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The Recommendations of a Consensus Panel for the Screening, Diagnosis, and Treatment of Neurogenic Orthostatic Hypotension and Associated Supine Hypertension

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The Recommendations of a Consensus Panel for the Screening, Diagnosis, and Treatment of Neurogenic Orthostatic Hypotension and Associated Supine Hypertension The recommendations of a consensus panel for the screening, diagnosis, and treatment of neurogenic orthostatic hypotension and associated supine hypertension The Harvard community has made this article openly available. Please share how this access benefits you. Your story matters Citation Gibbons, C. H., P. Schmidt, I. Biaggioni, C. Frazier-Mills, R. Freeman, S. Isaacson, B. Karabin, et al. 2017. “The recommendations of a consensus panel for the screening, diagnosis, and treatment of neurogenic orthostatic hypotension and associated supine hypertension.” Journal of Neurology 264 (8): 1567-1582. doi:10.1007/ s00415-016-8375-x. http://dx.doi.org/10.1007/s00415-016-8375-x. Published Version doi:10.1007/s00415-016-8375-x Citable link http://nrs.harvard.edu/urn-3:HUL.InstRepos:34375034 Terms of Use This article was downloaded from Harvard University’s DASH repository, and is made available under the terms and conditions applicable to Other Posted Material, as set forth at http:// nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of- use#LAA J Neurol (2017) 264:1567–1582 DOI 10.1007/s00415-016-8375-x REVIEW The recommendations of a consensus panel for the screening, diagnosis, and treatment of neurogenic orthostatic hypotension and associated supine hypertension 1 2 3 4 Christopher H. Gibbons • Peter Schmidt • Italo Biaggioni • Camille Frazier-Mills • 1 5 6 7 Roy Freeman • Stuart Isaacson • Beverly Karabin • Louis Kuritzky • 8 9 10 11 12 Mark Lew • Phillip Low • Ali Mehdirad • Satish R. Raj • Steven Vernino • Horacio Kaufmann13 Received: 11 November 2016 / Revised: 19 December 2016 / Accepted: 20 December 2016 / Published online: 3 January 2017 Ó The Author(s) 2016. This article is published with open access at Springerlink.com Abstract Neurogenic orthostatic hypotension (nOH) is 2016. This paper summarizes the panel members’ discus- common in patients with neurodegenerative disorders such sions held during the initial meeting along with continued as Parkinson’s disease, multiple system atrophy, pure deliberations among the panel members and provides autonomic failure, dementia with Lewy bodies, and essential recommendations based upon best available evi- peripheral neuropathies including amyloid or diabetic dence as well as expert opinion for the (1) screening, (2) neuropathy. Due to the frequency of nOH in the aging diagnosis, (3) treatment of nOH, and (4) diagnosis and population, clinicians need to be well informed about its treatment of associated supine hypertension. diagnosis and management. To date, studies of nOH have used different outcome measures and various methods of Keywords Neurogenic orthostatic hypotension Á Supine diagnosis, thereby preventing the generation of evidence- hypertension Á Autonomic dysfunction Á Droxidopa Á based guidelines to direct clinicians towards ‘best prac- Midodrine Á Fludrocortisone tices’ when treating patients with nOH and associated supine hypertension. To address these issues, the American Autonomic Society and the National Parkinson Foundation Introduction initiated a project to develop a statement of recommenda- tions beginning with a consensus panel meeting in Boston Neurogenic orthostatic hypotension (nOH) is a prevalent on November 7, 2015, with continued communications and disorder [1, 2]. Clinicians from a variety of specialties need to contributions to the recommendations through October of be well informed about diagnosis and management of nOH as it carries a significant burden of morbidity and has also been associated with increased mortality [3–5]. Clinicians should, Electronic supplementary material The online version of this therefore, familiarize themselves with this condition and article (doi:10.1007/s00415-016-8375-x) contains supplementary evolving management options, which offer substantial material, which is available to authorized users. & Christopher H. Gibbons 7 University of Florida College of Medicine, Gainesville, FL, [email protected] USA 8 Keck/USC School of Medicine, Los Angeles, CA, USA 1 Harvard Medical School and Beth Israel Deaconess Medical Center, Boston, MA, USA 9 Mayo Clinic, Rochester, MN, USA 2 National Parkinson Foundation, Miami, FL, USA 10 Saint Louis University Hospital, St. Louis, MO, USA 3 Vanderbilt University Medical Center, Nashville, TN, USA 11 University of Calgary, Calgary, BC, Canada 4 Duke University Hospital and Central Carolina Hospital, 12 University of Texas Southwestern Medical Center, Dallas, Durham, NC, USA TX, USA 5 Parkinson’s Disease and Movement Disorders Center of Boca 13 New York University Langone Medical Center, New York, Raton, Boca Raton, FL, USA NY, USA 6 University of Toledo Medical Center, Toledo, OH, USA 123 1568 J Neurol (2017) 264:1567–1582 symptomatic improvement. This communication will focus Screening for nOH primarily on nOH, while recognizing that orthostatic symp- toms are often multifactorial: i.e., patients with nOH may have There is no standardized or recommended screening protocol their symptoms worsened by medications, hypovolemia, for patients that present with symptoms of orthostatic intrinsic cardiovascular disease, and other factors [6, 7]. hypotension. Presenting symptoms and signs of OH include The literature on nOH is fraught with inconsistencies in postural lightheadedness or dizziness, the sensation of the definition and methods of diagnosis, and suffers from a blacking out, and falls with or without syncope. Less com- lack of evidence-based guidelines to direct clinicians mon symptoms include orthostatic cognitive dysfunction towards ‘best practice’. As nOH is a subset of orthostatic (executive function worsens significantly during the ortho- hypotension (OH), it should be noted that patients with nOH static challenge in patients with autonomic dysfunction, and OH may experience the same symptoms but for different possibly because of transient frontal lobe hypoperfusion), reasons. The following consensus definition of OH was mental dulling, generalized weakness, neck pain or dis- devised by the American Autonomic Society and the comfort in the suboccipital and paracervical region (‘coat American Academy of Neurology, and endorsed by the hanger’ configuration—a manifestation of hypotension-in- European Federation of Autonomic Societies and the World duced ischemia of the strap muscles of the neck), or Federation of Neurology: OH is ‘‘…a sustained reduction of platypnea (dyspnea while standing due to OH causing systolic blood pressure of at least 20 mmHg or diastolic inadequate perfusion of ventilated lung apices or ventilation blood pressure of 10 mmHg, or both, within 3 min of perfusion mismatch) [23–27]. Thus, screening for nOH starts standing or head-up tilt to at least 60° on a tilt table’’ [8]. In with questions to identify the symptoms of OH followed by addition to meeting the definition for OH, patients with nOH measurement of blood pressures from the supine (or seated) have impairment of the autonomic nervous system that is to standing position (recommended specific technique for characterized by failure to provide adequate autonomic timing of blood pressure measurements is detailed below) postural responses, most prominently systemic vasocon- [6]. It may be beneficial if screening questionnaires and striction and a compensatory increase in heart rate sufficient blood pressure measurements are conducted by a qualified to maintain blood pressure. This deficit is, in large part, non-physician (such as a nurse) prior to the patient’s visit attributed to insufficient norepinephrine release from sym- with the clinician. Patients in the following five categories pathetic nerves [9]. In addition, many patients with nOH also need to be routinely screened for OH: suffer from supine hypertension, which further confounds (1) Patients suspected of, or diagnosed with any neurode- therapy because pharmacologic treatments to normalize generative disorder associated with autonomic dys- standing blood pressure may worsen supine hypertension function, including Parkinson’s Disease (PD), [10]. Differences in study designs and endpoints, as well as a Multiple System Atrophy (MSA), Pure Autonomic paucity of data, preclude achieving definitive evidence- Failure (PAF), or Dementia with Lewy Bodies (DLB); based treatment regimens through a systematic review of (2) Patients who have reported an unexplained fall or trials [11–22]. To move forward in an effective and safe have had an episode of syncope; manner, consensus is required on the basics of screening, (3) Patients with peripheral neuropathies known to be diagnosing, and treating patients with nOH. Thus, an expert associated with autonomic dysfunction (e.g., dia- opinion statement to these basic approaches is needed. betes, amyloidosis, HIV); To address this issue, the American Autonomic Society (4) Patients who are elderly (C70 years of age) [28] and and the National Parkinson Foundation jointly held an frail or on multiple medications; initial consensus panel meeting to formulate essential (5) Patients with postural (orthostatic) dizziness or non- recommendations into a working guideline for the screen- specific symptoms that only occur when standing. ing, diagnosis, and treatment of nOH and associated supine hypertension. Results of the discussions held during the Patients in each of these groups have a higher risk of meeting, along with continued deliberations among the OH/nOH when compared to the normal population [29]. panel participants are presented here along with recom- For these five categories of patients, clinicians should ask mendations
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