Guest guest Posted February 19, 2007 Report Share Posted February 19, 2007 My daughter doesn't complain of spasm...but she does have a lot of difficulty swallowing pills. The doctor told us it was because the Lyme attacks the nerve in the throat. > > Has anyone else dealt with their child whose vocal cords spasm to the > point that they can't breathe? My daughter has been having an awful > time. We've tried many things. It has gotten a bit better but she's > missing a lot of school and the ER treats her like she's just being > hysterical. Her Herkheimer reactions to antibiotics has been a > challenge as I'm sure is usual. It's just hard for me to see her in so > much distress and feel helpless. I'm dealing with my own Lyme and I > feel like a nursemaid at times. I'm a single Mom. I feel like a whiner > but I just want to escape sometimes. > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted February 19, 2007 Report Share Posted February 19, 2007 Has the doctor found a way to relieve her symptoms? > > > > Has anyone else dealt with their child whose vocal cords spasm to the > > point that they can't breathe? My daughter has been having an awful > > time. We've tried many things. It has gotten a bit better but she's > > missing a lot of school and the ER treats her like she's just being > > hysterical. Her Herkheimer reactions to antibiotics has been a > > challenge as I'm sure is usual. It's just hard for me to see her in so > > much distress and feel helpless. I'm dealing with my own Lyme and I > > feel like a nursemaid at times. I'm a single Mom. I feel like a whiner > > but I just want to escape sometimes. > > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted February 19, 2007 Report Share Posted February 19, 2007 My entire family has lyme (me-44yo, my husband-39yo, daughter -6yo, son#1-almost 5, son#2-almost 2)... somehow I got the most powerful tick cocktail - with lyme, babesiosis, and bartonella. One of the severe symptoms I had were feelings of my throat closing... that actually led us down a path pursuing allergic reactions. I would also get swelling in my face and throat -- it is very frightening. What we did find that greatly helped these symptoms was Benadryl -- apparently the diseases are triggering the histamine system and therefore Benadryl does reduce the symptoms. I don't remember how old you said your daughter was, but they also have children's Benadryl. The other related symptoms we have had (me, my 6 yr old daughter and 4yo son all had this mostly in big herxes), is that horrible swallowing problem, where you just can't swallow correctly and it does feel like you're going to choke on your tongue - it is horrible. Again, Benadryl seemed to alleviate that as well. I don't know if you're also getting the blood pressure drops, but that is what ended me up with two 911 calls - my blood pressure dropped so low (76/48), it was frightening. I believe that a lot of these symptoms have to do with lyme that is in the nervous system and affecting the vagus nerve. Ask your doc about Benadryl and good luck! - in Southeast PA (Philadelphia suburbs) Quote Link to comment Share on other sites More sharing options...
Guest guest Posted February 21, 2007 Report Share Posted February 21, 2007 Thank you so much! My daughter is 12. We'll try the Benadryl. Do you only take it during the symptoms or can it be taken as a preventative? Annie - near Bloomsburg, PA. > > My entire family has lyme (me-44yo, my husband-39yo, daughter - 6yo, > son#1-almost 5, son#2-almost 2)... somehow I got the most powerful tick cocktail - > with lyme, babesiosis, and bartonella. One of the severe symptoms I had were > feelings of my throat closing... that actually led us down a path pursuing > allergic reactions. I would also get swelling in my face and throat -- it is > very frightening. What we did find that greatly helped these symptoms was > Benadryl -- apparently the diseases are triggering the histamine system and > therefore Benadryl does reduce the symptoms. I don't remember how old you said > your daughter was, but they also have children's Benadryl. The other related > symptoms we have had (me, my 6 yr old daughter and 4yo son all had this mostly > in big herxes), is that horrible swallowing problem, where you just can't > swallow correctly and it does feel like you're going to choke on your tongue - > it is horrible. Again, Benadryl seemed to alleviate that as well. I don't > know if you're also getting the blood pressure drops, but that is what ended me > up with two 911 calls - my blood pressure dropped so low (76/48), it was > frightening. I believe that a lot of these symptoms have to do with lyme that > is in the nervous system and affecting the vagus nerve. Ask your doc about > Benadryl and good luck! - in Southeast PA (Philadelphia suburbs) > > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted February 21, 2007 Report Share Posted February 21, 2007 I cant help but add that maybe you'd want to first check with your daughter's Drs?? Benadryl can have opposite and scary effects like nervousness, insomnia and even cardiac symptoms. Plus its been known to interact unpleasantly with Rx drugs and even some over the counter ones. I understand when all you want is to help your child! But personal experience has taught me to be very cautious. OTC drugs are as dangerous ( and sometimes even more dangerous) than RX ones. For me, the swallowing and throat things werent necessarily allergy or inflammation, but edema ( fluid swelling) of neck structures and also nerve damages ( at the same and different times). Neither of those 2 would have been helped by the Benadryl. Its really important to try to figure out the causes or IF youre going to do a trial and error ( hit or miss) approach to double check with Drs and be very cautious...like starting with TINY doses and gradually building up to the least dose that works. It also helps to keep a carefully detailed journal...time and dose and effects if any.This way you can see if her meds are the cause or make it worse, or anything in the environment. FYI: allergy has to do with H1 and H2 receptors. Both receive histamine as a messenger.H1 produce the typical " allergy symptoms " -itchy, burining , hives on skin. Fast heart and palpitations. Pressure headache. Stuffy or runny nose. Increased mucus, bronchial swelling ( asthma). Increased stomach acid and small intestine cramps. These receptors are EVERYWHERE in the body so any drug or herb that affects one area ( like nasal congestion) will certainly affect ALL the receptors!! In other words the Benedryl will affect far more than the throat! Benadryl, Atarax, Claritin etc block only HI receptors and may be sedating (OR have opposite reactions called paradoxical).They also cause dry mouth and throat which can worsen the feeling of " I cant swallow " . H2 receptors act as a " turn off " switch if working properly. H2 blockers like Tagamet etc, we know as acid blockers, however they may also be used as an " allergy modulator " to possibly balance an overactive allergy then rebound response. Prostaglandins and leukotrienes are also involved, so drugs working on these may help allergic responses. For example Singulair and Accolate. Not just being used for asthma, but for other general allergy....though I dont necessarily agree...Im suspicious of marketing ploys by Big Pharma!! But IF the throat symptoms are nerve related and there is a component of autonomic problems then the Benadryl will make it a LOT worse!! Feeling like you cant get air/thick throat, nausea, swallowing problems are sometimes cited by those of us with dysautonomia. You may also want to look up Dysautonomia on a good website: www.ndrf.org and see if there are any safe self-help measures for throat issues.BUT this site has very recently changed. I tried to navigate it and found it quite difficult plus apparently you have to join something called " groupee " . I have emailed the gal who founded the site and the NDRF to ask if thats the only way now to access info. If youre interested I will let you know what she says. Be wary of the site " dinet " dysautonomia info network--theyre very political and I have no confidence in any accuracy of info or in the folks that run that site...at all. dynakids.org is GREAT...its for kids with various dysauto's...and may even have self help ideas. they definitely have Dr referrals for more local Drs. It is extremely difficult for trained allergists to pinpoint the cause and proper treatment, and so almost impossible for us to guess safely. I always take symptoms like you describe to a good allergists/immunologist ( NOT the typical allergy shot, ragweed jockey neighborhood allergist). and ask for a histamine test. you need both histamine in bloods,and urine 24 hr histamine; AND a special 4 hr urine catch during symptoms to check for the breakdown product ( I think its N-methylhistamine but my brain cells arent cooperating-- Im sure its for " mastocytosis rule out " ),. If histamine isnt high or erratic why chance anything risky that blocks histamine?? and then I STILL approach with caution because allergists dont have a good handle on the Lyme aspect. And then if there are autonomic system issues...well, forget it. Ive found that there are only 3 or 4 true " specialists " in the entire country with enough experience to sort out dysautonomias, and then they arent able to deal with the Lyme...but many locals do confer with these biggies...and you can find them thru Dynakids etc. so step one- immunology/allergy; step 2- autonomic specialist and then only after and with a Dr's guidance would I try otc drugs. Re; BP drops: it may have nothing to do directly with a vasoVAGAL thing for fainting and/or BP drops. many Drs wrongly say this. Again I would direct you to the dysautonomi sites!!! its much more complex than I can explain here. and any real big drops in BP arent to be played with by trying Benadryl!! My own BP has dropped as low as 47 over ZERO ( palp) and I was conscious ( barely). Plus those on the Marshall Protocol for Lyme have constantly low bps of 60-85/38-60. I dont get it but they seem to function allright. Id be scared to have BP that low due to my hearts habit of stopping dead for several seconds!! they tell me that for me a bit higher than normal is better than very low. Good luck Finette [ ] Re: vocal cord dysfunction Thank you so much! My daughter is 12. We'll try the Benadryl. Do you only take it during the symptoms or can it be taken as a preventative? Annie - near Bloomsburg, PA. > > My entire family has lyme (me-44yo, my husband-39yo, daughter - 6yo, > son#1-almost 5, son#2-almost 2)... somehow I got the most powerful tick cocktail - > with lyme, babesiosis, and bartonella. One of the severe symptoms I had were > feelings of my throat closing... that actually led us down a path pursuing > allergic reactions. I would also get swelling in my face and throat -- it is > very frightening. What we did find that greatly helped these symptoms was > Benadryl -- apparently the diseases are triggering the histamine system and > therefore Benadryl does reduce the symptoms. I don't remember how old you said > your daughter was, but they also have children's Benadryl. The other related > symptoms we have had (me, my 6 yr old daughter and 4yo son all had this mostly > in big herxes), is that horrible swallowing problem, where you just can't > swallow correctly and it does feel like you're going to choke on your tongue - > it is horrible. Again, Benadryl seemed to alleviate that as well. I don't > know if you're also getting the blood pressure drops, but that is what ended me > up with two 911 calls - my blood pressure dropped so low (76/48), it was > frightening. I believe that a lot of these symptoms have to do with lyme that > is in the nervous system and affecting the vagus nerve. Ask your doc about > Benadryl and good luck! - in Southeast PA (Philadelphia suburbs) > > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted November 6, 2008 Report Share Posted November 6, 2008 GM all. I got my fourth shot yesterday and yet again was really sick to my stomach. I also got the flu shot and now have a fever too. I am wondering if anyone else gets this side effect from the shots. It is right away when i stand up I am dizzy and then the nausea hits. My number was down to a 12 yesterday, but winter has hit us, and I always have issues with the cold. NOW the dr. wants me tested for Vocal Cord Dysfunction, a $550 visit, that I am not totaly convinced I need. Does anyone have this and what is it? Thanks Dana Quote Link to comment Share on other sites More sharing options...
Guest guest Posted October 12, 2009 Report Share Posted October 12, 2009 Sunny, although running for the sake of running isn't my cup of tea, it is not, as you insinuate, bad for a healthy person... but for an individual who has not been physically active throughout live (a very un-healthy way to live) then running would be a challenge. Physical movement helps produce brain derived neurotrophic factor which helps the brain grow and maintain health, and keeps depression at bay. The point of my post is that asthma is often a mis-diagnosis, and that VCD may be the accurate dx. Did you read the article? The MD author points out that many individuals are wrongly medicated. Seitz, DC Tuality Physicians 730-D SE Oak St Hillsboro, OR 97123 (503)640-3724brian@...; From: skrndc1@...Date: Mon, 12 Oct 2009 14:50:35 -0700Subject: RE: vocal cord dysfunction So...once again, guys: think chiropracatically: running escalates compression. We live in a world that compresses us: riding in cars that pack us down like boxes of cornflakes; walkling on concrete that, with every step, compresses us; living in gravity for all of our days.... and all of that compression is BEFORE we carry a child on our hip or live 8 decades or have motor vehicle accidents or fall out of trees or drive and turn our heads a dozen times/mile to check our parameters. Then: you run! How compressive is that?! .... and how much does it effect the compressions you have encountered up to that point?! ...or that day? Exercise induced asthma, if you haven't already figured out, is also about lack of adequate calcium. Many time in this office we have shifted a person out of an asthma attack with the use of liquid calcium...and, yes, I usually provide a tab/cap of HCL with it as well. We can do SO So SO much for these conditions .... maybe what our students need is just to understand the difference between what the MDs call something versus what we call it .... and not get hung up on: "I can't fix that" just because it has a fancy medicalese name on it. my 2 cents this afternoon Sunny Sunny Kierstyn, RN DC Fibromyalgia Care Center of Oregon 2677 Willakenzie Road, 7CEugene, Oregon, 97401541- 654-0850; Fx; 541- 654-0834 From: briantualityphysiciansDate: Mon, 12 Oct 2009 12:13:43 -0700Subject: vocal cord dysfunction Group, I’ve recently become aware of this disorder. My wife and kids have a strange desire to run – without a ball or other reason! I am thus exposed to many runners of all ages. One particular high level Boise State runner had struggled with “exercise induced asthma”, and treated with bronchodilators and steroids for many years. Problem was, it wasn’t asthma!!! It was diagnosed as VCD and through proper treatment was able to take control of the problem. You would think we would all be aware of this ddx to asthma, but I wasn’t and I don’t think many MD’s are either. The following is an interesting article from Medscape: Mark T. O'Hollaren, MD, Director, Allergy Clinic; Clinical Professor of Medicine, Oregon Health and Science University, Portland, Oregon Dyspnea Due to Vocal Cord Dysfunction and Other Laryngeal Sources Mark T. O'Hollaren, MD Published: 08/26/2002 Introduction Both primary care and subspecialty physicians are frequently called upon to evaluate patients with shortness of breath. This dyspnea may be labeled "difficult or refractory asthma." In some cases, the site of origin of this dyspnea may in fact not be the bronchial airways or the lung parenchyma, but rather the larynx. Most of us are familiar with the clinical management of shortness of breath due to asthma or chronic obstructive pulmonary disease; however, a high index of suspicion is needed to carefully unravel a patient's symptom complex and pinpoint a diagnosis of pathology in the larynx. The diagnosis of laryngeal causes of dyspnea may escape accurate diagnosis for years, and may result in inappropriate and dangerous long-term treatment, including use of chronic maintenance corticosteroids. This may result in needless diagnostic tests, potentially invasive therapeutic interventions, and possible debilitating long-term side effects from inappropriate treatment. Patients with dyspnea originating in their larynx may complain of shortness of breath, which may be accompanied by a wheezing or stridorous sound. Others may state that their symptoms are worsened by physical exertion. The recognition of the laryngeal origin of these syndromes may lead to a more timely diagnosis. The highest yield diagnostic study in the majority of laryngeal disorders is the direct visualization of the larynx at the time a patient is experiencing symptoms. Careful examination with a flexible or rigid laryngoscope, or indirect visualization of the larynx with the laryngeal mirror, is needed to establish an appropriate or an accurate diagnosis. If appropriate examination cannot be done, or the diagnosis is in question, prompt referral to a competent otolaryngologist is necessary. In specialized centers, problems with the vocal cords and speech production may be further evaluated with specialized diagnostic equipment, such as a laryngostroboscope. This discussion will center around the laryngeal disorders that may lead to dyspnea, and disorders of voice will not be covered with this summary. The Amazing Larynx The larynx is a very complex and extremely important anatomic region that functions to join the airway and the superior portion of the gastrointestinal tract. Its sphincteric capabilities allow protection of the airway, prevent aspiration of fluid and food particles during swallowing, and also protect against aspiration of any potential foreign material when it enters the larynx during respiration. During swallowing, the airway closes naturally, and will close involuntarily with stimulation of the pharynx. The automatic reflex will take precedence over all voluntary controls of laryngeal function. To facilitate vocal communication, an elaborate mechanism of vocal cord vibration/oscillation is coordinated with movements of the tongue and mouth. For further information on the voice and vocal disorders, the reader is referred to an elegant summary by Cohn and colleagues.[1] Dyspnea and the Larynx There are 2 main ways in which patients may experience dyspnea originating in the larynx. First, there may be structural interference with air flow due to an anatomic abnormality. In other words, there is some structural interference with air flow due to a growth, tumor, swelling, anatomical narrowing, etc. The second mechanism by which dyspnea may originate in the larynx is abnormal motion of functioning of a laryngeal structure. This may include problems such as vocal cord dysfunction (VCD), neurologic disorders of the vocal cords, vocal cord paralysis, laryngospasm, etc. Air Flow Obstruction Resulting From Structural Interference A number of structural abnormalities may interfere with laryngeal air flow, and may or may not be accompanied by any change in the actual quality of the patient's voice. There are both infectious and noninfectious processes that can lead to air flow obstruction. One of the most rapidly developing and frightening infectious causes of dyspnea originating in the larynx is epiglottitis. Epiglottitis is almost always due to a bacterial pathogen, which may produce rapidly evolving inflammation and edema of the larynx in the supraglottic area. Causative organisms include Haemophilus influenzae type B, Pneumococcus, and group A beta hemolytic streptococci. This most commonly affects children, and may be clinically characterized by drooling, inspiratory stridor, high fever, and airway distress. As noted above, the symptoms may be rapid in onset and progression, and most commonly affect children between the ages of 2 and 8 years, but also may occur in adults. In a series of 129 cases, approximately 1 out of 7 adults with epiglottitis required airway intervention, by either tracheotomy or endotracheal intubation.[2] In this series, factors that were associated with the need for acute airway intervention were the presence of stridor or having the patient sitting up and erect at the time of presentation. Although there were no deaths, major complications occurred in 5% of patients. Visualization of the epiglottis is done with either a lateral neck radiograph or using a flexible fiberoptic rhinolaryngoscope via a nasal approach. A tongue blade is never used when epiglottitis is suspected because of the risk of precipitating acute airway closure. Medical management of acute epiglottitis involves the use of appropriate antibiotic therapy and, in some patients, corticosteroids. The immediate availability of medical personnel capable of securing an airway is also crucial, since tracheotomy or endotracheal intubation may be needed in the management of the patient. If a patient's symptoms are escalating rapidly, it is better to secure an airway sooner rather than later in this potentially life-threatening situation. The subglottic area may also be affected by viral infections, such as croup. Croup is commonly caused by a viral pathogen, frequently influenza or parainfluenza virus. Although croup is not a typical laryngeal cause of dyspnea, nonetheless, it is an important cause of stridor in children, with treatment consisting of hydration, humidification, corticosteroids, and racemic epinephrine in some patients. Bacterial tracheitis may be fatal, and typically presents with high fever, stridor, a barking cough, extreme leukocytosis, and thick mucopurulent discharge from the trachea. Staphylococcus is a frequent causative organism, although H influenzatype B and group A streptococci have also been reported to cause this condition. Occasionally, intubation and tracheostomy may be needed in these patients, and therapeutic intervention with antibiotics must be done without delay to minimize the need for acute airway intervention. Infections may also result in laryngeal abscesses, including those in both the larynx or hypopharyngeal area, and may compromise the airway, requiring surgical incision and drainage. These abscesses may occur following an episode of tonsillitis, and may be deceptively slow in their evolution. Finally, there are a number of less common infectious diseases that may involve the larynx, including tuberculosis, syphilis, trichinosis, diphtheria, histoplasmosis, and leprosy. Fungal infections may also involve the laryngeal airway, including infections with Aspergillus, Histoplasma, Coccidioides, Blastomyces, Actinomyces, Candida, Cryptococcus, and Nocardia. Both benign and malignant tumors of the larynx may also lead to shortness of breath; again, direct visualization is mandatory to accurately diagnose these disorders. The most common benign tumor of the larynx is squamous papilloma, which may occur either in a juvenile or adult form. It is seen in a higher frequency in children who are delivered vaginally from mothers who have venereal warts and are infected with the human papilloma virus. In this case, presenting symptoms may include hoarseness, respiratory compromise, or audible stridor. If untreated, this condition can result in fatal asphyxiation, and this has been reported in children.[3] This condition is difficult to treat, and a number of approaches have been used, including carbon dioxide laser, systemic interferon, and others. It is most important to refer such patients to an otolaryngologist for appropriate management. Noninfectious Causes of Laryngeal Air Flow Limitation Appropriate air flow through the larynx may be impeded by a number of noninfectious conditions. The most common cause of stridor in children is congenital laryngomalacia. This is a condition that results from a flaccidity of the larynx. A lack of rigidity of the framework that supports the larynx leads to this condition, in concert with some accompanying flaccidity of the supraglottic tissues of the larynx. Increased physician activity may lead to stridor, as may crying in infants. The symptoms may occur in infants and young children as early as a few weeks after birth and may last from 12 to 18 months. Direct visualization of the larynx may show a converging of the laryngeal structures during inspiration, and although the disorder usually spontaneously resolves in time, tracheostomy may be indicated in severe cases. A narrowing of the area just beneath the true vocal cords is referred to as subglottic stenosis. This may occur from a number of causes, including trauma to the larynx from prolonged endotracheal intubation. In addition, this narrowing may occur from vasculitic or other inflammatory conditions such as Wegener's granulomatosis, relapsing polychondritis, or systemic lupus erythematosus. The differential diagnosis of subglottic stenosis includes infection, tumor, trauma, thermal or chemical inhalation, live/acid ingestion, and tracheomalacia. In addition, sarcoidosis and amyloidosis may also cause inflammatory changes or masses within the larynx. An acute allergic reaction, such as anaphylaxis to food, insect sting, drug, or other cause, may also lead to laryngeal edema. Idiopathic angioedema, outside of the setting of acute anaphylaxis, may also lead to laryngeal swelling and may occur as either an idiopathic condition or as the hereditary form of C-1 esterase inhibitor deficiency. Prompt administration of subcutaneous epinephrine, systemic corticosteroids, and maintenance of an adequate airway are crucial in the management of acute laryngeal edema. In young children or toddlers with stridor, the question of foreign body aspiration frequently arises. The peak incidence of foreign body aspiration occurs between the ages of 12 and 36 months. In young children, the larynx is very pliable and is located in close proximity to the esophagus. Because of this fact, foreign bodies lodged within the esophagus may actually lead to respiratory compromise and stridor in young children. Elderly patients, especially those who are debilitated or have any type of swallowing dysfunction, may also suffer from foreign body aspiration. Those who have degenerative neurologic disease or have experienced a cerebrovascular accident may be at especially high risk. Finally, other noninfectious causes of laryngeal airway obstruction may include vocal cord polyps, laryngoceles, saccular cysts, and laryngeal vascular malformations. Goiters involving the cervical and substernal area may also interfere with tracheal and laryngeal air flow. The flow volume loop may be somewhat helpful in alerting a physician to a structural interference with air flow. A flattening of the inspiratory portion of the flow volume loop may suggest a variable extrathoracic obstruction, whereas a flattening of the expiratory portion may suggest a variable intrathoracic obstruction. Flattening of both the inspiratory and expiratory limbs raises the suspicion of a fixed airway narrowing. Laryngeal Air Flow Limitation Resulting From Abnormal Movement of Laryngeal Structures Background The boundaries of the larynx extend from the superior tip of the epiglottis to the cricoid cartilage. The cricoid cartilage serves as the foundation of the larynx, and is actually the only complete cartilaginous ring in the tracheal bronchial tree. The definitive configuration of the larynx is present by 28 weeks of gestation.[4] The true vocal cords serve as a "guardian of the airway." In addition, closing the glottis allows us to have fixation of the thorax, which aids in the mechanisms of heavy lifting using the arms. Finally, motion of the vocal cords allows us to produce vocal sounds for communication, and this process has required the development of a very complex neural control mechanism, which permits precise movements of the vocal cords to produce vocal sounds. Those unfamiliar with the mechanics of voice production feel the process is somewhat simplistic and automatic. However, it is immensely complex and requires the coordination of conceptualized thoughts to be placed in linguistic form, selection of appropriate words, and conversion of these thoughts into appropriate neural impulses. The various laryngeal articulatory structures are then used to produce vocal sounds. While this is taking place, the entire process is monitored using visual, auditory, and proprioceptive systems on an ongoing basis. It is usually when something goes wrong that this complex series of neural and muscular interactions comes to the attention of both the treating physician and the patient. The respiratory cycle consists of inspiration and expiration, and, in most patients, the glottal opening of the vocal cords is slightly wider on inspiration compared with expiration. In general, however, the average opening of the glottis is fairly constant. This glottic opening is controlled through the medullary respiratory center (via the vagus nerve), which leads to contraction of the posterior cricoarytenoid (PCA) muscle. Contraction of the PCA muscle then leads to opening (abduction) of the vocal cords, which functions to open the glottis and reduce resistance to air flow through the larynx. Contraction of the PCA muscle is also timed with contraction of the diaphragmatic musculature, and is also influenced by variations in both arterial carbon dioxide and oxygen concentrations as well as intrapulmonary pressure.[5] Of note, it appears that the vocal cords are sensitive to changes in airway caliber as well. Experimentally, histamine-induced bronchospasm may lead to an expiratory narrowing of the vocal cords. Because of this, some feel that the glottis is capable of reflex adjustments in parallel with changes in airway caliber. Dyspnea resulting from abnormal motion of laryngeal structures has been described in a number of clinical settings, including VCD (also sometimes referred as paradoxical vocal cord motion), vocal cord paralysis, laryngospasm, Meige syndrome, and spastic dysphonia. These disorders may occur in children, adolescents, and adults, and some may have at least a partial functional component. Most do not appear to be under the direct voluntary control of the patient experiencing these symptoms. As previously mentioned, the vocal cords are normally opened widest during inspiration, and may narrow slightly during expiration in a normal individual. VCD is an phenomenon in which the vocal cords come together (adduct), producing air flow obstruction at the level of the larynx.[6] This abnormal vocal cord motion may produce recurrent wheezing that may imitate asthma, and may be misdiagnosed as asthma for years. If vocal cords close during inspiration, this may lead to stridor, which may be misdiagnosed as an upper airway obstruction of life-threatening severity. The acute presentation, frequently seen in the emergency department, may be dramatic and lead to inappropriate endotracheal intubation, tracheotomy, or recurrent courses of high-dose corticosteroids.[6] VCD may affect either sex; however, the vast majority of cases described in the literature have been in females. For example, at the National Jewish Center for Respiratory Disease, in the excellent summary by Drs. Newman and Dubester,[6] 37 of 38 patients with VCD without asthma were women. The age of their patients at the time of presentation ranged from 9 to 74 years. However, the most common patient profile involves females between the ages of 20 and 40 years of age, with greater than a high school education and often some affiliation with a health-related field. Approximately 1 of every 4 patients with VCD seen at National Jewish fit this profile. Clinical presentations of VCD may include wheezing, which may suggest asthma, or stridor, which may suggest upper airway obstruction. The excellent summary by Newman characterizes the clinical and laboratory findings of VCD, as well as therapeutic recommendations.[6] VCD may follow a respiratory infection, although this history is not always given. It is also very common to have VCD occur in the presence of gastroesophageal reflux or significant postnasal drainage. Symptoms may occur with or without exercise, and VCD may occur as an isolated condition or may occur simultaneously in patients with pre-existing asthma. Diagnosis of VCD When interviewing a patient, a careful history may give some clues as to the correct diagnosis. Patients may point to their larynx when asked where they feel the site of air flow limitation exists, and may describe a sense of throat tightness or even changes in their voice during an acute attack. B. Newman, MD,[7] Medical Director of Respiratory Products of Forest Laboratories, Inc. in New York, NY, stated at the 58th Annual Meeting of the American Academy of Allergy, Asthma and Immunology that perhaps the most reliable question to ask a patient is whether they feel inhaled bronchodilators improved their breathing or not. Especially in patients with isolated VCD without asthma, bronchodilators have little benefit. Another important question is whether they experience dyspnea accompanying these episodes and waking them up at night. Nocturnal symptoms of shortness of breath are fairly common in patients with asthma, and are rare in patients with VCD. The physical examination of patients with VCD may be very unreliable. Because sounds may be transmitted throughout the chest through the excellent sound-conducting properties of the large airways, it is difficult to localize the site of origin for wheezing or stridor sounds. If a patient is suspected of having VCD, then the gold standard is direct visualization of the larynx during an acute attack to confirm that the vocal cords approximate during inspiration, during expiration, or both. The term "paradoxical vocal cord motion" is typically given to patients who have approximation of the vocal cords during an inspiratory maneuver, since the vocal cords typically abduct, or widen, during inspiration in patients without the VCD. Another potentially helpful diagnostic tip when suspecting VCD is to have the patient hold their breath or to use a panting pattern of breathing. Patients with acute asthma find it very difficult to hold their breath, although those with VCD may be able to do so more readily. This action may actually improve their symptoms of dyspnea. In addition, patients with VCD may have decreased symptoms of dyspnea if they breathe in a panting fashion. Patients with VCD may have a flattening of the inspiratory portion of the flow volume loop, consistent with variable extrathoracic obstruction. Dr. Newman described approximately 25% of patients who may have an abnormal inspiratory portion of the flow volume loop, even when asymptomatic. Another clue that a patient's dyspnea may be caused by VCD is that during an attack, the patient's alveolar-arterial (A-a) oxygen gradient is frequently normal.[8] In contrast, patients experiencing acute severe asthma will have a widening of the A-a oxygen gradient in greater than 90% of cases. Flow volume loop during the acute attack may also show some inspiratory flattening consistent with variable extrathoracic obstruction, but, alternatively, the flow volume loop may show both inspiratory and expiratory flattening more consistent with fixed obstruction. It should be pointed out, however, that virtually any type of air flow abnormality pattern could be present during an acute attack of VCD. Laryngoscopic Findings With VCD As discussed earlier, inspiration typically results in the widening of the glottic aperture. During VCD, there tends to be an inappropriate adduction of the anterior two thirds of the vocal cords, with the posterior one third typically remaining slightly open in a "diamond-shaped chink" pattern. This may occur during inspiration only, during both phases of respiration, or during expiration only. If needed, provocative challenges using exercise or other stimuli may be done where laryngoscopic confirmation of the diagnosis may be accomplished. Other Contributing Factors Psychological stress may also play a role in some patients with VCD. Clinical experience of those treating VCD has shown that stressful situations, especially in adolescent high-performance female athletes, may increase the chance that VCD may be playing a role in some patients with dyspnea, which do not respond to typical treatment for exercise-induced asthma. It is appropriate to consider each individual case, and explore areas of psychological difficulty that may be compounding a given patient's clinical presentation. There have been some reports of association of VCD with psychological trauma as well, including a past history of sexual abuse, although this appears to be only evident in a minority of patients. A retrospective review by Freedman and coworkers[9] of 47 female inpatients at National Jewish Center with discharge diagnoses of VCD showed that 36% of those patients had experienced childhood sexual abuse. This should be kept in the context that the prevalence of sexual abuse in the general female population ranges from 6% to 62%.[10] The prevalence of sexual abuse in patients with VCD may not, therefore, represent a defining characteristic of this population. It is clear that unrecognized and untreated psychological problems may, in fact, be associated with VCD and should be addressed as appropriate. Treatment of VCD The appropriate treatment of VCD is best initiated with a careful explanation of the disorder and treatment recommendations. It is helpful for patients to have a description of the anatomy of the vocal cords, as well as the abnormalities that occur that produce the symptoms. It may also be useful to compare the psychological factors related to VCD with asthma, in which emotions are also seen as a common trigger, but not the positive factor of the disorder. Patients need to be reassured that they are not being told that the physician does not believe their symptoms to be real, or that it is "all in their head." Speech therapy is the foundation of treatment of VCD. A speech therapist who is familiar with this disorder, and who can coach a patient on appropriate laryngeal and neck relaxation techniques, panting breathing, breath holding, slow relaxed expiration techniques, etc., may be extremely helpful in preventing and treating these episodes. Vocal cord paralysis may be unilateral or bilateral and may result from damage of the recurrent laryngeal nerve during past thyroid or parathyroid surgery. The left vocal cord is more commonly affected than the right due to the somewhat longer path of the recurrent laryngeal nerve and its anatomic relationship to structures in the mediastinum. There also may be other neuropathies and degenerative neurologic conditions that may result in vocal cord paralysis. This condition may result in an abnormal voice, but the voice may be near normal in other patients with unilateral vocal cord paralysis. There may be problems, including aspiration while drinking liquids or eating solid foods, and once again the appropriate diagnosis is made by direct visualization of the vocal cords with documentation of abnormal vocal cord movements while coughing or during phonation. Other neurologic problems such as Meige syndrome, a neurologic condition accompanied by episodic spastic closure of the vocal cords, may lead to episodic shortness of breath, which may be severe enough to result in loss of consciousness. Spastic dysphonia, a somewhat poorly understood condition causing abnormal motion of the vocal cords, may occur in both an abductive and an adductive variety. Some patients who have abductive spastic dysphonia may experience some dyspnea. Treatment may be difficult, but is best referred to an otolaryngologist and appropriate speech therapist for management. Conclusion It is clear that dyspnea may originate from a large number of conditions affecting air flow through the larynx. The foundational corner stone of diagnosis of laryngeal causes of dyspnea is direct visualization of the larynx, especially when symptoms are present. Close consultation with an otolaryngologist, and, in some cases, a speech therapist, may be extremely helpful in alleviating the symptoms that these patients experience and returning them to a healthy, active lifestyle. References Cohn JR, Spiegel JR, Sattaloff RT. Vocal disorders and the professional voice user: The allergist's role. Ann Allergy Asthma Immunol. 1995;74:363-376. Franz TD, Rasgone BM, Quesenberry CP. Acute epiglottitis in the adults: an analysis of 129 cases. JAMA. 1994;272:1358-1360. Sperry K. Lethal asphyxiating juvenile laryngeal papillomatosis. Am J Forensic Med Pathol. 1995;15:146-150. Baxter MRM. Congenital laryngomalacia. Canadian J Anesthesia. 1994;41:333-339. Wood RP, Jafek BW, Cherniak RM. Laryngeal dysfunction in pulmonary disorders. Otolaryngol Head Neck Surg. 1986;94:374. Newman KB, Dubester SN. Vocal cord dysfunction: masquerader of asthma. Sem Respir Crit Care Med. 1994;15:161-167. Newman KB. Seminar: Vocal cord dysfunction. Program and abstracts of the 58th Annual Meeting of the American Academy of Allergy, Asthma and Immunology; March 1-6, 2002; New York, NY. KL, Wood RP, Eckert RC, et al. Vocal cord dysfunction presenting as asthma. N Engl J Med. 1983;390:1566-1570. Freedman MR, Rosenberg SJ, Schmaling KB. Childhood sexual abuse in patients with paradoxical vocal cord dysfunction. J Nerv Ment Dis. 1991;179:295-298. s SD, Wyalt GE, Finkelhor D. Prevalence. In: Finkelhower D, ed. A Source Book on Child Sexual Abuse. Beverly Hills, California: Sage Publications; 1986:15-59. 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Guest guest Posted October 12, 2009 Report Share Posted October 12, 2009 Running may have compressive loads of 3-5 times body weight, however to imply that these loads are degenerative is a far reach. Running and soccer have less symptomatic knees and hips vs non-athletes. Studies show healthcare costs in the last 5 years of life is markedly less in runners. Thus these folks the compression could be therapeutic. I think the key is what position is your body in during compression. Ted Forcum, DC, DACBSP ACA Sports Council, President '08 US Olympic Sports Medicine Team Member Back In Motion Sports Injuries Clinic, LLC 11385 SW Scholls Ferry Road Beaverton, Oregon 97008 503.524.9040 www.bimsportsinjuries.com The information contained in this electronic message may contain protected health information confidential under applicable law, and is intended only for the use of the individual or entity named above. If the recipient of this message is not the intended recipient, you are hereby notified that any dissemination, copy or disclosure of this communication is strictly prohibited. If you have received this communication in error, please notify Back In Motion Sports Injuries Clinic, LLC at 11385 SW Scholls Ferry Road, Beaverton, OR-97008. and purge the communication immediately without making any copy or distribution. From: [mailto: ] On Behalf Of Sunny Kierstyn Sent: Monday, October 12, 2009 2:51 PM Seitz; Subject: RE: vocal cord dysfunction So...once again, guys: think chiropracatically: running escalates compression. We live in a world that compresses us: riding in cars that pack us down like boxes of cornflakes; walkling on concrete that, with every step, compresses us; living in gravity for all of our days.... and all of that compression is BEFORE we carry a child on our hip or live 8 decades or have motor vehicle accidents or fall out of trees or drive and turn our heads a dozen times/mile to check our parameters. Then: you run! How compressive is that?! .... and how much does it effect the compressions you have encountered up to that point?! ...or that day? Exercise induced asthma, if you haven't already figured out, is also about lack of adequate calcium. Many time in this office we have shifted a person out of an asthma attack with the use of liquid calcium...and, yes, I usually provide a tab/cap of HCL with it as well. We can do SO So SO much for these conditions .... maybe what our students need is just to understand the difference between what the MDs call something versus what we call it .... and not get hung up on: " I can't fix that " just because it has a fancy medicalese name on it. my 2 cents this afternoon Sunny Sunny Kierstyn, RN DC Fibromyalgia Care Center of Oregon 2677 Willakenzie Road, 7C Eugene, Oregon, 97401 541- 654-0850; Fx; 541- 654-0834 From: briantualityphysicians Date: Mon, 12 Oct 2009 12:13:43 -0700 Subject: vocal cord dysfunction Group, I’ve recently become aware of this disorder. My wife and kids have a strange desire to run – without a ball or other reason! I am thus exposed to many runners of all ages. One particular high level Boise State runner had struggled with “exercise induced asthma”, and treated with bronchodilators and steroids for many years. Problem was, it wasn’t asthma!!! It was diagnosed as VCD and through proper treatment was able to take control of the problem. You would think we would all be aware of this ddx to asthma, but I wasn’t and I don’t think many MD’s are either. The following is an interesting article from Medscape: Mark T. O'Hollaren, MD, Director, Allergy Clinic; Clinical Professor of Medicine, Oregon Health and Science University, Portland, Oregon Dyspnea Due to Vocal Cord Dysfunction and Other Laryngeal Sources Mark T. O'Hollaren, MD Published: 08/26/2002 Introduction Both primary care and subspecialty physicians are frequently called upon to evaluate patients with shortness of breath. This dyspnea may be labeled " difficult or refractory asthma. " In some cases, the site of origin of this dyspnea may in fact not be the bronchial airways or the lung parenchyma, but rather the larynx. Most of us are familiar with the clinical management of shortness of breath due to asthma or chronic obstructive pulmonary disease; however, a high index of suspicion is needed to carefully unravel a patient's symptom complex and pinpoint a diagnosis of pathology in the larynx. The diagnosis of laryngeal causes of dyspnea may escape accurate diagnosis for years, and may result in inappropriate and dangerous long-term treatment, including use of chronic maintenance corticosteroids. This may result in needless diagnostic tests, potentially invasive therapeutic interventions, and possible debilitating long-term side effects from inappropriate treatment. Patients with dyspnea originating in their larynx may complain of shortness of breath, which may be accompanied by a wheezing or stridorous sound. Others may state that their symptoms are worsened by physical exertion. The recognition of the laryngeal origin of these syndromes may lead to a more timely diagnosis. The highest yield diagnostic study in the majority of laryngeal disorders is the direct visualization of the larynx at the time a patient is experiencing symptoms. Careful examination with a flexible or rigid laryngoscope, or indirect visualization of the larynx with the laryngeal mirror, is needed to establish an appropriate or an accurate diagnosis. If appropriate examination cannot be done, or the diagnosis is in question, prompt referral to a competent otolaryngologist is necessary. In specialized centers, problems with the vocal cords and speech production may be further evaluated with specialized diagnostic equipment, such as a laryngostroboscope. This discussion will center around the laryngeal disorders that may lead to dyspnea, and disorders of voice will not be covered with this summary. The Amazing Larynx The larynx is a very complex and extremely important anatomic region that functions to join the airway and the superior portion of the gastrointestinal tract. Its sphincteric capabilities allow protection of the airway, prevent aspiration of fluid and food particles during swallowing, and also protect against aspiration of any potential foreign material when it enters the larynx during respiration. During swallowing, the airway closes naturally, and will close involuntarily with stimulation of the pharynx. The automatic reflex will take precedence over all voluntary controls of laryngeal function. To facilitate vocal communication, an elaborate mechanism of vocal cord vibration/oscillation is coordinated with movements of the tongue and mouth. For further information on the voice and vocal disorders, the reader is referred to an elegant summary by Cohn and colleagues.[1] Dyspnea and the Larynx There are 2 main ways in which patients may experience dyspnea originating in the larynx. First, there may be structural interference with air flow due to an anatomic abnormality. In other words, there is some structural interference with air flow due to a growth, tumor, swelling, anatomical narrowing, etc. The second mechanism by which dyspnea may originate in the larynx is abnormal motion of functioning of a laryngeal structure. This may include problems such as vocal cord dysfunction (VCD), neurologic disorders of the vocal cords, vocal cord paralysis, laryngospasm, etc. Air Flow Obstruction Resulting From Structural Interference A number of structural abnormalities may interfere with laryngeal air flow, and may or may not be accompanied by any change in the actual quality of the patient's voice. There are both infectious and noninfectious processes that can lead to air flow obstruction. One of the most rapidly developing and frightening infectious causes of dyspnea originating in the larynx is epiglottitis. Epiglottitis is almost always due to a bacterial pathogen, which may produce rapidly evolving inflammation and edema of the larynx in the supraglottic area. Causative organisms include Haemophilus influenzae type B, Pneumococcus, and group A beta hemolytic streptococci. This most commonly affects children, and may be clinically characterized by drooling, inspiratory stridor, high fever, and airway distress. As noted above, the symptoms may be rapid in onset and progression, and most commonly affect children between the ages of 2 and 8 years, but also may occur in adults. In a series of 129 cases, approximately 1 out of 7 adults with epiglottitis required airway intervention, by either tracheotomy or endotracheal intubation.[2] In this series, factors that were associated with the need for acute airway intervention were the presence of stridor or having the patient sitting up and erect at the time of presentation. Although there were no deaths, major complications occurred in 5% of patients. Visualization of the epiglottis is done with either a lateral neck radiograph or using a flexible fiberoptic rhinolaryngoscope via a nasal approach. A tongue blade is never used when epiglottitis is suspected because of the risk of precipitating acute airway closure. Medical management of acute epiglottitis involves the use of appropriate antibiotic therapy and, in some patients, corticosteroids. The immediate availability of medical personnel capable of securing an airway is also crucial, since tracheotomy or endotracheal intubation may be needed in the management of the patient. If a patient's symptoms are escalating rapidly, it is better to secure an airway sooner rather than later in this potentially life-threatening situation. The subglottic area may also be affected by viral infections, such as croup. Croup is commonly caused by a viral pathogen, frequently influenza or parainfluenza virus. Although croup is not a typical laryngeal cause of dyspnea, nonetheless, it is an important cause of stridor in children, with treatment consisting of hydration, humidification, corticosteroids, and racemic epinephrine in some patients. Bacterial tracheitis may be fatal, and typically presents with high fever, stridor, a barking cough, extreme leukocytosis, and thick mucopurulent discharge from the trachea. Staphylococcus is a frequent causative organism, although H influenzatype B and group A streptococci have also been reported to cause this condition. Occasionally, intubation and tracheostomy may be needed in these patients, and therapeutic intervention with antibiotics must be done without delay to minimize the need for acute airway intervention. Infections may also result in laryngeal abscesses, including those in both the larynx or hypopharyngeal area, and may compromise the airway, requiring surgical incision and drainage. These abscesses may occur following an episode of tonsillitis, and may be deceptively slow in their evolution. Finally, there are a number of less common infectious diseases that may involve the larynx, including tuberculosis, syphilis, trichinosis, diphtheria, histoplasmosis, and leprosy. Fungal infections may also involve the laryngeal airway, including infections with Aspergillus, Histoplasma, Coccidioides, Blastomyces, Actinomyces, Candida, Cryptococcus, and Nocardia. Both benign and malignant tumors of the larynx may also lead to shortness of breath; again, direct visualization is mandatory to accurately diagnose these disorders. The most common benign tumor of the larynx is squamous papilloma, which may occur either in a juvenile or adult form. It is seen in a higher frequency in children who are delivered vaginally from mothers who have venereal warts and are infected with the human papilloma virus. In this case, presenting symptoms may include hoarseness, respiratory compromise, or audible stridor. If untreated, this condition can result in fatal asphyxiation, and this has been reported in children.[3] This condition is difficult to treat, and a number of approaches have been used, including carbon dioxide laser, systemic interferon, and others. It is most important to refer such patients to an otolaryngologist for appropriate management. Noninfectious Causes of Laryngeal Air Flow Limitation Appropriate air flow through the larynx may be impeded by a number of noninfectious conditions. The most common cause of stridor in children is congenital laryngomalacia. This is a condition that results from a flaccidity of the larynx. A lack of rigidity of the framework that supports the larynx leads to this condition, in concert with some accompanying flaccidity of the supraglottic tissues of the larynx. Increased physician activity may lead to stridor, as may crying in infants. The symptoms may occur in infants and young children as early as a few weeks after birth and may last from 12 to 18 months. Direct visualization of the larynx may show a converging of the laryngeal structures during inspiration, and although the disorder usually spontaneously resolves in time, tracheostomy may be indicated in severe cases. A narrowing of the area just beneath the true vocal cords is referred to as subglottic stenosis. This may occur from a number of causes, including trauma to the larynx from prolonged endotracheal intubation. In addition, this narrowing may occur from vasculitic or other inflammatory conditions such as Wegener's granulomatosis, relapsing polychondritis, or systemic lupus erythematosus. The differential diagnosis of subglottic stenosis includes infection, tumor, trauma, thermal or chemical inhalation, live/acid ingestion, and tracheomalacia. In addition, sarcoidosis and amyloidosis may also cause inflammatory changes or masses within the larynx. An acute allergic reaction, such as anaphylaxis to food, insect sting, drug, or other cause, may also lead to laryngeal edema. Idiopathic angioedema, outside of the setting of acute anaphylaxis, may also lead to laryngeal swelling and may occur as either an idiopathic condition or as the hereditary form of C-1 esterase inhibitor deficiency. Prompt administration of subcutaneous epinephrine, systemic corticosteroids, and maintenance of an adequate airway are crucial in the management of acute laryngeal edema. In young children or toddlers with stridor, the question of foreign body aspiration frequently arises. The peak incidence of foreign body aspiration occurs between the ages of 12 and 36 months. In young children, the larynx is very pliable and is located in close proximity to the esophagus. Because of this fact, foreign bodies lodged within the esophagus may actually lead to respiratory compromise and stridor in young children. Elderly patients, especially those who are debilitated or have any type of swallowing dysfunction, may also suffer from foreign body aspiration. Those who have degenerative neurologic disease or have experienced a cerebrovascular accident may be at especially high risk. Finally, other noninfectious causes of laryngeal airway obstruction may include vocal cord polyps, laryngoceles, saccular cysts, and laryngeal vascular malformations. Goiters involving the cervical and substernal area may also interfere with tracheal and laryngeal air flow. The flow volume loop may be somewhat helpful in alerting a physician to a structural interference with air flow. A flattening of the inspiratory portion of the flow volume loop may suggest a variable extrathoracic obstruction, whereas a flattening of the expiratory portion may suggest a variable intrathoracic obstruction. Flattening of both the inspiratory and expiratory limbs raises the suspicion of a fixed airway narrowing. Laryngeal Air Flow Limitation Resulting From Abnormal Movement of Laryngeal Structures Background The boundaries of the larynx extend from the superior tip of the epiglottis to the cricoid cartilage. The cricoid cartilage serves as the foundation of the larynx, and is actually the only complete cartilaginous ring in the tracheal bronchial tree. The definitive configuration of the larynx is present by 28 weeks of gestation.[4] The true vocal cords serve as a " guardian of the airway. " In addition, closing the glottis allows us to have fixation of the thorax, which aids in the mechanisms of heavy lifting using the arms. Finally, motion of the vocal cords allows us to produce vocal sounds for communication, and this process has required the development of a very complex neural control mechanism, which permits precise movements of the vocal cords to produce vocal sounds. Those unfamiliar with the mechanics of voice production feel the process is somewhat simplistic and automatic. However, it is immensely complex and requires the coordination of conceptualized thoughts to be placed in linguistic form, selection of appropriate words, and conversion of these thoughts into appropriate neural impulses. The various laryngeal articulatory structures are then used to produce vocal sounds. While this is taking place, the entire process is monitored using visual, auditory, and proprioceptive systems on an ongoing basis. It is usually when something goes wrong that this complex series of neural and muscular interactions comes to the attention of both the treating physician and the patient. The respiratory cycle consists of inspiration and expiration, and, in most patients, the glottal opening of the vocal cords is slightly wider on inspiration compared with expiration. In general, however, the average opening of the glottis is fairly constant. This glottic opening is controlled through the medullary respiratory center (via the vagus nerve), which leads to contraction of the posterior cricoarytenoid (PCA) muscle. Contraction of the PCA muscle then leads to opening (abduction) of the vocal cords, which functions to open the glottis and reduce resistance to air flow through the larynx. Contraction of the PCA muscle is also timed with contraction of the diaphragmatic musculature, and is also influenced by variations in both arterial carbon dioxide and oxygen concentrations as well as intrapulmonary pressure.[5] Of note, it appears that the vocal cords are sensitive to changes in airway caliber as well. Experimentally, histamine-induced bronchospasm may lead to an expiratory narrowing of the vocal cords. Because of this, some feel that the glottis is capable of reflex adjustments in parallel with changes in airway caliber. Dyspnea resulting from abnormal motion of laryngeal structures has been described in a number of clinical settings, including VCD (also sometimes referred as paradoxical vocal cord motion), vocal cord paralysis, laryngospasm, Meige syndrome, and spastic dysphonia. These disorders may occur in children, adolescents, and adults, and some may have at least a partial functional component. Most do not appear to be under the direct voluntary control of the patient experiencing these symptoms. As previously mentioned, the vocal cords are normally opened widest during inspiration, and may narrow slightly during expiration in a normal individual. VCD is an phenomenon in which the vocal cords come together (adduct), producing air flow obstruction at the level of the larynx.[6] This abnormal vocal cord motion may produce recurrent wheezing that may imitate asthma, and may be misdiagnosed as asthma for years. If vocal cords close during inspiration, this may lead to stridor, which may be misdiagnosed as an upper airway obstruction of life-threatening severity. The acute presentation, frequently seen in the emergency department, may be dramatic and lead to inappropriate endotracheal intubation, tracheotomy, or recurrent courses of high-dose corticosteroids.[6] VCD may affect either sex; however, the vast majority of cases described in the literature have been in females. For example, at the National Jewish Center for Respiratory Disease, in the excellent summary by Drs. Newman and Dubester,[6] 37 of 38 patients with VCD without asthma were women. The age of their patients at the time of presentation ranged from 9 to 74 years. However, the most common patient profile involves females between the ages of 20 and 40 years of age, with greater than a high school education and often some affiliation with a health-related field. Approximately 1 of every 4 patients with VCD seen at National Jewish fit this profile. Clinical presentations of VCD may include wheezing, which may suggest asthma, or stridor, which may suggest upper airway obstruction. The excellent summary by Newman characterizes the clinical and laboratory findings of VCD, as well as therapeutic recommendations.[6] VCD may follow a respiratory infection, although this history is not always given. It is also very common to have VCD occur in the presence of gastroesophageal reflux or significant postnasal drainage. Symptoms may occur with or without exercise, and VCD may occur as an isolated condition or may occur simultaneously in patients with pre-existing asthma. Diagnosis of VCD When interviewing a patient, a careful history may give some clues as to the correct diagnosis. Patients may point to their larynx when asked where they feel the site of air flow limitation exists, and may describe a sense of throat tightness or even changes in their voice during an acute attack. B. Newman, MD,[7] Medical Director of Respiratory Products of Forest Laboratories, Inc. in New York, NY, stated at the 58th Annual Meeting of the American Academy of Allergy, Asthma and Immunology that perhaps the most reliable question to ask a patient is whether they feel inhaled bronchodilators improved their breathing or not. Especially in patients with isolated VCD without asthma, bronchodilators have little benefit. Another important question is whether they experience dyspnea accompanying these episodes and waking them up at night. Nocturnal symptoms of shortness of breath are fairly common in patients with asthma, and are rare in patients with VCD. The physical examination of patients with VCD may be very unreliable. Because sounds may be transmitted throughout the chest through the excellent sound-conducting properties of the large airways, it is difficult to localize the site of origin for wheezing or stridor sounds. If a patient is suspected of having VCD, then the gold standard is direct visualization of the larynx during an acute attack to confirm that the vocal cords approximate during inspiration, during expiration, or both. The term " paradoxical vocal cord motion " is typically given to patients who have approximation of the vocal cords during an inspiratory maneuver, since the vocal cords typically abduct, or widen, during inspiration in patients without the VCD. Another potentially helpful diagnostic tip when suspecting VCD is to have the patient hold their breath or to use a panting pattern of breathing. Patients with acute asthma find it very difficult to hold their breath, although those with VCD may be able to do so more readily. This action may actually improve their symptoms of dyspnea. In addition, patients with VCD may have decreased symptoms of dyspnea if they breathe in a panting fashion. Patients with VCD may have a flattening of the inspiratory portion of the flow volume loop, consistent with variable extrathoracic obstruction. Dr. Newman described approximately 25% of patients who may have an abnormal inspiratory portion of the flow volume loop, even when asymptomatic. Another clue that a patient's dyspnea may be caused by VCD is that during an attack, the patient's alveolar-arterial (A-a) oxygen gradient is frequently normal.[8] In contrast, patients experiencing acute severe asthma will have a widening of the A-a oxygen gradient in greater than 90% of cases. Flow volume loop during the acute attack may also show some inspiratory flattening consistent with variable extrathoracic obstruction, but, alternatively, the flow volume loop may show both inspiratory and expiratory flattening more consistent with fixed obstruction. It should be pointed out, however, that virtually any type of air flow abnormality pattern could be present during an acute attack of VCD. Laryngoscopic Findings With VCD As discussed earlier, inspiration typically results in the widening of the glottic aperture. During VCD, there tends to be an inappropriate adduction of the anterior two thirds of the vocal cords, with the posterior one third typically remaining slightly open in a " diamond-shaped chink " pattern. This may occur during inspiration only, during both phases of respiration, or during expiration only. If needed, provocative challenges using exercise or other stimuli may be done where laryngoscopic confirmation of the diagnosis may be accomplished. Other Contributing Factors Psychological stress may also play a role in some patients with VCD. Clinical experience of those treating VCD has shown that stressful situations, especially in adolescent high-performance female athletes, may increase the chance that VCD may be playing a role in some patients with dyspnea, which do not respond to typical treatment for exercise-induced asthma. It is appropriate to consider each individual case, and explore areas of psychological difficulty that may be compounding a given patient's clinical presentation. There have been some reports of association of VCD with psychological trauma as well, including a past history of sexual abuse, although this appears to be only evident in a minority of patients. A retrospective review by Freedman and coworkers[9] of 47 female inpatients at National Jewish Center with discharge diagnoses of VCD showed that 36% of those patients had experienced childhood sexual abuse. This should be kept in the context that the prevalence of sexual abuse in the general female population ranges from 6% to 62%.[10] The prevalence of sexual abuse in patients with VCD may not, therefore, represent a defining characteristic of this population. It is clear that unrecognized and untreated psychological problems may, in fact, be associated with VCD and should be addressed as appropriate. Treatment of VCD The appropriate treatment of VCD is best initiated with a careful explanation of the disorder and treatment recommendations. It is helpful for patients to have a description of the anatomy of the vocal cords, as well as the abnormalities that occur that produce the symptoms. It may also be useful to compare the psychological factors related to VCD with asthma, in which emotions are also seen as a common trigger, but not the positive factor of the disorder. Patients need to be reassured that they are not being told that the physician does not believe their symptoms to be real, or that it is " all in their head. " Speech therapy is the foundation of treatment of VCD. A speech therapist who is familiar with this disorder, and who can coach a patient on appropriate laryngeal and neck relaxation techniques, panting breathing, breath holding, slow relaxed expiration techniques, etc., may be extremely helpful in preventing and treating these episodes. Vocal cord paralysis may be unilateral or bilateral and may result from damage of the recurrent laryngeal nerve during past thyroid or parathyroid surgery. The left vocal cord is more commonly affected than the right due to the somewhat longer path of the recurrent laryngeal nerve and its anatomic relationship to structures in the mediastinum. There also may be other neuropathies and degenerative neurologic conditions that may result in vocal cord paralysis. This condition may result in an abnormal voice, but the voice may be near normal in other patients with unilateral vocal cord paralysis. There may be problems, including aspiration while drinking liquids or eating solid foods, and once again the appropriate diagnosis is made by direct visualization of the vocal cords with documentation of abnormal vocal cord movements while coughing or during phonation. Other neurologic problems such as Meige syndrome, a neurologic condition accompanied by episodic spastic closure of the vocal cords, may lead to episodic shortness of breath, which may be severe enough to result in loss of consciousness. Spastic dysphonia, a somewhat poorly understood condition causing abnormal motion of the vocal cords, may occur in both an abductive and an adductive variety. Some patients who have abductive spastic dysphonia may experience some dyspnea. Treatment may be difficult, but is best referred to an otolaryngologist and appropriate speech therapist for management. Conclusion It is clear that dyspnea may originate from a large number of conditions affecting air flow through the larynx. The foundational corner stone of diagnosis of laryngeal causes of dyspnea is direct visualization of the larynx, especially when symptoms are present. Close consultation with an otolaryngologist, and, in some cases, a speech therapist, may be extremely helpful in alleviating the symptoms that these patients experience and returning them to a healthy, active lifestyle. References Cohn JR, Spiegel JR, Sattaloff RT. Vocal disorders and the professional voice user: The allergist's role. Ann Allergy Asthma Immunol. 1995;74:363-376. Franz TD, Rasgone BM, Quesenberry CP. Acute epiglottitis in the adults: an analysis of 129 cases. JAMA. 1994;272:1358-1360. Sperry K. Lethal asphyxiating juvenile laryngeal papillomatosis. Am J Forensic Med Pathol. 1995;15:146-150. Baxter MRM. Congenital laryngomalacia. Canadian J Anesthesia. 1994;41:333-339. Wood RP, Jafek BW, Cherniak RM. Laryngeal dysfunction in pulmonary disorders. Otolaryngol Head Neck Surg. 1986;94:374. Newman KB, Dubester SN. Vocal cord dysfunction: masquerader of asthma. Sem Respir Crit Care Med. 1994;15:161-167. Newman KB. Seminar: Vocal cord dysfunction. Program and abstracts of the 58th Annual Meeting of the American Academy of Allergy, Asthma and Immunology; March 1-6, 2002; New York, NY. KL, Wood RP, Eckert RC, et al. Vocal cord dysfunction presenting as asthma. N Engl J Med. 1983;390:1566-1570. Freedman MR, Rosenberg SJ, Schmaling KB. Childhood sexual abuse in patients with paradoxical vocal cord dysfunction. J Nerv Ment Dis. 1991;179:295-298. s SD, Wyalt GE, Finkelhor D. Prevalence. In: Finkelhower D, ed. A Source Book on Child Sexual Abuse. Beverly Hills, California: Sage Publications; 1986:15-59. 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Guest guest Posted October 12, 2009 Report Share Posted October 12, 2009 Not to mention, as mentioned, the state of the underlying tone of the individual as they do/start this exercise. Sunny Sunny Kierstyn, RN DC Fibromyalgia Care Center of Oregon 2677 Willakenzie Road, 7CEugene, Oregon, 97401541- 654-0850; Fx; 541- 654-0834 Subject: RE: vocal cord dysfunctionDate: Mon, 12 Oct 2009 15:15:32 -0700From: TForcum@...To: skrndc1@...; brian@...; Running may have compressive loads of 3-5 times body weight, however to imply that these loads are degenerative is a far reach. Running and soccer have less symptomatic knees and hips vs non-athletes. Studies show healthcare costs in the last 5 years of life is markedly less in runners. Thus these folks the compression could be therapeutic. I think the key is what position is your body in during compression. Ted Forcum, DC, DACBSP ACA Sports Council, President '08 US Olympic Sports Medicine Team Member Back In Motion Sports Injuries Clinic, LLC 11385 SW Scholls Ferry Road Beaverton, Oregon 97008 503.524.9040 www.bimsportsinjuries.com The information contained in this electronic message may contain protected health information confidential under applicable law, and is intended only for the use of the individual or entity named above. If the recipient of this message is not the intended recipient, you are hereby notified that any dissemination, copy or disclosure of this communication is strictly prohibited. If you have received this communication in error, please notify Back In Motion Sports Injuries Clinic, LLC at 11385 SW Scholls Ferry Road, Beaverton, OR-97008. and purge the communication immediately without making any copy or distribution. From: [mailto: ] On Behalf Of Sunny KierstynSent: Monday, October 12, 2009 2:51 PM Seitz; Subject: RE: vocal cord dysfunction So...once again, guys: think chiropracatically: running escalates compression. We live in a world that compresses us: riding in cars that pack us down like boxes of cornflakes; walkling on concrete that, with every step, compresses us; living in gravity for all of our days.... and all of that compression is BEFORE we carry a child on our hip or live 8 decades or have motor vehicle accidents or fall out of trees or drive and turn our heads a dozen times/mile to check our parameters. Then: you run! How compressive is that?! .... and how much does it effect the compressions you have encountered up to that point?! ...or that day? Exercise induced asthma, if you haven't already figured out, is also about lack of adequate calcium. Many time in this office we have shifted a person out of an asthma attack with the use of liquid calcium...and, yes, I usually provide a tab/cap of HCL with it as well. We can do SO So SO much for these conditions .... maybe what our students need is just to understand the difference between what the MDs call something versus what we call it .... and not get hung up on: "I can't fix that" just because it has a fancy medicalese name on it. my 2 cents this afternoon Sunny Sunny Kierstyn, RN DC Fibromyalgia Care Center of Oregon 2677 Willakenzie Road, 7CEugene, Oregon, 97401541- 654-0850; Fx; 541- 654-0834 From: briantualityphysiciansDate: Mon, 12 Oct 2009 12:13:43 -0700Subject: vocal cord dysfunction Group, I’ve recently become aware of this disorder. My wife and kids have a strange desire to run – without a ball or other reason! I am thus exposed to many runners of all ages. One particular high level Boise State runner had struggled with “exercise induced asthma”, and treated with bronchodilators and steroids for many years. Problem was, it wasn’t asthma!!! It was diagnosed as VCD and through proper treatment was able to take control of the problem. You would think we would all be aware of this ddx to asthma, but I wasn’t and I don’t think many MD’s are either. The following is an interesting article from Medscape: Mark T. O'Hollaren, MD, Director, Allergy Clinic; Clinical Professor of Medicine, Oregon Health and Science University, Portland, Oregon Dyspnea Due to Vocal Cord Dysfunction and Other Laryngeal Sources Mark T. O'Hollaren, MD Published: 08/26/2002 Introduction Both primary care and subspecialty physicians are frequently called upon to evaluate patients with shortness of breath. This dyspnea may be labeled "difficult or refractory asthma." In some cases, the site of origin of this dyspnea may in fact not be the bronchial airways or the lung parenchyma, but rather the larynx. Most of us are familiar with the clinical management of shortness of breath due to asthma or chronic obstructive pulmonary disease; however, a high index of suspicion is needed to carefully unravel a patient's symptom complex and pinpoint a diagnosis of pathology in the larynx. The diagnosis of laryngeal causes of dyspnea may escape accurate diagnosis for years, and may result in inappropriate and dangerous long-term treatment, including use of chronic maintenance corticosteroids. This may result in needless diagnostic tests, potentially invasive therapeutic interventions, and possible debilitating long-term side effects from inappropriate treatment. Patients with dyspnea originating in their larynx may complain of shortness of breath, which may be accompanied by a wheezing or stridorous sound. Others may state that their symptoms are worsened by physical exertion. The recognition of the laryngeal origin of these syndromes may lead to a more timely diagnosis. The highest yield diagnostic study in the majority of laryngeal disorders is the direct visualization of the larynx at the time a patient is experiencing symptoms. Careful examination with a flexible or rigid laryngoscope, or indirect visualization of the larynx with the laryngeal mirror, is needed to establish an appropriate or an accurate diagnosis. If appropriate examination cannot be done, or the diagnosis is in question, prompt referral to a competent otolaryngologist is necessary. In specialized centers, problems with the vocal cords and speech production may be further evaluated with specialized diagnostic equipment, such as a laryngostroboscope. This discussion will center around the laryngeal disorders that may lead to dyspnea, and disorders of voice will not be covered with this summary. The Amazing Larynx The larynx is a very complex and extremely important anatomic region that functions to join the airway and the superior portion of the gastrointestinal tract. Its sphincteric capabilities allow protection of the airway, prevent aspiration of fluid and food particles during swallowing, and also protect against aspiration of any potential foreign material when it enters the larynx during respiration. During swallowing, the airway closes naturally, and will close involuntarily with stimulation of the pharynx. The automatic reflex will take precedence over all voluntary controls of laryngeal function. To facilitate vocal communication, an elaborate mechanism of vocal cord vibration/oscillation is coordinated with movements of the tongue and mouth. For further information on the voice and vocal disorders, the reader is referred to an elegant summary by Cohn and colleagues.[1] Dyspnea and the Larynx There are 2 main ways in which patients may experience dyspnea originating in the larynx. First, there may be structural interference with air flow due to an anatomic abnormality. In other words, there is some structural interference with air flow due to a growth, tumor, swelling, anatomical narrowing, etc. The second mechanism by which dyspnea may originate in the larynx is abnormal motion of functioning of a laryngeal structure. This may include problems such as vocal cord dysfunction (VCD), neurologic disorders of the vocal cords, vocal cord paralysis, laryngospasm, etc. Air Flow Obstruction Resulting From Structural Interference A number of structural abnormalities may interfere with laryngeal air flow, and may or may not be accompanied by any change in the actual quality of the patient's voice. There are both infectious and noninfectious processes that can lead to air flow obstruction. One of the most rapidly developing and frightening infectious causes of dyspnea originating in the larynx is epiglottitis. Epiglottitis is almost always due to a bacterial pathogen, which may produce rapidly evolving inflammation and edema of the larynx in the supraglottic area. Causative organisms include Haemophilus influenzae type B, Pneumococcus, and group A beta hemolytic streptococci. This most commonly affects children, and may be clinically characterized by drooling, inspiratory stridor, high fever, and airway distress. As noted above, the symptoms may be rapid in onset and progression, and most commonly affect children between the ages of 2 and 8 years, but also may occur in adults. In a series of 129 cases, approximately 1 out of 7 adults with epiglottitis required airway intervention, by either tracheotomy or endotracheal intubation.[2] In this series, factors that were associated with the need for acute airway intervention were the presence of stridor or having the patient sitting up and erect at the time of presentation. Although there were no deaths, major complications occurred in 5% of patients. Visualization of the epiglottis is done with either a lateral neck radiograph or using a flexible fiberoptic rhinolaryngoscope via a nasal approach. A tongue blade is never used when epiglottitis is suspected because of the risk of precipitating acute airway closure. Medical management of acute epiglottitis involves the use of appropriate antibiotic therapy and, in some patients, corticosteroids. The immediate availability of medical personnel capable of securing an airway is also crucial, since tracheotomy or endotracheal intubation may be needed in the management of the patient. If a patient's symptoms are escalating rapidly, it is better to secure an airway sooner rather than later in this potentially life-threatening situation. The subglottic area may also be affected by viral infections, such as croup. Croup is commonly caused by a viral pathogen, frequently influenza or parainfluenza virus. Although croup is not a typical laryngeal cause of dyspnea, nonetheless, it is an important cause of stridor in children, with treatment consisting of hydration, humidification, corticosteroids, and racemic epinephrine in some patients. Bacterial tracheitis may be fatal, and typically presents with high fever, stridor, a barking cough, extreme leukocytosis, and thick mucopurulent discharge from the trachea. Staphylococcus is a frequent causative organism, although H influenzatype B and group A streptococci have also been reported to cause this condition. Occasionally, intubation and tracheostomy may be needed in these patients, and therapeutic intervention with antibiotics must be done without delay to minimize the need for acute airway intervention. Infections may also result in laryngeal abscesses, including those in both the larynx or hypopharyngeal area, and may compromise the airway, requiring surgical incision and drainage. These abscesses may occur following an episode of tonsillitis, and may be deceptively slow in their evolution. Finally, there are a number of less common infectious diseases that may involve the larynx, including tuberculosis, syphilis, trichinosis, diphtheria, histoplasmosis, and leprosy. Fungal infections may also involve the laryngeal airway, including infections with Aspergillus, Histoplasma, Coccidioides, Blastomyces, Actinomyces, Candida, Cryptococcus, and Nocardia. Both benign and malignant tumors of the larynx may also lead to shortness of breath; again, direct visualization is mandatory to accurately diagnose these disorders. The most common benign tumor of the larynx is squamous papilloma, which may occur either in a juvenile or adult form. It is seen in a higher frequency in children who are delivered vaginally from mothers who have venereal warts and are infected with the human papilloma virus. In this case, presenting symptoms may include hoarseness, respiratory compromise, or audible stridor. If untreated, this condition can result in fatal asphyxiation, and this has been reported in children.[3] This condition is difficult to treat, and a number of approaches have been used, including carbon dioxide laser, systemic interferon, and others. It is most important to refer such patients to an otolaryngologist for appropriate management. Noninfectious Causes of Laryngeal Air Flow Limitation Appropriate air flow through the larynx may be impeded by a number of noninfectious conditions. The most common cause of stridor in children is congenital laryngomalacia. This is a condition that results from a flaccidity of the larynx. A lack of rigidity of the framework that supports the larynx leads to this condition, in concert with some accompanying flaccidity of the supraglottic tissues of the larynx. Increased physician activity may lead to stridor, as may crying in infants. The symptoms may occur in infants and young children as early as a few weeks after birth and may last from 12 to 18 months. Direct visualization of the larynx may show a converging of the laryngeal structures during inspiration, and although the disorder usually spontaneously resolves in time, tracheostomy may be indicated in severe cases. A narrowing of the area just beneath the true vocal cords is referred to as subglottic stenosis. This may occur from a number of causes, including trauma to the larynx from prolonged endotracheal intubation. In addition, this narrowing may occur from vasculitic or other inflammatory conditions such as Wegener's granulomatosis, relapsing polychondritis, or systemic lupus erythematosus. The differential diagnosis of subglottic stenosis includes infection, tumor, trauma, thermal or chemical inhalation, live/acid ingestion, and tracheomalacia. In addition, sarcoidosis and amyloidosis may also cause inflammatory changes or masses within the larynx. An acute allergic reaction, such as anaphylaxis to food, insect sting, drug, or other cause, may also lead to laryngeal edema. Idiopathic angioedema, outside of the setting of acute anaphylaxis, may also lead to laryngeal swelling and may occur as either an idiopathic condition or as the hereditary form of C-1 esterase inhibitor deficiency. Prompt administration of subcutaneous epinephrine, systemic corticosteroids, and maintenance of an adequate airway are crucial in the management of acute laryngeal edema. In young children or toddlers with stridor, the question of foreign body aspiration frequently arises. The peak incidence of foreign body aspiration occurs between the ages of 12 and 36 months. In young children, the larynx is very pliable and is located in close proximity to the esophagus. Because of this fact, foreign bodies lodged within the esophagus may actually lead to respiratory compromise and stridor in young children. Elderly patients, especially those who are debilitated or have any type of swallowing dysfunction, may also suffer from foreign body aspiration. Those who have degenerative neurologic disease or have experienced a cerebrovascular accident may be at especially high risk. Finally, other noninfectious causes of laryngeal airway obstruction may include vocal cord polyps, laryngoceles, saccular cysts, and laryngeal vascular malformations. Goiters involving the cervical and substernal area may also interfere with tracheal and laryngeal air flow. The flow volume loop may be somewhat helpful in alerting a physician to a structural interference with air flow. A flattening of the inspiratory portion of the flow volume loop may suggest a variable extrathoracic obstruction, whereas a flattening of the expiratory portion may suggest a variable intrathoracic obstruction. Flattening of both the inspiratory and expiratory limbs raises the suspicion of a fixed airway narrowing. Laryngeal Air Flow Limitation Resulting From Abnormal Movement of Laryngeal Structures Background The boundaries of the larynx extend from the superior tip of the epiglottis to the cricoid cartilage. The cricoid cartilage serves as the foundation of the larynx, and is actually the only complete cartilaginous ring in the tracheal bronchial tree. The definitive configuration of the larynx is present by 28 weeks of gestation.[4] The true vocal cords serve as a "guardian of the airway." In addition, closing the glottis allows us to have fixation of the thorax, which aids in the mechanisms of heavy lifting using the arms. Finally, motion of the vocal cords allows us to produce vocal sounds for communication, and this process has required the development of a very complex neural control mechanism, which permits precise movements of the vocal cords to produce vocal sounds. Those unfamiliar with the mechanics of voice production feel the process is somewhat simplistic and automatic. However, it is immensely complex and requires the coordination of conceptualized thoughts to be placed in linguistic form, selection of appropriate words, and conversion of these thoughts into appropriate neural impulses. The various laryngeal articulatory structures are then used to produce vocal sounds. While this is taking place, the entire process is monitored using visual, auditory, and proprioceptive systems on an ongoing basis. It is usually when something goes wrong that this complex series of neural and muscular interactions comes to the attention of both the treating physician and the patient. The respiratory cycle consists of inspiration and expiration, and, in most patients, the glottal opening of the vocal cords is slightly wider on inspiration compared with expiration. In general, however, the average opening of the glottis is fairly constant. This glottic opening is controlled through the medullary respiratory center (via the vagus nerve), which leads to contraction of the posterior cricoarytenoid (PCA) muscle. Contraction of the PCA muscle then leads to opening (abduction) of the vocal cords, which functions to open the glottis and reduce resistance to air flow through the larynx. Contraction of the PCA muscle is also timed with contraction of the diaphragmatic musculature, and is also influenced by variations in both arterial carbon dioxide and oxygen concentrations as well as intrapulmonary pressure.[5] Of note, it appears that the vocal cords are sensitive to changes in airway caliber as well. Experimentally, histamine-induced bronchospasm may lead to an expiratory narrowing of the vocal cords. Because of this, some feel that the glottis is capable of reflex adjustments in parallel with changes in airway caliber. Dyspnea resulting from abnormal motion of laryngeal structures has been described in a number of clinical settings, including VCD (also sometimes referred as paradoxical vocal cord motion), vocal cord paralysis, laryngospasm, Meige syndrome, and spastic dysphonia. These disorders may occur in children, adolescents, and adults, and some may have at least a partial functional component. Most do not appear to be under the direct voluntary control of the patient experiencing these symptoms. As previously mentioned, the vocal cords are normally opened widest during inspiration, and may narrow slightly during expiration in a normal individual. VCD is an phenomenon in which the vocal cords come together (adduct), producing air flow obstruction at the level of the larynx.[6] This abnormal vocal cord motion may produce recurrent wheezing that may imitate asthma, and may be misdiagnosed as asthma for years. If vocal cords close during inspiration, this may lead to stridor, which may be misdiagnosed as an upper airway obstruction of life-threatening severity. The acute presentation, frequently seen in the emergency department, may be dramatic and lead to inappropriate endotracheal intubation, tracheotomy, or recurrent courses of high-dose corticosteroids.[6] VCD may affect either sex; however, the vast majority of cases described in the literature have been in females. For example, at the National Jewish Center for Respiratory Disease, in the excellent summary by Drs. Newman and Dubester,[6] 37 of 38 patients with VCD without asthma were women. The age of their patients at the time of presentation ranged from 9 to 74 years. However, the most common patient profile involves females between the ages of 20 and 40 years of age, with greater than a high school education and often some affiliation with a health-related field. Approximately 1 of every 4 patients with VCD seen at National Jewish fit this profile. Clinical presentations of VCD may include wheezing, which may suggest asthma, or stridor, which may suggest upper airway obstruction. The excellent summary by Newman characterizes the clinical and laboratory findings of VCD, as well as therapeutic recommendations.[6] VCD may follow a respiratory infection, although this history is not always given. It is also very common to have VCD occur in the presence of gastroesophageal reflux or significant postnasal drainage. Symptoms may occur with or without exercise, and VCD may occur as an isolated condition or may occur simultaneously in patients with pre-existing asthma. Diagnosis of VCD When interviewing a patient, a careful history may give some clues as to the correct diagnosis. Patients may point to their larynx when asked where they feel the site of air flow limitation exists, and may describe a sense of throat tightness or even changes in their voice during an acute attack. B. Newman, MD,[7] Medical Director of Respiratory Products of Forest Laboratories, Inc. in New York, NY, stated at the 58th Annual Meeting of the American Academy of Allergy, Asthma and Immunology that perhaps the most reliable question to ask a patient is whether they feel inhaled bronchodilators improved their breathing or not. Especially in patients with isolated VCD without asthma, bronchodilators have little benefit. Another important question is whether they experience dyspnea accompanying these episodes and waking them up at night. Nocturnal symptoms of shortness of breath are fairly common in patients with asthma, and are rare in patients with VCD. The physical examination of patients with VCD may be very unreliable. Because sounds may be transmitted throughout the chest through the excellent sound-conducting properties of the large airways, it is difficult to localize the site of origin for wheezing or stridor sounds. If a patient is suspected of having VCD, then the gold standard is direct visualization of the larynx during an acute attack to confirm that the vocal cords approximate during inspiration, during expiration, or both. The term "paradoxical vocal cord motion" is typically given to patients who have approximation of the vocal cords during an inspiratory maneuver, since the vocal cords typically abduct, or widen, during inspiration in patients without the VCD. Another potentially helpful diagnostic tip when suspecting VCD is to have the patient hold their breath or to use a panting pattern of breathing. Patients with acute asthma find it very difficult to hold their breath, although those with VCD may be able to do so more readily. This action may actually improve their symptoms of dyspnea. In addition, patients with VCD may have decreased symptoms of dyspnea if they breathe in a panting fashion. Patients with VCD may have a flattening of the inspiratory portion of the flow volume loop, consistent with variable extrathoracic obstruction. Dr. Newman described approximately 25% of patients who may have an abnormal inspiratory portion of the flow volume loop, even when asymptomatic. Another clue that a patient's dyspnea may be caused by VCD is that during an attack, the patient's alveolar-arterial (A-a) oxygen gradient is frequently normal.[8] In contrast, patients experiencing acute severe asthma will have a widening of the A-a oxygen gradient in greater than 90% of cases. Flow volume loop during the acute attack may also show some inspiratory flattening consistent with variable extrathoracic obstruction, but, alternatively, the flow volume loop may show both inspiratory and expiratory flattening more consistent with fixed obstruction. It should be pointed out, however, that virtually any type of air flow abnormality pattern could be present during an acute attack of VCD. Laryngoscopic Findings With VCD As discussed earlier, inspiration typically results in the widening of the glottic aperture. During VCD, there tends to be an inappropriate adduction of the anterior two thirds of the vocal cords, with the posterior one third typically remaining slightly open in a "diamond-shaped chink" pattern. This may occur during inspiration only, during both phases of respiration, or during expiration only. If needed, provocative challenges using exercise or other stimuli may be done where laryngoscopic confirmation of the diagnosis may be accomplished. Other Contributing Factors Psychological stress may also play a role in some patients with VCD. Clinical experience of those treating VCD has shown that stressful situations, especially in adolescent high-performance female athletes, may increase the chance that VCD may be playing a role in some patients with dyspnea, which do not respond to typical treatment for exercise-induced asthma. It is appropriate to consider each individual case, and explore areas of psychological difficulty that may be compounding a given patient's clinical presentation. There have been some reports of association of VCD with psychological trauma as well, including a past history of sexual abuse, although this appears to be only evident in a minority of patients. A retrospective review by Freedman and coworkers[9] of 47 female inpatients at National Jewish Center with discharge diagnoses of VCD showed that 36% of those patients had experienced childhood sexual abuse. This should be kept in the context that the prevalence of sexual abuse in the general female population ranges from 6% to 62%.[10] The prevalence of sexual abuse in patients with VCD may not, therefore, represent a defining characteristic of this population. It is clear that unrecognized and untreated psychological problems may, in fact, be associated with VCD and should be addressed as appropriate. Treatment of VCD The appropriate treatment of VCD is best initiated with a careful explanation of the disorder and treatment recommendations. It is helpful for patients to have a description of the anatomy of the vocal cords, as well as the abnormalities that occur that produce the symptoms. It may also be useful to compare the psychological factors related to VCD with asthma, in which emotions are also seen as a common trigger, but not the positive factor of the disorder. Patients need to be reassured that they are not being told that the physician does not believe their symptoms to be real, or that it is "all in their head." Speech therapy is the foundation of treatment of VCD. A speech therapist who is familiar with this disorder, and who can coach a patient on appropriate laryngeal and neck relaxation techniques, panting breathing, breath holding, slow relaxed expiration techniques, etc., may be extremely helpful in preventing and treating these episodes. Vocal cord paralysis may be unilateral or bilateral and may result from damage of the recurrent laryngeal nerve during past thyroid or parathyroid surgery. The left vocal cord is more commonly affected than the right due to the somewhat longer path of the recurrent laryngeal nerve and its anatomic relationship to structures in the mediastinum. There also may be other neuropathies and degenerative neurologic conditions that may result in vocal cord paralysis. This condition may result in an abnormal voice, but the voice may be near normal in other patients with unilateral vocal cord paralysis. There may be problems, including aspiration while drinking liquids or eating solid foods, and once again the appropriate diagnosis is made by direct visualization of the vocal cords with documentation of abnormal vocal cord movements while coughing or during phonation. Other neurologic problems such as Meige syndrome, a neurologic condition accompanied by episodic spastic closure of the vocal cords, may lead to episodic shortness of breath, which may be severe enough to result in loss of consciousness. Spastic dysphonia, a somewhat poorly understood condition causing abnormal motion of the vocal cords, may occur in both an abductive and an adductive variety. Some patients who have abductive spastic dysphonia may experience some dyspnea. Treatment may be difficult, but is best referred to an otolaryngologist and appropriate speech therapist for management. Conclusion It is clear that dyspnea may originate from a large number of conditions affecting air flow through the larynx. The foundational corner stone of diagnosis of laryngeal causes of dyspnea is direct visualization of the larynx, especially when symptoms are present. Close consultation with an otolaryngologist, and, in some cases, a speech therapist, may be extremely helpful in alleviating the symptoms that these patients experience and returning them to a healthy, active lifestyle. References Cohn JR, Spiegel JR, Sattaloff RT. Vocal disorders and the professional voice user: The allergist's role. Ann Allergy Asthma Immunol. 1995;74:363-376. Franz TD, Rasgone BM, Quesenberry CP. Acute epiglottitis in the adults: an analysis of 129 cases. JAMA. 1994;272:1358-1360. Sperry K. Lethal asphyxiating juvenile laryngeal papillomatosis. Am J Forensic Med Pathol. 1995;15:146-150. Baxter MRM. Congenital laryngomalacia. Canadian J Anesthesia. 1994;41:333-339. Wood RP, Jafek BW, Cherniak RM. Laryngeal dysfunction in pulmonary disorders. Otolaryngol Head Neck Surg. 1986;94:374. Newman KB, Dubester SN. Vocal cord dysfunction: masquerader of asthma. Sem Respir Crit Care Med. 1994;15:161-167. Newman KB. Seminar: Vocal cord dysfunction. Program and abstracts of the 58th Annual Meeting of the American Academy of Allergy, Asthma and Immunology; March 1-6, 2002; New York, NY. KL, Wood RP, Eckert RC, et al. Vocal cord dysfunction presenting as asthma. N Engl J Med. 1983;390:1566-1570. Freedman MR, Rosenberg SJ, Schmaling KB. Childhood sexual abuse in patients with paradoxical vocal cord dysfunction. J Nerv Ment Dis. 1991;179:295-298. s SD, Wyalt GE, Finkelhor D. Prevalence. In: Finkelhower D, ed. A Source Book on Child Sexual Abuse. Beverly Hills, California: Sage Publications; 1986:15-59. 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