Clin Auton Res (2012) 22:207–258DOI 10.1007/s10286-012-0175-5 ABSTRACTS23rd INTERNATIONAL SYMPOSIUM ON THE AUTONOMICNERVOU...
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Clin Auton Res (2012) 22:207–258                                                                                          ...
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Clin Auton Res (2012) 22:207–258                                                                                          ...
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Clin Auton Res (2012) 22:207–258                                                                                          ...
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Clin Auton Res (2012) 22:207–258                                                                                          ...
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Clin Auton Res (2012) 22:207–258                                                                                          ...
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Clin Auton Res (2012) 22:207–258                                                                                          ...
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Clin Auton Res (2012) 22:207–258                                                                                          ...
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Clinical Autonomic Research, issue 22, 2012
Clinical Autonomic Research, issue 22, 2012
Clinical Autonomic Research, issue 22, 2012
Clinical Autonomic Research, issue 22, 2012
Clinical Autonomic Research, issue 22, 2012
Clinical Autonomic Research, issue 22, 2012
Clinical Autonomic Research, issue 22, 2012
Clinical Autonomic Research, issue 22, 2012
Clinical Autonomic Research, issue 22, 2012
Clinical Autonomic Research, issue 22, 2012
Clinical Autonomic Research, issue 22, 2012
Clinical Autonomic Research, issue 22, 2012
Clinical Autonomic Research, issue 22, 2012
Clinical Autonomic Research, issue 22, 2012
Clinical Autonomic Research, issue 22, 2012
Clinical Autonomic Research, issue 22, 2012
Clinical Autonomic Research, issue 22, 2012
Clinical Autonomic Research, issue 22, 2012
Clinical Autonomic Research, issue 22, 2012
Clinical Autonomic Research, issue 22, 2012
Clinical Autonomic Research, issue 22, 2012
Clinical Autonomic Research, issue 22, 2012
Clinical Autonomic Research, issue 22, 2012
Clinical Autonomic Research, issue 22, 2012
Clinical Autonomic Research, issue 22, 2012
Clinical Autonomic Research, issue 22, 2012
Clinical Autonomic Research, issue 22, 2012
Clinical Autonomic Research, issue 22, 2012
Clinical Autonomic Research, issue 22, 2012
Clinical Autonomic Research, issue 22, 2012
Clinical Autonomic Research, issue 22, 2012
Clinical Autonomic Research, issue 22, 2012
Clinical Autonomic Research, issue 22, 2012
Clinical Autonomic Research, issue 22, 2012
Clinical Autonomic Research, issue 22, 2012
Clinical Autonomic Research, issue 22, 2012
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Clinical Autonomic Research, issue 22, 2012

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ABSTRACTS
23rd INTERNATIONAL SYMPOSIUM ON THE AUTONOMIC
NERVOUS SYSTEM
Atlantis Resort, Paradise Island, Bahamas
October 31–November 3, 2012
Preliminary Program

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Transcript of "Clinical Autonomic Research, issue 22, 2012"

  1. 1. Clin Auton Res (2012) 22:207–258DOI 10.1007/s10286-012-0175-5 ABSTRACTS23rd INTERNATIONAL SYMPOSIUM ON THE AUTONOMICNERVOUS SYSTEMAtlantis ResortParadise Island, BahamasOctober 31–November 3, 2012Preliminary ProgramWEDNESDAY, OCTOBER 31, 20126:00–7:00 PM Registration Imperial Foyer South I7:00–7:15 PM Welcome—Dr. Michael Joyner, President Imperial Ballroom CDAutonomic Failure: PAF, MSA, Parkinson’s DiseaseChairs: Eduardo Benarroch & Steven Vernino7:15–7:30 PM Alpha synuclein as a cutaneous biomarker of Parkinson disease C.H. Gibbons, N. Wang, J. Lafo, R. Freeman Boston, MA, USA7:30–7:45 PM CSF biomarkers of central and peripheral catecholamine deficiency in synucleinopathies D.S. Goldstein, L. Sewell, C. Holmes, C. Sims-O’Neil, Y. Sharabi Bethesda, MD, USA7:45–8:00 PM Prognostic indicators and clinical spectrum of MSA based on autopsy-confirmed cases J.J. Figueroa, A.K. Parsaik, W. Singer, P. Sandroni, E.E. Benarroch, P.A. Low, J.H. Bower Rochester, MN, USA8:00–8:15 PM Mechanical stimulation of the feet improves gait and increases cardiac vagal profile in Parkinson’s disease F. Barbic, M. Galli, M. Canesi, A. Porta, V. Cimolin, V. Bari, L. Dalla Vecchia, F. Dipaola, V. Pacetti, F. Meda, I. Bianchi, E. Brunetta, R. Furlan Milan, Italy8:15–8:30 PM Profound myocardial catecholamine depletion in Lewy body diseases D.S. Goldstein, P. Sullivan, T. Jenkins, C. Holmes, M. Basile, D.C. Mash, I.J. Kopin, Y. Sharabi Bethesda, MD, USA8:30–8:45 PM Autonomic dysfunction in Parkinsonian LRRK2 mutation carriers ´ B. Tijero, J.C. Gomez Esteban, K. Berganzo, V. Llorens, H.J.J. Zarranz Bilbau, Spain8:45–9:00 PM Comparison of techniques for non-invasive assessment of systemic hemodynamics in autonomic function testing C. Sims-O’Neil, S. Pechnik, L. Sewell, L. Nez, D.S. Goldstein Bethesda, MD, USATHURSDAY, NOVEMBER 1, 20127:30–8:00 AM Breakfast & Exhibits Imperial Ballroom B 123
  2. 2. 208 Clin Auton Res (2012) 22:207–2588:00–8:45 AM Plenary Lecture Master and commander: the brain and the autonomic nervous system Vaughan G. Macefield, Ph.D University of Western Sydney & Neuroscience Research Australia Sydney, AustraliaCerebral Blood Flow, Neuroimaging in Brain and Heart & Pediatric Autonomic DisordersChairs: Lucy Norcliffe-Kaufmann & Jens Tank8:45–9:00 AM The middle cerebral artery dilates to sodium nitroprusside: a combined transcranial Doppler and near infrared spectroscopy study J.M Stewart, C.E. Schwartz, Z.R. Messer, C. Terilli, M.S. Medow, Valhalla, NY, USA9:00–9:15 AM Cerebral oxygenation, heart rate & blood pressure responses in congenital central hypoventilation syndrome (CCHS) during exogenous ventilatory challenges: PHOX2B genotype/CCHS phenotype association M.S. Carroll, P.P. Patwari, T.M. Stewart, C.D. Brogadir, A.S. Kenny, C.M. Rand, D.E. Weese-Mayer Chicago, IL, USA9:15–9:30 AM Time course of cardiac sympathetic denervation in Parkinson disease D.S. Goldstein Bethesda, MD, USA9:30–9:45 AM Parental attribution of symptoms in adolescents with postural tachycardia syndrome and its relation to child functioning and psychological variables E.M. Keating, R.M. Antiel, K.E. Weiss, D. Wallace, P.R. Fischer, C. Harbeck-Weber Rochester, MN, USA9:45–10:00 AM Cardiovagal sensitivity and orthostatic heart rate response in young patients with orthostatic intolerance W. Singer, A.K. Parsaik, E.E. Benarroch, P. Sandroni, P.A. Low Rochester, MN, USA10:00–10:15 AM Parental response to pain: the impact on functional disability, depression, anxiety, and pain acceptance in adolescents with chronic pain and orthostatic intolerance R.M. Antiel, E.M. Keating, K.E. Weiss, D.P. Wallace, P.R. Fischer, C. Harbeck-Weber Rochester, MN, USA10:15–10:30 AM Coffee Break Imperial Ballroom BAutonomic Regulation: Basic Science & Animal StudiesChairs: David Jardine & Imad Jarjour10:30–10:45 AM Relationship between ganglionic long-term potentiation (LTP) and homeostatic synaptic plasticity in experimental autoimmune autonomic ganglionopathy (EAAG) Z. Wang, S. Vernino Dallas, TX, USA10:45–11:00 AM Methionine sulfoxide reductase A: a novel molecular determinant of baroreflex sensitivity, blood pressure and hypertensive end-organ damage R. Sabharwal, R. El Accaoui, M.K. Davis, J.A. Goeken, R. Weiss, F.M. Abboud, D. Meyerholz, M.W. Chapleau Iowa City, IA, USA11:00–11:15 AM Baroreflex induced changes in stressed blood volume, not cardiac output curve, is the central mechanism preventing volume load induced pulmonary edema T. Sakamoto, T. Kakino, K. Sunagawa Fukuoka, Japan11:15–11:30 AM Prostaglandin D synthase is critical for development of chronic angiotensin II-salt hypertension in the rat G.D. Fink, N. Asirvatham-Jeyaraj East Lansing, MI, USA11:30–11:45 AM The central chemoreflex activation induces sympathoexcitation and resets the arterial baroreflex without compromising its pressure stabilizing function K. Saku, K. Sunagawa Fukuoka, Japan11:45–12:00 PM Advanced techniques and pitfalls of autonomic function assessment and arrhythmia analysis in the mouse model C.M. Welzig, J.B. Galper Charleston, SC, USA12:00–1:30 PM Lunch & Poster Session I Imperial Ballroom B1:30–3:30 PM Free Time3:30–4:00 PM AAS Business meeting Imperial Ballroom CD123
  3. 3. Clin Auton Res (2012) 22:207–258 209Awards SessionChairs: Michael Joyner & Wouter Wieling4:00–4:45 PM Streeten Lecture The ‘‘ups and downs’’ of blood pressure & baroreflex sensitivity—a historical and personal perspective Mark Chapleau, Ph.D University of Iowa and Veterans Affairs Medical Center, Iowa City, IA, USA4:45–5:00 PM Streeten Travel Fellowship Award Blunted osmopressor response in familial dysautonomia N. Goulding, L. Norcliffe-Kaufmann, J. Martinez, D. Roncevic, L. Stok, F. Axelrod, H. Kaufmann New York, NY, USA5:00–5:15 PM FMS/Penaz Wesseling Award Paradox elevations in angiotensin II, independent of plasma renin activity, contribute to the supine hypertension of primary autonomic failure A.C. Arnold, L.E Okamoto, C. Shibao, A. Gamboa, S.R. Raj, D. Robertson, I. Biaggioni Nashville, TN, USA5:15–5:30 PM FMS/Penaz Wesseling Award Chronic effects of aliskiren versus hydrochlorothiazide on sympathetic neural responses to head-up tilt in hypertensive seniors Y. Okada, S.S. Jarvis, S.A. Best, T.B. Bivens, R.L. Meier, B.D. Levine, Q. Fu Dallas, TX, USA5:30–5:45 PM AAS Travel Award Association between cerebral autoregulation and white matter hyperintensities in elderly individuals S. Purkayastha, B. Paccha, I. Iloputaife, D.K. Kiely, F.A. Sorond, L.A. Lipsitz Roslindale, MA, USA5:45–6:00 PM AAS Travel Award The change in arterial stiffness during ganglionic blockade is associated with sympathetic nerve activity in women J.N. Barnes, R.E. Harvey, E.C. Hart, N. Charkoudian, T.B. Curry, J.H. Eisenach, W.T. Nicholson, M.J. Joyner, D.P. Casey Rochester, MN, USAFRIDAY, NOVEMBER 2, 20127:00–7:30 AM Breakfast & Exhibits Imperial Ballroom B7:30–8:15 AM Plenary Lecture Autonomic responses to pregnancy Qi Fu, M.D., Ph.D Institute for Exercise and Environmental Medicine, Texas Health Presbyterian Hospital Dallas, and UT Southwestern Medical Center, Dallas, TX, USAMicroneurography & Cardiovascular Control in Humans/Cardiovascular Disease, Diabetes, Obesity & AgingChairs: Jill Barnes & Qi Fu8:15–8:30 AM Catheter based renal nerve ablation does not elicit a central sympatholytic response in difficult to control hypertensive patients J. Brinkmann, K. Heusser, B.M. Schmidt, J. Menne, G. Klein, H. Haller, A. Diedrich, J. Jordan, J. Tank Hanover, Germany8:30–8:45 AM Methodological considerations for assessing resting spontaneous baroreflex control of muscle sympathetic nerve activity in humans S.W. Holwerda, H. Yang, J.R. Carter, P.J. Fadel Columbia, MO, USA8:45–9:00 AM Sleep deprivation augments cardiovascular reactivity to acute stress in humans H. Yang, J.J. Durocher, R.A. Larson, J.P. DellaValla, J.R. Carter Houghton, MI, USA9:00–9:15 AM Susceptibility to inducible ventricular arrhythmia in type I diabetic Akita mice is dependent on abnormalities of Ca2+ handling H. Jin, M. Rajab, M. Aronovitz, B. Wang, K. Picard, H. Park, M. Link, J.B. Galper Boston, MA, USA9:15–9:30 AM Sympathetic hyper-responsiveness In takotsubo cardiomyopathy L. Norcliffe-Kaufmann, J. Martinez, H. Kaufmann, H. Reynolds New York, NY, USA 123
  4. 4. 210 Clin Auton Res (2012) 22:207–2589:30–9:45 AM Improvement of obesity-associated insulin resistance during autonomic blockade A. Gamboa, L. Okamoto, A. Arnold, S. Raj, A. Diedrich, N. Abumrad, I. Biaggioni Nashville, TN, USA9:45–11:15 AM Coffee & Poster Session II Imperial Ballroom BPostural Orthostatic Tachycardia Syndrome (POTS)Chairs: Satish Raj & Wolfgang Singer11:15–11:30 AM Beta-2 adrenergic receptor polymorphism and hemodynamics in patients with postural orthostatic tachycardia syndrome and healthy controls M.N. Manento, L.R. Gullixson, K.K. Nickander, P.A. Low, J.H. Eisenach Rochester, MN, USA11:30–11:45 AM The pathophysiology of neuropathic and non-neuropathic postural tachycardia syndrome C. Gibbons, I. Bonyhay, A. Benson, R. Freeman Boston, MA, USA11:45–12:00 PM Deconditioning in patients with orthostatic intolerance A. Parsaik, T.G. Allison, W. Singer, D.M. Sletten, M.J. Joyner, E.E. Benarroch, P.A. Low, P. Sandroni Rochester, MN, USA12:00–12:15 PM Preliminary data on the durability of improved symptoms, functioning, and psychological distress in adolescents with POTS treated in a multidisciplinary treatment program B.K. Bruce, T.E. Harrison, K.E. Weiss, P.R. Fischer, S.P. Ahrens, W.N. Timm Rochester, MN, USA12:15–12:30 PM Objective measures of sleep in patients with POTS S.J. Kizilbash, P.R. Fischer, R.M. Lloyd Rochester, MN, USA12:30–12:45 PM Reduced alpha-adrenergic vascular response: the physiological link between postural orthostatic tachycardia syndrome and neurally mediated syncope N. Mehta, M. Tavora-Mehta, J.C. Guzman, C.A. Morillo Hamilton, ON, Canada12:45–7:00 PM Free Time7:00–10:00 PM Presidential Dinner Ripples Pool DeckSATURDAY, NOVEMBER 3, 20127:30–8:00 AM Breakfast & Exhibits Imperial Ballroom BDiabetic, Autoimmune & Other Autonomic NeuropathiesChairs: Christopher Gibbons & Christoph Schroeder8:00–8:15 AM Multi-scale glycemic variability affects brain structure and functional outcomes in type 2 diabetes mellitus X. Cui, A. Galica, B. Manor, A. Abduljalil, C.-K. Peng, V. Novak Boston, MA, USA8:15–8:30 AM The laser Doppler imaging axon-reflex flare area—a novel regression thresholding based technique to assess neurovascular function T. Siepmann, B.M. Illigens, R. Freeman, C. Gibbons Boston, MA, USA8:30–8:45 AM Long-term outcomes in autoimmune autonomic ganglionopathy S. Muppidi, E.B. Spaeth, C. Gibbons, S. Vernino Dallas, TX, USA8:45–9:00 AM Type I diabetic Akita mice demonstrate decreased heart rate variability and increased inducibility of ventricular tachycardia which are reversed by statins C.M. Welzig, H.-J. Park, M. Rajab, M. Aronovitz, H. Jin, M.S. Link, J.B. Galper Charlston, SC, USA9:00–9:15 AM The quantification of sudomotor nerve fibers: a multicenter study in diabetes C.H. Gibbons, J. Lafo, G. Smith, R. Singleton, R. Freeman Boston, MA, USA9:15–10:45 AM Coffee & Poster Session III Imperial Ballroom B123
  5. 5. Clin Auton Res (2012) 22:207–258 211Orthostatic Hypotension and SyncopeChairs: Rasna Sabharwal & Darren Casey10:45–11:00 AM Treatment of neurogenic orthostatic hypotension (NOH) with droxidopa: results from a multicenter, double-blind, randomized, placebo-controlled, parallel group, induction design study H. Kaufmann, P. Low, I. Biaggioni, C.J. Mathias, R. Freeman, L.A. Hewitt New York, NY, USA11:00–11:15 AM What is MSNA doing at the onset of syncope? D.L. Jardine Christchurch, New Zealand11:15–11:30 AM A meta-analysis of pharmacologic treatments of orthostatic hypotension C.H. Gibbons, S. Raj Boston, MA, USA11:30–11:45 AM Increasing cardiac output does not change middle cerebral artery blood velocity in the hyperthermic human C.G. Crandall, T. Seifert, T.E. Wilson, M. Bundgaard-Nielsen, N.H. Secher Dallas, TX, USA11:45–12:00 PM Patterns of diagnosis and intervention in neurogenic orthostatic hypotension (NOH): a patient-flow study H. Kaufmann, R.E. Paquette New York, NY, USA12:00–12:30 PM Open Discussion & AdjournPOSTER SESSION IThursday, November 1, 201212:00–1:30 PMAutonomic Failure: PAF, MSA, Parkinson’s DiseasePoster #1 A randomized, double-blind, placebo-controlled clinical trial of Rifampicin in multiple system atrophy P.A. Low, S. Gilman, D. Robertson, I. Biaggioni, W. Singer, H. Kaufmann, S. Perlman, W. Cheshire, S. Vernino, R. Freeman, R.A. Hauser, S. Lessig Rochester, MN, USAPoster #2 Orthostatic hypotension in Parkinson disease: passive tilt vs. active standing J. Martinez, J.C. Esteban Gomez, B. Tijero Merino, K. Berganzo, H. Kaufmann New York, NY, USAPoster #3 Cerebellar and parkinsonian phenotypes in multiple system atrophy (MSA). Similarities and differences D. Roncevic, J. Martinez, L. Norcliffe-Kaufmann, H. Kaufmann New York, NY, USAPoster #4 A novel quantitative index of baroreflex-sympathoneural function: application to patients with chronic autonomic failure F. Rahman, D.S. Goldstein Bethesda, MD, USAPoster #5 Loss of cerebral blood flow rhythm in Parkinson’s disease and vascular parkinsonism S.-J. Yeh, B.-W. Chang, B.-Y. Liau, C.-C. Chiu Taichung, TaiwanPediatric Autonomic DisordersPoster #6 Temperature profile in congenital central hypoventilation syndrome (CCHS) and rapid-onset obesity with hypothalamic dysfunction, hypoventilation, and autonomic dysregulation (ROHHAD): ibutton measures of peripheral skin temperature R. Saiyed, C.M. Rand, M.S. Carroll, P.P. Patwari, T. Stewart, C. Koliboski, D.E. Weese-Mayer Chicago, IL, USAPoster #7 Heart rate variability in hospitalized children: autonomic response to laughter and engagement P.P. Patwari, M.S. Carroll, K. Gray, M.K. Janda, A.S. Kenny, T.H. Stewart, C. Brogadir, S.H. Wang, D.M. Steinhorn Chicago, IL, USAPoster #8 Cardiac stroke volume and sympathetic/parasympathetic measurements increase the sensitivity and specificity of HUTT in children and adolescents M.T. Numan, J.E. Lankford, A. Gourishankar, I.J. Butler Houston, TX, USA 123
  6. 6. 212 Clin Auton Res (2012) 22:207–258Autonomic Regulation: Basic Science & Animal StudiesPoster #9 Biogenic amine metabolism in juvenile neurocardiogenic syncope with dysautonomia I.J. Butler, J.E. Lankford, M.T. Numan Houston, TX, USAPoster #10 The iceman revisited: autonomic function tests during performance of the Asian Tummo meditation technique J.T. Groothuis, M.T.E. Hopman Nijmegen, The NetherlandsPoster #11 Evidence for central sensitization in bladder pain syndrome from the ICEPAC trial (Interstitial Cystitis: Elucidation of Psychophysiologic and Autonomic Characteristics)—preliminary psychometric findings J.W. Janata, F. Daneshgari, C.A.T. Buffington, G. Chelimsky, M.D. Louttit, D. Zhang, T.C. Chelimsky Cleveland, OH, USANovel Therapies & Clinical TrialsPoster #12 The antiemetic efficacy of carbidopa: a randomized, double-blind, placebo-controlled crossover study in patients with familial dysautonomia L. Norcliffe-Kaufmann, J. Martinez, F. Axelrod, H. Kaufmann New York, NY, USAPoster #13 Comparative efficacy between the norepinephrine transporter blocker, atomoxetine, against midodrine for the treatment of orthostatic hypotension C.E. Ramirez, L.E. Okamoto, A. Gamboa, S.R. Raj, A. Diedrich, D. Robertson, I. Biaggioni, C. Shibao Nashville, TN, USAPoster #14 Beneficial effects of oral rehydration solution on orthostatic intolerance M.S. Medow, D. Tewari, A. Aggarwal, Z. Messer, J.M. Stewart Valhalla, NY, USAGastrointestinal & Urogenital Systems, IBS, CystitisPoster #15 Musculoskeletal evaluation of patients with interstitial cystitis T.V. Sanses, G. Chelimsky, D. Zhang, J. Janata, T. Mahajan, B. Fenton, A. Askari, R. Elston, T. Chelimsky, ICEPAC Study Group Milwaukee, WI, USAPoster #16 Heart rate variability in pelvic pain P. Singh, J. Thayer, G. Chelimsky, T. Chelimsky Milwaukee, WI, USAPoster #17 Study of the P2X2 and 7 receptors in the enteric glial cells of ileum rat subjected to ischemia and reperfusion C.E. Mendes, K. Palombit, W. Tavares de Lima, P. Castelucci ˜ Sao Paulo, BrazilPoster #18 Brainstem neuropeptides and vagal protection of the gastric mucosal against injury: role of prostaglandins, nitric oxide and calcitonin-gene related peptide in capsaicin afferents Y. Tache Los Angeles, CA, USAPoster #19 Autonomic dysfunction and esophageal dysmotility in persons with spinal cord injury G.J. Schilero, M. Radulovic, C. Renzi, C. Yen, W.A. Bauman, M. Korsten Bronx, NY, USAPoster #20 Real time change of prefrontal cortex activity related to normal and abnormal bladder filling in Parkinson disease: a functional near-infrared spectroscopy (fNIRS) study C. Yamaguchi, T. Uchiyama, T. Yamamoto, R. Sakakibara, M. Fuse, M. Yanagisawa, T. Kamai, T. Ichikawa, K. Hirata, S. Kuwabara, T. Yamanishi Tochigi, JapanPoster #21 Effect of Brilliant Blue G on P2X7 receptor after intestinal ischemia and reperfusion K. Palombit, C.E. Mendes, W. Tavares de Lima, P. Castelucci Sao Paulo, BrazilPoster #22 Photo-stimulating effects of low reactive level laser on bladder dysfunction in neurological disease rats T. Uchiyama, C. Yamaguchi, T. Yamamoto, R. Sakakibara, M. Fuse, M. Yanagisawa, T. Kamai, T. Ichikawa, K. Hirata, S. Kuwabara, T. Yamanishi Tochigi, JapanCerebral Blood Flow RegulationPoster #23 Cerebral blood flow in autonomic failure L. Rivera Lara, P. Novak Worcester, MA, USA123
  7. 7. Clin Auton Res (2012) 22:207–258 213Poster #24 Added clinical value of cerebral blood flow in juveniles and young adults with neurocardiogenic syncope and dysautonomia as measured by near-infrared spectroscopy J.E. Lankford, M.T. Numan, A. Gourishankar, I.J. Butler Houston, TX, USAPOSTER SESSION IIFriday, November 2, 20129:45–11:15 AMMicroneurography & Cardiovascular Reflexes in HumansPoster #25 Do the chronic heart failure patients have limited sympathetic response to a transient baroreflex stress? P. Zubin Maslov, T. Breskovic, J.K. Shoemaker, Z. Dujic Split, CroatiaPoster #26 Assessment of cardiovascular adrenergic function using the Valsalva maneuver—reproducibility and validity of indices T.L. Gehrking, J.A. Gehrking, J.D. Schmelzer, P.A. Low, W. Singer Rochester, MN, USAPoster #27 Sex differences in limb vascular reactivity to mental stress in humans J.R. Carter, H. Yang, T.D. Drummer Houghton, MI, USAPoster #28 Melatonin does not alter skin sympathetic nerve responses to mental stress C.A. Ray, C.L. Sauder, M.D. Muller Hershey, PA, USAPoster #29 The arterial baroreflex resets with orthostasis C.E. Schwartz, J.M. Stewart Hawthorne, NY, USAPoster #30 Carotid chemoreflex and muscle metaboreflex interactions in humans H. Edgell, M.K. Stickland Edmonton, AB, CanadaPoster #31 Do multi-unit sympathetic discharge patterns change with age and cardiovascular disease? D.N. Brewer, P. Zubin Maslov, Z. Dujic, J.K. Shoemaker London, Ontario, CanadaCardiovascular Disease, Obesity & Aging: Human StudiesPoster #32 Acute baroreflex sensitivity impairment due to insulin-induced experimental hypoglycemia A. Rao, I. Bonyhay, S. Ballatori, G. Adler, R. Freeman Boston, MA, USAPoster #33 Autonomic contribution to blood pressure and resting energy expenditure in obese hispanics L.E. Okamoto, C. Shibao, A. Gamboa, A. Diedrich, G. Farley, S. Paranjape, I. Biaggioni Nashville, TN, USAPoster #34 The impact of injury to autonomic pathways on cardiovascular disease risk after spinal cord injury H.J.C. Ravensbergen, I.S. Sahota, S.A. Lear, V.E. Claydon Burnaby, British Columbia, CanadaPoster #35 What is the best marker for obesity in individuals with spinal cord injury? H.J.C. Ravensbergen, M.C. Keenleyside, S.A. Lear, V.E. Claydon Burnaby, British Columbia, CanadaPoster #36 Central arterial stiffness and autonomic modulation in active women P. Latchman, G. Gates, J. Pereira, R. Axtell, M. Bartels, R. De Meersman New Haven, CT, USAPoster #37 Impaired autonomic modulation in acute stroke improves with clinical recovery within 72 hours M.J. Hilz, H. Marthol, S. Moeller, J. Koehn, A. Akhundova, P. De Fina, S. Schwab Erlangen, Germany & New York, NY, USAPoster #38 Relation of cardiovagal baroreflex sensitivity to impaired carotid artery elastic function in patients with tetralogy of Fallot A. Pinter, T. Horvath, A. Sarkozi, D. Cseh, M. Kollai Budapest, HungaryPoster #39 Features of vascular neurogenic regulation in patients with atrial fibrillation and heart failure O.V. Mamontov, A.V. Kozlenok, E.R. Bernhard, E.V. Parmon, E.V. Shlyakhto Saint-Petersburg, Russian FederationPoster #40 Calcitonin gene related peptide level and endocannabinoid system activity in patients with abdominal obesity and arterial hypertension E. Shlyakhto, E. Bazhenova, O. Belyaeva, A. Berezina, O. Berkovich, E. Baranova Saint-Petersburg, Russian Federation 123
  8. 8. 214 Clin Auton Res (2012) 22:207–258Poster #41 Heart rate variability and high sensitivity C-reactive protein: influence of coronary artery lesions N.Y. Tamburus, V.C. Kunz, R.F.L. Paula, M.R. Salviati, T.A.G. Nery, E. da Silva ˜ Sao Paulo, BrazilSympathovagal Balance & Spectral AnalysisPoster #42 Oligofiber recordings detail single-fiber sympathetic nerve discharge C.-K. Su, C.-H. Chiang, C.-M. Ho, C.-M. Lee, Y.-P. Fan Taipei, TaiwanPoster #43 Cardiovascular autonomic control in the first year after spinal cord injury J. Inskip, M. McGrath, B. Kwon, V. Claydon Burnaby, BC, CanadaPoster #44 ‘‘Sympathovagal balance’’—a thermodynamic perspective R. Schondorf, J. Benoit, M.J. Lafitte Montreal, QC, CanadaPoster #45 The autonomic testing of normal subjects G. Chelimsky, S.M. Ialacci, T.C. Chelimsky Milwaukee, WI, USABlood Flow & AutonomicsPoster #46 Alpha-adrenergic blockade unmasks a greater compensatory vasodilation in hypoperfused contracting muscle D.P. Casey, M.J. Joyner Rochester, MN, USAPoster #47 COMPASS 31—a refined and abbreviated composite autonomic symptom score D.M. Sletten, G.A. Suarez, P.A. Low, J. Mandrekar, W. Singer Rochester, MN, USAPoster #48 Autonomic, Blood Flow and Sensory Small Fiber Scale (ABSS) P. Novak Worcester, MA, USAPoster #49 Systemic dysautonomia in complex regional pain syndrome—a feasibility study K.R. Chemali, K. McNeeley, L. Zhou, T. Chelimsky Norfolk, VA, USAPOSTER SESSION IIISaturday, November 3, 20129:15–10:45 AMExercise, Temperature Regulation & HypoxiaPoster #50 Thermophysiological consequences of an absent evening melatonin release in spinal cord injury H. Jones, J.T. Groothuis, T.M.H. Eijsvogels, J. Nyakayiru, R.J.M. Verheggen, A. Thompson, E.J.W. van Someren, G. Atkinson, M.T.E. Hopman, D.H.J. Thijssen Nijmegen, The NetherlandsPoster #51 Post-exercise recovery period in patients with idiopathic ventricular arrhythmias E. Parmon, T. Tulintseva, E. Berngardt, E. Panova, E. Shlaykto Saint Petersburg, Russian FederationPostural Orthostatic Tachycardia SyndromePoster #52 Regulation of circulation during exercise in adolescents with postural orthostatic tachycardia syndrome (POTS) A. Goodloe, D. Soma, C.K. Brands, P.R. Fischer, P.T. Pianosi Rochester, MN, USAPoster #53 Neuropsychological profiles in adolescents with postural tachycardia syndrome (POTS) K.D. Evankovich, L.K. Jarjour, A.M. Hernandez, I.T. Jarjour Houston, TX, USAPoster #54 How important is the T in POTS using pediatric versus adult diagnostic criteria for postural tachycardia? I.T. Jarjour, A.M. Hernandez, L.K. Jarjour Houston, TX, USAPoster #55 Palpitations in postural tachycardia syndrome: what do they tell? R.K. Khurana Baltimore, MD, USAPoster #56 The spectrum of neuropathic orthostatic tachycardia W. Singer, T.L. Gehrking, P.A. Low Rochester, MN, USA123
  9. 9. Clin Auton Res (2012) 22:207–258 215Poster #57 Origins of cognitive dysfunction in postural tachycardia syndrome A.C. Arnold, K. Haman, E.M. Garland, S.Y. Paranjape, C.A. Shibao, I. Biaggioni, D. Robertson, S.R. Raj Nashville, TN, USAPoster #58 Pharmacological I(f) pacemaker current inhibition in a human postural tachycardia syndrome (POTS) model C. Schroeder, K. Heusser, D. Rieck, F.C. Luft, J. Tank, J. Jordan Hannover, GermanyPoster #59 Cardiovascular autonomic response to nitric oxide inhibition in POTS patients I. Bonyhay, C. Gibbons, A. Benson, R. Freeman Boston, MA, USAPoster #60 Postural tachycardia syndrome: optimal duration of diagnostic orthostatic challenge W.B. Plash, V. Nwazue, A. Diedrich, I. Biaggioni, E.M. Garland, S.Y. Paranjape, B.K. Black, W.D. Dupont, C. Shibao, S.R. Raj Nashville, TN, USAPoster #61 Uncoupling of serum interleukin-6 and C-reactive protein in lean patients with postural tachycardia syndrome L.E. Okamoto, S.R. Raj, A. Gamboa, C. Shibao, A.C. Arnold, A. Diedrich, G. Farley, D. Robertson, I. Biaggioni Nashville, TN, USAOrthostatic Hypotension & SyncopePoster #62 Blood pressure effect of droxidopa in hypotensive individuals with spinal cord injury J. Wecht, D. Rosado-Rivera, C. Yen, M. Radulovic, W. Bauman Bronx, NY, USAPoster #63 Prevalence of orthostatic hypotension in asymptomatic veterans J. Wecht, C. Yen, S. Pena, A. Ivan, W. Bauman Bronx, NY, USAPoster #64 Combination ergotamine and caffeine for the treatment of orthostatic hypotension C. Shibao, C.E. Ramirez, L.E. Okamoto, A.C. Arnold, A. Gamboa, P. Muppa, S.R. Raj, A. Diedrich, D. Robertson, I. Biaggioni Nashville, TN, USAPoster #65 Abnormal autonomic findings in chronic subjective dizziness: sympathetic dysfunction or hyperactivity H. Lee, H.A. Kim Daegu, South KoreaPoster #66 Neurogenic mechanisms and venous physiology in patients with orthostatic intolerance L. Saju, Z. Sun, R. Shields, F. Fouad-Tarazi Cleveland, OH, USAPoster #67 Mechanisms underlying the relationships between cardiovascular dysfunction and fall susceptibility in older adults B.H. Shaw, S.N. Robinovitch, V.E. Claydon Burnaby, BC, CanadaPoster #68 Arterial baroreflex asymmetry: an additional mechanism of orthostatic insufficiency in patients with non-cardiac syncope O.V. Mamontov, M.I. Bogachev, E.V. Shlyakhto Saint-Petersburg, Russian FederationPoster #69 Myoclonic jerks in syncope are probably generated in the cortex J.G. van Dijk, R.D. Thijs, J. van Niekerk, W. Wieling, D.G. Benditt Leiden, The NetherlandsDiabetic, Autoimmune & Other Autonomic NeuropathiesPoster #70 Glucoregulation and autonomic function in older male patients with diabetes mellitus and obstructive sleep apnea J.L. Gilden, J. Cheng, B. Theckedath, P. Hung, J. Stoll North Chicago, IL, USAPoster #71 A case of paraneoplastic autonomic failure preceding Hodgkin’s lymphoma P. Muppa, C.E. Ramirez, B. Black, D. Robertson, A. Peltier, S.R. Raj, C. Shibao, I. Biaggioni Nashville, TN, USAPoster #72 11-year follow-up of a case of autoimmune autonomic ganglionopathy W. Singer, D.M. Sletten, T.L. Gehrking, A.K. Parsaik, P.A. Low Rochester, MN, USAPoster #73 Autonomic function test outcomes in diabetes mellitus L.B. Tay, S. Srinivasan, C. Kang, T. Umapathi Singapore 123
  10. 10. 216 Clin Auton Res (2012) 22:207–258Wednesday, October 31, 2012 (PAF), and Parkinson disease (PD). We hypothesized that cerebro- spinal fluid levels of neuronal metabolites of catecholamines provide neurochemical biomarkers of these disorders.Oral Presentations Methods: We measured cerebrospinal fluid levels of catechols includ- ing dopamine, norepinephrine, and their main respective neuronalAlpha-synuclein as a cutaneous metabolites dihydroxyphenylacetic acid and dihydroxyphenylglycol inbiomarker of Parkinson disease MSA, PAF, and PD. Cerebrospinal fluid catechols were assayed in 146 subjects—54 MSA, 20 PAF, 34 PD, and 38 controls. In 14 patients cerebrospinal fluid was obtained before or within 2 years after the onsetC.H. Gibbons, N. Wang, J. Lafo, R. Freeman of Parkinsonism.Department of Neurology, Beth Israel Deaconess Medical Center, Results: The MSA, PAF, and PD groups all had lower cerebrospinalHarvard Medical School, Boston, MA, USA fluid dihydroxyphenylacetic acid [1.32 ± (SEM) 0.12 nmol/l, 0.86 ± 0.09, 1.00 ± 0.09] than controls (2.15 ± 0.18 nmol/l;Background: Parkinson’s disease is a multisystem neurodegenerative p 0.0001, p = 0.0002, p 0.0001). Dihydroxyphenylglycol wasdisease characterized by the deposition of a-synuclein in the central, also lower in the three synucleinopathies (7.75 ± 0.42, 5.82 ± 0.65,peripheral and enteric nervous system. Although the most prominent 8.82 ± 0.44 nmol/l) than controls (11.0 ± 0.62 nmol/l; p = 0.009,manifestations of Parkinson’s disease are due to central, motor system p 0.0001, p 0.0001). Dihydroxyphenylacetic acid was lower andneurodegeneration, there is widespread peripheral, autonomic and dihydroxyphenylglycol higher in PD than in PAF. Dihydroxyphen-enteric nervous system degeneration with associated clinical features. ylacetic acid was 100 % sensitive at 89 % specificity in separatingObjective: To develop a biomarker for Parkinson disease. patients with recent onset of Parkinsonism from controls but was ofMethods: Fourteen patients with Parkinson disease and 10 age and no value in differentiating MSA from PD.gender matched control subjects underwent skin biopsies at the distal Conclusions: Synucleinopathies feature cerebrospinal fluid neuro-leg, distal thigh and proximal thigh. Skin biopsies were stained for chemical evidence for central dopamine and norepinephrinePGP9.5, tyrosine hydroxylase, vasoactive intestinal peptide and deficiency. PD and PAF involve differential central dopaminergica-synuclein. The density of nerve fibers within specific dermal versus noradrenergic lesions. Cerebrospinal fluid dihydroxyphenyl-organelles (pilomotor muscles and sweat glands) was calculated. acetic acid seems to provide a sensitive means to identify evenBecause normal subjects have low levels of a-synuclein and Parkin- early PD. (Ref.: Goldstein et al., Brain 2012; Mar 26. [Epub ahead ofsonian subjects have autonomic nerve degeneration, we chose a print])primary outcome as the proportion of these nerve fibers that containeda-synuclein (determined by a-synuclein overlap with PGP 9.5),defined as the a-synuclein ratio.Results: Patients with PD had a distal sensory and autonomic neu-ropathy expressed by loss of intra-epidermal, pilomotor and Prognostic indicators and clinical spectrum of MSAsudomotor fibers (P 0.05 vs. controls). Patients with PD had higher based on autopsy-confirmed casesa-synuclein ratios compared to controls within pilomotor nerves at thedistal leg (0.76 ± 0.19 vs. 0.26 ± 0.13, P 0.001), distal thigh J.J. Figueroa, A.K. Parsaik, W. Singer, P. Sandroni, E.E. Benarroch,(0.78 ± 0.16 vs. 0.28 ± 0.18; P 0.001) and proximal thigh P.A. Low, J.H. Bower(0.80 ± 0.13 vs. 0.32 ± 0.15; P 0.001). Patients with PD hadhigher a-synuclein ratios compared to controls within sudomotor Department of Neurology, Mayo Clinic, Rochester, MN, USAnerves at the distal leg (0.20 ± 0.11 vs. 0.02 ± 0.01, P 0.005),distal thigh (0.18 ± 0.12 vs. 0.02 ± 0.01, P 0.005) and proximal Multiple system atrophy (MSA) is a progressive neurodegenerativethigh (0.20 ± 0.14 vs. 0.02 ± 0.01, P 0.005). disorder characterized by motor dysfunction with autonomic failure.Discussion: We have developed novel techniques to quantify the The goal of our study was to evaluate phenotype at presentation, rate ofdensity of autonomic nerve fiber innervation within specific dermal motor deterioration, and survival time after onset of motor and auto-organelles, and have quantified the ratio of a-synuclein deposition nomic symptoms in a cohort of autopsy confirmed MSA patients. Wewithin these nerve fibers. We found significantly elevated a-synuclein retrospectively studied the Mayo Clinic cohort of 49 autopsy confirmeddeposition ratios within both sympathetic adrenergic pilomotor and MSA patients comprised of 33 (67 %) men and 16 (33 %) women.sympathetic cholinergic sudomotor fibers in patients with Parkinson Disease duration from motor symptom onset (age 55.8 ± 7.1 years) todisease. These findings suggest the a-synuclein ratio may be a bio- death (age 65.5 ± 8.6 years) was 9.7 ± 4.7 years. Clinical phenotypemarker in patients with Parkinson disease. at first evaluation was MSA-P in 29 (60 %), MSA-C in 16 (32 %),Acknowledgement: Study supported by NIH NINDS K23NS050209 MSA-PC in 2 (4 %), and pure autonomic failure in 2 (4 %). At pre-(CHG) and the RJG Foundation (CHG). sentation, patients had symmetric parkinsonism (27/32), retropulsion (12/14), absent resting tremor (37/44), poor levodopa responsiveness (18/22) and antecollis (5/7). Gait impairment was present at onset of motor symptoms in 80 %. Time from onset of motor symptoms to firstCSF biomarkers of central and peripheral fall, wheelchair dependency and dysphagia was 1.5 ± 0.8, 4.4 ± 2.9catecholamine deficiency in synucleinopathies and 6.1 ± 2.2 years respectively. Dysphagia requiring intervention was associated with the shortest survival time (1.4 ± 1.2 years), fol- lowed by wheelchair dependency (4.4 ± 2.9 years), fecal incontinenceD.S. Goldstein, L. Sewell, C. Holmes, C. Sims-O’Neil, Y. Sharabi (6.0 ± 3.8 years), presyncope and syncope (6.2 ± 4.3 years), needClinical Neurocardiology Section, NINDS/NIH, Bethesda, MD, USA for bladder catheterization (6.4 ± 4.1 years) and erectile dysfunction (8.9 ± 5.0 years). This study reveals important clinical characteris-Background: Central catecholamine deficiency characterizes primary tics and indicators of prognosis of MSA based on the natural historychronic autonomic failure syndromes, including alpha-synucleinopa- of a large cohort of well-characterized autopsy-confirmed cases ofthies such as multiple system atrophy (MSA), pure autonomic failure MSA.123
  11. 11. Clin Auton Res (2012) 22:207–258 217Mechanical stimulation of the feet improves gait loss of catecholaminergic neurons both in the striatum and the heart,and increases cardiac vagal profile in Parkinson’s by assaying putamen and left ventricular apical concentrations of catecholamines and the catecholamine precursor DOPA, the imme-disease diate product of tyrosine hydroxylation, in post-mortem tissue from patients with PD, pure autonomic failure (PAF, a rare Lewy bodyF. Barbic1, M. Galli2, M. Canesi3, A. Porta4, V. Cimolin2, V. Bari4, disease that does not involve clinical evidence of central neurode-L. Dalla Vecchia5, F. Dipaola1, V. Pacetti1, F. Meda1, I. Bianchi1, generation), or multiple system atrophy (MSA, a non-Lewy bodyE. Brunetta1, R. Furlan1 form of alpha-synucleinopathy).1 ` Unita Sincopi e Disturbi della Postura, Clinica Medica-IRCCS Methods: Putamen and apical myocardial tissue were obtained at `Istituto Clinico Humanitas, Rozzano (MI), Universita di Milano, autopsy within several hours of death in patients with end-stage PD,Milano, Italy; 2Laboratorio per l’analisi della postura e del PAF, or MSA, and control patients (N = 4, 1, 1, and 6 as of thismovimento ‘‘L. Divieti’’, Politecnico di Milano, Milano, Italy; writing).3 Centro Parkinson, CTO, Milano, Italy; 4Dipartimento di Tecnologie Results: PD patients had strikingly decreased myocardial norepi- `per la Salute, Istituto Ortopedico Galeazzi, Universita di Milano, nephrine and dopamine contents (by 93 and 94 %) compared toMilano, Italy; 5IRCCS, Fondazione Maugeri, Milano, Italy controls (p = 0.008, p = 0.001). Decreased myocardial catechol- amine contents were also evident in the PAF patient but were normalBackground: Alterations in sensorimotor central integration and/or in the MSA patient. Myocardial and putamen DOPA were decreasedperipheral sensory function might play a role in movement disorders in PD but to a lesser extent (about 2/3) than were the catecholamines.in Parkinson’s disease (PD). Body mechanical stimulations was Post-mortem findings confirmed neuroimaging and neurochemicalrecently found to improve gait in PD. In addition, alterations in car- data in the same patients during life.diovascular autonomic control are common in PD, although their Conclusions: Lewy body diseases are associated with drastic myo-relationships with movement disorders have not been fully addressed. cardial catecholamine depletion, demonstrating that PD is not only aAims: We tested the hypothesis that bilateral plantar stimulation can brain disease and movement disorder but is a more generalized dis-improve gait and autonomic control of heart rate up to 24 h. ease that involves a form of dysautonomia. The decreases inMethods: We studied 13 patients with idiopathic PD (mean age norepinephrine and dopamine in the putamen and myocardium seem66 ± 2 years, BMI 23 ± 1 kg/m2, Hoehn–Yahr scale 2–4) on their greater than explained by denervation alone, consistent withhabitual pharmacological treatment. Every subject underwent decreased vesicular storage in residual nerves.mechanical pressure (0.8 kg/mm2) at the big toe tip and at the big toemetatarsal joint (plantar stimulation, PL) on both feet. Gait analysisand spectral analysis of heart rate variability provided quantitativeindexes to assess movement disorders and cardiac autonomic profile(HFRR, marker of cardiac vagal modulation) before and 24 h after Autonomic dysfunction in Parkinsonian LRRK2plantar stimulation. mutation carriersResults: Twenty-four hour after PL step mean length and gait velocityincreased (23.3 ± 6.2 from 537.7 ± 40.8 mm and 0.06 ± 0.02 from B. Tijero1, J.C. Gomez Esteban1, K. Berganzo1, V. Llorens2, ´0.93 ± 0.09 m/s, respectively) and clock-wise rotation time H.J.J. Zarranz1decreased (-1.8 ± 0.8 from 8.8 ± 1.2 s). In addition, HFRR 1 Movement Disorders and Autonomic Unit, Neurology Service,increased (1.2E-04 ± 2.7E-04 from 4.5E-04 ± 1.9E-04 m/sec2) Cruces Hospital, Basque Health Service (Osakidetza), Departmentcompared to baseline, suggesting an enhancement of the cardiac vagal of Neurociences, University of the Basque Country, Spain; 2Nuclearmodulation. Medicine Service, Cruces Hospital, Baracaldo, SpainConclusions: 24 h after plantar stimulation, PD patients showedchanges in step length, gait velocity and body rotation time consistentwith an improvement of their movement disorder. Plantar stimulation Introduction: The aim of this study is to compare autonomic functioninduced a concomitant increase in the vagal modulatory activity of in carriers of the LRRK2 (G2019S and R1441S) mutations and thoseheart rate. with idiopathic Parkinson’s Disease (iPD) Patients. Patients and methods: We studied 25 patients with a diagnosis of PD according to the UK Parkinson’s Disease Society clinical diagnosis criteria (6 had the G2019S and 6 R1441G, and 13 had iPD without genetic mutations). All patients completed the SCOPA autonomicProfound myocardial catecholamine depletion in Lewy questionnaire, underwent blood pressure and heart rate monitoring during head up tilt with measurements of plasma norepinephrine,body diseases Valsalva maneuver and deep breathing, recording of sympathetic skin response (SSR), and cardiac MIBG scintigraphy.D.S. Goldstein, P. Sullivan, T. Jenkins, C. Holmes, M. Basile, Results: Scores of the SCOPA questionnaire were similar in patientsD.C. Mash, I.J. Kopin, Y. Sharabi with and without the LRRK2 mutations. Three of the iPD and one ofClinical Neurocardiology Section, NINDS/NIH, Bethesda, MD, USA the LRRK2 carriers have orthostatic hypotension. During passive tilt, iPD patients have minor Blood pressure increase than LRRK patients.Background: Striatal dopamine depletion is a neurochemical hallmark Arterial pressure ‘‘overshoot’’ during phase IV of the Valsalvaof Parkinson disease (PD) and a major cause of the characteristic maneuver was less pronounced in patients with iPD than LRRK2movement disorder. Accumulating evidence indicates that PD and mutation carriers. MIBG late (4 h) myocardial/mediastinal uptakeother Lewy body diseases also feature loss of cardiac sympathetic ratios are higher in LRRK2 mutation carriers than iPD patientsnerves, with decreased tyrosine hydroxylase, the rate-limiting enzyme (1.51 ± 0.28 vs. 1.32 ± 0.25, p = 0.05) Discussion: Carriers of thein catecholamine biosynthesis, measured by semi-quantitative LRRK2 gene mutation had less autonomic impairment than thoseimmunohistochemistry. We applied a quantitative neurochemical with iPD as shown by higher cardiac MIBG uptake and less impair-method to test whether Lewy body diseases characteristically involve ment of autonomic non-invasive test. 123
  12. 12. 218 Clin Auton Res (2012) 22:207–258Comparison of techniques for non-invasive assessment increase in blood pressure that we may be worried about. The point here isof systemic hemodynamics in autonomic function that the delegated system—the Commander—can operate without higher-order control to maintain our blood pressure, our heart rate, ourtesting temperature essentially constant. Yet, the Master can exert higher-order control that is either volitionally generated, such as during exercise or isC. Sims-O’Neil, S. Pechnik, L. Sewell, L. Nez, D.S. Goldstein the product of cognitive or affective processes, such as worrying or theClinical Neurocardiology Section, NINDS/NIH, Bethesda, MD, USA experience of pain. In this talk, I will consider recent neuroimaging data that highlight the different roles of cortical and subcortical structures inBackground: Neurogenic orthostatic hypotension is a cardinal mani- the generation of sympathetic outflow related to cardiovascular control.festation of chronic autonomic failure (CAF). Systemic hemodynamic In particular, I will discuss the advantages of concurrent microneurog-measurements include cardiac output (stroke volume times heart rate) raphy and functional magnetic resonance imaging (fMRI) in theand total peripheral resistance (TPR, mean arterial pressure divided identification of functional roles for various bulbar and suprabulbarby cardiac output). Normally, orthostasis decreases stroke volume, structures, with particular reference to medullary and hypothalamicand heart rate and TPR increase reflexively. In CAF, TPR should fail nuclei, the insula, precuneus and prefrontal cortex.to increase during orthostasis, because of baroreflex failure. Thisstudy compared three non-invasive methods for measuring orthostatichemodynamic changes in CAF-impedance cardiography (BioZ), fin-ger pulse contour (Nexfin), and gas rebreathing (Innocor).Methods: A total of 78 subjects, 29 with and 49 without CAF, The middle cerebral artery dilates to sodiumunderwent simultaneous hemodynamic measurements by BioZ, nitroprusside: a combined transcranial DopplerNexfin, or Innocor during supine rest and at 5 min of head-up tilt. and near infrared spectroscopy studyResults: Among supine subjects individual values by the three tech-niques agreed for stroke volume and TPR. CAF patients had higher J.M Stewart1,2, C.E. Schwartz1, Z.R. Messer2, C.Terilli2,TPR than did controls. During orthostasis, stroke volume decreased M.S. Medow1,2by all three measurements. Clear differences emerged for calculated 1 Department of Physiology, New York Medical College, Valhalla,orthostatic changes in TPR in CAF patients: BioZ reported a fall, NY, USA; 2Department of Pediatrics, New York Medical College,Nexfin no change, and Innocor an increase. In some patients, the Valhalla, NY, USAInnocor rebreathing maneuver itself decreased stroke volume asindicated by the Nexfin device, especially during orthostasis.Conclusions: All three non-invasive methods for tracking systemic Prior studies indicate that the middle cerebral artery (MCA) does nothemodynamics yield similar results for TPR in supine subjects, and dilate in response to moderate orthostatic stress or changes in carbonTPR during supine rest is increased in CAF. Impedance cardiography dioxide. Thus, measurements of cerebral blood flow velocity (CBFv) byunderestimates the orthostatic fall in stroke volume in CAF patients, transcranial Doppler ultrasound (TCD) are sufficient to estimate relativeresulting in a calculated orthostatic fall in TPR. Gas diffusion over- changes in cerebral blood flow under these conditions. Systemicallyestimates the orthostatic fall in stroke volume, resulting in a administered nitric oxide (NO) donors decrease CBFv. However, NOcalculated orthostatic increase in TPR, due to artifactual effects of the dilates cerebral arteries of all sizes in primate models. We investigatedrebreathing maneuver required for the cardiac output measurement. whether systemic bolus injection of the NO donor sodium nitroprussideOf the three methods, the finger pulse contour approach seems to (SNP) dilates the MCA and whether bolus phenylephrine constricts thetrack most validly effects of orthostasis on TPR in CAF. MCA in 10 supine healthy volunteer subjects 18–24 years old. We combined TCD of the MCA with near infrared spectroscopy (NIRS) over the frontal cortex. Cerebral oxygenation and total hemoglobin increased by 14 ± 1 and 15 ± 1 lM/L with 100 lg SNP despite hypotension, and were reduced by 6 ± 1 and 7 ± 1 lM with 150 lg phenylephrineThursday, November 1, 2012 despite hypertension. SNP increased NIRS derived cerebral blood flow estimates by approximately 40 % from baseline, while TCD derivedOral Presentations CBFv decreased by 15 %. Phenylephrine decreased NIRS derived cerebral blood flow estimates by approximately 11 % from baseline, while TCD derived CBFv increased by 5 %. Studies using upright tilt andPlenary Lecture lower body negative pressure were performed for comparison with the literature and demonstrated similar relative changes in NIRS derivedMaster and commander: the brain and the autonomic cerebral blood flow and TCD derived CBFv as orthostatic stress pro-nervous system gressed. We conclude that the middle cerebral artery dilates to sodium nitroprusside and constricts to phenylephrine but does not dilate during orthostatic stress.Vaughan G. Macefield, Ph.D.School of Medicine, University of Western Sydney; NeuroscienceResearch Australia, Sydney, Australia Cerebral oxygenation, heart rate & blood pressureThe autonomic nervous system, so named because it operates automat- responses in congenital central hypoventilationically—without the need for conscious control—is very much a syndrome (CCHS) during exogenous ventilatory‘‘delegated system’’: it faithfully follows a set of instructions to bring challenges: PHOX2B genotype/CCHS phenotypeabout homeostasis, and attempts to maintain a stable internal environ-ment in the presence of disease, yet these ‘‘presets’’ can be over-ridden by associationthe requirements of higher-order control. We have all experienced theracing heart rate, and the cold, clammy palms associated with anxiety. M.S. Carroll, P.P. Patwari, T.M. Stewart, C.D. Brogadir, A.S. Kenny,Some of us may be in a state of chronic stress and are experiencing an C.M. Rand, D.E. Weese-Mayer123
  13. 13. Clin Auton Res (2012) 22:207–258 219Center for Autonomic Medicine in Pediatrics, Ann and Robert H. mean. Diffuse denervation was defined by both septal and free wallLurie Children’s Hospital, Northwestern University Feinberg School radioactivity more than 2 standard deviations below the normal mean.of Medicine, Chicago, IL, USA Results: The time between localized and diffuse denervation averaged 2.5 ± (SEM) 0.8 years. The mean change in septal radioactivityCongenital central hypoventilation syndrome (CCHS) is a disorder of during this interval was -56 ± 10 %, corresponding to 22 % loss perrespiratory and autonomic regulation, characterized by hypoventila- year. In one patient followed over more than 12 years, cardiac sym-tion and diminished/absent ventilatory responses to hypoxia/ pathetic innervation was normal for 6 years, with subsequent rapidhypercarbia. However, ventilatory responses in CCHS have not been loss of free wall radioactivity and then equally rapid loss of septalevaluated subsequent to identification of PHOX2B as the disease- radioactivity with a delay of about 2 years.defining gene, and recognition that the longer polyalanine repeat Conclusions: In Parkinson disease, once there is evidence for loss ofexpansion mutations (PARMs) are typically associated with more sympathetic nerves in the left ventricular free wall, septal denervationsevere clinical features. We therefore hypothesized that cerebral rapidly ensues, resulting in remarkably swift diffuse denervation byoxygenation and cardiovascular metrics in response to exogenous 2–3 years later. Follow-up cardiac sympathetic neuroimaging inventilatory challenges (EVC) would show a graded deficit correlated patients with localized cardiac denervation therefore may be a basiswith PHOX2B genotype among CCHS patients with PARMs. Thirty- for a novel, quantitative means to assess potential treatments to retardone children and young adults (5 months–27 years; 14 female) with the loss of catecholaminergic neurons that characterizes ParkinsonCCHS were tested during wakefulness with 45 separate clinical EVCs disease.(each with 4 distinct gas mixtures) during continuous comprehensivephysiological monitoring. Three-minute challenges were adminis-tered between 3 min room-air periods, with minimal ventilatorysupport: Hyperoxia (100 % O2), hyperoxia-hypercarbia (95 % O2/ Parental attribution of symptoms in adolescents5 % CO2) and hypoxia-hypercarbia (14 % O2/7 % CO2). The fourthchallenge, hypoxia, consisted of 5 or 7 tidal breaths of N2. A com- with postural tachycardia syndrome and its relationparison group of 4 young men (18–21 years) were monitored while to child functioning and psychological variablesreceiving all but the hypoxia challenge. Percent change from baseline(±SEM) was calculated during each challenge for the cerebral near E.M. Keating1, R.M. Antiel2, K.E. Weiss3, D. Wallace4,infrared spectroscopy (cNIRS) channel, mean blood pressure, and P.R. Fischer5, C. Harbeck-Weber3heart rate. Significance was assessed at p 0.05 (paired t test). The 3 1 Mayo Medical School, Mayo Clinic, Rochester, MN, USA;most common PARM genotypes were compared to assess genotype- 2 Department of General Surgery, Mayo Clinic, Rochester, MN, USA;phenotype association. Though the cNIRS response was not consis- 3 Department of Psychiatry and Psychology, Mayo Clinic, Rochester,tently associated with polyalanine repeat length, it was impaired/ MN, USA; 4Integrative Pain Management, Children’s Mercyattenuated in CCHS versus controls during the hypoxia-hypercarbia Hospital, Kansas City, MO, USA; 5Department of Pediatricchallenge. Blood pressure responses were variable, but showed a and Adolescent Medicine, Mayo Clinic, Rochester, MN, USACO2-dependent increase in CCHS. Heart rate was suppressed byhyperoxia in CCHS, but increased in the combined hypoxia-hyper-carbia challenge. The heart rate response to the hypoxia-hypercarbia Background: Chronic pain is a common symptom in adolescents withchallenge was consistently correlated with polyalanine repeat length postural orthostatic tachycardia syndrome (POTS), and it is frequently(blunted response with increasing PARM length). Overall, compre- associated with impairment in functioning. The manner in whichhensive physiological evaluation during ventilatory challenges parents respond to children’s pain may predict children’s functionalindicated residual responsiveness in CCHS, providing a potential disability, and parental responses to the pain are related to parentalfulcrum for therapeutic interventions. beliefs about the causes of the pain. The Parent Attribution Ques- tionnaire (PAQ) was developed to assess these parental attributions regarding their child’s pain. We evaluated parent attributions of symptoms in adolescents with POTS in order to determine how theyTime course of cardiac sympathetic denervation are related to their child’s functioning.in Parkinson disease Methods: 141 adolescent patients with chronic pain and clinical symptoms suggestive of POTS were seen in a multidisciplinary chronic pain clinic at Mayo Clinic. Of these patients, 37 were iden-D.S. Goldstein tified as having POTS with a postural heart range change of at least 40Clinical Neurocardiology Section, NINDS/NIH, Bethesda, MD, USA beats per minute on tilt table testing. Parents of 114 of these patients completed a demographic questionnaire and PAQ. The PAQ is aBackground: Parkinson disease entails not only nigrostriatal dopa- 19-item questionnaire that asks parents to indicate the extent theyminergic but also cardiac noradrenergic denervation, which can occur believe medical (9 items) and psychosocial factors (10 items) accountbefore clinical onset of the movement disorder. The neuropathologic for their child’s health condition.process in the heart appears to proceed retrogradely and centripetally. Results: In patients with chronic pain who have symptoms suggestiveLocalized denervation in the left ventricular myocardial free wall of possible autonomic dysfunction, higher parental attribution ofprogresses to diffuse denervation, with late loss of interventricular symptoms to medical causes was associated with increased levelsseptal innervation. We analyzed neuroimaging data from patients with of functional disability (r = 0.33, p 0.001). Parental attribution oflocalized denervation to estimate the loss rate of cardiac catechol- symptoms to psychological causes was linked to depression only inaminergic neurons in Parkinson disease. patients without POTS (r = 0.53, p 0.01) but not in those withMethods: Serial 18F-dopamine positron emission tomographic scan- POTS.ning data in Parkinson disease patients were reviewed and 4 patients Conclusions: Functional disability in adolescents with POTS relatesidentified who had localized followed by diffuse denervation. to the degree to which parents attribute the child’s symptoms to aLocalized denervation was defined by free wall 18F-dopamine-derived medical problem. It is likely that helping parents avoid over-accep-radioactivity more than 2 standard deviations below the normal mean tance of incurable medical problems as causing pain could helpand septal radioactivity within 2 standard deviations of the normal children attain better functioning. 123
  14. 14. 220 Clin Auton Res (2012) 22:207–258Cardiovagal sensitivity and orthostatic heart rate Background: Parental responses to pain may have an importantresponse in young patients with orthostatic intolerance impact on adolescent pain outcomes. Approximately 10 % of adolescents suffer from autonomic dysfunction marked by ortho- static intolerance, severe fatigue, and chronic pain. We sought toW. Singer, A.K. Parsaik, E.E. Benarroch, P. Sandroni, P.A. Low examine if parental responses to these symptoms are related toDepartment of Neurology, Mayo Clinic, Rochester, MN, USA their child’s functioning, psychological well-being, and pain acceptance.Background and Objective: Orthostatic intolerance (OI) is increas- Methods: Participants included 141 adolescents with chronic painingly recognized among adolescents but pathophysiologic and symptoms of orthostatic intolerance who were seen in a mul-mechanisms underlying this condition remain poorly understood. tidisciplinary pain clinic at the Mayo Clinic. Of the 141 patients, 37These patients typically have normal autonomic function as assessed (26 %) had excessive postural tachycardia (PT) with a heart rateusing standardized autonomic testing. We frequently see high or very change of at least 40 bpm on tilt table testing. Participants com-high values for cardiovagal indices in these patients and made the pleted the Functional Disability Inventory, the Center ofobservation that those with unusually high HR responses to deep Epidemiological Studies—Depression Scale, the Spence Children’sbreathing (HRDB) and Valsalva maneuver (VM, Valsalva Anxiety Scale, and the Chronic Pain Acceptance Questionnaire,ratio = VR) also seem to have the most excessive HR responses to adolescent version. Parents of 103 of these patients completed thetilt. Such relationship—if present—would be intriguing in terms of Parent Response to Pain Questionnaire—Revised, which measures 4mechanisms underlying the magnitude of HR responses to tilt and of theoretically driven parental factors: solicitous behaviors, secondaryOI; factors such as excessive cardiac vagal modulation and baroreflex gain, promoting adaptive behavior, and encouragement of specificsensitivity might be implicated. We therefore sought to evaluate pain management.whether the magnitude of cardiovagal indices predicts the orthostatic Results: Parent solicitous behaviors were significantly related torise in HR and whether the pattern of findings reveals insights into the anxiety (r = 0.21, p 0.05). Parent report of secondary gain waspathophysiology underlying adolescent OI. correlated with depression (r = 0.57, p 0.01) and negatively relatedMethods: 100 adolescent patients were randomly selected from a to acceptance (r = -0.40, p 0.05). Upon further examination of thelarge cohort of patients referred to our laboratory for evaluation of sub-sample of patients with excessive PT, parent report of secondarysymptoms of OI. HRDB and VR were quantified using standard gain was related to functional disability (r = 0.39, p 0.05) andtechniques. Vagal baroreflex sensitivity (vBRS) was defined as slope parent encouragement to use specific pain management skills wasbetween systolic blood pressure (BP) decline during phase II and inversely associated with depression (r = -0.069, p 0.05).resulting change in RR interval. HR and BP responses to tilt were Conclusions: Differential parental responses to pain are significantlyassessed using 30 s data averages, BP responses to the VM were related to adolescent anxiety, depression, and pain acceptance. Fur-assessed using systolic BP at the different phases of the maneuver. thermore, in patients with co-morbid orthostatic intolerance parentalCorrelations between different parameters were tested using Pear- responses are associated with functional disability and depression.son’s r. These findings suggest that parental responses to adolescent pain areResults: HRDB and vBRS were not correlated with DHR or DBP related to patient outcomes and could have implications for effectiveduring tilt. However, VR was significantly correlated with DHR interventions.(p = 0.001). While VR was also strongly correlated with the BPchanges during early phase II and phase IV of the VM, as well as thesum of both, only one of these BP indices (phase IV) was weaklycorrelated with DHR during tilt. No correlations were seen between Relationship between ganglionic long-term potentiationBP and HR responses to tilt. (LTP) and homeostatic synaptic plasticityConclusions: These findings argue against excessive cardiac vagalmodulation or excessive BRS underlying the excessive orthostatic rise in experimental autoimmune autonomicin HR in adolescents with OI. The pattern of findings would rather ganglionopathy (EAAG)suggest that the mechanism underlying the excessive orthostatic risein HR also results in excessive BP responses to the VM and conse- Z. Wang, S. Verninoquently excessive VR. This putative mechanism remains subject to UT Southwestern University, Dallas, TX, USAfurther study. Supported by NIH (K23NS075141, U54NS065736,UL1RR24150) and Mayo Funds. The autonomic nervous system must be able to adapt to maintain homeostasis. Plasticity of ganglionic synaptic transmission repre- sents one important mechanism of autonomic adaptation. We have shown that homeostatic plasticity of ganglionic neurotransmissionParental response to pain: the impact on functional occurs in EAAG. In EAAG, there is a reduction in synaptic gan-disability, depression, anxiety, and pain acceptance glionic AChRs followed by a compensatory increase in neurotransmitter release to help offset the deficit in synaptic trans-in adolescents with chronic pain and orthostatic mission. Homeostatic plasticity is quite different from classical use-intolerance dependent LTP. Both types of plasticity occur in autonomic ganglia, so the ganglionic synapse is an ideal system in which to study theR.M. Antiel1, E.M. Keating2, K.E. Weiss3, D.P. Wallace4, interrelationship between these two forms of synaptic plasticity. WeP.R. Fischer5, C. Harbeck-Weber3 studied synaptic transmission in isolated mouse superior cervical1 Department of General Surgery, Mayo Clinic, Rochester, MN, USA; ganglia using microelectrode and patch clamp electrophysiology2 Mayo Medical School, Rochester, MN, USA; methods. High frequency stimulation (HFS) of the preganglionic3 Department of Psychiatry and Psychology, Mayo Clinic, Rochester, nerve (20 Hz for 20 s) in control ganglia induces a long-lastingMN, USA; 4Integrative Pain Management, Children’s Mercy increase in synaptic transmission due to increased probability ofHospital, Kansas City, MO, USA; 5Department of Pediatric synaptic release. A second HFS does not produce further enhance-and Adolescent Medicine, Mayo Clinic, Rochester, MN, USA ment. Ganglia from mice with EAAG fail to show LTP. Inhibitors123
  15. 15. Clin Auton Res (2012) 22:207–258 221of nitric oxide synthase prevent the induction of LTP in control baroreflex failure causes volume intolerance remains unknown. Theganglia and also cause a normalization of presynaptic release in aim of this investigation is to examine the mechanism of baroreflexEAAG ganglia. These findings indicate that homeostatic plasticity of failure induced volume intolerance.synaptic transmission (as occurs in the EAAG model) shares com- Method: In 6 anesthetized dogs, we isolated carotid sinuses andmon molecular mechanism with use-dependent plasticity (ganglionic controlled intra-carotid sinus pressure (CSP), while measuring the leftLTP). The implication is that pharmacological manipulation of (PLA) and right (PRA) atrial pressure, arterial pressure (AP) andganglionic LTP may be a useful therapeutic option for patients with aortic flow (CO). We closed the baroreflex feedback loop by matchingautonomic disorders. CSP to instantaneous AP, whereas opened by maintaining CSP con- stant independent of AP. We infused total of 22.5 ml/kg of dextran in an increment of 2.5 ml/kg. In each step, we measured PLA, PRA and CO in both open and closed loop conditions. We fitted the CO curveMethionine sulfoxide reductase A: a novel molecular to a logarithmic function and determined its functional slope S, as adeterminant of baroreflex sensitivity, blood pressure measure of cardiac performance, for the left (SL) and right (SR)and hypertensive end-organ damage ventricle. We determined stressed blood volume and mean circulatory filling pressure (Pmcf). Results: Increases in PLA was lower in the closed loop than in theR. Sabharwal, R. El Accaoui, M.K. Davis, J.A. Goeken, R. Weiss, open loop condition (9 ± 3 vs. 12 ± 5 mmHg, p 0.05). Both SLF.M. Abboud, D. Meyerholz, M.W. Chapleau and SR were lower in the closed loop than in the open loop conditionThe University of Iowa and Veterans Affairs Medical Center, (SL: 23 ± 5 vs. 27 ± 6 ml/kg/min, p 0.01, SR: 23 ± 5 vs.Iowa City, IA, USA 27 ± 6 ml/kg/min, p 0.01) indicating that the baroreflex lowers cardiac performance against volume overload. Pmcf after infusion ofMethionine sulfoxide reductase-A (MsrA) selectively reverses oxi- 22.5 ml/kg of dextran was lower in the closed loop than in the opendation of methionine residues in proteins, thereby protecting against loop condition (10.8 ± 0.5 vs. 12.8 ± 1.1 mmHg, p 0.005).oxidative stress-induced cellular damage and dysfunction. We Conclusion: In response to volume challenge, the baroreflex loweredhypothesized that MsrA is required for normal autonomic and blood cardiac performance and prevented the increases in Pmcf. Althoughpressure (BP) regulation, and protects against hypertension-induced those two responses have antagonizing impact on PLA, the fact thatend-organ damage. BP, heart rate (HR) and locomotor activity were the baroreflex lowered PLA indicates that the baroreflex inducedmeasured in MsrA deficient (n = 13) and control C57BL/6 (n = 7) changes in stressed volume is the central mechanism preventingmice by telemetry, before and during infusion of angiotensin II (Ang pulmonary edema.II) (1,000 ng/kg/min for 4 weeks). Under basal conditions, MsrA-/-mice exhibited mild hypertension (117 ± 3 vs. 107 ± 2 mmHg) anddecreased locomotor activity. During periods when activity levelswere similar, the hypertension in MsrA-/- mice was exacerbated Prostaglandin D synthase is critical for development(135 ± 2 vs. 103 ± 2 mmHg). MsrA-/- mice also exhibited of chronic angiotensin II-salt hypertension in the ratdecreases in spontaneous baroreflex sensitivity (BRS, sequencetechnique) (0.9 ± 0.1 vs. 2.2 ± 0.1 ms/mmHg) and cardiovagal tone G.D. Fink, N. Asirvatham-Jeyaraj(HR response to cholinergic receptor blocker methylatro- Department of Pharmacology and Toxicology, Michigan Statepine = +32 ± 5 vs. +100 ± 17 bpm); and increases in BP variability University, East Lansing, MI, USA(BPV) and sympathetic tone (HR response to beta adrenergic receptorblocker propranolol) (P 0.05). Ang II increased mean BP, BPV andsympathetic tone; and decreased BRS and vagal tone, with MsrA-/- Chronic infusion of angiotensin II (150 ng/kg/min, sc) into ratsmice exhibiting markedly enhanced responses (P 0.05). Adminis- ingesting a high salt diet (4.0 % NaCl) produces sustained hyper-tration of the antioxidant tempol (1 mM, drinking water) reversed the tension (AngII-salt HT) caused in part by increased splanchnicAng II-induced hypertension and autonomic dysregulation. Ang II- sympathetic nerve activity. Previous work suggests that cyclooxy-infused MsrA-/- mice (n = 10) exhibited left ventricular dysfunc- genase products generated in the brain during the first few days oftion, increased diameter of the ascending aorta (echocardiography), exposure to angiotensin II are necessary for these effects. Analyses ofand abdominal aortic aneurysms. We conclude that MsrA: (1) is eicosanoid pathway gene expression in the brain during the earlyrequired for normal BP, BRS and sympathovagal balance under basal phase of AngII-salt HT highlighted lipocalin-type prostaglandin Dconditions; (2) protects against Ang II-induced hypertension, auto- synthase (L-PGDS) as a possible critical element in the response. Tonomic dysfunction and end-organ damage; and (3) is a novel test that idea we continuously administered the highly selectivetherapeutic target in hypertension. (HL14388, VA) L-PGDS inhibitor AT-56 into the brain of rats via intracerebroven- tricular (icv) infusion (6.6 lmol/h). We then induced our standard 14-day model of AngII-salt HT starting 5 days after icv AT-56 administration had begun. Rats receiving only icv vehicle served asBaroreflex induced changes in stressed blood volume, controls. Blood pressure was measured continuously throughout thenot cardiac output curve, is the central mechanism experiment by radiotelemetry. Sympathetic control of blood pressure was estimated from the depressor response to acute ganglion blockadepreventing volume load induced pulmonary edema with hexamethonium (30 mg/kg, ip). Control rats showed typical elevations in blood pressure during AngII infusion and a significantlyT. Sakamoto, T. Kakino, K. Sunagawa enhanced depressor response to ganglion blockade on day 8 afterDepartment of Cardiovascular Medicine, Kyushu University, starting AngII. Rats receiving icv AT-56 exhibited no change in basalFukuoka, Japan blood pressure but had a markedly and significantly reduced blood pressure and sympathetic response to AngII infusion compared toBackground: We previously demonstrated that baroreflex failure control rats. Systemic administration of AT-56 via continuous sub-predisposes volume induced pulmonary edema. Since the baroreflex cutaneous infusion (6.6 lmol/h) also completely prevented thechanges both cardiac and vascular properties, how exactly the increases in blood pressure and sympathetic pressor activity normally 123
  16. 16. 222 Clin Auton Res (2012) 22:207–258observed during AngII infusion. These studies reveal that L-PGDS, well as cardiac arrhythmia is relatively uncommon compared to largerlikely in the brain, is a necessary component of AngII-salt HT and animals or humans, since high quality continuous long term ECG andsympathoexcitation. Since systemic inflammation, sleep deprivation arterial blood pressure (APB) recordings as well as the techniques forand obesity are all associated with increased brain levels of prosta- analysis of heart rate (HR), heart rate variability (HRV) andglandin D and sympathoexcitation, our results may have broad arrhythmia detection in the mouse present technical and computa-implications for understanding neurogenic forms of hypertension. tional challenges. Methods: We present data from several studies involving murine ECG and ABP signals from implanted wireless radiofrequency transmitters. We describe and compare different methods of digital signal pro-The central chemoreflex activation induces cessing, heart beat and arrhythmia detection and classification,sympathoexcitation and resets the arterial baroreflex computation of baroreflex sensitivity, time domain and frequencywithout compromising its pressure stabilizing function domain HRV parameters, construction of composite plots for dynamics of HR and HRV data over time during interventional studies from an aspect specific to the mouse model. We illustrateK. Saku, K. Sunagawa technical challenges, common mistakes and solutions throughout theDepartment of Cardiovascular Medicine, Kyushu University, process from telemetry to the analysis results presentation.Fukuoka, Japan Results: During a decade of experience with murine ECG signal analysis, we have developed a toolbox of techniques specificallyBackground: The augmented chemoreflex and impaired baroreflex in tailored to the mouse model. Here we demonstrate the technicalheart failure result in excessive sympathoexcitation and poor prog- requirements for signal quality and processing, how wavelet basednosis. However, how the chemoreflex interacts with the baroreflex visualizations and spectrograms can significantly aid in the charac-remains unknown. The purpose of this investigation was to examine terization of dynamic changes and the detection of anomalies andthe impact of chemoreflex on the baroreflex function under the open- artifacts and how specific plotting techniques can reveal unexpectedloop condition. findings such as multiple transient atrial pacemakers during carbacholMethods and Results: In 7 vagotomized rats, we vascularily isolated challenge experiments. We show the use of machine learning algo-the bilateral carotid sinuses, controlled carotid sinus pressure (CSP) rithms for the automatic detection and reliable subclassification ofand measured SNA at the celiac ganglia and arterial pressure (AP). ventricular tachycardia and premature contractions after myocardialWe activated the central chemoreflex by hypercapnia (inhalation of infarction with pattern recognition techniques such as artificial neural3 % CO2). Under the open baroreflex loop, we compared the changes networks in large data sets from long term ECG signals. Finally, wein AP and SNA in response to CSP with/without hypercapnia. show that parallel processing and general-purpose computing onIncreasing CSP stepwise from 60 to 170 mmHg sigmoidally sup- graphics processing units allow for accelerated analysis of continuouspressed SNA, whereas the SNA suppression linearly decreased AP. mouse ECG recordings over days with millions of heart beats as wellHypercapnia markedly increased SNA (DSNA = 53.4 ± 7.1 %, as for providing near real-time computation of advanced analysisp 0.01) irrespective of CSP indicating the resetting of the CSP– output during experiments.SNA relationship (the neural arc). Hypercapnia increased the setpointpressure (168.6 ± 8.2 vs. 188.3 ± 8.1 mmHg, p 0.01) of neuralarc, whereas did not alter the SNA–AP relationship (peripheral arc).The total loop gain from CSP to AP at the operating point remained Streeten Lectureunchanged (-1.09 ± 0.13 vs. -1.43 ± 0.18, p = ns). Random per-turbation of CSP with binary white noise sequences indicated that The ‘‘ups and downs’’ of blood pressure & baroreflexhypercapnia did not affect the transfer functions of the neural or sensitivity—a historical and personal perspectiveperipheral arcs. Therefore, the chemoreflex activation did not impact onthe baroreflex dynamic characteristics of pressure stabilizing function.Conclusion: Hypercapnia resets the baroreflex neural arc upward and Mark W. Chapleau, Ph.D.increases arterial pressure, while does not affect baroreflex pressure University of Iowa and Veterans Affairs Medical Center, Iowa City,stabilizing characteristics. We conclude that the central chemoreflex IA, USAmodifies hemodynamics via sympathoexcitation without compro-mising baroreflex function. The augmented chemoreflex in heart The baroreceptor reflex is a powerful regulator of blood pressurefailure cannot be responsible for the baroreflex dysfunction. How (BP). Increases and decreases in BP are buffered by baroreflex-chemoreflex induced changes in hemodynamics contribute to CO2 mediated autonomic and circulatory adjustments. By minimizing BPhomeostasis remains to be seen. variability, the baroreflex protects against ischemia, syncope and end- organ damage (e.g., vascular and cardiac hypertrophy, renal failure, stroke). The baroreflex also favorably influences cardiac sympath- ovagal balance, and consequently affects the electrical properties ofAdvanced techniques and pitfalls of autonomic function the heart. Decreased baroreflex sensitivity (BRS) for control of heartassessment and arrhythmia analysis in the mouse model rate (HR) predicts future arrhythmias and decreased survival in patients with myocardial infarction, heart failure and diabetes; increased BRS is protective. In my presentation, I will reviewC.M. Welzig1, J.B. Galper2 experimental approaches and key discoveries related to the physiol-1 Department of Neurosciences, Medical University of South Carolina, ogy and pathophysiology of the baroreceptor reflex, with emphasis onCharleston, SC, USA; 2Molecular Cardiology Research Institute, studies leading up to and including work in my laboratory. ResultsTufts Medical Center, Boston, MA, USA obtained using a variety of approaches will be presented including recordings of baroreceptor afferent and sympathetic efferent nerveBackground: Mice are very frequently employed as a mammalian activity; telemetry-based measurements of cardiovascular and derivedresearch model and are used in a wide spectrum of experimental autonomic indices in conscious, genetically modified mice; electro-protocols. However, the study of autonomic function and disorders as physiological and imaging studies of isolated baroreceptor neurons in123

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