The Action of L(-)-Dopa on Baroreflexes in Parkinsonism

Reid, John L.; Calne, D. B.; George, Charles F.; Vakil, S. D.

doi:10.1042/cs0430851

Cited by 21 publications

(14 citation statements)

References 23 publications

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“…With regard to possible iatrogenic effects of dopamine agonists, which have been shown to produce or worsen OH and cause cognitive deficits, we controlled for levodopa equivalent dosages and found no associated differences in OH severity or cognitive performance. 36,37 We also addressed potential confounds that would have otherwise affected interpretation of our neuropsychological test findings. As noted, we ensured that no participants had severe (hence distracting) symptoms during tilt, and while reliance on the subjective report has some inherent flaws, we are confident that the cognitive changes as observed in this study were not driven by state-based factors related to somatic stress.…”

Section: Memory the Consortium To Establish A Registry Formentioning

confidence: 99%

Effects of orthostatic hypotension on cognition in Parkinson disease

et al. 2017

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Objective: To investigate the relation between orthostatic hypotension (OH) and posturemediated cognitive impairment in Parkinson disease (PD) using a cross-sectional and withingroup design.Methods: Individuals without dementia with idiopathic PD included 18 with OH (PDOH) and 19 without OH; 18 control participants were also included. Neuropsychological tests were conducted in supine and upright-tilted positions. Blood pressure was assessed in each posture. Results:The PD groups performed similarly while supine, demonstrating executive dysfunction in sustained attention and response inhibition, and reduced semantic fluency and verbal memory (encoding and retention). Upright posture exacerbated and broadened these deficits in the PDOH group to include phonemic fluency, psychomotor speed, and auditory working memory. When group-specific supine scores were used as baseline anchors, both PD groups showed cognitive changes following tilt, with the PDOH group exhibiting a wider range of deficits in executive function and memory as well as significant changes in visuospatial function. Conclusions:Cognitive deficits in PD have been widely reported with assessments performed in the supine position, as seen in both our PD groups. Here we demonstrated that those with PDOH had transient, posture-mediated changes in excess of those found in PD without OH. These observed changes suggest an acute, reversible effect. Understanding the effects of OH due to autonomic failure on cognition is desirable, particularly as neuroimaging and clinical assessments collect data only in the supine or seated positions. Identification of a distinct neuropsychological profile in PD with OH has quality of life implications, and OH presents itself as a possible target for intervention in cognitive disturbance. Orthostatic hypotension (OH) is among the most commonly reported nonmotor manifestations in persons with Parkinson disease (PD), with prevalence as high as 53%.1 Symptoms include lightheadedness, fatigue, neck pain, presyncope, and syncope.2,3 The causes can include both CNS and peripheral nervous system degeneration.4 Dopamine replacement therapies have been implicated as well. 5OH is associated with cognitive impairment. Even when controlling for systolic blood pressure (SBP), both elderly and younger individuals with OH show relative deficits in verbal memory and sustained attention, both of which are predictors of subsequent cognitive decline that is greater than would be expected in the context of normal aging. 6Idiopathic PD is itself associated with cognitive deficits. Historically, these were thought to be limited to psychomotor/information processing speeds and caused by disease-specific subcortical pathologies.7 However, deficits across executive functions are present, even in cases without

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Section: Memory the Consortium To Establish A Registry Formentioning

confidence: 99%

Effects of orthostatic hypotension on cognition in Parkinson disease

et al. 2017

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“…6,7 Reflexive cardiovagal gain has been reported to be variably decreased in PD 8,9 and markedly decreased in PDϩOH. 10 Levodopa treatment of PD can affect reflexive cardiovagal function, 11 and decreased reflexive cardiovagal gain is more prominent in patients with long-standing PD, 12 who would be expected to be on levodopa. This study explored whether levodopa treatment is related to abnormal neurocirculatory function in PDϩOH.…”

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confidence: 99%

Neurocirculatory Abnormalities in Parkinson Disease With Orthostatic Hypotension

et al. 2005

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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-͓ 18 F͔fluorodopamine-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 (Ϫ52Ϯ6 ͓SEM͔ versus Ϫ49Ϯ5 mm Hg systolic). The 2 groups had similarly low reflexive cardiovagal gain (0.84Ϯ0.23 versus 1.33Ϯ0.35 ms/mm Hg during Valsalva; 0.43Ϯ0.09 versus 0.27Ϯ0.06 bpm/mm Hg during orthostasis); and had similarly attenuated reflexive sympathoneural responses (97Ϯ29 versus 71Ϯ23 pg/mL during orthostasis; Ϫ82Ϯ10 versus Ϫ73Ϯ8 mm Hg during Valsalva). In patients off levodopa, plasma norepinephrine was lower in those with (193Ϯ19 pg/mL) than without (348Ϯ46 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. Key Words: hypotension Ⅲ sympathetic nervous system Ⅲ norepinephrine Ⅲ baroreflex P rimary chronic autonomic failure syndromes have been classified clinically in 3 forms: pure autonomic failure (PAF), multiple system atrophy (MSA), and Parkinson disease (PD) with autonomic failure. 1 All 3 forms feature neurogenic orthostatic hypotension (OH), supine hypertension, 2,3 and attenuation of the orthostatic increase in the plasma level of norepinephrine (NE), the sympathetic neurotransmitter. 4,5 Levodopa is a precursor of dopamine and therefore of NE. In the treatment of PD, levodopa is usually combined with an inhibitor of L-aromatic-acid-decarboxylase, such as carbidopa, which does not penetrate the blood-brain barrier. Combined levodopa/carbidopa treatment therefore augments delivery of levodopa to the brain and mitigates nausea and vomiting thought to result from occupation of dopamine receptors outside the blood-brain barrier. Combined levodopa/carbidopa treatment attenuates but does not prevent catecholamine synthesis from levodopa outside the brain. 6,7 Reflexive cardiovagal gain has been reported to be variably decreased in PD 8,9 and markedly decreased in PDϩOH. 10 Levodopa treatment of PD can affect reflexive cardiov...

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“…The atrial tachyarrhythmia spontaneously reverted to sinus rhythm within 24 h after stopping bromocriptine. There has been no clinical or electrocardi6graphic (Reid et al, 1972). Animal investigations suggest that levodopa exerts its central hypotensive effect through formation of noradrenaline which interacts with noradrenergic receptors similar to \unable alpha-adrenoceptors (Henning & Rubenson, 1970).…”

Section: Resultsmentioning

confidence: 99%

The Cardiovascular Effects of Bromocriptine in Parkinsonism

Greenacre¹,

Teychenne

Petrie³

et al. 1976

Brit J Clinical Pharma

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1 The cardiovascular effects of bromocriptine, a dopamine receptor agonist, were investigated in twenty-eight Parkinsonian patients. 2 Bromocriptine caused a significant impairment of postural compensation with a fall in systolic pressure and an absence of the rise in diastolic pressure after standing for 1 min when patients taking active drug were compared to the same patients on placebo. The hypotensive effect persisted for at least 6 weeks of treatment. There was also a significant reduction in supine heart rate. 3 One patient had marked falls in supine and erect blood pressure after a single oral dose of bromocriptine (2.5 mg) and a further patient developed paroxysmal atrial tachyarrhythmias. Both blood pressure and heart rate changes reversed spontaneously after stopping bromocriptine. 4 It is proposed that dopaminergic mechanisms either in the central nervous system or the periphery contribute to cardiovascular regulation in man.

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The Action of L(-)-Dopa on Baroreflexes in Parkinsonism

Cited by 21 publications

References 23 publications

Effects of orthostatic hypotension on cognition in Parkinson disease

Effects of orthostatic hypotension on cognition in Parkinson disease

Neurocirculatory Abnormalities in Parkinson Disease With Orthostatic Hypotension

The Cardiovascular Effects of Bromocriptine in Parkinsonism

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