# Orthostatic Intolerance and Vertigo



## M&M (Jan 20, 2002)

Sorry, this is very long. If you have the energy, it might be worth the read (I'll honestly admit I haven't made it through the whole thing yet myself)...Posted to the Co-Cure list:


> quote:Orthostatic Intolerance and VertigoOrthostatic IntoleranceWhat is Orthostatic Intolerance?When orthostatic symptoms occur in patients, but blood pressure does notfall as much as 20/10 mmHg on assumption of upright posture, the patienthas orthostatic intolerance (OI). Additional criteria used for thediagnosis of OI at Vanderbilt's Autonomic Dysfunction Center include anincrease in heart rate of at least 30 beats per minute with standing, and astanding plasma norepinephrine level of at least 600 pg/ml. Because uprightheart rate is usually greatly increased, the term Postural TachycardiaSyndrome (POTS) is also used.DemographicsOrthostatic intolerance affects an estimated 500,000 Americans and causes awide range of disabilities. It is a disorder that more frequently affectsyoung women (female-to-male ratio at least 4:1), often less than 35 yearsof age. Most of these patients experience an excessive heart rate increasewhen they stand. This heart rate increase is a sign that the cardiovascularsystem is working hard to maintain blood pressure and blood flow to thebrain in the presence of a disordered cardiovascular regulation. Other thanessential hypertension, OI is the most common disorder of blood pressureregulation. OI is also the most frequently encountered dysautonomia,accounting for the bulk of patients referred to centers specializing inautonomic disorders.Symptoms and SignsOrthostatic intolerance is present when patients experience symptoms suchas lightheadedness, palpitations, and tremulousness during standing. Manypatients also note other symptoms with upright posture: visual changes,discomfort in the head or neck, throbbing of the head, poor concentration,tiredness, weakness and occasionally fainting. Patients can be severelyimpaired by these symptoms and signs, such as a bluish-red suffusion ofskin in the lower extremities on standing, which are relieved by lyingdown. Similar orthostatic symptoms of inadequate cerebral perfusion canoccur transiently after serious debilitating illness, substantial weightloss and deconditioning or spaceflight.HeterogenityMany diagnoses have been given to such patients (Table 1). There areseveral features shared by these various entities, although in some ofthem, there appear to be abnormalities that are unrelated to thecardiovascular effects of the disorder.Table 1. Names Sometimes Used for Orthostatic Intolerance SyndromesHyperadrenergic orthostatic hypotensionPartial dysautonomiaOrthostatic tachycardia syndromeSympathicotonic orthostatic hypotensionPostural orthostatic tachycardia syndrome (POTS)Mitral valve prolapse syndromePostural tachycardia syndromeSoldier's heartHyperadrenergic postural hypotensionVasoregulatory astheniaSympathotonic orthostatic hypotensionNeurocirculatory astheniaHyperdynamic beta-adrenergic stateIrritable heartIdiopathic hypovolemiaOrthostatic anemiaEtiologyThe etiology of OI is unknown. For many years, such patients were felt tohave deconditioning and were encouraged to pursue a more vigorous exerciseregimen. However, recently it has become clear that many individuals withthese symptoms have a more serious problem than mere deconditioning. Theonset of OI is often predated by a recent viral infection. Patients canundergo extensive clinical evaluation without identification of a specificabnormality, and therefore most patients remained undiagnosed. Thesedifficulties are compounded by the heterogeneity of disease states inpatients with orthostatic symptoms, spontaneous fluctuations in diseaseseverity, and no uniformity in nomenclature of disease classification.Another problem in the diagnosis of OI is its overlap with other conditionssuch as Chronic Fatigue Syndrome (CFS), Neurally Mediated Syncope (NMS),physical deconditioning, etc. Improving characterization of the underlyingcirculatory responses may lead to a clarification of some of those issues,and will facilitate the discovery of the pathophysiology of OI.PathophysiologyPatients with OI typically have tachycardia on standing, usually a 30 beatper minute increment over a normal or slightly raised supine baselinevalue. Blood volume is usually reduced (5-25%). Plasma norepinephrine isnormal, high normal, or raised. Standing plasma norepinephrine levelsgreater than 2000 pg/ml have been encountered and such patients much becarefully studied to rule out pheochromocytoma.It is likely that the causes of OI are heterogeneous, but potentialpathophysiological mechanisms include a partial autonomic neuropathy,excessive venous pooling, a gravity-dependent fluid shift, diminishedplasma volume or red cell mass, cardiac beta-adrenergic hypersensitivity,diminished cardiovagal baroreflex sensitivity, brainstem dysfunction, andenhanced baseline sympathetic activity. It is suggested that the finding ofabnormally enhanced sympathetic drive to the cardiovascular system is afinal common pathophysiological mechanism in the majority of patients.A partial dysautonomia could account for the warm dry feet (loss ofsudomotor nerve), the gravity-dependent dusky skin (blood suffusion of theskin), the leg vein hyper-responsiveness to norepinephrine, the reducedgalvanic responses, abnormal sweating of the extremities, the excessiveorthostatic blood pooling, the tachycardia, and the reduced stroke volumeseen in OI patients.The hyperadrenergic subgroup of OI is characterized by a clinical spectrumincluding attenuated plasma renin activity and aldosterone, reduced supineblood volume coupled with dynamic orthostatic hypovolemia, elevated plasmanorepinephrine and epinephrine, impaired clearance of norepinephrine fromthe circulation and evidence of partial dysautonomia. When the uprightposture is assumed, there is a loss of plasma volume from the blood intothe surrounding tissue. In normal subjects, about 14% of the plasma volumemay leave the blood within 30 minutes of standing. This loss of plasmavolume into interstitial tissues is greatly enhanced in patients with OI;occasional patients will lose more than twice this amount of fluid. It islittle wonder such patients with supine hypovolemia to begin with developsymptoms in a setting of this excessive dynamic orthostatic hypovolemia.Normal subjects reduce urinary sodium excretion on assumption of uprightposture, but patients with OI do so ineffectively. This probablycontributes to the severity of their hypovolemia. In patients with floridsymptoms of orthostatic intolerance in a setting of hypovolemia andincreased plasma norepinephrine, several interesting findings emerge. Theplasma renin activity and aldosterone are generally slightly reduced inproportion to the degree of the hypovolemia. This suggests that the reducedrenin level may be responsible for the hypovolemia. It is possible thatimpaired sympathetic innervation of the juxtoglomerular apparatus in thekidney may underlie this renin deficit.Autoimmune mechanisms are probably also important. An antibody against thealpha-3 subunit of the nicotinic receptor on autonomic ganglia has beendetected in a subgroup of patients with autonomic problems, includingorthostatic intolerance.OI is significantly overrepresented in young women, and the severity oforthostatic symptoms sometimes shows a cyclical change. Possible reasonsfor these cyclical changes would be an estrogen-dependent change of theplasma volume or a direct estrogen receptor-mediated modulation of vascularreactivity.Our understanding of orthostatic intolerance was greatly expanded in 2000when norepinephrine transporter (NET) deficiency was reported. In a probandwith significant orthostatic symptoms and tachycardia, we founddisproportionately elevated plasma norepinephrine with standing, impairedsystemic and local clearance of infused tritiated norepinephrine, impairedtyramine responsiveness, and a dissociation between stimulated plasmanorepinephrine and DHPG elevation. Studies of NET gene structure in theproband revealed a coding mutation which converts a highly conservedtransmembrane domain Ala residue to Pro. Analysis of the protein producedby the mutant cDNA in transfected cells demonstrated greater than 98%reduction in activity relative to normal. Studies of the proband and herfamily revealed correlations of plasma NE, DHPG/NE, and heart rate with themutant allele. These results represent the first identification of aspecific genetic defect in OI and the first disease linked to a codingalteration in a Na+/Cl- dependent neurotransmitter transporter.Identification of this mechanism may facilitate our understanding ofgenetic causes of OI and lead to the development of more effectivetherapeutic modalities.Long-Term Outlook for PatientsThe majority of patients with OI have a relatively mild disorder whichimproves over succeeding weeks and months. Most patients will eventually befree of symptoms. However, in some patients, the symptoms are more severe,the duration of the illness may be longer, and the expected recovery maynot occur. Overall, on follow-up, the majority of patients with OI haveimproved. More than half of the patients remained on treatment. Thosepatients with antecedent events, such as a viral infection, appeared to dobetter overall than those who developed the condition spontaneously.UncertaintiesWe need to understand more about where normal ends and where OI begins. Weneed to know the interrelationships of OI and deconditioning. Both OI anddeconditioning share many clinical features and their separation can provechallenging. Perhaps more challenging is the fact that many patients withOI respond to their illness by reducing their physical activity. When theypresent to physicians, they therefore present with both OI and deconditioning.ProspectusOrthostatic intolerance takes a significant toll on lifestyle and workcapacity. OI is a category of diseases, which implies that various otherdiseases fall under the umbrella of OI and contribute to orthostatictachycardia. These encompass absolute and orthostatic hypovolemia,hyperadrenergic (central autonomic dysregulation or NET deficiency),neuropathic, autoimmune reaction and cardiovascular diseases. It isunlikely that all patients with OI employ precisely the same mechanisms,and a clearer understanding of the pathophysiology in individual patientswill be helpful toward developing therapeutic strategies.TherapyIn individual patients, different therapeutic regimens may result inimprovement of symptoms. These include (1) orthostatic "exercise", (2)water, (3) salt and /or fludrocortisone,(4) low dose beta blockade, (5) lowdose alpha 2 agonist (clonidine), (6) low dose alpha-1 agonist (midodrine). web page ____________________________________The following exercises and links to more information may be helpful tothose with various balance & dizziness problems not caused by OI or ME/CFS. LKWPosted on Mon, Jul. 26, 2004Exercises might ease vertigo symptoms9302ba.jpgBY DAFFODIL J. ALTANLos Angeles TimesVertigo. For most people, the word summons images of Jimmy Stewart danglingfrom high places in Alfred Hitchcock's classic thriller by the same name.It means something else, however, to hundreds of thousands of people whoexperience the strange, dizzying affliction.The most common cause of vertigo, known as benign paroxysmal positionalvertigo, usually can be treated with one visit to the doctor. Because theproblem is caused by loose crystal particles floating in the inner earcanal, doctors usually maneuver the head and upper body so the particlesfall out.Sometimes, however, the vertigo persists or reoccurs and requires repeatedtreatments.But researchers in Germany have found that many sufferers can treat theirvertigo at home, without another visit to the doctor. A few simplehead-turning exercises appear to be able to relieve the stomach-churningsensation of spinning and whirling that occurs when the head is suddenlyturned.Patients who can treat themselves feel more confident if it recurs "becausethey have learned how to manage their vertigo independently," saysprincipal investigator Dr. Andrea Radtke, a neurologist at Charite CampusVirchow Clinic in Berlin.The study, which was published in the July 13, 2004, issue of Neurology,involved 70 people, all of whom were about 60 years old.The group was split in half, with each group performing one of twotreatments. Both techniques took less than two minutes and involved headand neck movements while sitting on a bed. Patients performed the movementsthree times a day until the vertigo stopped for at least 24 hours.After one week, 95 percent of people who did the "modified Epley" procedurehad no more symptoms. The exercise, developed by Portland, Ore., physicianJohn Epley, requires patients to lie on their backs and tilt their heads toone side for 30 seconds, then to the other side for 30 seconds. They thenturn their bodies on that same side without moving their head, holding thatposition for 30 more seconds before sitting up.At the end of the study, 58 percent of people who performed the "modifiedSemont" maneuver reported no more symptoms. That maneuver requires patientsto sit up and then drop quickly to one side, holding their ear against thebed for 30 seconds, and then sit up and drop quickly to the other side,with their ear down for 30 more seconds.A video showing the maneuver is available on the Neurology journal Website, <www.neurology.org" web page . Go tothe July 13, 2004,issue, then to the "Brief Communications" section. Look for the studybeginning "Self-treatment" and click on "videos."For even more information: From the National Institutes of Health:Balance Disorders: web page (National Institute on Deafness and Other Communication Disorders)Balance, Dizziness, and You: web page (National Institute on Deafness and Other Communication Disorders)Also available in Spanish: web page OverviewsDizziness: web page (Mayo Foundation for Medical Education and Research)Dizziness and Motion Sickness: web page (American Academy of Otolaryngology--Head and Neck Surgery)Vestibular Disorders: An Overview: web page (Vestibular Disorders Association)Anatomy/PhysiologyHuman Balance System: web page (Vestibular Disorders Association)Diagnosis/SymptomsDiagnostic Tests: web page (Vestibular Disorders Association)Possible Symptoms of Vestibular Disorders: web page (Vestibular Disorders Association)Trouble Getting a Diagnosis? web page (Vestibular Disorders Association)TreatmentGeneral Hydrops and Meniere's Diet Suggestions: web page (Vestibular Disorders Association)Surgical Treatments of Vertigo: web page (American Hearing Research Foundation)Specific ConditionsBarotrauma: web page (American Hearing Research Foundation)Benign Paroxysmal Positional Vertigo(BPPV): web page (American Hearing Research Foundation)Bilateral Vestibulopathy: web page (American Hearing Research Foundation)Cervical Vertigo: web page (American Hearing Research Foundation)Endolymphatic Hydrops: web page (Vestibular Disorders Association)Epileptic Vertigo: web page (American Hearing Research Foundation)Mal de Debarquement (MDD): web page (American Hearing Research Foundation)Migraine and Vertigo: web page (Vestibular Disorders Association)Ototoxicity: web page (Vestibular Disorders Association)Post-Traumatic Vertigo: web page (American Hearing Research Foundation)Vestibular Neuritis and Labyrinthitis: web page (American Hearing Research Foundation)Prevention/ScreeningPreventing Balance and Hearing Problems: web page (Vestibular Disorders Association)NutritionSpecific Dietary Concerns: web page (Vestibular Disorders Association)CopingDining Out: web page (Vestibular Disorders Association)RehabilitationVestibular Rehabilitation: web page (Vestibular Disorders Association)GeneticsResearchers find gene important for helping body maintain balance web page (National Institute on Deafness and Other Communication Disorders)Dictionaries/GlossariesNIDCD Glossary: web page (National Institute on Deafness and Other Communication Disorders)Peripheral Vestibular System: web page (Vestibular Disorders Association)DirectoriesDirectory of Organizations: web page (National Institute on Deafness and Other Communication Disorders) - listsorganizations that focus on health issues relating to hearing, balance,smell, taste, voice, speech, and languageFind an Otolaryngologist: web page (American Academy of Otolaryngology--Head and Neck Surgery)Resource Lists by Geographic Region: web page (Vestibular Disorders Association)OrganizationsAmerican Hearing Research Foundation: web page National Institute on Deafness and Other Communication Disorders: web page (Vestibular Disorders Association (VEDA): web page ChildrenChildhood Vestibular Disorders: web page (Vestibular Disorders Association)SeniorsAging Vestibular System: web page (Vestibular Disorders Association)Balance Problems: web page (National Institute on Deafness and Other Communication Disorders)What You Need To Know About Balance And Falls: web page (American Physical Therapy Association)


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## Susan Purry (Nov 6, 2001)

Gosh, _thank you_ for posting that!







I'll look at those vertigo resources when I've more energy. Maybe I'll find some exercises to help me. The OI article was v. interesting too.


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## M&M (Jan 20, 2002)

> quote: I'll look at those vertigo resources when I've more energy


And maybe when you're not _quite_ so dizzy







haha, But really, I hope some of the information is helpful. There just seems to be so very little that will help with Vertigo, I hope some of this will help.


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