Orville : I have suffered with episodic cluster migraines for years they usually come every other fall. the only thing that has helped me besides oxygen is zomig but I have to take more than the manufacturer recomends. What are the possible complications associated with Glycerol facial injections
Dr Shapira response: Glycerol injections are usually safe and effective but can have advers effects.
I have quoted a reference below that discusses adverse effects such as refractory pain that becomes non-remitting and possibly worse and unresponsive to treatment.
I would recommend utilizing Sphenopalatine Ganglion Blocks (SPG), an autonomic block that can be done transnasaly with no risk almost no risk. Patients can do SPG blocks at home to turn off or prevent attacks. Oxygen is obviously an excellent therap and can be used alone or with SPG blocks. SPG blocks before bed can often prevent an attack if they occur primarily in the night.
Taking more than rx dose of ZOMIG should be discussed with your physician.
Trigeminal Cistern Glycerol Injections for Facial Pain†
Thomas A. Waltz M.D., Donald J. Dalessio M.D., Kenneth H. Ott M.D., Brian Copeland M.D., Gaye Abbott C.M.A.-C.Article first published online: 22 JUN 2005
Headache: The Journal of Head and Face Pain
Volume 25, Issue 7, pages 354–357, October 1985
Dalessio, D. J., Ott, K. H., Copeland, B. and Abbott, G. (1985), Trigeminal Cistern Glycerol Injections for Facial Pain. Headache: The Journal of Head and Face Pain, 25: 354–357.
Publication History Issue published online: 22 JUN 2005
Article first published online: 22 JUN 2005
SYNOPSIS
The treatment of paroxysmal facial pain is often easily accomplished. At times, however, the converse occurs; the pain becomes more refractory, and unresponsive to therapy. This is especially the case when trigeminal neuralgia, cluster headache, and atypical facial pain become chronic. This report will summarize our experience with injection of glycerol into the region of the trigeminal cistern for intractable facial pain in 71 patients; 58 with trigeminal neuralgia, 5 with chronic cluster headache, and 8 with atypical facial pain.
Thursday, September 23, 2010
Increased Cortical Activity that causes headaches is increased with sleep apnea.
A recent study in Sleep Med on altered Cortical Excitability in sleep apnea concluded that " This TMS-based study suggests that untreated severe OSAS patients have imbalanced cortical excitabilities that enhanced inhibition or decreased brain excitability when awake during the day."
This may be a major cause of chronic headaches or migraines or other biochemical imbalances leading to stress disorders ofr depression. Many patients do not reach the clinical definition of sleep apnea but have UARS (upper respiratory resistance syndrome). This has been implicated in fibromyalgia and central sensitization as well.
I have included a few relevant pubmed articles below.
Sleep apne is the result of a TMJ disorder (http://www.nhlbi.nih.gov/meetings/workshops/tmj_wksp.pdf)
Neuromuscular Dentistry can help reduce incresed corticl activity, Treatment of sleep apnea can do the same.
Patients with sleep apnea have a smaller airway 24/7 that collapses at night. Correction of apnea and daytime jaw position may be ideal for all patients with chronic pain and sleep apnea.
Sleep Med. 2010 Oct;11(9):857-61.
Altered cortical excitability in patients with untreated obstructive sleep apnea syndrome.
Joo EY, Kim HJ, Lim YH, Koo DL, Hong SB.
Sleep Center, Department of Neurology, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Republic of Korea.
Comment in:
Sleep Med. 2010 Oct;11(9):820-1.
Abstract
OBJECTIVE: To investigate cortical excitability in patients with obstructive sleep apnea syndrome (OSAS) during wakefulness.
METHODS: The authors recruited 45 untreated severe OSAS (all males, mean age 47.2 years, mean apnea-hypopnea index=44.6h(-1)) patients and 44 age-matched healthy male volunteers (mean apnea-hypopnea index=3.4h(-1)). The TMS parameters measured were resting motor threshold (RMT), motor evoked potential (MEP) amplitude, cortical silent period (CSP), and short-interval intracortical inhibition (SICI) and intracortical facilitation (ICF). These parameters were measured in the morning (9-10 am) more than 2h after arising and the parameters of patients and controls were compared. The Epworth Sleepiness Scale (ESS) and the Stanford Sleepiness Scale (SSS) were also measured before the TMS study.
RESULTS: OSAS patients had a significantly higher RMT and a longer CSP duration (t-test, p<0.001) compared to healthy volunteers. No significant difference was observed between MEP amplitudes at any stimulus intensity or between the SICI (2, 3, 5ms) and ICF (10, 15, 20ms) values of OSAS patients and healthy volunteers (p>0.05).
CONCLUSIONS: This TMS-based study suggests that untreated severe OSAS patients have imbalanced cortical excitabilities that enhanced inhibition or decreased brain excitability when awake during the day.
PMID: 20817550 [PubMed - in process]
Handb Clin Neurol. 2010;97:73-83.
Biological science of headache channels.
Pietrobon D.
Abstract
Several episodic neurological diseases, including familial hemiplegic migraine (FHM) and different types of epilepsy, are caused by mutations in ion channels, and hence classified as channelopathies. The classification of FHM as a channelopathy has introduced a new perspective in headache research and has strengthened the idea of migraine as a disorder of neural excitability. Here we review recent studies of the functional consequences of mutations in the CACNA1A and SCNA1A genes (encoding the pore-forming subunit of Ca(V)2.1 and Na(V)1.1 channels) and the ATPA1A2 gene (encoding the alpha(2) subunit of the Na(+)/K(+) pump), responsible for FHM1, FHM3, and FHM2, respectively. These studies show that: (1) FHM1 mutations produce gain-of-function of the Ca(V)2.1 channel and, as a consequence, increased glutamate release at cortical synapses and facilitation of induction and propagation of cortical spreading depression (CSD); (2) FHM2 mutations produce loss-of-function of the alpha(2) Na(+)/K(+)-ATPase; and (3) the FHM3 mutation accelerates recovery from fast inactivation of Na(V)1.5 channels. These findings are consistent with the hypothesis that FHM mutations share the ability to render the brain more susceptible to CSD, by causing excessive synaptic glutamate release (FHM1) or decreased removal of K(+) and glutamate from the synaptic cleft (FHM2) or excessive extracellular K(+) (FHM3).
PMID: 20816411 [PubMed - in pr
Handb Clin Neurol. 2010;97:47-71.
Pharmacology.
Bolay H, Durham P.
Department of Neurology, Gazi Hospital and Neuropsychiatry Centre, Gazi University, Besevler, Ankara, Turkey.
Abstract
Headache treatment has been based primarily on experiences with non-specific drugs such as analgesics, non-steroidal anti-inflammatory drugs, or drugs that were originally developed to treat other diseases, such as beta-blockers and anticonvulsant medications. A better understanding of the basic pathophysiological mechanisms of migraine and other types of headache has led to the development over the past two decades of more target-specific drugs. Since activation of the trigeminovascular system and neurogenic inflammation are thought to play important roles in migraine pathophysiology, experimental studies modeling those events successfully predicted targets for selective development of pharmacological agents to treat migraine. Basically, there are two fundamental strategies for the treatment of migraine, abortive or preventive, based to a large degree on the frequency of attacks. The triptans, which exhibit potency towards selective serotonin (5-hydroxytryptamine, 5-HT) receptors expressed on trigeminal nerves, remain the most effective drugs for the abortive treatment of migraine. However, numerous preventive medications are currently available that modulate the excitability of the nervous system, particularly the cerebral cortex. In this chapter, the pharmacology of commercially available medications as well as drugs in development that prevent or abort headache attacks will be discussed.
PMID: 20816410 [PubMed - in process]
Cephalalgia. 2010 Sep;30(9):1101-9. Epub 2010 Mar 19.
Cortical hyperexcitability and mechanism of medication-overuse headache.
Supornsilpchai W, le Grand SM, Srikiatkhachorn A.
Department of Physiology, Faculty of Medicine, Chulalongkorn University, Patumwan, Bangkok, Thailand.
Abstract
The present study was conducted to determine the effect of acute (1 h) and chronic (daily dose for 30 days) paracetamol administration on the development of cortical spreading depression (CSD), CSD-evoked cortical hyperaemia and CSD-induced Fos expression in cerebral cortex and trigeminal nucleus caudalis (TNC). Paracetamol (200 mg/kg body weight, intraperitonealy) was administered to Wistar rats. CSD was elicited by topical application of solid KCl. Electrocorticogram and cortical blood flow were recorded. Results revealed that acute paracetamol administration substantially decreased the number of Fos-immunoreactive cells in the parietal cortex and TNC without causing change in CSD frequency. On the other hand, chronic paracetamol administration led to an increase in CSD frequency as well as CSD-evoked Fos expression in parietal cortex and TNC, indicating an increase in cortical excitability and facilitation of trigeminal nociception. Alteration of cortical excitability which leads to an increased susceptibility of CSD development can be a possible mechanism underlying medication-overuse headache.
PMID: 20713560 [PubMed - in process]
This may be a major cause of chronic headaches or migraines or other biochemical imbalances leading to stress disorders ofr depression. Many patients do not reach the clinical definition of sleep apnea but have UARS (upper respiratory resistance syndrome). This has been implicated in fibromyalgia and central sensitization as well.
I have included a few relevant pubmed articles below.
Sleep apne is the result of a TMJ disorder (http://www.nhlbi.nih.gov/meetings/workshops/tmj_wksp.pdf)
Neuromuscular Dentistry can help reduce incresed corticl activity, Treatment of sleep apnea can do the same.
Patients with sleep apnea have a smaller airway 24/7 that collapses at night. Correction of apnea and daytime jaw position may be ideal for all patients with chronic pain and sleep apnea.
Sleep Med. 2010 Oct;11(9):857-61.
Altered cortical excitability in patients with untreated obstructive sleep apnea syndrome.
Joo EY, Kim HJ, Lim YH, Koo DL, Hong SB.
Sleep Center, Department of Neurology, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Republic of Korea.
Comment in:
Sleep Med. 2010 Oct;11(9):820-1.
Abstract
OBJECTIVE: To investigate cortical excitability in patients with obstructive sleep apnea syndrome (OSAS) during wakefulness.
METHODS: The authors recruited 45 untreated severe OSAS (all males, mean age 47.2 years, mean apnea-hypopnea index=44.6h(-1)) patients and 44 age-matched healthy male volunteers (mean apnea-hypopnea index=3.4h(-1)). The TMS parameters measured were resting motor threshold (RMT), motor evoked potential (MEP) amplitude, cortical silent period (CSP), and short-interval intracortical inhibition (SICI) and intracortical facilitation (ICF). These parameters were measured in the morning (9-10 am) more than 2h after arising and the parameters of patients and controls were compared. The Epworth Sleepiness Scale (ESS) and the Stanford Sleepiness Scale (SSS) were also measured before the TMS study.
RESULTS: OSAS patients had a significantly higher RMT and a longer CSP duration (t-test, p<0.001) compared to healthy volunteers. No significant difference was observed between MEP amplitudes at any stimulus intensity or between the SICI (2, 3, 5ms) and ICF (10, 15, 20ms) values of OSAS patients and healthy volunteers (p>0.05).
CONCLUSIONS: This TMS-based study suggests that untreated severe OSAS patients have imbalanced cortical excitabilities that enhanced inhibition or decreased brain excitability when awake during the day.
PMID: 20817550 [PubMed - in process]
Handb Clin Neurol. 2010;97:73-83.
Biological science of headache channels.
Pietrobon D.
Abstract
Several episodic neurological diseases, including familial hemiplegic migraine (FHM) and different types of epilepsy, are caused by mutations in ion channels, and hence classified as channelopathies. The classification of FHM as a channelopathy has introduced a new perspective in headache research and has strengthened the idea of migraine as a disorder of neural excitability. Here we review recent studies of the functional consequences of mutations in the CACNA1A and SCNA1A genes (encoding the pore-forming subunit of Ca(V)2.1 and Na(V)1.1 channels) and the ATPA1A2 gene (encoding the alpha(2) subunit of the Na(+)/K(+) pump), responsible for FHM1, FHM3, and FHM2, respectively. These studies show that: (1) FHM1 mutations produce gain-of-function of the Ca(V)2.1 channel and, as a consequence, increased glutamate release at cortical synapses and facilitation of induction and propagation of cortical spreading depression (CSD); (2) FHM2 mutations produce loss-of-function of the alpha(2) Na(+)/K(+)-ATPase; and (3) the FHM3 mutation accelerates recovery from fast inactivation of Na(V)1.5 channels. These findings are consistent with the hypothesis that FHM mutations share the ability to render the brain more susceptible to CSD, by causing excessive synaptic glutamate release (FHM1) or decreased removal of K(+) and glutamate from the synaptic cleft (FHM2) or excessive extracellular K(+) (FHM3).
PMID: 20816411 [PubMed - in pr
Handb Clin Neurol. 2010;97:47-71.
Pharmacology.
Bolay H, Durham P.
Department of Neurology, Gazi Hospital and Neuropsychiatry Centre, Gazi University, Besevler, Ankara, Turkey.
Abstract
Headache treatment has been based primarily on experiences with non-specific drugs such as analgesics, non-steroidal anti-inflammatory drugs, or drugs that were originally developed to treat other diseases, such as beta-blockers and anticonvulsant medications. A better understanding of the basic pathophysiological mechanisms of migraine and other types of headache has led to the development over the past two decades of more target-specific drugs. Since activation of the trigeminovascular system and neurogenic inflammation are thought to play important roles in migraine pathophysiology, experimental studies modeling those events successfully predicted targets for selective development of pharmacological agents to treat migraine. Basically, there are two fundamental strategies for the treatment of migraine, abortive or preventive, based to a large degree on the frequency of attacks. The triptans, which exhibit potency towards selective serotonin (5-hydroxytryptamine, 5-HT) receptors expressed on trigeminal nerves, remain the most effective drugs for the abortive treatment of migraine. However, numerous preventive medications are currently available that modulate the excitability of the nervous system, particularly the cerebral cortex. In this chapter, the pharmacology of commercially available medications as well as drugs in development that prevent or abort headache attacks will be discussed.
PMID: 20816410 [PubMed - in process]
Cephalalgia. 2010 Sep;30(9):1101-9. Epub 2010 Mar 19.
Cortical hyperexcitability and mechanism of medication-overuse headache.
Supornsilpchai W, le Grand SM, Srikiatkhachorn A.
Department of Physiology, Faculty of Medicine, Chulalongkorn University, Patumwan, Bangkok, Thailand.
Abstract
The present study was conducted to determine the effect of acute (1 h) and chronic (daily dose for 30 days) paracetamol administration on the development of cortical spreading depression (CSD), CSD-evoked cortical hyperaemia and CSD-induced Fos expression in cerebral cortex and trigeminal nucleus caudalis (TNC). Paracetamol (200 mg/kg body weight, intraperitonealy) was administered to Wistar rats. CSD was elicited by topical application of solid KCl. Electrocorticogram and cortical blood flow were recorded. Results revealed that acute paracetamol administration substantially decreased the number of Fos-immunoreactive cells in the parietal cortex and TNC without causing change in CSD frequency. On the other hand, chronic paracetamol administration led to an increase in CSD frequency as well as CSD-evoked Fos expression in parietal cortex and TNC, indicating an increase in cortical excitability and facilitation of trigeminal nociception. Alteration of cortical excitability which leads to an increased susceptibility of CSD development can be a possible mechanism underlying medication-overuse headache.
PMID: 20713560 [PubMed - in process]
My Headaches are throbbing, nausea, stabbing ....Renee
Heeadaches related to the trigeminal nerves and jaw function frequently have all of those qualities. This relates to the vascular, hemodynamic and autonomic functions of the trigeminal nerve. Neuromuscular dentistry can frequently allieve and eliminate these sypmtoms as well as the more common tender, aching, and penetrating headaches. Painful TM Joint symptoms may or may not be present.
HEADACHES,TMJ AND ORTHOMOLECULAR MEDICINE
Question rrom Phil Bohnert, MD How about ortho-molecular treatments?
Reply: Orthomolecular Medicine is a term originally coined by Linus Pauling one of the greatest minds of the last century. It is medicine that idealizes the health of the total individual by correcting or optimizing the nutritional and biochemical stautus of the body.
Neuromuscular Dentistry is a form of orthomolecular medicine optimizing and correcting not nutritional but neurological input into the trigeminal nerve. The trigeminal nerve accounts for almost half of total input to the brain.
There are corrections in biochemical homeostasis at neurojunctions when it is optimized. There are also major changes to brain chemistry from control of blood flow to the brain br the trigeminal nerve.
Thank You Dr Bonnert
Reply: Orthomolecular Medicine is a term originally coined by Linus Pauling one of the greatest minds of the last century. It is medicine that idealizes the health of the total individual by correcting or optimizing the nutritional and biochemical stautus of the body.
Neuromuscular Dentistry is a form of orthomolecular medicine optimizing and correcting not nutritional but neurological input into the trigeminal nerve. The trigeminal nerve accounts for almost half of total input to the brain.
There are corrections in biochemical homeostasis at neurojunctions when it is optimized. There are also major changes to brain chemistry from control of blood flow to the brain br the trigeminal nerve.
Thank You Dr Bonnert
Sunday, August 22, 2010
TMJ Treatment: Is Neuromuscular Dentistry the TMJ Treatment?
Neuromuscular Dentistry treats TMJ disorders by correcting the underlying problems rather than just treating the symptoms. The old fashioned mechanical approach to TMD treatment only addresses the current symptoms. Long term correction of chronic headaches, joint pain and muscle pain is actually the result of healing when underlying pathology is eliminated. Neuromuscular Dentistry is the best way to correct function and permit long term healing.
Monday, August 16, 2010
Headaches after wisdom teeth extractions and residual paresthesia.
Question from ELMA:
What is the correlation between the removal of the third molar and migraine headaches? I have permanent paresthesia on the lower left lip and chin. This occured in 1987 and I never suffered with headaches or sinus problems until the surgery. I remember hearing the dentist asking his assistant "What is that?" once he extracted that particular tooth.
Dr Shapira Response: Dear Elma I have seen many patients who trace TMJ problems and headaches back to wisdom teeth extractions. This can be due to many reasons. You had damage to your trigeminal nerve during the surgery that causes parasthesia or permanent numbness.
It is also traumatic to the joints, ligaments and muscles to have third molars extracted. Injuries may not always heal correctly and bites can change leading to neuromuscular problems.
Frequently there were always underlying problems that do not express themselves until after extractions. Clicking can start in the TM Joints due to direct trauma to the joint or secondary to bite changes.
I am hoping my patented devices for early prophylactic removal or third molars before they calcify will eliminate most of this type of problem in the future. There is virtually no morbidity when the developing tooth bud is removed before calcification and it is a quick atraumatic procedure with the added benefit of allowing collection and storage of stem cells for future use.
What is the correlation between the removal of the third molar and migraine headaches? I have permanent paresthesia on the lower left lip and chin. This occured in 1987 and I never suffered with headaches or sinus problems until the surgery. I remember hearing the dentist asking his assistant "What is that?" once he extracted that particular tooth.
Dr Shapira Response: Dear Elma I have seen many patients who trace TMJ problems and headaches back to wisdom teeth extractions. This can be due to many reasons. You had damage to your trigeminal nerve during the surgery that causes parasthesia or permanent numbness.
It is also traumatic to the joints, ligaments and muscles to have third molars extracted. Injuries may not always heal correctly and bites can change leading to neuromuscular problems.
Frequently there were always underlying problems that do not express themselves until after extractions. Clicking can start in the TM Joints due to direct trauma to the joint or secondary to bite changes.
I am hoping my patented devices for early prophylactic removal or third molars before they calcify will eliminate most of this type of problem in the future. There is virtually no morbidity when the developing tooth bud is removed before calcification and it is a quick atraumatic procedure with the added benefit of allowing collection and storage of stem cells for future use.
Relief of 30 years of constant Headache: Brief relief may provide clue to long term relief.
KEN:I Have had headaches for 30 years going away only once when having a root canal done on an upper tooth. While everything was numbed up I had complete brain function and no headache. They are located directly behind my nose area and I feel a constant pressure.
Dr Shapira response: The anaesthetic relieved the pain probably confirming that it is from the trigeminal nerve. I would be very interested is a spenopalatine ganglion block could give more long term relief. It is a easy procedure that I have taught patients to do at home with a q-tip and anaesthetic thru the nose. There are also other diagnostic blocks that can be done to determine the cause of your headaches.
A diagnostic neuromuscular orthotic would be an excellent first step in treatment. If the headaches are eliminated or significantly relieved a permenant stabilization could be done. I have referred you to an excellent Dr who knows both of the procedures mentioned.
Dr Shapira response: The anaesthetic relieved the pain probably confirming that it is from the trigeminal nerve. I would be very interested is a spenopalatine ganglion block could give more long term relief. It is a easy procedure that I have taught patients to do at home with a q-tip and anaesthetic thru the nose. There are also other diagnostic blocks that can be done to determine the cause of your headaches.
A diagnostic neuromuscular orthotic would be an excellent first step in treatment. If the headaches are eliminated or significantly relieved a permenant stabilization could be done. I have referred you to an excellent Dr who knows both of the procedures mentioned.
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