Guillaume Lamotte1,2, Makoto Takahashi3,4, Tianxia Wu5, Patricia Sullivan3, Jamie Cherup3, Courtney Holmes3, David S Goldstein3. 1. Autonomic Medicine Section, National Institute of Neurological, Disorders and Stroke (NINDS), National Institutes of Health (NIH), 9000 Rockville Pike 10/8C260, Bethesda, MD, 20892, USA. guillaume.lamotte@nih.gov. 2. Department of Neurology, Mayo Clinic, Rochester, MN, USA. guillaume.lamotte@nih.gov. 3. Autonomic Medicine Section, National Institute of Neurological, Disorders and Stroke (NINDS), National Institutes of Health (NIH), 9000 Rockville Pike 10/8C260, Bethesda, MD, 20892, USA. 4. Department of Neurology, Kanto Central Hospital, Tokyo, Japan. 5. Clinical Trials Unit, NINDS, NIH, Bethesda, MD, USA.
Abstract
INTRODUCTION: Patients with neurogenic orthostatic hypotension in the setting of Lewy body diseases (LBnOH) typically have baroreflex failure and peripheral noradrenergic deficiency. Either or both of these abnormalities might determine the magnitude of OH in individual patients. We retrospectively correlated the orthostatic fall in systolic blood pressure (∆BPs) during active standing or 5 min of head-up tilt at 90° from horizontal as a function of several baroreflex and sympathetic noradrenergic indices. METHODS: Physiological, neurochemical, and sympathetic neuroimaging data from the Valsalva maneuver, head-up tilt table testing, and thoracic 18F-dopamine positron emission tomographic scanning (18F-DA PET) were analyzed from 72 patients with LBnOH [44 with Parkinson disease (PD) and nOH, 28 with pure autonomic failure]. Comparison subjects had PD without OH (N = 44) or PD risk factors without parkinsonism or OH (N = 28) or were healthy volunteers (N = 8). Indices of baroreflex function included the Valsalva maneuver-associated baroreflex areas in Phase II (BRA-II) and IV (BRA-IV), the pressure recovery time (PRT), and baroreflex-cardiovagal and adrenergic sensitivities (BRS-V and BRS-A). The fractional orthostatic increment in plasma norepinephrine (Fx∆NE) provided a neurochemical index of baroreflex-sympathoneural function. RESULTS: As expected, the LBnOH group had baroreflex-sympathoneural and baroreflex-cardiovagal impairment and low cardiac 18F-DA-derived radioactivity. Among patients, values for ∆BPs correlated with BRA-II, BRA-IV, BRS-V, and Fx∆NE but not with values for PRT, BRS-A, supine plasma NE, or 18F-DA-derived radioactivity. CONCLUSION: Across individual patients with LBnOH, quantitative indices of baroreflex dysfunctions and peripheral noradrenergic deficiency are inconsistently associated with the magnitude of OH, even under controlled laboratory conditions.
INTRODUCTION:Patients with neurogenic orthostatic hypotension in the setting of Lewy body diseases (LBnOH) typically have baroreflex failure and peripheral noradrenergic deficiency. Either or both of these abnormalities might determine the magnitude of OH in individual patients. We retrospectively correlated the orthostatic fall in systolic blood pressure (∆BPs) during active standing or 5 min of head-up tilt at 90° from horizontal as a function of several baroreflex and sympathetic noradrenergic indices. METHODS: Physiological, neurochemical, and sympathetic neuroimaging data from the Valsalva maneuver, head-up tilt table testing, and thoracic 18F-dopamine positron emission tomographic scanning (18F-DA PET) were analyzed from 72 patients with LBnOH [44 with Parkinson disease (PD) and nOH, 28 with pure autonomic failure]. Comparison subjects had PD without OH (N = 44) or PD risk factors without parkinsonism or OH (N = 28) or were healthy volunteers (N = 8). Indices of baroreflex function included the Valsalva maneuver-associated baroreflex areas in Phase II (BRA-II) and IV (BRA-IV), the pressure recovery time (PRT), and baroreflex-cardiovagal and adrenergic sensitivities (BRS-V and BRS-A). The fractional orthostatic increment in plasma norepinephrine (Fx∆NE) provided a neurochemical index of baroreflex-sympathoneural function. RESULTS: As expected, the LBnOH group had baroreflex-sympathoneural and baroreflex-cardiovagal impairment and low cardiac 18F-DA-derived radioactivity. Among patients, values for ∆BPs correlated with BRA-II, BRA-IV, BRS-V, and Fx∆NE but not with values for PRT, BRS-A, supine plasma NE, or 18F-DA-derived radioactivity. CONCLUSION: Across individual patients with LBnOH, quantitative indices of baroreflex dysfunctions and peripheral noradrenergic deficiency are inconsistently associated with the magnitude of OH, even under controlled laboratory conditions.
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