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Monday, June 28, 2010

CLUSTER HEADACHES TREATMENT WITH ELECTRICAL STIMULATION OF SPHENOPALATINE GANGLION BLOCK.

Cluster Headaches are a type of primary headache that frequently occur at night and are characterize by autonomic phenomena and bouts of severe unilateral head pain. Spenopalatine Ganglion blocks are frequently used by neuromuscular dentists as an adjunct procedure in treating a multitue of painful conditions. A popular book "Miracles on Park Avenue: Technique for Treating Arthritis and Other Chronic Pain by Albert B. Gerber (Hardcover - Nov 1986)" discussed how SPG blocks were used to treat a multitude of diverse pain conditions with minmal risk. Many Neuromuscular Dentists utilize this valuable technique. I teach the technique of SPG blocks at my courses in treating sleep apnea (http://www.ihatecpap.com).

PATIENTS WITH MIGRAINES, CLUSTER HEADACHES AND OTHER PAINFUL CONDITIONS CAN BE TAUGHT A SIMPLE TECHNIQUE FOR SELF ADMINISTERED SPG BLOCKS (WITH LIDOCAINE)
THAT CAN COMPLETELY OR PARTIALLY ABORT ATTACKS AND REDUCE OR ELIMINATE SYMPTOMS AFTER AN ATTACK BEGINS.

An article in April Headache (SEE PUBMED abstract below) discusses the use of acute electrical stimulation in test subjects to relieve acute cluster headache symptoms.

Neuromuscular dentistry is unique in that the autonomic fibers of the Trigeminal Nerve that pass thru the Sphenopalatine Ganglion (also called the pterygopalatine ganglion) are stimulated with the use of ultra-low frequency TENS and is frequently effectiving in treating many types of headaches and migraines including cluster headaches. The Sphenoplatine Ganglion contains sensory fibers of the Maxillary division of the Trigeminal Nerve.

ACCORDING TO WIKIPEDIA:
The Sphenopalatine Ganglion "receives a sensory, a motor, and a sympathetic root.
Sensory root.
Its sensory root is derived from two sphenopalatine branches of the maxillary nerve; their fibers, for the most part, pass directly into the palatine nerves; a few, however, enter the ganglion, constituting its sensory root."

IT IS BELIEVED THAT NEUROMUSCULAR DENTISTRY HAS A MAJOR EFFECT ON THIS STRUCTURE THRU ITS SENSORY ROOT THAT NEUROMUSCULAR DENTISTRY STIMULATES WITH ULTRA LOW FREQUENCY ANTI-DROMIC STIMULATION . IT IS WELL KNOWN THAT MANY TYPES OF TREATMENT RESISTANT HEADACHES ARE IMPROVED OR ELIMINATED AFTER USE OF A DIAGNOSTIC NEUROMUSCULAR ORTHOTIC.

WIKIPEDIA ALSO STATES:
"Parasympathetic root
Its parasympathetic root is derived from the nervus intermedius (a part of the facial nerve) through the greater petrosal nerve.
In the pterygopalatine ganglion, the preganglionic parasympathetic fibers from the greater petrosal branch of the facial nerve synapse with neurons whose postganglionic axons, vasodilator and secretory fibers, are distributed with the deep branches of the TRIGEMINAL NERVE to the mucous membrane of the nose, soft palate, tonsils, uvula, roof of the mouth, upper lip and gums, and to the upper part of the pharynx. It also sends postganglionic parasympathetic fibers to the lacrimal gland via the zygomatic nerve, a branch of the maxillary nerve (from the trigeminal nerve) which then connects with the lacrimal nerve (a branch of the ophthalmic nerve, also part of the trigeminal nerve) to arrive at the lacrimal gland.
The nasal glands are innervated with secretomotor from the nasopalatine and greater palatine nerve. Similarly, the palatine glands are innervated by the nasopalatine, greater palatine nerve and lesser palatine nerves. The pharyngeal nerve innervates pharyngeal glands. These are all branches of maxillary nerve."

THIS EXPLAINS WHY NEUROMUSCULAR DENTISTRY FREQUENTLY RELIEVES AUTONOMIC ASPECTS OF HEADACHES. THERE IS A DECREASE IN NOCICEPTIVE (PAIN) INPUT TO THIS SENSORY CENTER THEREBY REDUCING THE AUTONOMIC SYMPTOMS ASSOCIATED WITH CLUSTER HEADACHES AND OTHER VASCULAR HEADACHES.

ANOTHER ARTICLE Curr Pain Headache Rep. 2010 Apr;14(2):160-3.
Role of sphenopalatine ganglion neuroablation in the management of cluster headache discusse electrical ablation of the sphenopalatine ganglion. I strong urge patients avoid this procedure except as a last resort. Previous attempts at Mayo met with disaster.

WIKIPEDIA ON THE SYMPATHETIC ROOT:
"The ganglion also consists of sympathetic efferent (postganglionic) fibers from the superior cervical ganglion. These fibers, from the superior cervical ganglion, travel through the carotid plexus, and then through the deep petrosal nerve. The deep petrosal nerve joins with the greater petrosal nerve to form the nerve of the pterygoid canal, which enters the ganglion. "

THE CONNECTIONS TO THE CERVICAL GANGLION AND CAROTID PLEXUS EXPLAIN THE CERVICAL CONNECTION AND EFFECTS ON BLOOD FLOW. THE TRIGEMNAL NERVE ALSO CONTROLS THE BLOOD FLOW TO THE BRAIN BY CONTROL OF BLOOD FLOWTHRU THE MEMINGES OF THE BRAIN.

Another study J Neurophysiol. 2010 Jan;103(1):172-82. Epub 2009 Nov 4.
Muscarinic acetylcholine receptor modulation of mu (mu) opioid receptors in adult rat sphenopalatine ganglion neurons. showed that "These results suggest that in rat SPG neurons activation of M(2) mAChR likely modulates opioid transmission in the brain vasculature to adequately maintain cerebral blood flow." THE MODULATION OF OPIOD RECEPTORS AND CONTROL OF VASCULAR FLOW TO THE BRAIN IS CENTRAL TO MANAGEMENT OF CLUSTER HEADACHES, MIGRAINES ANDOTHER TYPES OF VASCULAR HEADACHES.

NEUROMUSCULAR DENTISTRY IS EXTREMELY EFFECTIVE IN TREATING A WIDE VARIETY OF HEADACHES INCLUDING CLUSTER HEADACHES, SUNCT, CLASSICAL MIGRAINE, ATYPICAL MIGRANE AND OTHER VASCULAR HEADACHES AS WELL AS TENSION-TYPE HEADACHES, CHRONIC DAILY HEADACHES, SINUS HEADACHES AND A WIDE VARIETY OF FACIAL AND CRANIAL PAIN AND/OR DYSFUNCTION.

THE USE OF OXYGEN ON CLUSTER HEADACHE IS EFFECTIVE DUE TO INHIBITION OFTRIGEMINOCERVIAL COMPLEX ACCORDING TO AN ARTICLE IN Headache. 2009 Sep;49(8):1131-43. (SEE PUBMED ABSTRACT BELOW)
Oxygen inhibits neuronal activation in the trigeminocervical complex after stimulation of trigeminal autonomic reflex, but not during direct dural activation of trigeminal afferents. THE ARTICLE CLEARLY STATES THAT CLUSTER HEADACHES ARE A TRIGEMINAL AUTONOMIC CONDITION "To understand the mechanism of action of oxygen treatment in cluster headache. BACKGROUND: Trigeminal autonomic cephalalgias, including cluster headache, are characterized by unilateral head pain in association with ipsilateral cranial autonomic features. They are believed to involve activation of the trigeminovascular system and the parasympathetic outflow to the cranial vasculature from the superior salivatory nucleus (SuS) projections through the sphenopalatine ganglion, via the greater petrosal nerve of the VIIth (facial) cranial nerve. Cluster headache is remarkably responsive to treatment with oxygen, and yet our understanding of its mode of action is unknown"

IT SHOULD BE NOTED THAT THE MODE OF ACTION IS NOT WELL UNDERSTOOD. NEUROMUSCULAR DENTISTRY IS WELL UNDERSTOOD BUT IT IS NOT COMPLETELY UNDERSTOOD WHY SO MANY PATIENTS EXPERIENCE DRAMATIC RELIEF THAT SURPASSES STANDARD MEDICAL TECHNIQUES. NEUROMUSCULAR DENTISTRY IS ONE OF THE SAFEST METHODS OF TREATING ALL TYPES OF CHRONIC PAIN. THE TRIGEMINAL NERVE IS FREQUENTLY REFERRED TO AS THE DENTIST'S NERVE. AN EXCELLENT REFERENCE ON NEUROMUSCULAR DENTISTRY CAN BE FOUND IN SLEEP AND HEALTH JOURNAL http://www.sleepandhealth.com/neuromuscular-dentistry


Headache. 2010 Apr 22. [Epub ahead of print]
Electrical Stimulation of Sphenopalatine Ganglion for Acute Treatment of Cluster Headaches.
Ansarinia M, Rezai A, Tepper SJ, Steiner CP, Stump J, Stanton-Hicks M, Machado A, Narouze S.

From the Headache Specialists, Las Vegas, NV, USA (M. Ansarinia); Department of Neurosurgery and Center for Neuromodulation, The Ohio State University, Columbus, OH, USA (A. Rezai and J. Stump); Cleveland Clinic Centers for Headache and Pain and Neurological Restoration and Department of Neurology, Cleveland, OH, USA (S.J. Tepper); Cleveland Clinic Innovations, Product Development Manager, Center for Neurological Restoration, Cleveland, OH, USA (C.P. Steiner); Cleveland Clinic Center for Pain Anesthesia, Cleveland, OH, USA (M. Stanton-Hicks); Cleveland Clinic Center for Neurological Restoration and Department of Neurosurgery, Cleveland, OH, USA (A. Machado); Cleveland Clinic Center for Pain Anesthesia, Cleveland, OH, USA (S. Narouze).
Abstract
(Headache 2010;**:**-**) Introduction.- Cluster headaches (CH) are primary headaches marked by repeated short-lasting attacks of severe, unilateral head pain and associated autonomic symptoms. Despite aggressive management with medications, oxygen therapy, nerve blocks, as well as various lesioning and neurostimulation therapies, a number of patients are incapacitated and suffering. The sphenopalatine ganglion (SPG) has been implicated in the pathophysiology of CH and has been a target for blocks, lesioning, and other surgical approaches. For this reason, it was selected as a target for an acute neurostimulation study. Methods.- Six patients with refractory chronic CH were treated with short-term (up to 1 hour) electrical stimulation of the SPG during an acute CH. Headaches were spontaneously present at the time of stimulation or were triggered with agents known to trigger clusters headache in each patient. A standard percutaneous infrazygomatic approach was used to place a needle at the ipsilateral SPG in the pterygopalatine fossa under fluoroscopic guidance. Electrical stimulation was performed using a temporary stimulating electrode. Stimulation was performed at various settings during maximal headache intensity. Results.- Five patients had CH during the initial evaluation. Three returned 3 months later for a second evaluation. There were 18 acute and distinct CH attacks with clinically maximal visual analog scale (VAS) intensity of 8 (out of 10) and above. SPG stimulation resulted in complete resolution of the headache in 11 attacks, partial resolution (>50% VAS reduction) in 3, and minimal to no relief in 4 attacks. Associated autonomic features of CH were resolved in each responder. Pain relief was noted within several minutes of stimulation. Conclusion.- Sphenopalatine ganglion stimulation can be effective in relieving acute severe CH pain and associated autonomic features. Chronic long-term outcome studies are needed to determine the utility of SPG stimulation for management and prevention of CH.

PMID: 20438584 [PubMed - as supplied by publisher]

Curr Pain Headache Rep. 2010 Apr;14(2):160-3.
Role of sphenopalatine ganglion neuroablation in the management of cluster headache.
Narouze SN.

Pain Management Department, Anesthesiology Institute, Cleveland Clinic, OH 44195, USA. narouzs@ccf.org
Abstract
Cluster headache is a primary neurovascular headache. It is a strictly unilateral head pain that is associated with cranial autonomic symptoms and usually follows circadian and circannual patterns. Chronic cluster headache, which accounts for about 10% to 15% of patients with cluster headache, lacks the circadian pattern and is often resistant to pharmacological management. The sphenopalatine ganglion (SPG), located in the pterygopalatine fossa, is involved in the pathophysiology of cluster headache and has been a target for blocks and other surgical approaches. Percutaneous radiofrequency ablation of the SPG was shown to have encouraging results in those patients with intractable cluster headaches.

PMID: 20425206 [PubMed - in process]

J Neurophysiol. 2010 Jan;103(1):172-82. Epub 2009 Nov 4.
Muscarinic acetylcholine receptor modulation of mu (mu) opioid receptors in adult rat sphenopalatine ganglion neurons.
Margas W, Mahmoud S, Ruiz-Velasco V.

Department of Anesthesiology, Penn State University College of Medicine, 500 University Drive, Hershey, PA 17033-0850, USA.
Abstract
The sphenopalatine ganglion (SPG) neurons represent the parasympathetic branch of the autonomic nervous system involved in controlling cerebral blood flow. In the present study, we examined the coupling mechanism between mu (mu) opioid receptors (MOR) and muscarinic acetylcholine receptors (mAChR) with Ca(2+) channels in acutely dissociated adult rat SPG neurons. Successful MOR activation was recorded in approximately 40-45% of SPG neurons employing the whole cell variant of the patch-clamp technique. In addition, immunofluorescence assays indicated that MOR are not expressed in all SPG neurons while M(2) mAChR staining was evident in all neurons. The concentration-response relationships generated with morphine and [d-Ala2-N-Me-Phe4-Glycol5]-enkephalin (DAMGO) showed IC(50) values of 15.2 and 56.1 nM and maximal Ca(2+) current inhibition of 26.0 and 38.7%, respectively. Activation of MOR or M(2) mAChR with morphine or oxotremorine-methiodide (Oxo-M), respectively, resulted in voltage-dependent inhibition of Ca(2+) currents via coupling with Galpha(i/o) protein subunits. The acute prolonged exposure (10 min) of neurons to morphine or Oxo-M led to the homologous desensitization of MOR and M(2) mAChR, respectively. The prolonged stimulation of M(2) mAChR with Oxo-M resulted in heterologous desensitization of morphine-mediated Ca(2+) current inhibition, and was sensitive to the M(2) mAChR blocker methoctramine. On the other hand, when the neurons were exposed to morphine or DAMGO for 10 min, heterologous desensitization of M(2) mAChR was not observed. These results suggest that in rat SPG neurons activation of M(2) mAChR likely modulates opioid transmission in the brain vasculature to adequately maintain cerebral blood flow.

PMID: 19889856 [PubMed - indexed for MEDLINE]PMCID: PMC2807216 [Available on 2011/1/1]

Headache. 2009 Sep;49(8):1131-43.
Oxygen inhibits neuronal activation in the trigeminocervical complex after stimulation of trigeminal autonomic reflex, but not during direct dural activation of trigeminal afferents.
Akerman S, Holland PR, Lasalandra MP, Goadsby PJ.

Headache Group, Department of Neurology, University of California, San Francisco, San Francisco, CA 94143-0114, USA.
Abstract
OBJECTIVE: To understand the mechanism of action of oxygen treatment in cluster headache. BACKGROUND: Trigeminal autonomic cephalalgias, including cluster headache, are characterized by unilateral head pain in association with ipsilateral cranial autonomic features. They are believed to involve activation of the trigeminovascular system and the parasympathetic outflow to the cranial vasculature from the superior salivatory nucleus (SuS) projections through the sphenopalatine ganglion, via the greater petrosal nerve of the VIIth (facial) cranial nerve. Cluster headache is remarkably responsive to treatment with oxygen, and yet our understanding of its mode of action is unknown. METHODS: Combining models of trigeminovascular nociception and a novel approach that activates the trigeminal-autonomic reflex, using SuS/facial nerve stimulation, we explored the effect of oxygen on trigeminal nerve activation as well as on autonomic responses through blood flow observations of the lacrimal duct/sac. RESULTS: Meningeal vasodilation and neuronal firing in the trigeminocervical complex (TCC), in response to dural electrical stimulation, was unaffected by treatment with 100% oxygen. Stimulation of the SuS via the facial nerve caused only marginal changes in dural blood vessel diameter, but did result in evoked firing in the TCC. Two populations of neurons were characterized, those responsive to 100% oxygen treatment, with a maximal inhibition of 33%, 20 minutes after the start of oxygen treatment (t(15) = 4.4, P < .0001). A second population of neurons were not inhibited by oxygen and tended to have shorter latency. Oxygen also inhibited evoked blood flow changes in the lacrimal sac/duct caused by SuS stimulation. CONCLUSIONS: The data provide the first systematic, experimental evidence for a mechanism of action of oxygen in cluster headache. The data show oxygen has no direct effect on trigeminal afferents, acting specifically on the parasympathetic/facial nerve projections to the cranial vasculature to inhibit both evoked trigeminovascular activation and activation of the autonomic pathway during cluster headache attacks. Moreover, the studies begin to characterize a novel laboratory model for the most painful primary headache syndrome known--cluster headache.

PMID: 19719541 [PubMed - indexed for MEDLINE

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posted by Dr Shapira at 5:25 AM

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