Obstructive sleep apnea affects around 20 million Americans and can lead to hypertension, heart attack, stroke, depression, muscle pain, fibromyalgia, morning headaches, and excessive daytime sleepiness.
Friday, February 26, 2010
Sleep Apnea, TMD, Myofascial Pain and Headaches
The American Equilibration Society hed its 2010 meeting and Sleep apnea and sleep disordered breathing were continually reference as comorbidities for headaches, TMD (TMJ), fibromyalgia and muscle and joint disorders. Patients who visit this site and suffer from headaches, myofascial pain, fibromyalgia or TMJ disorders should go to http://www.ihateheadaches.org and read my blog http://www.ihateheadaches.org/blogs/illinois/2010/02/myofascial-trigger-points-are-explained.html covering muscle pain and how the newest research agrees with neuromuscular dental concepts.
New surgery to treat obstructive sleep apnea.
There is a new surgery designed to treat sleep apnea. Permanent sutures are placed to secure the tongu to the jaw preventing it from blocking the airway. The is a logic to this procedure and it may require more than 1 surgical procedure. There is no long term data. In general surgery has been ineffective for treating apnea unless major surgical prcedures are done. Soft palate surgery carried high risk of morbidity and poor results. Tongue reduction was more successful,especially base of the tongue reduction. A recent article showed similar rsults with base of tongue reduction and somnoplasty on the base of the tongue. The somnoplasty proceedure had lower risk and morbidity.
CPAP remains the "Gold Standard" for treatment of obstructive sleep apnea but the majority of patients do not tolerate CPAP or BiPAP. Oral appliances are the only other therapy considerd a first line treatment of mild to moderate sleep apnea. Oral Appliances are considered an alternative treatment for severe sleep apnea when patients do not tolerate CPAP. Even when sleep apnea is severe the majority of patients do not tolerate CPAP.
Bimaxillary advancement is the most successful surgical proceedure but is a major orthopedic procedure with significant risks of morbidity. The surgery works in a similar method to oral appliances. Prior to surgery a trial oral appliance can help determine the best position to place the jaws to prevent additional future surgeries.
Suturing the tongue to the jaw is a novel approach to treating sleep apnea. Hopefully it will be more successful and less painful that soft palate surgery has proven to be.
CPAP remains the "Gold Standard" for treatment of obstructive sleep apnea but the majority of patients do not tolerate CPAP or BiPAP. Oral appliances are the only other therapy considerd a first line treatment of mild to moderate sleep apnea. Oral Appliances are considered an alternative treatment for severe sleep apnea when patients do not tolerate CPAP. Even when sleep apnea is severe the majority of patients do not tolerate CPAP.
Bimaxillary advancement is the most successful surgical proceedure but is a major orthopedic procedure with significant risks of morbidity. The surgery works in a similar method to oral appliances. Prior to surgery a trial oral appliance can help determine the best position to place the jaws to prevent additional future surgeries.
Suturing the tongue to the jaw is a novel approach to treating sleep apnea. Hopefully it will be more successful and less painful that soft palate surgery has proven to be.
Wednesday, February 24, 2010
The Palate and Obstructive Sleep Apnea
In describing obstructive sleep apnea, we often talk about the collapse of the airways during sleep. Now, the Journal Archives of Otolaryngology reports that at least one of these anatomical changes has been imaged during actual apnea/hypoxia events. In a study reported in the February issue, researchers investigated changes to the soft palate experienced by sleepers to determine whether particular soft palate changes could be used to distinguish between obstructive sleep apnea sufferers and simple snorers.
The palate is the roof of the mouth. The front of the palate is the hard palate, and behind it is the soft palate, which extends back to the uvula (the fleshy, dangling protuberance at the back of the mouth). Using sleep videofluoroscopy to measure anatomical changes and polysomnography to identify apnea/hypoxia events, researchers found that the soft palate behaved very differently in sleep apnea sufferers than it did in simple snorers. Sleep apnea sufferers were more likely to see the soft palate expand backward during sleep. And this expansion was linked to instances of apnea and hypoxia.
The distinction between simple snorers and obstructive sleep apnea sufferers is a crucial part of delivering the right solution for those with sleep disordered breathing. Simple snoring is just a nuisance, but the dangers of sleep apnea make it a deadly condition that can dramatically reduce a person's life expectancy.
If you need help getting the best solution for your sleep apnea, please schedule a sleep apnea consultation with dentist, Dr. Ira Shapria at the Snoring and Sleep Apnea Treatment Center in Gurnee, Illinois today.
The palate is the roof of the mouth. The front of the palate is the hard palate, and behind it is the soft palate, which extends back to the uvula (the fleshy, dangling protuberance at the back of the mouth). Using sleep videofluoroscopy to measure anatomical changes and polysomnography to identify apnea/hypoxia events, researchers found that the soft palate behaved very differently in sleep apnea sufferers than it did in simple snorers. Sleep apnea sufferers were more likely to see the soft palate expand backward during sleep. And this expansion was linked to instances of apnea and hypoxia.
The distinction between simple snorers and obstructive sleep apnea sufferers is a crucial part of delivering the right solution for those with sleep disordered breathing. Simple snoring is just a nuisance, but the dangers of sleep apnea make it a deadly condition that can dramatically reduce a person's life expectancy.
If you need help getting the best solution for your sleep apnea, please schedule a sleep apnea consultation with dentist, Dr. Ira Shapria at the Snoring and Sleep Apnea Treatment Center in Gurnee, Illinois today.
Monday, February 22, 2010
Researcher Develops Urine Test for identifying Sleep Apnea in Children. Will this change lead to early diagnosis and prevention of ADD and ADHD
WFPL news reported
"University of Louisville researcher Dr. Saeed Jortani has developed a urine test that could soon be used to screen or diagnose children with obstructive sleep apnea. He says children have been difficult to diagnose because of the required overnight stay in a sleep clinic.
Jortani says they looked for another way to screen children, so fewer would have to get tested, and found the answer in urine.
“Whatever the body does throughout the day, urine is basically a record of what’s going on for the previous several hours,” says Jortani, “and we thought if the child is under stress or if the child is having difficulty breathing, that has to affect some of the proteins in their body.”
Jortani says children who suffer from the sleep disorder have a high level of stress-related protein in their urine. He says in the future, children who test positive in the urine test will then go on to tests in a sleep clinic.
He says in future research, he may develop the test for adults"
Screening for sleep apnea was also the subject of a recent repot from the University of Chicago (see PubMed abstract below). They concluded in Am J Respir Crit Care Med. 2009 Dec 15;180(12):1253-61 "CONCLUSIONS: Proteomic approaches reveal that pediatric OSA is associated with specific and consistent alterations in urinary concentrations of specific protein clusters. Future studies aiming to validate this approach as a screening method of habitually snoring children appears warranted."
Their study showed extremely high sensitivity and specificity.
Another study in Chest. 2009 Jun;135(6):1496-501 (see PUBMED abstract below) showed that "Urine concentrations of cysteinyl leukotrienes in children with obstructive sleep-disordered breathing" could be used to predict severity of pediatric sleep apnea. It is well known that neurocognitive effects of sleep apnea include increases in ADD, ADHD, Dyslexia and other behavioral disorders as recently reported in Pediatr Pulmonol. 2009 May;44(5):417-22 in an article titled "Neurocognitive and behavioral impact of sleep disordered breathing in children."
The question is do these metabolic changes measured in the urine act just as a marker to identify sleep apnea or can the chemical changes measured actually be causing the toxic effects on brain development and maturation?
The development of the craniomandibular articulation and the size of the palate and oral cavity are easily correctable at early ages to eliminate snoring and sleep apnea. The NHLBI considers Sleep Apnea to be a TMJ disorder. Correction of aberrant oral devlopment can probably prevent sleep apnea, and tmj problems and headaches in adults. Babies who are breastfed are less likely to develop these problems to begin with. Dentistry and early orthodontic airway orthopedics may be ables to drastically reduce future medical and educational costs by preventing sleep apnea and/or diagnosing and treating at an early stage prior to adverse neurocognitive changes.
PubMed abstracts below:
Am J Respir Crit Care Med. 2009 Dec 15;180(12):1253-61. Epub 2009 Sep 24.
Two-dimensional differential in-gel electrophoresis proteomic approaches reveal urine candidate biomarkers in pediatric obstructive sleep apnea.
Gozal D, Jortani S, Snow AB, Kheirandish-Gozal L, Bhattacharjee R, Kim J, Capdevila OS.
Section of Pediatric Sleep Medicine, Department of Pediatrics, University of Chicago, Chicago, Illinois, USA. dgozal@peds.bsd.uchicago.edu
RATIONALE: Sleep studies are laborious, expensive, inaccessible, and inconvenient for diagnosing obstructive sleep apnea (OSA) in children. OBJECTIVES: To examine whether the urinary proteome uncovers specific clusters that are differentially expressed in the urine of children with OSA. METHODS: Two-dimensional differential in-gel electrophoresis (2D-DIGE) and mass spectrometry proteomics followed by validation with western blot of ELISA. MEASUREMENTS AND MAIN RESULTS: Morning urine proteins from 60 children with polysomnographically confirmed OSA and from matched children with primary snoring (n = 30) and control subjects (n = 30) were assessed. A total of 16 proteins that are differentially expressed in OSA were identified, and 7 were confirmed by either immunoblots or ELISA. Among the latter, receiver-operator curve analyses of urinary concentrations of uromodulin, urocortin-3, orosomucoid-1, and kallikrein assigned favorable predictive properties to these proteins. Furthermore, combinatorial approaches indicated that the presence of values beyond the calculated cutoff concentrations for three or more of the proteins yielded a sensitivity of 95% and a specificity of 100%. CONCLUSIONS: Proteomic approaches reveal that pediatric OSA is associated with specific and consistent alterations in urinary concentrations of specific protein clusters. Future studies aiming to validate this approach as a screening method of habitually snoring children appears warranted.
PMID: 19797158 [PubMed - indexed for MEDLINE]
Chest. 2009 Jun;135(6):1496-501. Epub 2009 Jan 13.
Urine concentrations of cysteinyl leukotrienes in children with obstructive sleep-disordered breathing.
Kaditis AG, Alexopoulos E, Chaidas K, Ntamagka G, Karathanasi A, Tsilioni I, Kiropoulos TS, Zintzaras E, Gourgoulianis K.
Sleep Disorders Laboratory, University of Thessaly School of Medicine and Larissa University Hospital, Larissa, Greece. Kaditia@hotmail.com
BACKGROUND: Adenotonsillar tissue of children with obstructive sleep-disordered breathing (SDB) has increased content of cysteinyl leukotrienes (CysLTs) and expression of CysLTs receptors. Furthermore, CysLTs concentrations in the nasal exhaled breath condensate of children with sleep apnea are elevated. OBJECTIVE: To investigate the relationship between urine levels of CysLTs and severity of SDB in children. METHODS: Morning urine concentrations of CysLTs were measured in children with symptoms of SDB and in control subjects with recurrent tonsillitis and without snoring who underwent polysomnography and were expressed in pg/mL per mg/dL of urine creatinine. RESULTS: Nineteen children with moderate-to-severe SDB (mean [+/- SD] age, 5.4 +/- 1.6 years; obstructive apnea-hypopnea index [OAHI]: 14.4 +/- 9.6 episodes/h), 29 subjects with mild SDB (5.1 +/- 1.5 years; OAHI: 2.9 +/- 0.8 episodes/h), 26 children with primary snoring (PS) [7 +/- 2.6 years; OAHI: 1.1 +/- 0.3 episodes/h], and 18 control subjects (6.4 +/- 2.5 years; OAHI: 0.7 +/- 0.3 episodes/h) were studied. Children with moderate-to severe SDB had higher log-transformed urine CysLTs levels than those with mild SDB, PS, or control subjects (2.39 +/- 0.51 vs 2.06 +/- 0.26 vs 2.11 +/- 0.25 vs 1.86 +/- 0.28; p < 0.05). Log-transformed CysLTs concentration, tonsillar size, and body mass index z score were significant predictors of log-transformed OAHI (p < 0.01). CONCLUSIONS: Urine excretion of CysLTs is related to SDB severity in children. This finding indicates that 5-lipoxygenase pathway products participate in the pathogenesis of obstructive sleep apnea in childhood or alternatively that SDB promotes CysLTs biosynthesis.
PMID: 19141528 [PubMed - indexed for MEDLINE]
Pediatr Pulmonol. 2009 May;44(5):417-22.
Neurocognitive and behavioral impact of sleep disordered breathing in children.
Owens JA.
Department of Ambulatory Pediatrics, Rhode Island Hospital, Providence, Rhode Island 02903, USA. owensleep@gmail.com
The consequences of poor quality and/or inadequate sleep in children and adolescents have become a major public health concern, and one in which pediatric health care professionals have become increasingly involved. In particular, insufficient and/or fragmented sleep resulting from primary sleep disorders such as obstructive sleep apnea (OSA), often compounded by the presence of comorbid sleep disorders as well as by voluntary sleep curtailment related to lifestyle and environmental factors, has been implicated in a host of negative consequences. These range from metabolic dysfunction and increased cardiovascular morbidity to impairments in mood and academic performance. The following review will focus on what is currently known about the effects of sleep disordered breathing (SDB) specifically on neurobehavioral and neurocognitive function in children. Because of the scarcity of literature on the cognitive and behavioral impact of sleep disorders in infants and very young children, this review will target largely the preschool/school-aged child and adolescent populations. In addition, the focus will be on a review of the most recent literature, as a supplement to several excellent previous reviews on the topic. (c) 2009 Wiley-Liss, Inc.
PMID: 19382210 [PubMed - indexed for MEDLINE]
"University of Louisville researcher Dr. Saeed Jortani has developed a urine test that could soon be used to screen or diagnose children with obstructive sleep apnea. He says children have been difficult to diagnose because of the required overnight stay in a sleep clinic.
Jortani says they looked for another way to screen children, so fewer would have to get tested, and found the answer in urine.
“Whatever the body does throughout the day, urine is basically a record of what’s going on for the previous several hours,” says Jortani, “and we thought if the child is under stress or if the child is having difficulty breathing, that has to affect some of the proteins in their body.”
Jortani says children who suffer from the sleep disorder have a high level of stress-related protein in their urine. He says in the future, children who test positive in the urine test will then go on to tests in a sleep clinic.
He says in future research, he may develop the test for adults"
Screening for sleep apnea was also the subject of a recent repot from the University of Chicago (see PubMed abstract below). They concluded in Am J Respir Crit Care Med. 2009 Dec 15;180(12):1253-61 "CONCLUSIONS: Proteomic approaches reveal that pediatric OSA is associated with specific and consistent alterations in urinary concentrations of specific protein clusters. Future studies aiming to validate this approach as a screening method of habitually snoring children appears warranted."
Their study showed extremely high sensitivity and specificity.
Another study in Chest. 2009 Jun;135(6):1496-501 (see PUBMED abstract below) showed that "Urine concentrations of cysteinyl leukotrienes in children with obstructive sleep-disordered breathing" could be used to predict severity of pediatric sleep apnea. It is well known that neurocognitive effects of sleep apnea include increases in ADD, ADHD, Dyslexia and other behavioral disorders as recently reported in Pediatr Pulmonol. 2009 May;44(5):417-22 in an article titled "Neurocognitive and behavioral impact of sleep disordered breathing in children."
The question is do these metabolic changes measured in the urine act just as a marker to identify sleep apnea or can the chemical changes measured actually be causing the toxic effects on brain development and maturation?
The development of the craniomandibular articulation and the size of the palate and oral cavity are easily correctable at early ages to eliminate snoring and sleep apnea. The NHLBI considers Sleep Apnea to be a TMJ disorder. Correction of aberrant oral devlopment can probably prevent sleep apnea, and tmj problems and headaches in adults. Babies who are breastfed are less likely to develop these problems to begin with. Dentistry and early orthodontic airway orthopedics may be ables to drastically reduce future medical and educational costs by preventing sleep apnea and/or diagnosing and treating at an early stage prior to adverse neurocognitive changes.
PubMed abstracts below:
Am J Respir Crit Care Med. 2009 Dec 15;180(12):1253-61. Epub 2009 Sep 24.
Two-dimensional differential in-gel electrophoresis proteomic approaches reveal urine candidate biomarkers in pediatric obstructive sleep apnea.
Gozal D, Jortani S, Snow AB, Kheirandish-Gozal L, Bhattacharjee R, Kim J, Capdevila OS.
Section of Pediatric Sleep Medicine, Department of Pediatrics, University of Chicago, Chicago, Illinois, USA. dgozal@peds.bsd.uchicago.edu
RATIONALE: Sleep studies are laborious, expensive, inaccessible, and inconvenient for diagnosing obstructive sleep apnea (OSA) in children. OBJECTIVES: To examine whether the urinary proteome uncovers specific clusters that are differentially expressed in the urine of children with OSA. METHODS: Two-dimensional differential in-gel electrophoresis (2D-DIGE) and mass spectrometry proteomics followed by validation with western blot of ELISA. MEASUREMENTS AND MAIN RESULTS: Morning urine proteins from 60 children with polysomnographically confirmed OSA and from matched children with primary snoring (n = 30) and control subjects (n = 30) were assessed. A total of 16 proteins that are differentially expressed in OSA were identified, and 7 were confirmed by either immunoblots or ELISA. Among the latter, receiver-operator curve analyses of urinary concentrations of uromodulin, urocortin-3, orosomucoid-1, and kallikrein assigned favorable predictive properties to these proteins. Furthermore, combinatorial approaches indicated that the presence of values beyond the calculated cutoff concentrations for three or more of the proteins yielded a sensitivity of 95% and a specificity of 100%. CONCLUSIONS: Proteomic approaches reveal that pediatric OSA is associated with specific and consistent alterations in urinary concentrations of specific protein clusters. Future studies aiming to validate this approach as a screening method of habitually snoring children appears warranted.
PMID: 19797158 [PubMed - indexed for MEDLINE]
Chest. 2009 Jun;135(6):1496-501. Epub 2009 Jan 13.
Urine concentrations of cysteinyl leukotrienes in children with obstructive sleep-disordered breathing.
Kaditis AG, Alexopoulos E, Chaidas K, Ntamagka G, Karathanasi A, Tsilioni I, Kiropoulos TS, Zintzaras E, Gourgoulianis K.
Sleep Disorders Laboratory, University of Thessaly School of Medicine and Larissa University Hospital, Larissa, Greece. Kaditia@hotmail.com
BACKGROUND: Adenotonsillar tissue of children with obstructive sleep-disordered breathing (SDB) has increased content of cysteinyl leukotrienes (CysLTs) and expression of CysLTs receptors. Furthermore, CysLTs concentrations in the nasal exhaled breath condensate of children with sleep apnea are elevated. OBJECTIVE: To investigate the relationship between urine levels of CysLTs and severity of SDB in children. METHODS: Morning urine concentrations of CysLTs were measured in children with symptoms of SDB and in control subjects with recurrent tonsillitis and without snoring who underwent polysomnography and were expressed in pg/mL per mg/dL of urine creatinine. RESULTS: Nineteen children with moderate-to-severe SDB (mean [+/- SD] age, 5.4 +/- 1.6 years; obstructive apnea-hypopnea index [OAHI]: 14.4 +/- 9.6 episodes/h), 29 subjects with mild SDB (5.1 +/- 1.5 years; OAHI: 2.9 +/- 0.8 episodes/h), 26 children with primary snoring (PS) [7 +/- 2.6 years; OAHI: 1.1 +/- 0.3 episodes/h], and 18 control subjects (6.4 +/- 2.5 years; OAHI: 0.7 +/- 0.3 episodes/h) were studied. Children with moderate-to severe SDB had higher log-transformed urine CysLTs levels than those with mild SDB, PS, or control subjects (2.39 +/- 0.51 vs 2.06 +/- 0.26 vs 2.11 +/- 0.25 vs 1.86 +/- 0.28; p < 0.05). Log-transformed CysLTs concentration, tonsillar size, and body mass index z score were significant predictors of log-transformed OAHI (p < 0.01). CONCLUSIONS: Urine excretion of CysLTs is related to SDB severity in children. This finding indicates that 5-lipoxygenase pathway products participate in the pathogenesis of obstructive sleep apnea in childhood or alternatively that SDB promotes CysLTs biosynthesis.
PMID: 19141528 [PubMed - indexed for MEDLINE]
Pediatr Pulmonol. 2009 May;44(5):417-22.
Neurocognitive and behavioral impact of sleep disordered breathing in children.
Owens JA.
Department of Ambulatory Pediatrics, Rhode Island Hospital, Providence, Rhode Island 02903, USA. owensleep@gmail.com
The consequences of poor quality and/or inadequate sleep in children and adolescents have become a major public health concern, and one in which pediatric health care professionals have become increasingly involved. In particular, insufficient and/or fragmented sleep resulting from primary sleep disorders such as obstructive sleep apnea (OSA), often compounded by the presence of comorbid sleep disorders as well as by voluntary sleep curtailment related to lifestyle and environmental factors, has been implicated in a host of negative consequences. These range from metabolic dysfunction and increased cardiovascular morbidity to impairments in mood and academic performance. The following review will focus on what is currently known about the effects of sleep disordered breathing (SDB) specifically on neurobehavioral and neurocognitive function in children. Because of the scarcity of literature on the cognitive and behavioral impact of sleep disorders in infants and very young children, this review will target largely the preschool/school-aged child and adolescent populations. In addition, the focus will be on a review of the most recent literature, as a supplement to several excellent previous reviews on the topic. (c) 2009 Wiley-Liss, Inc.
PMID: 19382210 [PubMed - indexed for MEDLINE]
Sunday, February 21, 2010
SLEEP APNEA AND TMJ DISORDERS ARE CLOSELY RELATED.
TMJ DISORDERS AND SLEEP APNEA DISORDERS ARE CLOSELY RELATED. THE BITE CHANGES THAT OCCUR WITH ORAL APPLIANCE THERAPY CAN BE CONTROLLED WITH REGULAR EXERCISE IN THE MORNING (EXERCISES ARE USUALLY FOR A COUPLE OF MINUTES ONLY) BUT MANY PAIENTS DISCONTINUE THEIR EXERCISES. I BELIEVE THE PRIMARY REASON IS THAT THEY ARE MORE COMFORTABLE WITH THEIR MANDIBLE (LOWER JAW) IN A FORWARD POSITION.
THE ANTERIOR POSITION OF THE JAW IS USUALLY NOT A PROBLEM FOR THE JOINTS BUT CAN CAUSE BITE CHANGES.
NEUROMUSCULAR DENTISTRY IS A EXCELLENT MANNER TO HANDLE BITE CHANGES WHEN PATIENTS DO NOT WISH TO RETURN TO THEIR ORIGINAL PATHOLOGIC BITES.
I CALL THE BITES PATHOLOGICAL BECAUSE IT DOES NOT MAINTAIN AN INTACT AIRWAY. THESE PATIENTS FREQUENTLY HAVE A FORWARD HEAD POSTURE THAT IS AN ADAPTATION TO INCREASE THE AIRWAY WHEN WE ARE AWAKE. UNFORTUNATELY FORWARD HEAD POSTURE IS IMPLICATED IN HEAD AND NECK PAIN AS WELL AS LOW BACK PAIN. IT IS THE ELIMINATION OF PAIN THAT IS A FREQUENT REASON PATIENTS DO NOT OBJECT TO THE BITE CHANGES OR FAIL TO DO THE EXERCISES TO PREVENT THEM.
IF YOU HAVE ANY HEAD OR NECK PAIN PLEASE CHECK OUT MY OTHER SITE HTTP://WWW.IHATEHEADACHES.ORG WHICH IS AN EXCELLENT SITE TO LEARN HOW CHRONIC HEADACHES AND/OR MIGRAINES CAN BE TREATED AND/OR ELIMINATED WITH A DIAGNOSTIC NEUROMUSCULAR ORTHOTIC. WHEN THE ORTHOTIC RELIEVES THE PAIN LONG TERM MANAGEMENT CAN BE ADDRESSED.
THE ANTERIOR POSITION OF THE JAW IS USUALLY NOT A PROBLEM FOR THE JOINTS BUT CAN CAUSE BITE CHANGES.
NEUROMUSCULAR DENTISTRY IS A EXCELLENT MANNER TO HANDLE BITE CHANGES WHEN PATIENTS DO NOT WISH TO RETURN TO THEIR ORIGINAL PATHOLOGIC BITES.
I CALL THE BITES PATHOLOGICAL BECAUSE IT DOES NOT MAINTAIN AN INTACT AIRWAY. THESE PATIENTS FREQUENTLY HAVE A FORWARD HEAD POSTURE THAT IS AN ADAPTATION TO INCREASE THE AIRWAY WHEN WE ARE AWAKE. UNFORTUNATELY FORWARD HEAD POSTURE IS IMPLICATED IN HEAD AND NECK PAIN AS WELL AS LOW BACK PAIN. IT IS THE ELIMINATION OF PAIN THAT IS A FREQUENT REASON PATIENTS DO NOT OBJECT TO THE BITE CHANGES OR FAIL TO DO THE EXERCISES TO PREVENT THEM.
IF YOU HAVE ANY HEAD OR NECK PAIN PLEASE CHECK OUT MY OTHER SITE HTTP://WWW.IHATEHEADACHES.ORG WHICH IS AN EXCELLENT SITE TO LEARN HOW CHRONIC HEADACHES AND/OR MIGRAINES CAN BE TREATED AND/OR ELIMINATED WITH A DIAGNOSTIC NEUROMUSCULAR ORTHOTIC. WHEN THE ORTHOTIC RELIEVES THE PAIN LONG TERM MANAGEMENT CAN BE ADDRESSED.
TMJ,TMD,Snoring, Sleep Apnea,Neuromuscular Dentistry,Freedom from Headaches in LaCrosse Wisconsin
I am constantly receiving e-mails that tell me that the I HATE CPAP site is the best site on the web with information on Sleep Apnea,Sleep Apnea treatment, information on Dental Sleep Medicine, oral appliances foor treating sleep apnea. I recently received a post from LaCrosse Wisconsin. The patient who did not tolerate CPAP was thrilled to learn that there was a comfortable alternative to CPAP and that Dr Kevin Ladesic in La Crosse was an expert at those prosdures. She was also happy to learn that he understood neurmuscular dentistry and how it could treat migraines, tension-type headaches and chronic daily headaches as well as the more typical TMJ disorders (TMJ)
Nap 'boosts' brain learning power according to article on BBC news.
"Sleep not only rights the wrong of prolonged wakefulness, but, at a neurocognitive level, it moves you beyond where you were before you took a nap" according to Dr Matthew Walker,at UC Berkeley.
I found this post on BBC news " The latest study, from the University of California at Berkeley, suggests that the brain may need sleep to process short-term memories, creating "space" for new facts to be learned. " http://news.bbc.co.uk/2/hi/health/8524549.stm
The quality of sleep at night as well as during naps determine how successfully are brains function cognitively and in terms of short term memory.
According to the BBC news "Dr Matthew Walker, who led the study, reported at the AAAS conference in San Diego, said: "Sleep not only rights the wrong of prolonged wakefulness, but, at a neurocognitive level, it moves you beyond where you were before you took a nap.
"It's as though the e-mail inbox in your hippocampus is full, and, until you sleep and clear out all those fact e-mails, you're not going to receive any more mail.
"It's just going to bounce until you sleep and move it into another folder."
However, Professor Derk-Jan Dijk, the director of the Surrey Sleep Research Centre, said that there was no clear evidence that daytime napping offered a distinct advantage over sleeping just once over 24 hours.
"The sleep-wake cycle is not as rigid as we might think - we have the capability to sleep in different ways."
He said that while the brain effect reported in the study might be spotted in a laboratory setting, the picture became more clouded in the "real world".
"The size of these effects are much more difficult to assess - if I have to learn something, for example, it's easier to do this when I'm feeling awake and alert than when I'm sleepy.""
I will try to read original studies and post again.
Dr Shapira
I found this post on BBC news " The latest study, from the University of California at Berkeley, suggests that the brain may need sleep to process short-term memories, creating "space" for new facts to be learned. " http://news.bbc.co.uk/2/hi/health/8524549.stm
The quality of sleep at night as well as during naps determine how successfully are brains function cognitively and in terms of short term memory.
According to the BBC news "Dr Matthew Walker, who led the study, reported at the AAAS conference in San Diego, said: "Sleep not only rights the wrong of prolonged wakefulness, but, at a neurocognitive level, it moves you beyond where you were before you took a nap.
"It's as though the e-mail inbox in your hippocampus is full, and, until you sleep and clear out all those fact e-mails, you're not going to receive any more mail.
"It's just going to bounce until you sleep and move it into another folder."
However, Professor Derk-Jan Dijk, the director of the Surrey Sleep Research Centre, said that there was no clear evidence that daytime napping offered a distinct advantage over sleeping just once over 24 hours.
"The sleep-wake cycle is not as rigid as we might think - we have the capability to sleep in different ways."
He said that while the brain effect reported in the study might be spotted in a laboratory setting, the picture became more clouded in the "real world".
"The size of these effects are much more difficult to assess - if I have to learn something, for example, it's easier to do this when I'm feeling awake and alert than when I'm sleepy.""
I will try to read original studies and post again.
Dr Shapira
Wednesday, February 17, 2010
SWEDISH EPIDEMIOLOGY: OBSTRUCTIVE SLEEP APNEA INCREASE CARDIOVASCULAR MORBIDITY AND MORTALITY
Obstructive sleep apnea increases cardiovascular morbidity and mortality according to Swedish article. This increase suggests that OSA is an increased (additive) risk above and beyond established risk factors of obesity, hypertension, smoking and hyperlipidemia. (see PubMed Abstract below).
A second article (see PubMed abstract below) published in the Journal of Cardiology 2010 Jan;55(1):92-98 concluded that Sleep Apnea Syndrom increased nocturnal blood pressure even in patients without hypertension. Patients with severe apnea demomstrated more sever elevations in nocturnal blood pressure.
A Japanese study (Heart Vessels. 2010 Jan;25(1):63-9) showed effectiveness of CPAP in treating arrythmias. Sleep apnea treatment with oral appliances and dental sleep medicine should show identical results based on other studies comparing treatment outcomes. This study showed " The results of this study demonstrate a significant relationship between OSA and several cardiac disorders, and also demonstrate the efficacy of CPAP in preventing OSA-associated arrhythmias in a large population of Japanese patients." Again I expect that apnea treated with oral appliances would have similar outcomes to CPAP use. This study again relates cardiac disorders to obstructive sleep apnea.
Another review article (Curr Opin Pulm Med. 2009 Aug 2) "Heart failure and sleep-disordered breathing: mechanisms, consequences and treatment." reviews recent articles on Sleep disordered breathing and Heart Failure. The article's summary (see PubMed abstract below) say "The relationship between CHF (congestive heart failure) and SDB (sleep disordered breathing) is likely to be bidirectional, CHF impacting on SDB severity and vice versa. Identification of SDB in the CHF population appears to be important as it is probably associated with greater mortality, but whether SDB intervention significantly influences CHF survival still remains to be determined. The effects of each conition worsens the other. Treatment that eliminates sleep disordered breathing should result in positive effects on cardiac symptoms. The article also discusses patients with central sleep apnea associated with Cheyne-Stokes breathing. Unfortunately CPAP and Oral appliances are not effective for central sleep apnea but adaptive servo-ventilation shows encouraging results. "Small, short-term studies are discussed, however long-term randomized trials with objective cardiac outcomes are still lacking" in regards to aaptive servo-ventilation.
A key point from all of these studies is that sleep apnea is a dangerous condition with multiple associated morbidities and with treatment improvement in morbidities and mortality is seen. While CPAP is extremely effective studies show it is rejected by the majority of patients. Dental Sleep Medicine and oral appliances provide needed alternatives to CPAP. Oral appliances are a first line treatment for mild to moderate sleep apnea. Patients with severe apnea who do not tolerate CPAP will benefit from an oral appliances. Patients with central sleep apnea may want to consider sero-ventilation.
Anadolu Kardiyol Derg. 2010 Feb;10(1):75-80.
Cardiovascular consequences of sleep apnea: I -Epidemiology.
Turgut Celen Y, Peker Y.
Sleep Medicine Unit, Department of Neurology and Rehabilitation Medicine, Skaraborg Hospital, Skövde, Sweden. yuksel.peker@lungall.gu.se.
Obstructive sleep apnea (OSA) is common in general population. There is an accumulating research evidence for an independent relationship between OSA and cardiovascular morbidity and mortality. This relationship is stronger in clinical cohorts compared with the general population, which suggests that concomitant OSA in subjects with traditionally recognized risk factors such as obesity, hypertension, smoking, and hyperlipidemia may provide an additive risk factor for the cardiovascular consequences. In the current article, the clinic-and population-based epidemiologic data will be reviewed in this context.
PMID: 20150011 [PubMed - in process]
J Cardiol. 2010 Jan;55(1):92-98. Epub 2009 Nov 22.
Relationship between sleep apnea syndrome and sleep blood pressure in patients without hypertension.
Sekizuka H, Kida K, Akashi YJ, Yoneyama K, Osada N, Omiya K, Miyake F.
Division of Cardiology, Department of Internal Medicine, St. Marianna University School of Medicine, 2-16-1 Sugao Miyamae-ku, Kawasaki-city, Kanagawa-prefecture 216-8511, Japan.
BACKGROUND AND PURPOSE: Ambulatory blood pressure monitoring (ABPM) provides an accurate assessment of blood pressure (BP) and shows non-dipper BP pattern in many sleep apnea syndrome (SAS) patients with hypertension (HTN); however, little information is available on the relationship between the severity of SAS and circadian BP changes in SAS patients without HTN. This study investigated whether SAS patients without HTN would have different BP courses in the severity of SAS. METHODS AND SUBJECTS: Seventy-four consecutive outpatients without HTN [systolic BP (BPs) at clinic <140mmHg and/or diastolic BP (BPd) at clinic <90mmHg], who received no antihypertensives, underwent overnight polysomnography (PSG) and ABPM. The apnea-hypopnea index (AHI) was calculated from the PSG results; patients were stratified into the following 4 groups based on their AHI: non-SAS, mild-, moderate-, or severe-SAS. RESULTS: The diurnal BPs and BPd showed no differences in the severity of SAS; however, the sleep BPs, lowest BPs, and pre-awake BPs were significantly higher in the severe-SAS group than the non-SAS group (p=0.02, p=0.04, and p=0.006, respectively). The sleep BPd and pre-awake BPd were significantly higher in the severe-SAS than the non-SAS (p=0.01 and p=0.0003, respectively) and mild-SAS (p=0.01 and p=0.008, respectively) groups. CONCLUSIONS: The results of this study suggested that SAS affected nocturnal BP elevation even in SAS patients without HTN. The diurnal BP showed no difference in the severity of SAS; however, the severe-SAS group revealed significant nocturnal BP elevation. Copyright © 2009 Japanese College of Cardiology. Published by Elsevier Ltd. All rights reserved.
PMID: 20122554 [PubMed - as supplied by publisher]
Heart Vessels. 2010 Jan;25(1):63-9. Epub 2010 Jan 21.
Efficacy of continuous positive airway pressure on arrhythmias in obstructive sleep apnea patients.
Abe H, Takahashi M, Yaegashi H, Eda S, Tsunemoto H, Kamikozawa M, Koyama J, Yamazaki K, Ikeda U.
Division of Cardiovascular Medicine, Shinshu University Graduate School of Medicine, 3-1-1 Asahi, Matsumoto, Nagano 390-8621, Japan.
The purpose of this study was to determine the relationship between obstructive sleep apnea (OSA) and cardiovascular disorders in a large Japanese population, and to assess the efficacy of continuous positive airway pressure (CPAP) in the treatment of OSA-associated arrhythmias. The study population comprised 1394 Japanese subjects (1086 men and 308 women) who were divided into four groups on the basis of polysomnography (PSG) analysis as follows: the no sleep apnea (N-SA) group (n = 44, apnea-hypopnea index [AHI] < 5), the mild OSA (Mi-OSA) group (n = 197, 5 < AHI < 15), the moderate OSA (Mo) group (n = 368, 15 < AHI < 30), and severe OSA (SOSA) group (n = 785, AHI < 30). The following baseline characteristics were significantly associated with OSA: age (P < 0.001), gender (P < 0.001), body mass index (P < 0.001), hypertension (P < 0.001), diabetes (P = 0.009), and hyperlipidemia (P = 0.013). In the OSA group, PSG revealed the predominance of paroxysmal atrial fibrillation (PAF) (P = 0.051), premature atrial complex short run (P < 0.005), premature ventricular complex (PVC, P = 0.004), sinus bradycardia (P = 0.036), and sinus pause (arrest >2 s, P < 0.001) during the PSG recording. A total of 316 patients from the group underwent CPAP titration and were then re-evaluated. Continuous positive airway pressure therapy significantly reduced the occurrences of PAF (P < 0.001), PVC (P = 0.016), sinus bradycardia (P = 0.001), and sinus pause (P = 0.004). The results of this study demonstrate a significant relationship between OSA and several cardiac disorders, and also demonstrate the efficacy of CPAP in preventing OSA-associated arrhythmias in a large population of Japanese patients.
PMID: 20091401 [PubMed - in process]
Curr Opin Pulm Med. 2009 Aug 26. [Epub ahead of print]
Heart failure and sleep-disordered breathing: mechanisms, consequences and treatment.
Kee K, Naughton MT.
Department of Allergy, Immunology and Respiratory Medicine, Alfred Hospital and Monash University, Melbourne, Victoria, Australia.
PURPOSE OF REVIEW: This review examines the recently published articles pertaining to sleep-disordered breathing (SDB) and heart failure. RECENT FINDINGS: The recent findings can be classified into pulmonary, upper airway and treatment trials. Pulmonary complications of heart failure include loss of surfactant, increased pulmonary dry weight and reduced lung volume, which are likely to increase plant gain and thus predispose to central sleep apnea with Cheyne-Stokes respiration. Upper airway narrowing in normal individuals has been shown to occur with lower limb compression and the supine body position, thus suggesting that rostral fluid shifts may narrow the upper airway and aggravate obstructive sleep apnea. Extrapolating this to congestive heart failure (CHF), it is possible that CHF fluid status may impact upon obstructive sleep apnea severity. Following the Canadian Continuous Positive Airway Pressure for Patients with Central Sleep Apnoea and Heart Failure trial, further SDB intervention studies have been reported using adaptive servo-ventilation. Although encouraging, small, short-term studies are discussed, however long-term randomized trials with objective cardiac outcomes are still lacking. SUMMARY: The relationship between CHF and SDB is likely to be bidirectional, CHF impacting on SDB severity and vice versa. Identification of SDB in the CHF population appears to be important as it is probably associated with greater mortality, but whether SDB intervention significantly influences CHF survival still remains to be determined.
PMID: 19713849 [PubMed - as supplied by publisher]
Anonymous has left a new comment on your post "SWEDISH EPIDEMIOLOGY: OBSTRUCTIVE SLEEP APNEA INC...":
Nice post and this enter helped me alot in my college assignement. Say thank you you on your information.
Dr Shapira: I get dozens of thank you's from high school and college students who use my site as a research source. I take pride in supplying the highest quality information. I recently spoke at Integrate Chicago a course on integrative medicine for medical stuents and many who attended my lectures had spent a considerable amount of time doing research on treatment of sleep apnea. The general response was that it was one of the best sites on the internet if you were looking for alternative treatments for sleep apnea.
Dr Shapira
A second article (see PubMed abstract below) published in the Journal of Cardiology 2010 Jan;55(1):92-98 concluded that Sleep Apnea Syndrom increased nocturnal blood pressure even in patients without hypertension. Patients with severe apnea demomstrated more sever elevations in nocturnal blood pressure.
A Japanese study (Heart Vessels. 2010 Jan;25(1):63-9) showed effectiveness of CPAP in treating arrythmias. Sleep apnea treatment with oral appliances and dental sleep medicine should show identical results based on other studies comparing treatment outcomes. This study showed " The results of this study demonstrate a significant relationship between OSA and several cardiac disorders, and also demonstrate the efficacy of CPAP in preventing OSA-associated arrhythmias in a large population of Japanese patients." Again I expect that apnea treated with oral appliances would have similar outcomes to CPAP use. This study again relates cardiac disorders to obstructive sleep apnea.
Another review article (Curr Opin Pulm Med. 2009 Aug 2) "Heart failure and sleep-disordered breathing: mechanisms, consequences and treatment." reviews recent articles on Sleep disordered breathing and Heart Failure. The article's summary (see PubMed abstract below) say "The relationship between CHF (congestive heart failure) and SDB (sleep disordered breathing) is likely to be bidirectional, CHF impacting on SDB severity and vice versa. Identification of SDB in the CHF population appears to be important as it is probably associated with greater mortality, but whether SDB intervention significantly influences CHF survival still remains to be determined. The effects of each conition worsens the other. Treatment that eliminates sleep disordered breathing should result in positive effects on cardiac symptoms. The article also discusses patients with central sleep apnea associated with Cheyne-Stokes breathing. Unfortunately CPAP and Oral appliances are not effective for central sleep apnea but adaptive servo-ventilation shows encouraging results. "Small, short-term studies are discussed, however long-term randomized trials with objective cardiac outcomes are still lacking" in regards to aaptive servo-ventilation.
A key point from all of these studies is that sleep apnea is a dangerous condition with multiple associated morbidities and with treatment improvement in morbidities and mortality is seen. While CPAP is extremely effective studies show it is rejected by the majority of patients. Dental Sleep Medicine and oral appliances provide needed alternatives to CPAP. Oral appliances are a first line treatment for mild to moderate sleep apnea. Patients with severe apnea who do not tolerate CPAP will benefit from an oral appliances. Patients with central sleep apnea may want to consider sero-ventilation.
Anadolu Kardiyol Derg. 2010 Feb;10(1):75-80.
Cardiovascular consequences of sleep apnea: I -Epidemiology.
Turgut Celen Y, Peker Y.
Sleep Medicine Unit, Department of Neurology and Rehabilitation Medicine, Skaraborg Hospital, Skövde, Sweden. yuksel.peker@lungall.gu.se.
Obstructive sleep apnea (OSA) is common in general population. There is an accumulating research evidence for an independent relationship between OSA and cardiovascular morbidity and mortality. This relationship is stronger in clinical cohorts compared with the general population, which suggests that concomitant OSA in subjects with traditionally recognized risk factors such as obesity, hypertension, smoking, and hyperlipidemia may provide an additive risk factor for the cardiovascular consequences. In the current article, the clinic-and population-based epidemiologic data will be reviewed in this context.
PMID: 20150011 [PubMed - in process]
J Cardiol. 2010 Jan;55(1):92-98. Epub 2009 Nov 22.
Relationship between sleep apnea syndrome and sleep blood pressure in patients without hypertension.
Sekizuka H, Kida K, Akashi YJ, Yoneyama K, Osada N, Omiya K, Miyake F.
Division of Cardiology, Department of Internal Medicine, St. Marianna University School of Medicine, 2-16-1 Sugao Miyamae-ku, Kawasaki-city, Kanagawa-prefecture 216-8511, Japan.
BACKGROUND AND PURPOSE: Ambulatory blood pressure monitoring (ABPM) provides an accurate assessment of blood pressure (BP) and shows non-dipper BP pattern in many sleep apnea syndrome (SAS) patients with hypertension (HTN); however, little information is available on the relationship between the severity of SAS and circadian BP changes in SAS patients without HTN. This study investigated whether SAS patients without HTN would have different BP courses in the severity of SAS. METHODS AND SUBJECTS: Seventy-four consecutive outpatients without HTN [systolic BP (BPs) at clinic <140mmHg and/or diastolic BP (BPd) at clinic <90mmHg], who received no antihypertensives, underwent overnight polysomnography (PSG) and ABPM. The apnea-hypopnea index (AHI) was calculated from the PSG results; patients were stratified into the following 4 groups based on their AHI: non-SAS, mild-, moderate-, or severe-SAS. RESULTS: The diurnal BPs and BPd showed no differences in the severity of SAS; however, the sleep BPs, lowest BPs, and pre-awake BPs were significantly higher in the severe-SAS group than the non-SAS group (p=0.02, p=0.04, and p=0.006, respectively). The sleep BPd and pre-awake BPd were significantly higher in the severe-SAS than the non-SAS (p=0.01 and p=0.0003, respectively) and mild-SAS (p=0.01 and p=0.008, respectively) groups. CONCLUSIONS: The results of this study suggested that SAS affected nocturnal BP elevation even in SAS patients without HTN. The diurnal BP showed no difference in the severity of SAS; however, the severe-SAS group revealed significant nocturnal BP elevation. Copyright © 2009 Japanese College of Cardiology. Published by Elsevier Ltd. All rights reserved.
PMID: 20122554 [PubMed - as supplied by publisher]
Heart Vessels. 2010 Jan;25(1):63-9. Epub 2010 Jan 21.
Efficacy of continuous positive airway pressure on arrhythmias in obstructive sleep apnea patients.
Abe H, Takahashi M, Yaegashi H, Eda S, Tsunemoto H, Kamikozawa M, Koyama J, Yamazaki K, Ikeda U.
Division of Cardiovascular Medicine, Shinshu University Graduate School of Medicine, 3-1-1 Asahi, Matsumoto, Nagano 390-8621, Japan.
The purpose of this study was to determine the relationship between obstructive sleep apnea (OSA) and cardiovascular disorders in a large Japanese population, and to assess the efficacy of continuous positive airway pressure (CPAP) in the treatment of OSA-associated arrhythmias. The study population comprised 1394 Japanese subjects (1086 men and 308 women) who were divided into four groups on the basis of polysomnography (PSG) analysis as follows: the no sleep apnea (N-SA) group (n = 44, apnea-hypopnea index [AHI] < 5), the mild OSA (Mi-OSA) group (n = 197, 5 < AHI < 15), the moderate OSA (Mo) group (n = 368, 15 < AHI < 30), and severe OSA (SOSA) group (n = 785, AHI < 30). The following baseline characteristics were significantly associated with OSA: age (P < 0.001), gender (P < 0.001), body mass index (P < 0.001), hypertension (P < 0.001), diabetes (P = 0.009), and hyperlipidemia (P = 0.013). In the OSA group, PSG revealed the predominance of paroxysmal atrial fibrillation (PAF) (P = 0.051), premature atrial complex short run (P < 0.005), premature ventricular complex (PVC, P = 0.004), sinus bradycardia (P = 0.036), and sinus pause (arrest >2 s, P < 0.001) during the PSG recording. A total of 316 patients from the group underwent CPAP titration and were then re-evaluated. Continuous positive airway pressure therapy significantly reduced the occurrences of PAF (P < 0.001), PVC (P = 0.016), sinus bradycardia (P = 0.001), and sinus pause (P = 0.004). The results of this study demonstrate a significant relationship between OSA and several cardiac disorders, and also demonstrate the efficacy of CPAP in preventing OSA-associated arrhythmias in a large population of Japanese patients.
PMID: 20091401 [PubMed - in process]
Curr Opin Pulm Med. 2009 Aug 26. [Epub ahead of print]
Heart failure and sleep-disordered breathing: mechanisms, consequences and treatment.
Kee K, Naughton MT.
Department of Allergy, Immunology and Respiratory Medicine, Alfred Hospital and Monash University, Melbourne, Victoria, Australia.
PURPOSE OF REVIEW: This review examines the recently published articles pertaining to sleep-disordered breathing (SDB) and heart failure. RECENT FINDINGS: The recent findings can be classified into pulmonary, upper airway and treatment trials. Pulmonary complications of heart failure include loss of surfactant, increased pulmonary dry weight and reduced lung volume, which are likely to increase plant gain and thus predispose to central sleep apnea with Cheyne-Stokes respiration. Upper airway narrowing in normal individuals has been shown to occur with lower limb compression and the supine body position, thus suggesting that rostral fluid shifts may narrow the upper airway and aggravate obstructive sleep apnea. Extrapolating this to congestive heart failure (CHF), it is possible that CHF fluid status may impact upon obstructive sleep apnea severity. Following the Canadian Continuous Positive Airway Pressure for Patients with Central Sleep Apnoea and Heart Failure trial, further SDB intervention studies have been reported using adaptive servo-ventilation. Although encouraging, small, short-term studies are discussed, however long-term randomized trials with objective cardiac outcomes are still lacking. SUMMARY: The relationship between CHF and SDB is likely to be bidirectional, CHF impacting on SDB severity and vice versa. Identification of SDB in the CHF population appears to be important as it is probably associated with greater mortality, but whether SDB intervention significantly influences CHF survival still remains to be determined.
PMID: 19713849 [PubMed - as supplied by publisher]
Anonymous has left a new comment on your post "SWEDISH EPIDEMIOLOGY: OBSTRUCTIVE SLEEP APNEA INC...":
Nice post and this enter helped me alot in my college assignement. Say thank you you on your information.
Dr Shapira: I get dozens of thank you's from high school and college students who use my site as a research source. I take pride in supplying the highest quality information. I recently spoke at Integrate Chicago a course on integrative medicine for medical stuents and many who attended my lectures had spent a considerable amount of time doing research on treatment of sleep apnea. The general response was that it was one of the best sites on the internet if you were looking for alternative treatments for sleep apnea.
Dr Shapira
Monday, February 15, 2010
Exploding Head Syndrome is a real sleep disorder
Exploding Head Syndrome is a real sleep disorder that I wrote about on my I HATE HEADACHES blog. You can find that blog at http://www.ihateheadaches.org/blogs/illinois/2010/01/exploding-head-syndrome-usually-does.html
I have received large numbers of patients ho have responded to the Exploding head syndrome blog. Here is a sample response.
"Not only is it real, it is terrifying to experience. I hope to find some more information, but it is a comfort to have a name for this and the knowledge that I am not (completely) crazy."
Patients find it terrifying but find comfort in having a name, Exploding head syndrome. I am posting the entire blog below:
Dr. Shapira's Chicago Headache Blog
* Tell us about your headaches...
*
*
*
*
*
*
* required |Privacy Policy
Friday, January 29, 2010
EXPLODING HEAD SYNDROME USUALLY DOES NOT HAVE SIGNIFICANT PAIN ASSOCIATED WITH IT.
Exploding head syndrome is an interesting syndrome of unknown pathogenisis. It is documented and accepted in the International Classification of Sleep Disorders (ICSD).
An article by Casucci G, d'Onofrio F, Torelli P. discusses " trigeminal autonomic cephalalgias (TACs) and hemicrania continua, while the latter comprise classical trigeminal neuralgia, hypnic headache, primary thunderclap headache, and exploding head syndrome." This article in Neurol Sci. 2004 Oct;25 Suppl 3:S77-83 and discusses Rare primary headaches: clinical insights.
The symptoms (according to ICSD) are:
"The patient complains of a sudden loud noise or sense of explosion in the head at either the wake-sleep transition or upon waking during the night."
" The experience is not associated with significant pain complaints"
"The patient rouses immediately after the event, usually with a sense of fright"
It is considered to be a seperate entity from Idiopathic Stabbing Headache (ice pick headache) which is benign and characterized by brief stabs of pain on the side of the head.
It is also different than Thunderclap Headache which is a severe sudden-onset pain that must be considered a warning sign of a subarachnoid hemorrhage but can also be benign.
There are also cluster headaches, sleep related migraines and nocturnal paroxysmal hemicrania. It is possible that Exploding Head Syndrome is a pain free version of one of these disorders.
Severe migraines can be related to sleep apnea as well. See I HATE CPAP!! (http://www.ihatecpap.com)
PubMed abstract below:
J Neurol Neurosurg Psychiatry. 1989 Jul;52(7):907-10.
Clinical features of the exploding head syndrome.
Pearce JM.
Department of Neurology, Hull Royal Infirmary, UK.
Fifty patients suffering from the "exploding head syndrome" are described. This hitherto unreported syndrome is characterised by a sense of an explosive noise in the head usually in the twilight stage of sleep. The associated symptoms are varied, but the benign nature of the condition is emphasised and neither extensive investigation nor treatment are indicated.
PMID: 2769286 [PubMed - indexed for MEDLINE]
Neurol Sci. 2004 Oct;25 Suppl 3:S77-83.
Rare primary headaches: clinical insights.
Casucci G, d'Onofrio F, Torelli P.
U. O. di Medicina Generale, Casa di Cura San Francesco, Viale Europa 21, I-82037 Telese Terme (BN), Italy. gerardocasucci@tin.it
So-called "rare" headaches, whose prevalence rate is lower than 1% or is not known at all and have been reported in only a few dozen cases to date, constitute a very heterogeneous group. Those that are best characterised from the clinical point of view can be classified into forms with prominent autonomic features and forms with sparse or no autonomic features. Among the former are trigeminal autonomic cephalalgias (TACs) and hemicrania continua, while the latter comprise classical trigeminal neuralgia, hypnic headache, primary thunderclap headache, and exploding head syndrome. The major clinical discriminating factor for the differential diagnosis of TACs is the relationship between duration and frequency of attacks: the forms in which pain is shorter lived are those with the higher frequency of daily attacks. Other aspects to be considered are the time pattern of symptoms, intensity and timing of attacks, the patient's behaviour during the attacks, the presence of any triggering factors and of the refractory period after an induced attack, and response to therapy, especially with indomethacin. Often these are little known clinical entities, which are not easily detected in clinical practice. For some of them, e. g., thunderclap headache, it is always necessary to perform instrumental tests to exclude the presence of underlying organic diseases.
PMID: 15549575 [PubMed - indexed for MEDLINE]
Labels: nocturnal migraine, SLEEP APNEA, thunderclap headache
I have received large numbers of patients ho have responded to the Exploding head syndrome blog. Here is a sample response.
"Not only is it real, it is terrifying to experience. I hope to find some more information, but it is a comfort to have a name for this and the knowledge that I am not (completely) crazy."
Patients find it terrifying but find comfort in having a name, Exploding head syndrome. I am posting the entire blog below:
Dr. Shapira's Chicago Headache Blog
* Tell us about your headaches...
*
*
*
*
*
*
* required |Privacy Policy
Friday, January 29, 2010
EXPLODING HEAD SYNDROME USUALLY DOES NOT HAVE SIGNIFICANT PAIN ASSOCIATED WITH IT.
Exploding head syndrome is an interesting syndrome of unknown pathogenisis. It is documented and accepted in the International Classification of Sleep Disorders (ICSD).
An article by Casucci G, d'Onofrio F, Torelli P. discusses " trigeminal autonomic cephalalgias (TACs) and hemicrania continua, while the latter comprise classical trigeminal neuralgia, hypnic headache, primary thunderclap headache, and exploding head syndrome." This article in Neurol Sci. 2004 Oct;25 Suppl 3:S77-83 and discusses Rare primary headaches: clinical insights.
The symptoms (according to ICSD) are:
"The patient complains of a sudden loud noise or sense of explosion in the head at either the wake-sleep transition or upon waking during the night."
" The experience is not associated with significant pain complaints"
"The patient rouses immediately after the event, usually with a sense of fright"
It is considered to be a seperate entity from Idiopathic Stabbing Headache (ice pick headache) which is benign and characterized by brief stabs of pain on the side of the head.
It is also different than Thunderclap Headache which is a severe sudden-onset pain that must be considered a warning sign of a subarachnoid hemorrhage but can also be benign.
There are also cluster headaches, sleep related migraines and nocturnal paroxysmal hemicrania. It is possible that Exploding Head Syndrome is a pain free version of one of these disorders.
Severe migraines can be related to sleep apnea as well. See I HATE CPAP!! (http://www.ihatecpap.com)
PubMed abstract below:
J Neurol Neurosurg Psychiatry. 1989 Jul;52(7):907-10.
Clinical features of the exploding head syndrome.
Pearce JM.
Department of Neurology, Hull Royal Infirmary, UK.
Fifty patients suffering from the "exploding head syndrome" are described. This hitherto unreported syndrome is characterised by a sense of an explosive noise in the head usually in the twilight stage of sleep. The associated symptoms are varied, but the benign nature of the condition is emphasised and neither extensive investigation nor treatment are indicated.
PMID: 2769286 [PubMed - indexed for MEDLINE]
Neurol Sci. 2004 Oct;25 Suppl 3:S77-83.
Rare primary headaches: clinical insights.
Casucci G, d'Onofrio F, Torelli P.
U. O. di Medicina Generale, Casa di Cura San Francesco, Viale Europa 21, I-82037 Telese Terme (BN), Italy. gerardocasucci@tin.it
So-called "rare" headaches, whose prevalence rate is lower than 1% or is not known at all and have been reported in only a few dozen cases to date, constitute a very heterogeneous group. Those that are best characterised from the clinical point of view can be classified into forms with prominent autonomic features and forms with sparse or no autonomic features. Among the former are trigeminal autonomic cephalalgias (TACs) and hemicrania continua, while the latter comprise classical trigeminal neuralgia, hypnic headache, primary thunderclap headache, and exploding head syndrome. The major clinical discriminating factor for the differential diagnosis of TACs is the relationship between duration and frequency of attacks: the forms in which pain is shorter lived are those with the higher frequency of daily attacks. Other aspects to be considered are the time pattern of symptoms, intensity and timing of attacks, the patient's behaviour during the attacks, the presence of any triggering factors and of the refractory period after an induced attack, and response to therapy, especially with indomethacin. Often these are little known clinical entities, which are not easily detected in clinical practice. For some of them, e. g., thunderclap headache, it is always necessary to perform instrumental tests to exclude the presence of underlying organic diseases.
PMID: 15549575 [PubMed - indexed for MEDLINE]
Labels: nocturnal migraine, SLEEP APNEA, thunderclap headache
Sunday, February 14, 2010
Restless Legs and Celiac Disease
Below is an interesting abstract that ties restless legs to low serum feritin and restless legs to Celiac disease.. Sometimes restless legs is tied to UARS or RERA's other times it is due to low feritin levels or other problems.
Sleep Med. 2009 Aug;10(7):763-5. Epub 2009 Jan 12.
Celiac disease as a possible cause for low serum ferritin in patients with restless legs syndrome.
Manchanda S, Davies CR, Picchietti D.
University of Illinois at Urbana-Champaign, College of Medicine, 506 S. Mathews Avenue, Suite 190, Urbana, IL 61801, USA. smanchan@illinois.edu
OBJECTIVE: To describe celiac disease (CD) as a possible cause for low serum ferritin in patients with restless legs syndrome (RLS). BACKGROUND: Low iron stores have been found to be a risk factor for RLS with serum ferritin levels less than 45-50 ng/mL associated with increased severity of RLS. It has become routine clinical practice to test serum ferritin in the initial assessment of RLS. CD is a common genetic disorder that can cause iron deficiency. METHODS: Consecutive case series of four patients with RLS and serum ferritin below 25 ng/mL, who had positive screening tests for celiac disease. RESULTS: We report four patients who had serum ferritin < 12 ng/mL and positive screening tests for CD. All had CD confirmed by duodenal biopsy and response to a gluten-free diet. RLS symptoms improved in all four, with two able to discontinue RLS medication and two responding without medication. CONCLUSIONS: In patients with RLS and low serum ferritin who do not have an obvious cause for iron deficiency, we suggest looking for CD by simple, inexpensive serologic testing. Diagnosis and treatment of CD is likely to improve the outcome for RLS, as well as identify individuals who are at risk for the significant long-term complications of CD.
PMID: 19138881 [PubMed - indexed for MEDLINE]
Sleep Med. 2009 Aug;10(7):763-5. Epub 2009 Jan 12.
Celiac disease as a possible cause for low serum ferritin in patients with restless legs syndrome.
Manchanda S, Davies CR, Picchietti D.
University of Illinois at Urbana-Champaign, College of Medicine, 506 S. Mathews Avenue, Suite 190, Urbana, IL 61801, USA. smanchan@illinois.edu
OBJECTIVE: To describe celiac disease (CD) as a possible cause for low serum ferritin in patients with restless legs syndrome (RLS). BACKGROUND: Low iron stores have been found to be a risk factor for RLS with serum ferritin levels less than 45-50 ng/mL associated with increased severity of RLS. It has become routine clinical practice to test serum ferritin in the initial assessment of RLS. CD is a common genetic disorder that can cause iron deficiency. METHODS: Consecutive case series of four patients with RLS and serum ferritin below 25 ng/mL, who had positive screening tests for celiac disease. RESULTS: We report four patients who had serum ferritin < 12 ng/mL and positive screening tests for CD. All had CD confirmed by duodenal biopsy and response to a gluten-free diet. RLS symptoms improved in all four, with two able to discontinue RLS medication and two responding without medication. CONCLUSIONS: In patients with RLS and low serum ferritin who do not have an obvious cause for iron deficiency, we suggest looking for CD by simple, inexpensive serologic testing. Diagnosis and treatment of CD is likely to improve the outcome for RLS, as well as identify individuals who are at risk for the significant long-term complications of CD.
PMID: 19138881 [PubMed - indexed for MEDLINE]
Sleep Med. 2009 Aug;10(7):763-5. Epub 2009 Jan 12.
Celiac disease as a possible cause for low serum ferritin in patients with restless legs syndrome.
Manchanda S, Davies CR, Picchietti D.
University of Illinois at Urbana-Champaign, College of Medicine, 506 S. Mathews Avenue, Suite 190, Urbana, IL 61801, USA. smanchan@illinois.edu
OBJECTIVE: To describe celiac disease (CD) as a possible cause for low serum ferritin in patients with restless legs syndrome (RLS). BACKGROUND: Low iron stores have been found to be a risk factor for RLS with serum ferritin levels less than 45-50 ng/mL associated with increased severity of RLS. It has become routine clinical practice to test serum ferritin in the initial assessment of RLS. CD is a common genetic disorder that can cause iron deficiency. METHODS: Consecutive case series of four patients with RLS and serum ferritin below 25 ng/mL, who had positive screening tests for celiac disease. RESULTS: We report four patients who had serum ferritin < 12 ng/mL and positive screening tests for CD. All had CD confirmed by duodenal biopsy and response to a gluten-free diet. RLS symptoms improved in all four, with two able to discontinue RLS medication and two responding without medication. CONCLUSIONS: In patients with RLS and low serum ferritin who do not have an obvious cause for iron deficiency, we suggest looking for CD by simple, inexpensive serologic testing. Diagnosis and treatment of CD is likely to improve the outcome for RLS, as well as identify individuals who are at risk for the significant long-term complications of CD.
PMID: 19138881 [PubMed - indexed for MEDLINE]
Celiac disease as a possible cause for low serum ferritin in patients with restless legs syndrome.
Manchanda S, Davies CR, Picchietti D.
University of Illinois at Urbana-Champaign, College of Medicine, 506 S. Mathews Avenue, Suite 190, Urbana, IL 61801, USA. smanchan@illinois.edu
OBJECTIVE: To describe celiac disease (CD) as a possible cause for low serum ferritin in patients with restless legs syndrome (RLS). BACKGROUND: Low iron stores have been found to be a risk factor for RLS with serum ferritin levels less than 45-50 ng/mL associated with increased severity of RLS. It has become routine clinical practice to test serum ferritin in the initial assessment of RLS. CD is a common genetic disorder that can cause iron deficiency. METHODS: Consecutive case series of four patients with RLS and serum ferritin below 25 ng/mL, who had positive screening tests for celiac disease. RESULTS: We report four patients who had serum ferritin < 12 ng/mL and positive screening tests for CD. All had CD confirmed by duodenal biopsy and response to a gluten-free diet. RLS symptoms improved in all four, with two able to discontinue RLS medication and two responding without medication. CONCLUSIONS: In patients with RLS and low serum ferritin who do not have an obvious cause for iron deficiency, we suggest looking for CD by simple, inexpensive serologic testing. Diagnosis and treatment of CD is likely to improve the outcome for RLS, as well as identify individuals who are at risk for the significant long-term complications of CD.
PMID: 19138881 [PubMed - indexed for MEDLINE]
Neuromuscular Dentistry: Treatment and Elimination of Migraines,Tension-Type Headaches, Chronic Daily Headaches and Facial Pain
The following is a reprint of my article I was asked to write for the American Equilibation society. There are a couple of pictures that are not included in the text but can be found on the Sleep and Health Journal Site @ http://www.sleepandhealth.com/neuromuscular-dentistry
This article was written to explain Neuromuscular Dentistry to TMJ dentists who are not familiar with the field. I firmly believe that all TMJ treatment is better if neuromuscular dental techniques are used to perfect position.
Neuromuscular Dentistry
NEUROMUSCULAR DENTISTRY (originally published in the American Equilibration Society magazine)
Ira L Shapira DDS, DABDSM, DAAPM, FICCMO
Neuromuscular Dentistry remains an enigma to many dentists who do not understand the purposes of the electrodes, the TENS, the computers and more. It has unfairly become a target of poor and misleading definitions by doctors who do not understand its basic principles.
There are several basic premises that underlie Neuromuscular Dentistry. The first premise is that the stomatognathic muscles are the primary determinate of the mandibles position during all jaw functions (when the teeth are not in occlusion) and that rest position is one of the most important positions in dentistry. Rest position is a maxillary to mandibular jaw relation where the teeth are not in occlusion but are prepared to occlude. In Neuromuscular Dentistry Rest is a position of bilaterally equal and low muscle tonicity from which the mandible moves into full occlusion with minimal muscle accommodation. Following closure from rest position the mandible should return to rest with similarly balanced low muscle tonicity. Rest position is determined not only by the mandible’s relation to the cranium but also by the position of the head relative to the body, the suprahyoid and infrahyoid muscles and the position of the hyoid bone. To fully understand the relation of jaw movement to head posture read the Quadrant Theorem of GUZAY (Available from the ADA Library). In essence it shows in engineering terms that after accounting for both rotation and translation of the mandible the actual axis of rotation of the mandible is at the odontoid process of the second vertebrae not at the mandible condylar head.
The second premise is that occlusion is important in neuromuscular dentistry as a resetting mechanism of the trigeminal nervous system’s control of the stomatognathic muscles. Myocentric occlusion is ideally a position in which the muscles move the mandible from a non-torqued rest position into full occlusion with minimal muscle accommodation and no interferences of occlusal contacts until full closure is attained thus eliminating all torque during closure. This means that there are no noxious contacts received by the periodontal ligaments or the muscular proprioceptors that must be avoided by the muscles (accommodation) but rather allow “free” entry into myocentric occlusion. The jaw muscles will return to rest position after closure with the muscles maintaining their healthy low tonicity. Relaxed healthy musculature is the gold standard of neuromuscular dentistry.
Swallowing is a primary activity when the jaw is closed into full occlusion. In order to swallow it is necessary to fixate the mandible and this happens as the teeth occlude. During chewing, speaking and other jaw functions the teeth do not actually occlude in normal function but are separated (during chewing by a bolus of food). Typically swallowing occurs approximately 2000 times a day and is momentary accounting for 6-10 minutes maximum time in occlusion over the course of the day and acts as a neuromuscular reset switch for trigeminally innervated muscles. During a healthy swallow the teeth will move freely without interference into full occlusion with bilateral equal contact and bilateral equal muscle activity and then return to rest position with low muscle tonicity. A deviate swallow as evidenced by scalloping of the tongue is a sign of a possible TMJ disorder and is also 80% predictive of sleep apnea (80% predictive in Dental study- 70% predictive ENT study)
Neuromuscular occlusion (myocentric) occurs when centric occlusion (maximum non-torqued intercuspation of teeth) is coincidental with a balanced muscle closure where the muscles will return to their relaxed state following closure. Myocentric is the ideal position for swallowing.
The dentist utilizing neuromuscular techniques does not determine a specific position of the condyles in the fossa. The position of the disk and condyle are determined primarily by the teeth (bite or orthotic during occlusal correction therapy) in occlusion (myocentric) and the application of muscle activity. Neuromuscular dentistry allows the patients healthy relaxed muscles to determine the joint relations with the teeth serving as a neuromuscular reset switch during closure. Neuromuscular dentistry rejects the notion that manipulation of the patient’s jaw by the intervention of the clinician muscles are more important in determining the relation of the components of the TM Joint than the muscles of the patient. Centric relation is not used as a reference position for mounting casts on an articulator. Centric Relation is considered a border movement of the mandible and as reported in orthopedic literature joints are rarely used in their border positions.
The HIP plane (defined by hamular notches, incisive papilla and the occipital condyles) and/or Campers plane is used to relate the maxilla to an articulator. When cosmetic considerations are involved photos are used to to incorporate this physiologic plane to soft tissues of the face. Ideally the occlusal plane (parallel to the HIP Plane) will bisect the odontoid process of the axis of the atlantoaxial joint the actual center of rotation for the mandible after accounting for translation and rotation according to the quadrant theorem.
This occlusal plane will be at a 90-degree angle to gravitational force when the head is in an upright position. A neuromuscular bite is used to mount the
mandibular casts according to data from EMG recordings and jaw tracings with TENS. The incorporation of the Curve of Spee based on Centro Masticale (CM) point which continues thru the mandibular condyle and the Curve of Wilson also based on CM point that is involved is stimulation of the autonomic nervous system via tongue reflexes when the lateral border of the tongue touches the lingual surfaces of the teeth. (Critical Reviews in Oral Biology & Medicine, Vol. 13, No. 5, 409-425 (2002)) This excellent article is available online at http://cro.sagepub.com/cgi/content/full/13/5/409
Neuromuscular dentistry considers many of the problems associated with TMD to be repetitive strain injuries. Movements become harmful when closure requires excessive accommodation and then the system fails at its weakest link. If the weakest link is muscle health we will see formation of tender sore muscles with eventual formation of taut bands and trigger points. If there is muscle overuse from clenching and/or grinding there will be post exercise pain secondary to anaerobic lactic acid build-up. If the weakest point is in the TM Joint then when repetitive strain occurs the muscle accommodation will lead to increased intra-articular pressure. This again will break down the joint at its weakest point. This may occur as a displaced disk or as wear of articular surfaces or many other conditions. It may come at the expense of the bone of the condyle leading to flattening or beaking of the condyle. Clenching and bruxism are two particularly well-known and harmful parafunctional habits that lead to varied repetitive strain injuries. There are many other parafunctions that can lead to problems. Some parafunctions are actually protective muscle accommodation such as the deviated or reversed swallow that protects the TM Joints and masticatory muscles at the expense of altered head, hyoid and spine position and consequent muscle problems.
The second type of problems would be described as I/O or Input/ output errors in computer lingo. The CNS is essentially a biological computer and is affected by input from afferent nerves from the body. Autonomic system function include the fight or flight response with concomitant release of adrenaline that alters the heart rate, blood pressure, muscle tone etc. This system effects the Hypothalamus pituitary complex with feedback to the adrenals and effects on ACTH and cortisol levels. During periods of acute stress these effects have a positive survival value but during chronic stress become a liability to the individual as described by Hans Selye in his book “The Stress of Life” and his discussion of the General Adaptation Syndrome. There are numerous biochemical changes that occur in the brain secondary to aberrant or nociceptive input into the brain these can be affected by correction of the neurological input, by using drugs to change the brain chemistry or a combination of these approaches. Ideally correction of the underlying cause of these biochemical changes is the preferred method of treatment.
The utilization of TENS or transcutaneous neural stimulation over the coronoid notch has been shown by Mitani and Fujii (1974 J. Dent Res.) to block the motor division of the trigeminal nerve and relax the musculature via anti-dromic impulses (hyperpolarisation) to both the alpha and gamma motor neurons without influence from proprioceptive and nocioceptive (tooth contacts) inputs The TENS is then use to create a balanced synchronize pulsing to find the trajectory of closure where a myocentric registration can be obtained. The muscles will return to their relaxed position following closure into myocentric.
The use of Computerized mandibular jaw tracking allows the dentist to measure and record resting jaw position relative to the cranium at a given head position. The location of myocentric occlusion is determined by the dentist with the aid of information from tracings recorded.
Electromyography or EMG is used to record relative values of resting muscle activity of masticatory muscles as well as muscles such as Sternocleidomastoid or Trapezius. While there are no absolute “normal values” of resting muscles the clinician uses his information to compare muscle activity within a given patient. Muscles should be approximately equal activity bilaterally. Thomas 1990 in Frontiers of Oral Physiology vol 7 pp162-170 demonstrated that Spectral analysis of the post TENS EMG may be utilized to evaluate muscle fatigue and differentiate between muscle atrophy or fatigue or relaxed muscle states. This was later confirmed by Frucht, Jonas and Kappert at Frieberg University in 1995 (Fortschr.Kieferorthop vol 56 pp 245-253)
Utilizing the two modalities together allows the clinician to evaluate the rest position of the jaw and simultaneously the health and functional activity of the muscles.
The EMG also allows tests to evaluate the functional capacity of the muscles and again compare the right and left sides for symmetry. The use of functional recordings (during clenching and closure into centric occlusion) allows the clinician to evaluate whether or not muscle function is satisfactory and functional. The use of EMG also allows evaluation and correction of first contact of closure position within microseconds bases on firing order of the masseter and temporalis muscles. The first point of contact on closure is vitally important and equilibration of orthotics and dentition must be finely adjusted until first contact is evenly dispersed on posterior dentition.
Neuromuscular dentistry is very concerned with the effects of mandibular position on the body as a whole and on the effects of the body on jaw and head position. The work of Sherrington and the righting reflex explains how ascending and descending disorders affect a patient. These phenomena have been best explained by Norman Thomas BDS, PhD. I will not attempt to explain this complicated topic in this agenda, which may be found in Anthology of ICCMO vol V pp159-170. It obviously must incorporate the Quadrant Theorem of Casey Guzay, the physiological aspects of the balance organ of the inner ear and the vestibular apparatus located in the brainstem as well as visual feedback. The control of sympathetic and parasympathetic systems by the cerebellum is quite intricate and also affected by head position.
Correction of the chewing cycle is an important part of occlusal finalization. It must be understood that the chewing cycle is different on the each side and that interferences can occur on both the opening and closing strokes of the chewing cycle. Interferences in chewing strokes are easiest to detect by study of the chewing strokes on computerized mandibular scans (MKG). Head position during chewing is not is normally in the upright head position but in the feeding position approximately a 30-degree anterior head flexion. Correction of the chewing cycle is at least as important as correction of right, left and protrusive excursions. Chewing is a healthy function of the craniomandibular apparatus where as excursive movements are actually exercises in parafunctional movements.
There is more commonality to treatment of TMJ disorders by neuromuscular and non-neuromuscular dentists than differences and complications caused by neural intensification in the reticular activating system, emotional aspects and the relation to the limbic system, connections to the sympathetic and parasympathetic nervous systems via the Sphenopalatine Ganglion and sympathetic chain, and chemical changes and cerebroplastic changes that occur during chronic pain leading to hyperalgesia and allodynia all can be discussed in greater detail and explained in relation to neuromuscular dentistry. The basics physiology including effects of Golgi tendon organs and muscle spindles on jaw muscles remain constant and must always be carefully considered during treatment.
Barney Jankelson’s famous quote, “if it is measured it is a fact otherwise it is an opinion “ rings as true today as when he first said it. Neuromuscular dentistry is about making accurate measurements and the use of those measurements to improve the doctor’s ability to make a differential diagnosis and tailor treatment to relieve pain and create stable restorative dentistry with healthy relaxed musculature.
I would like to make a disclaimer that this is my personal definition of Neuromuscular dentistry from 30 years of practice and to thank my mentors Barney Jankelson, Barry Cooper, Dayton Krajiec, Richard Coy, Harold Gelb, Peter Neff, Robert Jankelson and especially Jim Garry who first made me understand the connections between increased upper airway resistance and the common developmental aspects of sleep apnea and craniomandibular disorders. A special thank you for Dr Norman Thomas for his extraordinary help in understanding the complex physiology and anatomy underlying neuromuscular dentistry and in reviewing this paper prior to presentation.
My personal research in the 1980’s as a visiting assistant professor at Rush Medical School examined the jaw relations of patients with obstructive sleep apnea based on neuromuscular evaluations of jaw relations with a Myotronic's kinesiograph and a myomonitor to find neuromuscular rest position. These studies showed jaw relations in the male apnea patients that were strikingly similar to those found in female TMD patients. The National Heart Lung and Blood Institute considers sleep apnea to be a TMJ disorder. The NHLBI published a report, “Cardiovascular and Sleep Related Consequences of TMJ Disorders” in 2001 that can be found at http://www.nhlbi.nih.gov/meetings/workshops/tmj_wksp.pdf
Dr Shapira returned to Rush as an assistant professor at the sleep center in the 1990’s where he treated a wide variety of obstructive apnea patients with commercial and customized intraoral sleep appliances. He was a founding and credentialed member of the Sleep Disorder Dental Society that has become the American Academy of Dental Sleep Medicine, He is a Diplomate of the American Board of Dental Sleep Medicine, on the board of the Illinois Sleep Society, a Diplomat of the American Academy of Pain Management, a Regent Fellow of the International College of Cranio-Manibular Orthopedics and a representative of that group to the TMD Alliance. He is a long time member of AES, AACFP, Academy of Sleep Medicine and the Chicago Dental Society. Dr Shapira teaches hands-on in-depth Dental Sleep Medicine courses to small groups at his Gurnee office. A family history of genetic cancer led Dr Shapira into research on stem cells an he also holds several patents (method and device) on the collection of stem cells during early minimally invasive removal of the uncalcified tooth bud of developing third molars. This procedure can be complete in minutes with greatly reduced morbidity compared to current surgical techniques used for removal of developed third molars. He hopes in the future that patients will routinely remove the tooth buds and collect and save the stem cells for anti-aging and regenerative medical uses.
This article was written to explain Neuromuscular Dentistry to TMJ dentists who are not familiar with the field. I firmly believe that all TMJ treatment is better if neuromuscular dental techniques are used to perfect position.
Neuromuscular Dentistry
NEUROMUSCULAR DENTISTRY (originally published in the American Equilibration Society magazine)
Ira L Shapira DDS, DABDSM, DAAPM, FICCMO
Neuromuscular Dentistry remains an enigma to many dentists who do not understand the purposes of the electrodes, the TENS, the computers and more. It has unfairly become a target of poor and misleading definitions by doctors who do not understand its basic principles.
There are several basic premises that underlie Neuromuscular Dentistry. The first premise is that the stomatognathic muscles are the primary determinate of the mandibles position during all jaw functions (when the teeth are not in occlusion) and that rest position is one of the most important positions in dentistry. Rest position is a maxillary to mandibular jaw relation where the teeth are not in occlusion but are prepared to occlude. In Neuromuscular Dentistry Rest is a position of bilaterally equal and low muscle tonicity from which the mandible moves into full occlusion with minimal muscle accommodation. Following closure from rest position the mandible should return to rest with similarly balanced low muscle tonicity. Rest position is determined not only by the mandible’s relation to the cranium but also by the position of the head relative to the body, the suprahyoid and infrahyoid muscles and the position of the hyoid bone. To fully understand the relation of jaw movement to head posture read the Quadrant Theorem of GUZAY (Available from the ADA Library). In essence it shows in engineering terms that after accounting for both rotation and translation of the mandible the actual axis of rotation of the mandible is at the odontoid process of the second vertebrae not at the mandible condylar head.
The second premise is that occlusion is important in neuromuscular dentistry as a resetting mechanism of the trigeminal nervous system’s control of the stomatognathic muscles. Myocentric occlusion is ideally a position in which the muscles move the mandible from a non-torqued rest position into full occlusion with minimal muscle accommodation and no interferences of occlusal contacts until full closure is attained thus eliminating all torque during closure. This means that there are no noxious contacts received by the periodontal ligaments or the muscular proprioceptors that must be avoided by the muscles (accommodation) but rather allow “free” entry into myocentric occlusion. The jaw muscles will return to rest position after closure with the muscles maintaining their healthy low tonicity. Relaxed healthy musculature is the gold standard of neuromuscular dentistry.
Swallowing is a primary activity when the jaw is closed into full occlusion. In order to swallow it is necessary to fixate the mandible and this happens as the teeth occlude. During chewing, speaking and other jaw functions the teeth do not actually occlude in normal function but are separated (during chewing by a bolus of food). Typically swallowing occurs approximately 2000 times a day and is momentary accounting for 6-10 minutes maximum time in occlusion over the course of the day and acts as a neuromuscular reset switch for trigeminally innervated muscles. During a healthy swallow the teeth will move freely without interference into full occlusion with bilateral equal contact and bilateral equal muscle activity and then return to rest position with low muscle tonicity. A deviate swallow as evidenced by scalloping of the tongue is a sign of a possible TMJ disorder and is also 80% predictive of sleep apnea (80% predictive in Dental study- 70% predictive ENT study)
Neuromuscular occlusion (myocentric) occurs when centric occlusion (maximum non-torqued intercuspation of teeth) is coincidental with a balanced muscle closure where the muscles will return to their relaxed state following closure. Myocentric is the ideal position for swallowing.
The dentist utilizing neuromuscular techniques does not determine a specific position of the condyles in the fossa. The position of the disk and condyle are determined primarily by the teeth (bite or orthotic during occlusal correction therapy) in occlusion (myocentric) and the application of muscle activity. Neuromuscular dentistry allows the patients healthy relaxed muscles to determine the joint relations with the teeth serving as a neuromuscular reset switch during closure. Neuromuscular dentistry rejects the notion that manipulation of the patient’s jaw by the intervention of the clinician muscles are more important in determining the relation of the components of the TM Joint than the muscles of the patient. Centric relation is not used as a reference position for mounting casts on an articulator. Centric Relation is considered a border movement of the mandible and as reported in orthopedic literature joints are rarely used in their border positions.
The HIP plane (defined by hamular notches, incisive papilla and the occipital condyles) and/or Campers plane is used to relate the maxilla to an articulator. When cosmetic considerations are involved photos are used to to incorporate this physiologic plane to soft tissues of the face. Ideally the occlusal plane (parallel to the HIP Plane) will bisect the odontoid process of the axis of the atlantoaxial joint the actual center of rotation for the mandible after accounting for translation and rotation according to the quadrant theorem.
This occlusal plane will be at a 90-degree angle to gravitational force when the head is in an upright position. A neuromuscular bite is used to mount the
mandibular casts according to data from EMG recordings and jaw tracings with TENS. The incorporation of the Curve of Spee based on Centro Masticale (CM) point which continues thru the mandibular condyle and the Curve of Wilson also based on CM point that is involved is stimulation of the autonomic nervous system via tongue reflexes when the lateral border of the tongue touches the lingual surfaces of the teeth. (Critical Reviews in Oral Biology & Medicine, Vol. 13, No. 5, 409-425 (2002)) This excellent article is available online at http://cro.sagepub.com/cgi/content/full/13/5/409
Neuromuscular dentistry considers many of the problems associated with TMD to be repetitive strain injuries. Movements become harmful when closure requires excessive accommodation and then the system fails at its weakest link. If the weakest link is muscle health we will see formation of tender sore muscles with eventual formation of taut bands and trigger points. If there is muscle overuse from clenching and/or grinding there will be post exercise pain secondary to anaerobic lactic acid build-up. If the weakest point is in the TM Joint then when repetitive strain occurs the muscle accommodation will lead to increased intra-articular pressure. This again will break down the joint at its weakest point. This may occur as a displaced disk or as wear of articular surfaces or many other conditions. It may come at the expense of the bone of the condyle leading to flattening or beaking of the condyle. Clenching and bruxism are two particularly well-known and harmful parafunctional habits that lead to varied repetitive strain injuries. There are many other parafunctions that can lead to problems. Some parafunctions are actually protective muscle accommodation such as the deviated or reversed swallow that protects the TM Joints and masticatory muscles at the expense of altered head, hyoid and spine position and consequent muscle problems.
The second type of problems would be described as I/O or Input/ output errors in computer lingo. The CNS is essentially a biological computer and is affected by input from afferent nerves from the body. Autonomic system function include the fight or flight response with concomitant release of adrenaline that alters the heart rate, blood pressure, muscle tone etc. This system effects the Hypothalamus pituitary complex with feedback to the adrenals and effects on ACTH and cortisol levels. During periods of acute stress these effects have a positive survival value but during chronic stress become a liability to the individual as described by Hans Selye in his book “The Stress of Life” and his discussion of the General Adaptation Syndrome. There are numerous biochemical changes that occur in the brain secondary to aberrant or nociceptive input into the brain these can be affected by correction of the neurological input, by using drugs to change the brain chemistry or a combination of these approaches. Ideally correction of the underlying cause of these biochemical changes is the preferred method of treatment.
The utilization of TENS or transcutaneous neural stimulation over the coronoid notch has been shown by Mitani and Fujii (1974 J. Dent Res.) to block the motor division of the trigeminal nerve and relax the musculature via anti-dromic impulses (hyperpolarisation) to both the alpha and gamma motor neurons without influence from proprioceptive and nocioceptive (tooth contacts) inputs The TENS is then use to create a balanced synchronize pulsing to find the trajectory of closure where a myocentric registration can be obtained. The muscles will return to their relaxed position following closure into myocentric.
The use of Computerized mandibular jaw tracking allows the dentist to measure and record resting jaw position relative to the cranium at a given head position. The location of myocentric occlusion is determined by the dentist with the aid of information from tracings recorded.
Electromyography or EMG is used to record relative values of resting muscle activity of masticatory muscles as well as muscles such as Sternocleidomastoid or Trapezius. While there are no absolute “normal values” of resting muscles the clinician uses his information to compare muscle activity within a given patient. Muscles should be approximately equal activity bilaterally. Thomas 1990 in Frontiers of Oral Physiology vol 7 pp162-170 demonstrated that Spectral analysis of the post TENS EMG may be utilized to evaluate muscle fatigue and differentiate between muscle atrophy or fatigue or relaxed muscle states. This was later confirmed by Frucht, Jonas and Kappert at Frieberg University in 1995 (Fortschr.Kieferorthop vol 56 pp 245-253)
Utilizing the two modalities together allows the clinician to evaluate the rest position of the jaw and simultaneously the health and functional activity of the muscles.
The EMG also allows tests to evaluate the functional capacity of the muscles and again compare the right and left sides for symmetry. The use of functional recordings (during clenching and closure into centric occlusion) allows the clinician to evaluate whether or not muscle function is satisfactory and functional. The use of EMG also allows evaluation and correction of first contact of closure position within microseconds bases on firing order of the masseter and temporalis muscles. The first point of contact on closure is vitally important and equilibration of orthotics and dentition must be finely adjusted until first contact is evenly dispersed on posterior dentition.
Neuromuscular dentistry is very concerned with the effects of mandibular position on the body as a whole and on the effects of the body on jaw and head position. The work of Sherrington and the righting reflex explains how ascending and descending disorders affect a patient. These phenomena have been best explained by Norman Thomas BDS, PhD. I will not attempt to explain this complicated topic in this agenda, which may be found in Anthology of ICCMO vol V pp159-170. It obviously must incorporate the Quadrant Theorem of Casey Guzay, the physiological aspects of the balance organ of the inner ear and the vestibular apparatus located in the brainstem as well as visual feedback. The control of sympathetic and parasympathetic systems by the cerebellum is quite intricate and also affected by head position.
Correction of the chewing cycle is an important part of occlusal finalization. It must be understood that the chewing cycle is different on the each side and that interferences can occur on both the opening and closing strokes of the chewing cycle. Interferences in chewing strokes are easiest to detect by study of the chewing strokes on computerized mandibular scans (MKG). Head position during chewing is not is normally in the upright head position but in the feeding position approximately a 30-degree anterior head flexion. Correction of the chewing cycle is at least as important as correction of right, left and protrusive excursions. Chewing is a healthy function of the craniomandibular apparatus where as excursive movements are actually exercises in parafunctional movements.
There is more commonality to treatment of TMJ disorders by neuromuscular and non-neuromuscular dentists than differences and complications caused by neural intensification in the reticular activating system, emotional aspects and the relation to the limbic system, connections to the sympathetic and parasympathetic nervous systems via the Sphenopalatine Ganglion and sympathetic chain, and chemical changes and cerebroplastic changes that occur during chronic pain leading to hyperalgesia and allodynia all can be discussed in greater detail and explained in relation to neuromuscular dentistry. The basics physiology including effects of Golgi tendon organs and muscle spindles on jaw muscles remain constant and must always be carefully considered during treatment.
Barney Jankelson’s famous quote, “if it is measured it is a fact otherwise it is an opinion “ rings as true today as when he first said it. Neuromuscular dentistry is about making accurate measurements and the use of those measurements to improve the doctor’s ability to make a differential diagnosis and tailor treatment to relieve pain and create stable restorative dentistry with healthy relaxed musculature.
I would like to make a disclaimer that this is my personal definition of Neuromuscular dentistry from 30 years of practice and to thank my mentors Barney Jankelson, Barry Cooper, Dayton Krajiec, Richard Coy, Harold Gelb, Peter Neff, Robert Jankelson and especially Jim Garry who first made me understand the connections between increased upper airway resistance and the common developmental aspects of sleep apnea and craniomandibular disorders. A special thank you for Dr Norman Thomas for his extraordinary help in understanding the complex physiology and anatomy underlying neuromuscular dentistry and in reviewing this paper prior to presentation.
My personal research in the 1980’s as a visiting assistant professor at Rush Medical School examined the jaw relations of patients with obstructive sleep apnea based on neuromuscular evaluations of jaw relations with a Myotronic's kinesiograph and a myomonitor to find neuromuscular rest position. These studies showed jaw relations in the male apnea patients that were strikingly similar to those found in female TMD patients. The National Heart Lung and Blood Institute considers sleep apnea to be a TMJ disorder. The NHLBI published a report, “Cardiovascular and Sleep Related Consequences of TMJ Disorders” in 2001 that can be found at http://www.nhlbi.nih.gov/meetings/workshops/tmj_wksp.pdf
Dr Shapira returned to Rush as an assistant professor at the sleep center in the 1990’s where he treated a wide variety of obstructive apnea patients with commercial and customized intraoral sleep appliances. He was a founding and credentialed member of the Sleep Disorder Dental Society that has become the American Academy of Dental Sleep Medicine, He is a Diplomate of the American Board of Dental Sleep Medicine, on the board of the Illinois Sleep Society, a Diplomat of the American Academy of Pain Management, a Regent Fellow of the International College of Cranio-Manibular Orthopedics and a representative of that group to the TMD Alliance. He is a long time member of AES, AACFP, Academy of Sleep Medicine and the Chicago Dental Society. Dr Shapira teaches hands-on in-depth Dental Sleep Medicine courses to small groups at his Gurnee office. A family history of genetic cancer led Dr Shapira into research on stem cells an he also holds several patents (method and device) on the collection of stem cells during early minimally invasive removal of the uncalcified tooth bud of developing third molars. This procedure can be complete in minutes with greatly reduced morbidity compared to current surgical techniques used for removal of developed third molars. He hopes in the future that patients will routinely remove the tooth buds and collect and save the stem cells for anti-aging and regenerative medical uses.
Tongue Reduction Surgery for Treating Obstructive Sleep Apnea
I am frequently asked by patients what the best sleep apnea surgery. I have decided to do a series of posts on surgery to treat sleep apnea. I am going to cover tongue reduction surgery today. The tongue is much more important than the soft palate when obstructive sleep apnea is being treated.
The soft palate is basically a free swinging door. When you breathe in it opens and directs air down the oropharynx and into the lungs via the bronchi. If the tongue is back against the posterior pharyngeal wall it prevents the soft palate from opening. You can reduce the soft palate thru numerous painful surgeries with associated morbidities but the airway will remain obstructed due to the position of the tongue. A second alternative is to move the tongue out of the way of the soft palate to allow it to open freely. This is the primary method that oral appliances use to open the airway. They move the jaw forward and the tongue comes forward due to the genioglossus attatchment, you use a TRD or tongue retaining device to pull the tongue forward or you use a tongue restraining device to prevent the tongue from falling back (Full Breath Appliance).
The tongue is the strongest muscle in the body and when we look in the mouth only see about 20% of the total tongue. The rest is under the floor of the mouth down to the hyoid bone. The easies way to understand how the tongue blocks the airway is compare the tongue and the mouth to a car and a garage.
If we have an economy size tongue (car) and an economy size mouth (garage) the system works fine. If we have a Hummer size tongue and a Hummer size garage it also works fine. The problems begin when we have a Hummer size tongue and try to fit it in an economy size garage.
In this example the only way a Hummer fits in the economy size garage with the door closed it to drive it thru the back wall. This is exactly what happens with sleep apnea, the tongue goes back against the posterior pharyngeal wall and and down toward the epiglottis and blocks the airway and prevents the soft palate from swinging open to allow in air.
To complicate matters inspiration or breathing in causes a vaccumn that actually sucks the tongue downward and backward it the direction of the vacumn creating the airway blockage.
There are several surgeries that can be used to reduce the size and position of the tongue.
The first is a median Rhomboid Glossectomy, which is the removal of a rhomboid shaped area in the middle of the tongue. I have never had a patient who has had this procedure but I have talked to three surgeons who each did the proceedure once and never planned on doing it again. It has been described as a nightmare surgery to me. My rule of thumb is that surgeons like to do surgery and you probably do not want a surgery they do not want to do.
The second surgical reduction is an anterior wedge removal and closure. Basically a pizza slice is taken out of the front of the tongu and the parts are sewn together. This is a very easy surgery that could be done awake in an oral surgeons or ENT's office. It is done frequently in South America because it is easy and efficient. The tongue then postures forward out of the posterior pharyngeal areas (throat). The downside to this surgery is that all the goood tastebuds are primarily in this region of the tongue and the bitter or nasty taste buds are left after the surgery. The bad news is that nothing will ever taste good again, the good news is that this will make it easier to lose weight. For red wine lovers from now on you will only taste the tannins, need I say more.
It is also possible to do a base of the tongue reduction, this is not recommended for the severely obese (see abstract at end of post). This study showed a higher morbidity with a base of tongue surgery relative to radiofrequency surgery when combined uvulopalatopharyngealplasty (UP3). The success rate was over 50% however success was defined as a 50% reduction in apnea. Even the successful cases may still require CPAP or Oral Appliance therapy because the definition for success was set very low. In obese patients the success rate was significantly lower, only 10-12 1/2 % .
This can be done as a single surgical visit where an opening is made across the back of the tongue and and the insides are grossly scooped out. The coblation proceedure is much less traumatic and can be seen at: http://www.youtube.com/watch?v=uq4WcVQg__c The somnoplasty proceedure is the least traumatic with the lowest morbidity but will require several surgeries. I do not see successful base of tongue reduction patients because they are not looking for oral appliance therapy but patients I have seen who have been thru one or two somnoplasty treatment sessions in the base of the tongue and refuse additional surgery are always very easy to treat with oral appliances. This is much different than failed UP3 surgeries which are sometimes more difficult to treat du to scarring.
Tongue advancements are another group of surgeries that we will discuss in the future but include hyoid suspension, genioglossus advancement (several types).
Whie I am not a big fan of surgery for treating sleep apnea in most patient coblation and especially somnoplasty can significantly improve sleep apnea. The Somnoplasty proceedure has the lowest risk and morbidity of all tongue reduction procedures.
There is a quote I love "There is no disease or disorder known to man that cannot be made worse by sticking a knife in it!" This does not mean not to have surgery done but ask lots of questions about the procedure, what can go wrong and if there is a problem can it be fixed. Treatment of Sleep Apnea is essential but we want the cure to improve your quality of life.
Excellent questions are:
How many surgeries have you done?
can I talk to a patient who had successful surgery?
What are possible side effects?
Can I speak to patients who had those side effects?
Are the side effects permanent if they occur?
What is the recovery time?
etc
Make sure all of your questions and concerns are addressed before having surgery done. Bring your list of questions to your consult so you do not forget to ask them. Check them off as you go.
An excellent study on base of tongue surgery was done in Otolaryngol Head Neck Surg. 2009 Jun;140(6):917-23.
The Pub Med abstract is listed below for your convenience.
1: Otolaryngol Head Neck Surg. 2009 Jun;140(6):917-23. Epub 2009 Apr 15.Links
Randomized study comparing two tongue base surgeries for moderate to severe obstructive sleep apnea syndrome.
Fernández-Julián E, Muñoz N, Achiques MT, GarcÃa-Pérez MA, Orts M, Marco J.
Otorhinolaryngology Department, Hospital ClÃnico Universitario, University of Valencia, Valencia, Spain. fernandez_enr@gva.es
OBJECTIVE: To compare the effectiveness and morbidity of the tongue base radiofrequency and tongue base suspension techniques combined with uvulopalatopharyngoplasty for moderate to severe obstructive sleep apnea. STUDY DESIGN AND SETTING: Prospective and randomized surgical trial at a university hospital. METHODS: In total, 57 patients received either tongue base radiofrequency reduction (n = 29) or tongue base suspension (n = 28). Apnea-hypopnea index, lowest oxygen saturation (polysomnography), Epworth score, and side effects were assessed. Success was defined as a > or =50 percent reduction and final apneahypopnea index < 15/h, and an Epworth score < 11. RESULTS: The success rates of the two procedures were 57.1 percent and 51.7 percent, respectively (P = 0.79), but only 12.5 percent and 10 percent, respectively (P = 0.87), in obese patients. Body mass index (P = 0.0002) was the main predictor of success in a logistic regression analysis. Tongue base suspension demonstrated higher morbidity (P < 0.05). CONCLUSIONS: The effectiveness of tongue base suspension was similar to that of tongue base radiofrequency reduction, although with significantly higher morbidity, for moderate to severe obstructive sleep apnea. The effectiveness of both techniques was lower in obese patients. SIGNIFICANCE: Neither technique should be used in obese patients who have moderate to severe obstructive sleep apnea.
PMID: 19467415 [PubMed - indexed for MEDLINE]
The soft palate is basically a free swinging door. When you breathe in it opens and directs air down the oropharynx and into the lungs via the bronchi. If the tongue is back against the posterior pharyngeal wall it prevents the soft palate from opening. You can reduce the soft palate thru numerous painful surgeries with associated morbidities but the airway will remain obstructed due to the position of the tongue. A second alternative is to move the tongue out of the way of the soft palate to allow it to open freely. This is the primary method that oral appliances use to open the airway. They move the jaw forward and the tongue comes forward due to the genioglossus attatchment, you use a TRD or tongue retaining device to pull the tongue forward or you use a tongue restraining device to prevent the tongue from falling back (Full Breath Appliance).
The tongue is the strongest muscle in the body and when we look in the mouth only see about 20% of the total tongue. The rest is under the floor of the mouth down to the hyoid bone. The easies way to understand how the tongue blocks the airway is compare the tongue and the mouth to a car and a garage.
If we have an economy size tongue (car) and an economy size mouth (garage) the system works fine. If we have a Hummer size tongue and a Hummer size garage it also works fine. The problems begin when we have a Hummer size tongue and try to fit it in an economy size garage.
In this example the only way a Hummer fits in the economy size garage with the door closed it to drive it thru the back wall. This is exactly what happens with sleep apnea, the tongue goes back against the posterior pharyngeal wall and and down toward the epiglottis and blocks the airway and prevents the soft palate from swinging open to allow in air.
To complicate matters inspiration or breathing in causes a vaccumn that actually sucks the tongue downward and backward it the direction of the vacumn creating the airway blockage.
There are several surgeries that can be used to reduce the size and position of the tongue.
The first is a median Rhomboid Glossectomy, which is the removal of a rhomboid shaped area in the middle of the tongue. I have never had a patient who has had this procedure but I have talked to three surgeons who each did the proceedure once and never planned on doing it again. It has been described as a nightmare surgery to me. My rule of thumb is that surgeons like to do surgery and you probably do not want a surgery they do not want to do.
The second surgical reduction is an anterior wedge removal and closure. Basically a pizza slice is taken out of the front of the tongu and the parts are sewn together. This is a very easy surgery that could be done awake in an oral surgeons or ENT's office. It is done frequently in South America because it is easy and efficient. The tongue then postures forward out of the posterior pharyngeal areas (throat). The downside to this surgery is that all the goood tastebuds are primarily in this region of the tongue and the bitter or nasty taste buds are left after the surgery. The bad news is that nothing will ever taste good again, the good news is that this will make it easier to lose weight. For red wine lovers from now on you will only taste the tannins, need I say more.
It is also possible to do a base of the tongue reduction, this is not recommended for the severely obese (see abstract at end of post). This study showed a higher morbidity with a base of tongue surgery relative to radiofrequency surgery when combined uvulopalatopharyngealplasty (UP3). The success rate was over 50% however success was defined as a 50% reduction in apnea. Even the successful cases may still require CPAP or Oral Appliance therapy because the definition for success was set very low. In obese patients the success rate was significantly lower, only 10-12 1/2 % .
This can be done as a single surgical visit where an opening is made across the back of the tongue and and the insides are grossly scooped out. The coblation proceedure is much less traumatic and can be seen at: http://www.youtube.com/watch?v=uq4WcVQg__c The somnoplasty proceedure is the least traumatic with the lowest morbidity but will require several surgeries. I do not see successful base of tongue reduction patients because they are not looking for oral appliance therapy but patients I have seen who have been thru one or two somnoplasty treatment sessions in the base of the tongue and refuse additional surgery are always very easy to treat with oral appliances. This is much different than failed UP3 surgeries which are sometimes more difficult to treat du to scarring.
Tongue advancements are another group of surgeries that we will discuss in the future but include hyoid suspension, genioglossus advancement (several types).
Whie I am not a big fan of surgery for treating sleep apnea in most patient coblation and especially somnoplasty can significantly improve sleep apnea. The Somnoplasty proceedure has the lowest risk and morbidity of all tongue reduction procedures.
There is a quote I love "There is no disease or disorder known to man that cannot be made worse by sticking a knife in it!" This does not mean not to have surgery done but ask lots of questions about the procedure, what can go wrong and if there is a problem can it be fixed. Treatment of Sleep Apnea is essential but we want the cure to improve your quality of life.
Excellent questions are:
How many surgeries have you done?
can I talk to a patient who had successful surgery?
What are possible side effects?
Can I speak to patients who had those side effects?
Are the side effects permanent if they occur?
What is the recovery time?
etc
Make sure all of your questions and concerns are addressed before having surgery done. Bring your list of questions to your consult so you do not forget to ask them. Check them off as you go.
An excellent study on base of tongue surgery was done in Otolaryngol Head Neck Surg. 2009 Jun;140(6):917-23.
The Pub Med abstract is listed below for your convenience.
1: Otolaryngol Head Neck Surg. 2009 Jun;140(6):917-23. Epub 2009 Apr 15.Links
Randomized study comparing two tongue base surgeries for moderate to severe obstructive sleep apnea syndrome.
Fernández-Julián E, Muñoz N, Achiques MT, GarcÃa-Pérez MA, Orts M, Marco J.
Otorhinolaryngology Department, Hospital ClÃnico Universitario, University of Valencia, Valencia, Spain. fernandez_enr@gva.es
OBJECTIVE: To compare the effectiveness and morbidity of the tongue base radiofrequency and tongue base suspension techniques combined with uvulopalatopharyngoplasty for moderate to severe obstructive sleep apnea. STUDY DESIGN AND SETTING: Prospective and randomized surgical trial at a university hospital. METHODS: In total, 57 patients received either tongue base radiofrequency reduction (n = 29) or tongue base suspension (n = 28). Apnea-hypopnea index, lowest oxygen saturation (polysomnography), Epworth score, and side effects were assessed. Success was defined as a > or =50 percent reduction and final apneahypopnea index < 15/h, and an Epworth score < 11. RESULTS: The success rates of the two procedures were 57.1 percent and 51.7 percent, respectively (P = 0.79), but only 12.5 percent and 10 percent, respectively (P = 0.87), in obese patients. Body mass index (P = 0.0002) was the main predictor of success in a logistic regression analysis. Tongue base suspension demonstrated higher morbidity (P < 0.05). CONCLUSIONS: The effectiveness of tongue base suspension was similar to that of tongue base radiofrequency reduction, although with significantly higher morbidity, for moderate to severe obstructive sleep apnea. The effectiveness of both techniques was lower in obese patients. SIGNIFICANCE: Neither technique should be used in obese patients who have moderate to severe obstructive sleep apnea.
PMID: 19467415 [PubMed - indexed for MEDLINE]
Friday, February 12, 2010
Using an Aqualizer to relieve jaw discomfort
Jaw pain is relatively infrequent with oral appliance therapy. If it affects you it is a major problem. Always discuss pain with your doctor because there are many easy fixes to the pain. Two of the best are spray and stretch to eliminate muscle pain using Dr Travell's techniques (see previous post) and an Aqualizer.
The Aqualizer was invented by Dr Marty Lerman and it can give remarkable relief to some patients with jaw pain. It is quick and easy to use and costs under $35 for an appliance. Wearing an Aqualizer for as little as 20 minutes can relieve jaw pain and for many other pains.
It is a simple form of Neuromuscular Dentistry that can be extremely helpful for patients using oral appliances to treat slep apnea.
The Aqualizer was invented by Dr Marty Lerman and it can give remarkable relief to some patients with jaw pain. It is quick and easy to use and costs under $35 for an appliance. Wearing an Aqualizer for as little as 20 minutes can relieve jaw pain and for many other pains.
It is a simple form of Neuromuscular Dentistry that can be extremely helpful for patients using oral appliances to treat slep apnea.
Thursday, February 11, 2010
Excellent Feedback on Sleep Apnea Treatment by Dr Poe
I have recently received excellent feedback from 2 patients on Dr William Poe in Los Alamitos, California. Bill took his initial course in oral appliances and Dental Sleep Medicine at my Gurnee office. Dental Sleep Medicine has grown to be a significant portion of his practice. Dr Poe loves improving lives and marriages by treating sleep apnea and eliminating snoring. Dr Poe is also a trained neuromuscular dentist who enjoys treating TMJ problems and headaches. The following is a recent post on http://www.ihateheadaches.org by Bill Poe.
"Am I Crazy or are my Headaches making me crazy?"
True statement made by a new patient during our first getting to know you meeting. "Am I Crazy or are my headaches making me crazy?" Can pain cause mental illness? I will have to look into that but I do see pain being the cause of irritability, a short fuse, and down right mean.
I try to concentrate on decreasing or eliminating the discomfort and then check your mental state. Its amazing how many of my non-neuromuscular dental colleagues do not treat TMJ/TMD. Their comments are usually something like "Those patients are crazy".
I have found just the opposite, that TMJ/TMD patients, once feeling better are the best patients and become their old selves again. Or at least that is what their family and friends say. And their demeanor in the office is 100% different from their 1st visit.
Constant pain can have a debilitating effect. Just ask someone who is in pain, and if it is you, then I wish you are on your way to reducing or better yet eliminating it.
Patients with snoring and/or sleep apnea will apprciate both the knowledge and care the Dr Poe gives each of his patients.
William C. Poe V, D.D.S.
4012 Katella Ave. Suite 203
Los Alamitos, California 9072
562.594.5067
E-mail contact form: http://www.orangecounty.ihatecpap.com/contact.html
"Am I Crazy or are my Headaches making me crazy?"
True statement made by a new patient during our first getting to know you meeting. "Am I Crazy or are my headaches making me crazy?" Can pain cause mental illness? I will have to look into that but I do see pain being the cause of irritability, a short fuse, and down right mean.
I try to concentrate on decreasing or eliminating the discomfort and then check your mental state. Its amazing how many of my non-neuromuscular dental colleagues do not treat TMJ/TMD. Their comments are usually something like "Those patients are crazy".
I have found just the opposite, that TMJ/TMD patients, once feeling better are the best patients and become their old selves again. Or at least that is what their family and friends say. And their demeanor in the office is 100% different from their 1st visit.
Constant pain can have a debilitating effect. Just ask someone who is in pain, and if it is you, then I wish you are on your way to reducing or better yet eliminating it.
Patients with snoring and/or sleep apnea will apprciate both the knowledge and care the Dr Poe gives each of his patients.
William C. Poe V, D.D.S.
4012 Katella Ave. Suite 203
Los Alamitos, California 9072
562.594.5067
E-mail contact form: http://www.orangecounty.ihatecpap.com/contact.html
Wednesday, February 10, 2010
OSA and Sleepwalking
According to a research study, almost 1 in 10 people suffering from obstructive sleep apnea also suffer from some form of parasomnia (sleepwalking). While obstructive sleep apnea may not cause parasomnia, it can make the condition worse if you are already predisposed to it. An experienced sleep dentist can help people determine if they are suffering from either parasomnia or sleep apnea.
Parasomnia is a sleeping condition many people suffer from that includes a few different symptoms like sleepwalking, sleep paralysis, acting-out dreams, hallucinations, and even eating or driving.
New research looked at the sleep records of 537 sleep patients and found that 51 patients who suffered from sleep apnea also suffered from one or more symptoms of parasomnia. This means that about 10 percent of sleep apnea sufferers may also be suffering from the symptoms of parasomnia. Parasomnia can be very dangerous, sleepwalking or driving while asleep can injure you or the people around you.
One of the reasons sleep apnea can put people more at risk for parasomnia is because the brain becomes active the going through a sleep apnea episode. During one of these episodes, the soft tissue in the throat closes and the body is momentarily deprived of oxygen; the brain is then aroused so that you can breathe again.
This brain arousal can cause the symptoms of parasomnia. Sleep apnea can have other hazardous affects on your health like an increased risk of heart attack, high blood pressure, and stroke. Some of the symptoms of sleep apnea include being tired during the day, snoring, depression, and weight gain.
If you believe that you or your sleeping partner is suffering from sleep apnea or parasomnia, there are solutions available to you. To put an end to your sleep problems, please contact Dr. Ira Shapira, Gurnee, Illinois sleep dentist today.
Parasomnia is a sleeping condition many people suffer from that includes a few different symptoms like sleepwalking, sleep paralysis, acting-out dreams, hallucinations, and even eating or driving.
New research looked at the sleep records of 537 sleep patients and found that 51 patients who suffered from sleep apnea also suffered from one or more symptoms of parasomnia. This means that about 10 percent of sleep apnea sufferers may also be suffering from the symptoms of parasomnia. Parasomnia can be very dangerous, sleepwalking or driving while asleep can injure you or the people around you.
One of the reasons sleep apnea can put people more at risk for parasomnia is because the brain becomes active the going through a sleep apnea episode. During one of these episodes, the soft tissue in the throat closes and the body is momentarily deprived of oxygen; the brain is then aroused so that you can breathe again.
This brain arousal can cause the symptoms of parasomnia. Sleep apnea can have other hazardous affects on your health like an increased risk of heart attack, high blood pressure, and stroke. Some of the symptoms of sleep apnea include being tired during the day, snoring, depression, and weight gain.
If you believe that you or your sleeping partner is suffering from sleep apnea or parasomnia, there are solutions available to you. To put an end to your sleep problems, please contact Dr. Ira Shapira, Gurnee, Illinois sleep dentist today.
Secret Weight Loss Hormone Now Available for Free. Leptin Can Be Your Answer! Lose Weight /Cure Sleep Apnea
Sleep Apnea and weight(BMI)have long been linked. Leptin and ghrelin are two hormones that are intimately linked to sleep and weight loss or weight gain. Leptin is the hormone that helps suppress your appetite and increase your metabolism. Increases in Leptin will make it easier to lose wieght because the cravings and nervous eating are decreased by this powerful appetite suppressant. It is not available at pharmacies and not covered by insurance but you can start to receive free doses immediately.
People who sleep less hours produce less leptin and tend to have lower blood levels of leptin. Low levels of this important hormone that helps suppress your appetite and increase your metabolism causes weight gain. Poor sleep,as seen with untreated sleep apnea will aslo decrease leptin production. Sleep loss also tends to increase your level of the hormone ghrelin. Grehlin stimulates your appetite which makes trying to diet a difficult ordeal. As a result of these two hormones people who sleep less may crave more and eat more. They especially may crave and eat more foods that are unhealthy. Patients in studies with sleep restriction have been shown to crave sweets, starch and salty snacks as a result of that sleep restriction.
TO RECEIVE YOUR FREE LEPTIN: SEVEN AND ONE HALF HOURS OF GOOD SLEEP IS THE ANSWER. iF YOU HAVE SLEEP APNEA MAKE SURE IT IS TREATED ALL NIGHT/ EVERY NIGHT.
Dieters have stuggled for years with every conceivable type of diet to produce weight loss. Sleeping better may be the easy answer to solving your weight issues.
There are several cycles in sleep and control of thyroid hormone and insulin hormone as well as cortisol the stress hormone are also affected by poor sleep. Disrupted sleep seen with sleep apnea can exacerbate all of these issues. With better sleep we are more active during the day which also increases our metabolism. With sleep apnea our oxygen levels are lower and our physiology slows down. The first period of Delta Sleep is where our body produces the majority of Growth Hormone. If that is disrupted by sleep apnea we are more likely to build up fat in our bodies at the expense of lean muscles according to a Universit of Chicago study.
The "Sleep Diet" may be the answer you have been looking for and a part of solving our national health crisis. Obesity in the U.S. is rising at an alarming pace among all age groups and all races and both sexes. The majority of Americans are overweight or obese with estimates of 60-75% of the population falling in these categories. The weight alone increases risks of high blood pressure,cancer and cardiovacular diseases including atherosclerosis, heart attack and stroke.
Research has shown many intriguing links between sleep quality, sleep quantity and BMI. Sleeping fewer hours tends increse the BMI to higher levels than people who sleep longer. Numerous studies have linked sleep to some of the hormones that help control body weight and appetite. There is no question about the link of sleep to insulin resistance and sugar metabolism. Obstructive sleep apnea probably repesents the single biggest risk of obesity because apnea is resposible fer massive in several health risks. Even mild sleep apnea and/or snoring related arousals can disrupt sleep patterns sufficienty to destroy normal sleep patterns and hormonal controls.
While good sleep may not be a total answer for obesity there is no doubt that improving the quality and quantity of healthy sleep will make weight loss easier both emotionally and physically on patients.
People who sleep less hours produce less leptin and tend to have lower blood levels of leptin. Low levels of this important hormone that helps suppress your appetite and increase your metabolism causes weight gain. Poor sleep,as seen with untreated sleep apnea will aslo decrease leptin production. Sleep loss also tends to increase your level of the hormone ghrelin. Grehlin stimulates your appetite which makes trying to diet a difficult ordeal. As a result of these two hormones people who sleep less may crave more and eat more. They especially may crave and eat more foods that are unhealthy. Patients in studies with sleep restriction have been shown to crave sweets, starch and salty snacks as a result of that sleep restriction.
TO RECEIVE YOUR FREE LEPTIN: SEVEN AND ONE HALF HOURS OF GOOD SLEEP IS THE ANSWER. iF YOU HAVE SLEEP APNEA MAKE SURE IT IS TREATED ALL NIGHT/ EVERY NIGHT.
Dieters have stuggled for years with every conceivable type of diet to produce weight loss. Sleeping better may be the easy answer to solving your weight issues.
There are several cycles in sleep and control of thyroid hormone and insulin hormone as well as cortisol the stress hormone are also affected by poor sleep. Disrupted sleep seen with sleep apnea can exacerbate all of these issues. With better sleep we are more active during the day which also increases our metabolism. With sleep apnea our oxygen levels are lower and our physiology slows down. The first period of Delta Sleep is where our body produces the majority of Growth Hormone. If that is disrupted by sleep apnea we are more likely to build up fat in our bodies at the expense of lean muscles according to a Universit of Chicago study.
The "Sleep Diet" may be the answer you have been looking for and a part of solving our national health crisis. Obesity in the U.S. is rising at an alarming pace among all age groups and all races and both sexes. The majority of Americans are overweight or obese with estimates of 60-75% of the population falling in these categories. The weight alone increases risks of high blood pressure,cancer and cardiovacular diseases including atherosclerosis, heart attack and stroke.
Research has shown many intriguing links between sleep quality, sleep quantity and BMI. Sleeping fewer hours tends increse the BMI to higher levels than people who sleep longer. Numerous studies have linked sleep to some of the hormones that help control body weight and appetite. There is no question about the link of sleep to insulin resistance and sugar metabolism. Obstructive sleep apnea probably repesents the single biggest risk of obesity because apnea is resposible fer massive in several health risks. Even mild sleep apnea and/or snoring related arousals can disrupt sleep patterns sufficienty to destroy normal sleep patterns and hormonal controls.
While good sleep may not be a total answer for obesity there is no doubt that improving the quality and quantity of healthy sleep will make weight loss easier both emotionally and physically on patients.
Sunday, February 7, 2010
"Oral appliance therapy for obstructive sleep apnea is an effective treatment and ideal for use in military recruits" ACCORDING TO NEW STUDY
A study reported in the January, 2010 Sleep and Breathing discusses effectiveness of oral appliances in treating sleep apnea. The study also showed that periodic leg movements occured in a small subset of patients during oral appliance titration. This problem has been shown previously to occur with CPAP as well. This can be a cause of continued tiredness after treatment with CPAP or an Oral Appliance and is another reason to always have a sleep study to evaluate CPAP OR ORAL APPLIANCE THERAPY SUCCESS.
Frequently low (normal) ferritin levels can cause periodic leg movements and this should be evaluated prior to drug therapy for restless leggs.
I have also had patients see relief of leg movements by taking calcium/magnesium supplements.
(PubMed abstract)
Sleep Breath. 2010 Jan 23. [Epub ahead of print]
Oral appliance titration in patients with obstructive sleep apnea induces the appearance of periodic limb movements.
Guerrero ML, Kim D, Rupp TL, Balkin TJ.
Department of Behavioral Biology, Walter Reed Army Institute of Research, 503 Robert Grant Avenue, Silver Spring, MD, 20910, USA, Melanie.guerrero@us.army.mil.
STUDY OBJECTIVES: Oral appliance (OA) therapy is considered a first line choice of therapy for some patients with mild or moderate obstructive sleep apnea (OSA) and an alternative form of treatment in those intolerant of continuous positive airway pressure (CPAP) use. According to several studies, periodic limb movements (PLM) appear during effective treatment of OSA with CPAP, but a similar phenomenon has not been described with the use of oral appliance. Herein, we describe the incidence of PLM in patients with OSA who underwent oral appliance therapy titration. DESIGN: This is a prospective, observational study set in a six-bed sleep center in an academic, military referral hospital. PATIENTS AND METHODS: Patients with OSA (n = 21; 15 men and six women; mean age, 43 years; and age range, 25 to 53 years) treated with OA during a 1-year period were enrolled. Patients were categorized according to the severity of sleep apnea and incidence of PLM on diagnostic polysomnography. Effective treatment of OSA and appearance or disappearance of PLM with arousal on subsequent oral appliance titration polysomnography were recorded and compared. RESULTS: Twenty-one patients were enrolled. During baseline polysomnography, three of 21 (14%) patients had five or more PLM with arousal per hour while 11 of 21 (52%) patients had PLM with arousal during the oral appliance titration trial. CONCLUSION: Oral appliance therapy for obstructive sleep apnea is an effective treatment and ideal for use in military recruits. The appearance of periodic limb movements with arousal during oral appliance use should be considered as a cause of persistent daytime sleepiness despite effective treatment of obstructive sleep apnea in this subset of patients.
Frequently low (normal) ferritin levels can cause periodic leg movements and this should be evaluated prior to drug therapy for restless leggs.
I have also had patients see relief of leg movements by taking calcium/magnesium supplements.
(PubMed abstract)
Sleep Breath. 2010 Jan 23. [Epub ahead of print]
Oral appliance titration in patients with obstructive sleep apnea induces the appearance of periodic limb movements.
Guerrero ML, Kim D, Rupp TL, Balkin TJ.
Department of Behavioral Biology, Walter Reed Army Institute of Research, 503 Robert Grant Avenue, Silver Spring, MD, 20910, USA, Melanie.guerrero@us.army.mil.
STUDY OBJECTIVES: Oral appliance (OA) therapy is considered a first line choice of therapy for some patients with mild or moderate obstructive sleep apnea (OSA) and an alternative form of treatment in those intolerant of continuous positive airway pressure (CPAP) use. According to several studies, periodic limb movements (PLM) appear during effective treatment of OSA with CPAP, but a similar phenomenon has not been described with the use of oral appliance. Herein, we describe the incidence of PLM in patients with OSA who underwent oral appliance therapy titration. DESIGN: This is a prospective, observational study set in a six-bed sleep center in an academic, military referral hospital. PATIENTS AND METHODS: Patients with OSA (n = 21; 15 men and six women; mean age, 43 years; and age range, 25 to 53 years) treated with OA during a 1-year period were enrolled. Patients were categorized according to the severity of sleep apnea and incidence of PLM on diagnostic polysomnography. Effective treatment of OSA and appearance or disappearance of PLM with arousal on subsequent oral appliance titration polysomnography were recorded and compared. RESULTS: Twenty-one patients were enrolled. During baseline polysomnography, three of 21 (14%) patients had five or more PLM with arousal per hour while 11 of 21 (52%) patients had PLM with arousal during the oral appliance titration trial. CONCLUSION: Oral appliance therapy for obstructive sleep apnea is an effective treatment and ideal for use in military recruits. The appearance of periodic limb movements with arousal during oral appliance use should be considered as a cause of persistent daytime sleepiness despite effective treatment of obstructive sleep apnea in this subset of patients.
Acne, ulcers, sores and other skin irritation from CPAP masks leads to dermatologists referrals
Several years ago I treated a patient with severe obstructive sleep apnea who had facial sores and acne from her CPAP mask. I treated her with a TAP appliance and we eliminated the sleep apnea. She has worn an appliance now for several years with no problems and loves it. Her dermatologist who had treated her sores, ulcers and acne did not see her after the oral appliance because the probleems were eliminated. Later she went in for a different problem and told her doctor about theTAP appliance and he came in shortly after and was fitted for an appliance. He did not mind the CPAP but his wife hated the CPAP noise. He has worn an appliance for several years now.
The interesting part of the story is this dermatologist became one of my best referring physicians. I have a few pulmonologists and neurologists who frequently refer patients and many internists. What is interesting is that I only have one cardiologist who ever refers patients for oral appliances, and he owns a sleep lab. With over half of patients not using their CPAP you would think that cardiologists would be on top of this critical patient care concern. Cardiologists are very good at referring patients to sleep centers but do not seem to follow-up to evaluate continued CPAP use.
A frequent time for diagnosis of apnea is after a first heart attack and apnea is witnessed by nurses in intensive care. I have seen more than a few patients who were diagnosed with sleep apne, rejected CPAP and went untreated until a cardiac event put the issue back on the table.
It is crucial that sleep apnea be treated, especially in cardiac patients. It does not matter if the treatment is CPAP, Oral Appliances or surgical intervention but treatment is essential.
The interesting part of the story is this dermatologist became one of my best referring physicians. I have a few pulmonologists and neurologists who frequently refer patients and many internists. What is interesting is that I only have one cardiologist who ever refers patients for oral appliances, and he owns a sleep lab. With over half of patients not using their CPAP you would think that cardiologists would be on top of this critical patient care concern. Cardiologists are very good at referring patients to sleep centers but do not seem to follow-up to evaluate continued CPAP use.
A frequent time for diagnosis of apnea is after a first heart attack and apnea is witnessed by nurses in intensive care. I have seen more than a few patients who were diagnosed with sleep apne, rejected CPAP and went untreated until a cardiac event put the issue back on the table.
It is crucial that sleep apnea be treated, especially in cardiac patients. It does not matter if the treatment is CPAP, Oral Appliances or surgical intervention but treatment is essential.
Thursday, February 4, 2010
PERMENANT BRAIN DAMAGE FROM SLEEP APNEA : FROM CHILDHOOD TO ADULT.
A RECENT ARTICLE IN JADA SPELLS OUT HOW PERMENANT CHANGES IN THE BRAIN CAN BE CAUSED BY UNTREATED SLEEP APNEA. CHANGES IN THE GRAY MATTER OF THE BRAIN HAVE BEEN SHOWN TO BE RELATED TO SLEEP APNEA. THE PUBMED ARTICLE IS COPIE BELOW.
J Am Dent Assoc. 2009 May;140(5):536-42.
The potentially harmful medical consequences of untreated sleep-disordered breathing: the evidence supporting brain damage.
Simmons MS, Clark GT.
Division of Diagnostic Sciences, University of Southern California School of Dentistry, Los Angeles, Calif., USA. drmichaelsimmons@aol.com
BACKGROUND: The authors conducted a literature review to evaluate whether current scientific evidence supports the fact that brain damage results from episodic hypoxia (EH) as seen during sleep-disordered breathing (SDB). TYPES OF STUDIES REVIEWED: In their review, the authors included models that re-created circumstances seen in EH during SDB. They reviewed animal and human studies, including those with children and animal pups as subjects. These studies addressed neurocognitive and neurobehavioral effects, physical changes found on a cellular level as seen in brain imaging and the effects of treatment. RESULTS: The evidence suggests that EH as seen during SDB causes damage to the brain with specific areas of gray- and white-matter loss, alteration in autonomic and motor regulation, and damage to higher cognitive functions. While there is evidence of spontaneous reactive mechanisms, it is not clear if they limit ongoing brain damage or contribute to additional damage. Retention of deficits in the brain even after treatment suggests long-term injury. CLINICAL IMPLICATIONS: Evidence shows that EH during SDB may cause permanent brain changes and can start early in the progression of sleep disorders even in childhood. SDB should be identified and treated early to reduce and possibly prevent brain damage and permanently decreased cognitive function. Dentists are in the unique position of being able to screen patients for SDB during periodic examinations while providing routine dental health care. When dentists catch SDB early in the progression and refer patients to and coordinate care with patients' physicians, they can provide better service to their patients and may prolong and improve their patients' quality of life.
PMID: 19411520 [PubMed - indexed for MEDLINE]
J Am Dent Assoc. 2009 May;140(5):536-42.
The potentially harmful medical consequences of untreated sleep-disordered breathing: the evidence supporting brain damage.
Simmons MS, Clark GT.
Division of Diagnostic Sciences, University of Southern California School of Dentistry, Los Angeles, Calif., USA. drmichaelsimmons@aol.com
BACKGROUND: The authors conducted a literature review to evaluate whether current scientific evidence supports the fact that brain damage results from episodic hypoxia (EH) as seen during sleep-disordered breathing (SDB). TYPES OF STUDIES REVIEWED: In their review, the authors included models that re-created circumstances seen in EH during SDB. They reviewed animal and human studies, including those with children and animal pups as subjects. These studies addressed neurocognitive and neurobehavioral effects, physical changes found on a cellular level as seen in brain imaging and the effects of treatment. RESULTS: The evidence suggests that EH as seen during SDB causes damage to the brain with specific areas of gray- and white-matter loss, alteration in autonomic and motor regulation, and damage to higher cognitive functions. While there is evidence of spontaneous reactive mechanisms, it is not clear if they limit ongoing brain damage or contribute to additional damage. Retention of deficits in the brain even after treatment suggests long-term injury. CLINICAL IMPLICATIONS: Evidence shows that EH during SDB may cause permanent brain changes and can start early in the progression of sleep disorders even in childhood. SDB should be identified and treated early to reduce and possibly prevent brain damage and permanently decreased cognitive function. Dentists are in the unique position of being able to screen patients for SDB during periodic examinations while providing routine dental health care. When dentists catch SDB early in the progression and refer patients to and coordinate care with patients' physicians, they can provide better service to their patients and may prolong and improve their patients' quality of life.
PMID: 19411520 [PubMed - indexed for MEDLINE]
Sleep Disorderd Breathing and All-Cause Mortality in 40 to 70 Year Old Men in Sleep Heart Health Study
An article in the September-October issud of Sleep Diagnosis and Therapy (vol4 No 6) reports on the results from the Sleep Heart Helth Study based on 6441 men and women in the study. With an average follow-up of over 8 years during which time 1047 participants died. There was a statistically significant increased risk of death particularly in men aged 40- 70 y/o. Intermittent hypoxia was independently associated with increases in all cause mortality.
The study concluded that "Sleep-disordered breathing is associated with all-cause mortality and specifically that due to coronary artery disease, particularly in men aged 40-70 years.
The study concluded that "Sleep-disordered breathing is associated with all-cause mortality and specifically that due to coronary artery disease, particularly in men aged 40-70 years.
Dr Shapira's Dental Sleep Medicine Course
I will be teaching my next course in Dental Sleep Medicine in April 2010. As always the course will be limited to 6 doctors and their teams. My course is limited to this small number to insure that each dentist walks and all team members are prepared to offer the finest in Dental Sleep Medicine to their patients. All doctors have a full year of follow-up consultation and mentoring as they improve their diagnostic and treatment skill.
The course includes two sleep appliances for the dentist taking the course and chairside experience in fitting appliances and taking bites. In addition numerous tricks and pearls as for treating pain and TMj disorders are taught including use of trigger point injections and sphenopalatine ganglion blocks.
If your dentist is not currently treating sleep apnea this is an excellent course for doctors serious about wanting to practice dental sleep medicine. It is not a large lecture format where the doctor is not ready to treat patients after the course.
The course includes two sleep appliances for the dentist taking the course and chairside experience in fitting appliances and taking bites. In addition numerous tricks and pearls as for treating pain and TMj disorders are taught including use of trigger point injections and sphenopalatine ganglion blocks.
If your dentist is not currently treating sleep apnea this is an excellent course for doctors serious about wanting to practice dental sleep medicine. It is not a large lecture format where the doctor is not ready to treat patients after the course.
New Medicare Guidelines for CPAP
The new medicare guidelines for CPAP coverage state that patients must have compliance of at least 4 hours a night and wear CPAP 70% of the time for a 30 consequtive day period.
These guidelines reflect how little CPAP is uded. Even with these looose standards medicare expects to save substantial dollars. $-5 hours is the average amount of time patients wear CPAP. 7-71/2 hours of nightly use is recommended. Ideally CPAP should be worn nightly.
If medicare required 90% usage or 6 hours of wear almost no one would qualify for coverage. I think the new standard for coverage is appropriate because it will save medicare the cost of buyiny CPAP machines that are not used (wasted taxpayer money)and patients who wear CPAP 4 hours nightly (average use for all patients) will have coverage. Medicare will cover CPAP based on low expectations of use that history and published studies have shown to be the case.
These guidelines reflect how little CPAP is uded. Even with these looose standards medicare expects to save substantial dollars. $-5 hours is the average amount of time patients wear CPAP. 7-71/2 hours of nightly use is recommended. Ideally CPAP should be worn nightly.
If medicare required 90% usage or 6 hours of wear almost no one would qualify for coverage. I think the new standard for coverage is appropriate because it will save medicare the cost of buyiny CPAP machines that are not used (wasted taxpayer money)and patients who wear CPAP 4 hours nightly (average use for all patients) will have coverage. Medicare will cover CPAP based on low expectations of use that history and published studies have shown to be the case.
Experimental reduction in slow wave sleep vs reduction in slow wave sleep in aging.
An interesting study in Sleep, the Journal of Sleep and Sleep disorder Research compares the effects on daytime sleepiness of experimental awakenings from slow wave sleep in different age groups. Experimental reductions in slow wave sleep (SWS)lead to increases in daytime sleepiness (measured by MSLT) but normal age related declies in Slow Wave Sleep seen in health aging do not increase daytime sleepiness.
The article concludes that "age-related declines inSWS and reduction in daytime sleep propensity may reflect a lessening in homeostatic sleep requirement." "Healthy adults without sleep disorders can expect to be less sleepy during the daytime than young adults."
Older adults frequently complain of sllep disruptions, early morning wakening, wakening not refreshed, daytime sleepiness, and daytime napping. According to this study older adults with healthy sleep should not be subject to daytime tiredness so the question is are they tired due to poor sleep, sleep apnea or other health related disturbances. Daytime tiredness can be considered not a normal consequence of aging but a sign of loss of good sleep. The percentage of Slow Wave Sleep declines with age but should not cause problems of tiredness in otherwise healthy older adults.
Older adults with excessive daytime sleepiness, napping or other signs of excessive daytime sleepiness should be evaluated for sleep disorders and/or disturbed sleep. These symptoms should not be written off as normal consequences of aging. Better sleep will result in a better quality of life for older adults.
The article concludes that "age-related declines inSWS and reduction in daytime sleep propensity may reflect a lessening in homeostatic sleep requirement." "Healthy adults without sleep disorders can expect to be less sleepy during the daytime than young adults."
Older adults frequently complain of sllep disruptions, early morning wakening, wakening not refreshed, daytime sleepiness, and daytime napping. According to this study older adults with healthy sleep should not be subject to daytime tiredness so the question is are they tired due to poor sleep, sleep apnea or other health related disturbances. Daytime tiredness can be considered not a normal consequence of aging but a sign of loss of good sleep. The percentage of Slow Wave Sleep declines with age but should not cause problems of tiredness in otherwise healthy older adults.
Older adults with excessive daytime sleepiness, napping or other signs of excessive daytime sleepiness should be evaluated for sleep disorders and/or disturbed sleep. These symptoms should not be written off as normal consequences of aging. Better sleep will result in a better quality of life for older adults.
SHORT SLEEP DURATION AND WEIGHT GAIN REPORTED IN THE JOURNAL OF SLEEP DISORDER RESEARCH
An article in the February 2010 Journal Sleep reported that short sleep duration was associated with weight gain in ,ale patients after 1 year. This effect did not carry over to female patients. In the study 5.8% of non-obese men with short sleep became obese 1 year later. Dhort sleep duration was defined as 5-6 hours of sleep vs 7-8 hours of sleep as reference group. There was also higher of obesity in groups showing short sleep duration.
Previous studies have shown weight gain associated with obstructive sleep apnea. Other studies consistently show that weight gain also increases obstructive sleep apnea. The world health organization describes obesity as on of the most visible and neglected public health problems. The effects of sleep duration and quality are an important factor in obesity. Obesity to some extent must be considered a disease of inadequate or poor quality sleep and quality of sleep is adversely affected by obesity.
Previous studies have shown weight gain associated with obstructive sleep apnea. Other studies consistently show that weight gain also increases obstructive sleep apnea. The world health organization describes obesity as on of the most visible and neglected public health problems. The effects of sleep duration and quality are an important factor in obesity. Obesity to some extent must be considered a disease of inadequate or poor quality sleep and quality of sleep is adversely affected by obesity.
Wednesday, February 3, 2010
I HATE CPAP is an important public service for patients diagnosed with obstructive sleep apnea
I recently rceived this email from a patient.
comments : Your site is an important public service for those of us diagnosed with obstructive sleep apnea. Like most doctors, mine told me the only treatment worth considering for my mild OSA was CPAP. She scoffed at the mention of oral appliances, dismissing them as suited only to a special category of patients with TMJ symptoms. I mistrusted her absolutist statement,. Although I've been using the CPAP since she prescribed it, I have also been researching other professionally accepted treatments for OSA. Thanks to your website and many peer-reviewed journal articles, I've come to the conclusion that s I've I've learned there are a number of alternative treatments worth considering. Having been forced to uncover this information on my own has made me disillusioned with my pulmonologist-sleep specialist. I am in the process of finding a sleep center with a broader, more cutting-edge, and more personal approach to treating OSA. One factor I would like them to consider -- a
nd would appreciate your addressing -- is that I have esophageal problems secondary to systemic sclerosis. Also secondary to the SSc is mild pulmonary hypertension. Does the pre-existing condition of systemic sclerosis that includes these symptoms suggest any particular approach to the treatment of OSA? Thank you for all of your good work.
ESA
It is not uncommon for patients to wall into walls of ignorance or self interest. No sleep specialist should be unaware of the enormous successes with oral appliances. It is because oral appliances are so successful that they are considerd a first line treatment for mild to moderate sleep apnea by the American Academy of Sleep Medicine. Many sleep physicians and sleep centers have economic interests in DME companies that supply CPAP machines to patients. Sometimes these companies are owne by family members to evade federal Stark laws on self referral. Othertimes it is merely ignorance that causes doctors to make statements like this writer reports. When CPAP fails the majority of patients there must be alternatives presented to patients. CPAP is still an excellent and successful treatment but not for most patients. Oral appliances are also not for all patients. There must be honesty in the field of sleep medicine.
Dear Dr. Shapira,
Thank you for your thoughtful and encouraging reply to my questions.
I did a little bit of research about sleep centers in Houston, and you are right. Even though the lab I started with was little more than an extension of the hospital's pulmanology department, there are others out there that take a more modern approach to sleep medicine. Baylor, for one, seems to have a decent lab that emphasizes interdisciplinary treatment. I'll keep looking, but they're on the short list.
Thanks again for your excellent public education work on the internet. BTW, when I tell my various doctors about the eye-opening information you've posted on oral appliances, they inevitably ask the name of the site. It gets a laugh every time.
Regards,
Elizabeth S.
comments : Your site is an important public service for those of us diagnosed with obstructive sleep apnea. Like most doctors, mine told me the only treatment worth considering for my mild OSA was CPAP. She scoffed at the mention of oral appliances, dismissing them as suited only to a special category of patients with TMJ symptoms. I mistrusted her absolutist statement,. Although I've been using the CPAP since she prescribed it, I have also been researching other professionally accepted treatments for OSA. Thanks to your website and many peer-reviewed journal articles, I've come to the conclusion that s I've I've learned there are a number of alternative treatments worth considering. Having been forced to uncover this information on my own has made me disillusioned with my pulmonologist-sleep specialist. I am in the process of finding a sleep center with a broader, more cutting-edge, and more personal approach to treating OSA. One factor I would like them to consider -- a
nd would appreciate your addressing -- is that I have esophageal problems secondary to systemic sclerosis. Also secondary to the SSc is mild pulmonary hypertension. Does the pre-existing condition of systemic sclerosis that includes these symptoms suggest any particular approach to the treatment of OSA? Thank you for all of your good work.
ESA
It is not uncommon for patients to wall into walls of ignorance or self interest. No sleep specialist should be unaware of the enormous successes with oral appliances. It is because oral appliances are so successful that they are considerd a first line treatment for mild to moderate sleep apnea by the American Academy of Sleep Medicine. Many sleep physicians and sleep centers have economic interests in DME companies that supply CPAP machines to patients. Sometimes these companies are owne by family members to evade federal Stark laws on self referral. Othertimes it is merely ignorance that causes doctors to make statements like this writer reports. When CPAP fails the majority of patients there must be alternatives presented to patients. CPAP is still an excellent and successful treatment but not for most patients. Oral appliances are also not for all patients. There must be honesty in the field of sleep medicine.
Dear Dr. Shapira,
Thank you for your thoughtful and encouraging reply to my questions.
I did a little bit of research about sleep centers in Houston, and you are right. Even though the lab I started with was little more than an extension of the hospital's pulmanology department, there are others out there that take a more modern approach to sleep medicine. Baylor, for one, seems to have a decent lab that emphasizes interdisciplinary treatment. I'll keep looking, but they're on the short list.
Thanks again for your excellent public education work on the internet. BTW, when I tell my various doctors about the eye-opening information you've posted on oral appliances, they inevitably ask the name of the site. It gets a laugh every time.
Regards,
Elizabeth S.
Tuesday, February 2, 2010
# year old with (OSA) Sleep Apnea. Are there alternatives to tonsil and adenoid removal
comments : my 3yr old grandaughter has been diagnosed with OSA, they are referring surgery to remove adenoids & tonsils. would like to know if there are any alternatives out there. we are going to try the oxygen therapy 1st. is there anythings else we can do
This is an interesting question for several reasons. The first is that they have discussed oxygen therapy, unfortunately oxygen therapy is not helpful for obstructive sleep apnea because the airway is obstructed and therefore the oxygen does not get to the lungs.
The second part of the question is there an alterrnative to tonsil and adenoid removal. Rapid maxillary expansion can open the airway in children and is often indicated IN ADDITION to removal of tonsils and/or adenoids. A Swedish researcher suggested at the Dental Sleep Meeting that doing maxillary expansion prior to surgery make reduce complications and create easier and/or faster healing. Another recent report has shown that even if tonsils and adenoids are removed there will remain orthopedic jaw problems that will still usually require widening of the palate.
The question which should be done first surgery or widening of the maxilla is still open.
What is not open is that pediatric patients with sleep apnea should be treated ASAP. ADD, ADHD and other learning and behavioral disorders have been linked to pediatric sleep apnea and time is of the essence.
Various studies have shown delayed brain development and/or permanent changes in brain development as a consequence to sleep apnea in children. Read the story in my profile about my sons sleep apnea and how treating it changed his life.
This is an interesting question for several reasons. The first is that they have discussed oxygen therapy, unfortunately oxygen therapy is not helpful for obstructive sleep apnea because the airway is obstructed and therefore the oxygen does not get to the lungs.
The second part of the question is there an alterrnative to tonsil and adenoid removal. Rapid maxillary expansion can open the airway in children and is often indicated IN ADDITION to removal of tonsils and/or adenoids. A Swedish researcher suggested at the Dental Sleep Meeting that doing maxillary expansion prior to surgery make reduce complications and create easier and/or faster healing. Another recent report has shown that even if tonsils and adenoids are removed there will remain orthopedic jaw problems that will still usually require widening of the palate.
The question which should be done first surgery or widening of the maxilla is still open.
What is not open is that pediatric patients with sleep apnea should be treated ASAP. ADD, ADHD and other learning and behavioral disorders have been linked to pediatric sleep apnea and time is of the essence.
Various studies have shown delayed brain development and/or permanent changes in brain development as a consequence to sleep apnea in children. Read the story in my profile about my sons sleep apnea and how treating it changed his life.
Monday, February 1, 2010
CPAP: Still the Gold Standard?
For over two decades, CPAP has been considered the "gold standard" in treatment of obstructive sleep apnea (OSA) but has always had poor patient compliance. Because of ease of use and comfort, oral appliances are the much-preferred method of treatment. Even with making CPAP machines smaller, quieter and sometimes heated, the masks are still quite uncomfortable for many patients with sleep apnea. If you suffer from sleep apnea and CPAP just is not working for you, please contact Dr. Ira Shapira at our Gurnee, Illinois dental office today. For years, we have heard our patients declare, "I hate CPAP!" and we responded by offering more comfortable treatment modalities such as the very successful oral appliances we offer.
Oral appliances to treat sleep apnea are custom-fitted to help you sleep soundly and minimize the effects of sleep apnea. These devices are FDA approved and allow you to breath easily and continuously throughout the night. They are worn in the mouth and keep the soft tissue from collapsing and interrupting your normal breathing pattern.
If you suffer from sleep apnea and would like to explore more comfortable treatments than CPAP, please contact Dr. Ira Shapira today.
Oral appliances to treat sleep apnea are custom-fitted to help you sleep soundly and minimize the effects of sleep apnea. These devices are FDA approved and allow you to breath easily and continuously throughout the night. They are worn in the mouth and keep the soft tissue from collapsing and interrupting your normal breathing pattern.
If you suffer from sleep apnea and would like to explore more comfortable treatments than CPAP, please contact Dr. Ira Shapira today.
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