270–R274. Google Scholar|
|40.||Lang R, Zimmer R. Neurogenic control of cerebral blood flow. Exp Neurol 1974; 43: 143–161. Google Scholar Crossref, Medline|
|41.||Lambert GA, Bogduk N, Goadsby PJ, . Decreased carotid arterial resistance in cats in response to trigeminal stimulation. J Neurosurg 1984; 61: 307–315. Google Scholar Crossref, Medline|
|42.||Frese A, Evers S, May A. Autonomic activation in experimental trigeminal pain. Cephalalgia 2003; 23: 67–68. Google Scholar Link|
|43.||May A, Büchel C, Turner R, . Magnetic resonance angiography in facial and other pain: Neurovascular mechanisms of trigeminal sensation. J Cereb Blood Flow Metab 2001; 21: 1171–1176. Google Scholar Link|
|44.||Drummond PD. Lacrimation and cutaneous vasodilatation in the face induced by painful stimulation of the nasal ala and upper lip. J Auton Nerv Syst 1995; 51: 109–116. Google Scholar Crossref, Medline|
|45.||Olesen J, Goadsby PJ, Ramadan NH, . The Headaches, 3rd edn. Philadelphia: Lippincott Williams & Wilkins, 2006. Google Scholar|
|46.||Avnon Y, Nitzan M, Sprecher E, . Autonomic asymmetry in migraine: augmented parasympathetic activation in left unilateral migraineurs. Brain 2004; 127: 2099–2108. Google Scholar Crossref, Medline|
|47.||Drummond PD. Photophobia and autonomic responses to facial pain in migraine. Brain 1997; 120 (Pt 10): 1857–1864. Google Scholar Crossref, Medline|
|48.||Micieli G, Tassorelli C, Magri M, . Vegetative imbalance in migraine. A dynamic TV pupillometric evaluation. Funct Neurol 1989; 4: 105–111. Google Scholar Medline|
|49.||Havanka-Kanniainen H, Tolonen U, Myllylä VV. Autonomic dysfunction in adult migraineurs. Headache 1986; 26: 425–430. Google Scholar Crossref, Medline|
|50.||Pogacnik T, Sega S, Pecnik B, . Autonomic function testing in patients with migraine. Headache 1993; 33: 545–550. Google Scholar Crossref, Medline|
|51.||Yakinci C, Mungen B, Er H, et al. Autonomic nervous system function in childhood migraine. Pediatr Int 1999; 41: 529–53352. Google Scholar|
|52.||Mosek A, Novak V, Opfer-Gehrking TL, et al. Autonomic dysfunction in migraineurs. Headache 1999; 39: 108–117. Google Scholar|
|53.||Sanya EO, Brown CM, von Wilmowsky C, . Impairment of parasympathetic baroreflex responses in migraine patients. Acta Neurol Scand 2005; 111: 102–107. Google Scholar Crossref, Medline|
|54.||Thomsen LL, Olesen J. The autonomic nervous system and the regulation of arterial tone in migraine. Clin Auton Res 1995; 5: 243–250. Google Scholar Crossref, Medline|
|55.||Avnon Y, Nitzan M, Sprecher E, . Different patterns of parasympathetic activation in uni- and bilateral migraineurs. Brain 2003; 126: 1660–1670. Google Scholar Crossref, Medline|
|56.||Goadsby PJ, Edvinsson L, Ekman R. Vasoactive peptide release in the extracerebral circulation of humans during migraine headache. Ann Neurol 1990; 28: 183–187. Google Scholar Crossref, Medline|
|57.||Burstein R, Jakubowski M. Unitary hypothesis for multiple triggers of the pain and strain of migraine. J Comp Neurol 2005; 493: 9–14. Google Scholar Crossref, Medline|
|58.||Levy D, Strassman AM, Burstein R. A critical view on the role of migraine triggers in the genesis of migraine pain. Headache 2009; 49: 953–957. Google Scholar Crossref, Medline|
|59.||Yarnitsky D, Goor-Aryeh I, Bajwa ZH, . 2003 Wolff Award: Possible parasympathetic contributions to peripheral and central sensitization during migraine. Headache 2003; 43: 704–714. Google Scholar Crossref, Medline|
|60.||Hilz MJ, Dutsch M, Perrine K, . Hemispheric influence on autonomic modulation and baroreflex sensitivity. Ann Neurol 2001; 49: 575–584. Google Scholar Crossref, Medline|
|61.||Oppenheimer SM, Gelb A, Girvin JP, . Cardiovascular effects of human insular cortex stimulation. Neurology 1992; 42: 1727–1732. Google Scholar Crossref, Medline|
|62.||Yoon BW, Morillo CA, Cechetto DF, . Cerebral hemispheric lateralization in cardiac autonomic control. Arch Neurol 1997; 54: 741–744. Google Scholar Crossref, Medline|
|63.||Zamrini EY, Meador KJ, Loring DW, . Unilateral cerebral inactivation produces differential left/right heart rate responses. Neurology 1990; 40: 1408–1411. Google Scholar Crossref, Medline|
|64.||Akerman S, Holland PR, Lasalandra MP, . Oxygen inhibits neuronal activation in the trigeminocervical complex after stimulation of trigeminal autonomic reflex, but not during direct dural activation of trigeminal afferents. Headache 2009; 49: 1131–1143. Google Scholar Crossref, Medline|
|65.||Tepper SJ, Rezai A, Narouze S, . Acute treatment of intractable migraine with sphenopalatine ganglion electrical stimulation. Headache 2009; 49: 983–989. Google Scholar Crossref, Medline|
|66.||Ansarinia M, Rezai A, Tepper SJ, . Electrical stimulation of sphenopalatine ganglion for acute treatment of cluster headaches. Headache 2010; 50: 1164–1174. Google Scholar Crossref, Medline|
|67.||Schoenen J, Jensen RH, Lantéri-Minet M, . Stimulation of the sphenopalatine ganglion (SPG) for cluster headache treatment. Pathway CH-1: A randomized, sham-controlled study. Cephalalgia 2013; 33: 816–830. Google Scholar Link|
|68.||Magis D, Gerardy PY, Remacle JM, . Sustained effectiveness of occipital nerve stimulation in drug-resistant chronic cluster headache. Headache 2011; 51: 1191–1201. Google Scholar Crossref, Medline|
|69.||Magis D, Schoenen J. Advances and challenges in neurostimulation for headaches. Lancet Neurol 2012; 11: 708–719. Google Scholar Crossref, Medline|
|70.||Magis D, Bruno MA, Fumal A, . Central modulation in cluster headache patients treated with occipital nerve stimulation: An FDG-PET study. BMC Neurol 2011; 11: 25–25. Google Scholar Crossref, Medline|
|71.||Bartsch T, Goadsby PJ. Stimulation of the greater occipital nerve induces increased central excitability of dural afferent input. Brain 2002; 125: 1496–1509. Google Scholar Crossref, Medline|
|72.||Burns B, Watkins L, Goadsby PJ. Treatment of intractable chronic cluster headache by occipital nerve stimulation in 14 patients. Neurology 2009; 72: 341–345. Google Scholar Crossref, Medline|
|73.||Magis D, Allena M, Bolla M, . Occipital nerve stimulation for drug-resistant chronic cluster headache: A prospective pilot study. Lancet Neurol 2007; 6: 314–321. Google Scholar Crossref, Medline|
|74.||Schoenen J, Vandersmissen B, Jeangette S, . Migraine prevention with a supraorbital transcutaneous stimulator: A randomized controlled trial. Neurology 2013; 80: 697–704. Google Scholar Crossref, Medline|
|75.||Melzack R, Wall PD. Pain mechanisms: A new theory. Science 1965; 150: 971–979. Google Scholar Crossref, Medline|
|76.||DeSantana JM, Da Silva LF, De Resende MA, . Transcutaneous electrical nerve stimulation at both high and low frequencies activates ventrolateral periaqueductal grey to decrease mechanical hyperalgesia in arthritic rats. Neuroscience 2009; 163: 1233–1241. Google Scholar Crossref, Medline|
|77.||Burns B, Watkins L, Goadsby PJ. Treatment of medically intractable cluster headache by occipital nerve stimulation: Long-term follow-up of eight patients. Lancet 2007; 369: 1099–1106. Google Scholar Crossref, Medline|
|78.||Blau JN. Migraine prodromes separated from the aura: Complete migraine. Br Med J 1980; 281: 658–660. Google Scholar Crossref, Medline|
|79.||Blau JN. Migraine pathogenesis: The neural hypothesis reexamined. J Neurol Neurosurg Psychiatry 1984; 47: 437–442. Google Scholar Crossref, Medline|
|80.||Maniyar F, Sprenger T, Schankin C, . Imaging the premonitory phase of migraine—new insights into generation of the migraine attack. J Headache Pain 2013; 14(Suppl 1): P112–P112. Google Scholar Crossref|
|81.||Koo B. EEG changes with vagus nerve stimulation. J Clin Neurophysiol 2001; 18: 434–441. Google Scholar Crossref, Medline|
|82.||Englot DJ, Chang EF, Auguste KI. Vagus nerve stimulation for epilepsy: A meta-analysis of efficacy and predictors of response. J Neurosurg 2011; 115: 1248–1255. Google Scholar Crossref, Medline|
|83.||Krahl SE. Vagus nerve stimulation for epilepsy: A review of the peripheral mechanisms. Surg Neurol Int 2012; 3(Suppl 1): S47–S52. Google Scholar Crossref, Medline|