title: Neurocirculatory abnormalities in Parkinson disease with orthostatic hypotension: independence from levodopa treatment.
abstract: Patients with Parkinson disease often have orthostatic hypotension. Neurocirculatory abnormalities underlying orthostatic hypotension might reflect levodopa treatment. Sixty-six Parkinson disease patients (36 with orthostatic hypotension, 15 off and 21 on levodopa; 30 without orthostatic hypotension) had tests of reflexive cardiovagal gain (decrease in interbeat interval per unit decrease in systolic pressure during the Valsalva maneuver; orthostatic increase in heart rate per unit decrease in pressure); reflexive sympathoneural function (decrease in pressure during the Valsalva maneuver; orthostatic increment in plasma norepinephrine); and cardiac and extracardiac noradrenergic innervation (septal myocardial 6-[18F]fluorodopamine-derived radioactivity; supine plasma norepinephrine). Severity of orthostatic hypotension did not differ between the levodopa-untreated and levodopa-treated groups with Parkinson disease and orthostatic hypotension (-52+/-6 [SEM] versus -49+/-5 mm Hg systolic). The 2 groups had similarly low reflexive cardiovagal gain (0.84+/-0.23 versus 1.33+/-0.35 ms/mm Hg during Valsalva; 0.43+/-0.09 versus 0.27+/-0.06 bpm/mm Hg during orthostasis); and had similarly attenuated reflexive sympathoneural responses (97+/-29 versus 71+/-23 pg/mL during orthostasis; -82+/-10 versus -73+/-8 mm Hg during Valsalva). In patients off levodopa, plasma norepinephrine was lower in those with (193+/-19 pg/mL) than without (348+/-46 pg/mL) orthostatic hypotension. Low values for reflexive cardiovagal gain, sympathoneural responses, and noradrenergic innervation were strongly related to orthostatic hypotension. Parkinson disease with orthostatic hypotension features reflexive cardiovagal and sympathoneural failure and cardiac and partial extracardiac sympathetic denervation, independent of levodopa treatment.
authors.affiliation: Clinical Neurocardiology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892-1620, USA. goldsteind@ninds.nih.gov
authors.forename: David S
authors.initials: DS
authors.lastname: Goldstein
authors.forename: Basil A
authors.initials: BA
authors.lastname: Eldadah
authors.forename: Courtney
authors.initials: C
authors.lastname: Holmes
authors.forename: Sandra
authors.initials: S
authors.lastname: Pechnik
authors.forename: Jeffrey
authors.initials: J
authors.lastname: Moak
authors.forename: Ahmed
authors.initials: A
authors.lastname: Saleem
authors.forename: Yehonatan
authors.initials: Y
authors.lastname: Sharabi
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000978:Antiparkinson Agents / Q000627:therapeutic use*; D001775:Blood Circulation; D005260:Female; D006321:Heart / Q000503:physiopathology; D006801:Humans; D007024:Hypotension, Orthostatic / Q000097:blood / Q000209:etiology*; D007980:Levodopa / Q000627:therapeutic use*; D008297:Male; D008875:Middle Aged; D009638:Norepinephrine / Q000097:blood; D010300:Parkinson Disease / Q000150:complications / Q000188:drug therapy / Q000503:physiopathology*; D012018:Reflex; D013564:Sympathetic Nervous System / Q000098:blood supply*; D014630:Vagus Nerve / Q000503:physiopathology; D014636:Valsalva Maneuver
chemical_list: D000978:Antiparkinson Agents; D007980:Levodopa; D009638:Norepinephrine