The Experts below are selected from a list of 342144 Experts worldwide ranked by ideXlab platform

Katie Kingwell - One of the best experts on this subject based on the ideXlab platform.

David S Goldstein - One of the best experts on this subject based on the ideXlab platform.

  • catechols in post mortem brain of patients with Parkinson Disease
    European Journal of Neurology, 2011
    Co-Authors: David S Goldstein, Patti Sullivan, Courtney Holmes, Irwin J Kopin, M J Basile, Deborah C Mash
    Abstract:

    Background: Dihydroxyphenylacetaldehyde (DOPAL), a cytotoxic metabolite of dopamine, is the focus of the catecholaldehyde hypothesis about the pathogenesis of Parkinson Disease. This study explored whether DOPAL is detectable in human striatum – especially in the putamen (Pu), the main site of dopamine depletion in Parkinson Disease – and is related to other neurochemical indices of catecholamine stores and metabolism in Parkinson Disease. Methods: Putamen, caudate (Cd), and frontal cortex (Ctx) catechols were measured in tissue from patients with pathologically proven end-stage Parkinson Disease (N = 15) and control subjects (N = 14) of similar age with similar post-mortem intervals. Results: Putamen DOPAL (3% of dopamine in controls) correlated with dopamine and dihydroxyphenylacetic acid both across all subjects and within the Parkinson Disease and control groups. Pu dopamine was decreased by 93% and dihydroxyphenylacetic acid 95% in Parkinson Disease vs. controls, with smaller decreases of DOPAL (83%) and norepinephrine (73%) in Pu and of dopamine (74%) and dihydroxyphenylacetic acid (82%) in Cd. In Parkinson Disease, Pu DOPAL:dihydroxyphenylacetic acid averaged 3.4 times and DOPAL:dopamine 4.4 times control (P = 0.03 each). The main catecholamine in Ctx was norepinephrine, which was decreased by 51% in Parkinson Disease patients. Conclusions: Correlated decreases of DOPAL, dopamine, and dihydroxyphenylacetic acid in Parkinson Disease reflect severe loss of Pu dopamine stores, which seems more extensive than loss of Pu norepinephrine or Cd dopamine stores. Increased Pu DOPAL:dihydroxyphenylacetic acid ratios in Parkinson Disease suggest decreased detoxification of DOPAL by aldehyde dehydrogenase. Elevated levels of cytosolic DOPAL might contribute to loss of dopaminergic neurons in Parkinson Disease.

  • cardiac sympathetic denervation preceding motor signs in Parkinson Disease
    Cleveland Clinic Journal of Medicine, 2009
    Co-Authors: David S Goldstein, Ahmed Saleem, Yehonatan Sharabi, Barbara I Karp, Oladi Bentho, Karel Pacak, Graeme Eisenhofer
    Abstract:

    There is substantial interest in identifying biomarkers to detect early Parkinson Disease (PD). Cardiac noradrenergic denervation and attenuated baroreflex-cardiovagal function occur in de novo PD, but whether these abnormalities can precede PD has been unknown. Here we report the case of a patient who had profoundly decreased left ventricular myocardial 6-[18F]fluorodopamine-derived radioactivity and low baroreflex-cardiovagal gain, 4 years before the onset of symptoms and signs of PD. The results lead us to hypothesize that cardiac noradrenergic denervation and decreased baroreflex-cardiovagal function may occur early in the pathogenesis of PD.

  • neurocirculatory abnormalities in Parkinson Disease with orthostatic hypotension independence from levodopa treatment
    Hypertension, 2005
    Co-Authors: David S Goldstein, C Holmes, Basil A Eldadah, Sandra Pechnik, Jeffrey Moak, Ahmed Saleem, Yehonatan Sharabi
    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 F]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.

Michaela Mathews - One of the best experts on this subject based on the ideXlab platform.

  • Treatment of Visual Disorders in Parkinson Disease
    Current Treatment Options in Neurology, 2018
    Co-Authors: Joseph Savitt, Michaela Mathews
    Abstract:

    Purpose of review This article discusses visual disorders in both Parkinson Disease (PD) and other Parkinsonian disorders. It is organized largely by the anatomical site of pathology and emphasizes practical treatments. Targeted treatment options include medications, surgery, occupational, and physical therapies as well as optical aids. Recent findings The causes of visual complaints in Parkinson Disease and other similar disorders are being more clearly identified. A new medication approved specifically to treat hallucinations in PD now is available. There is increased understanding of the important role that an ophthalmologist can play in the care of these patients. Finally, research and therapeutic development are unmet needs in accessing and treating visual complaints in PD and Parkinsonian disorders. Summary A better understanding of Parkinson-related visual complaints and of available treatment options is important to optimize patient safety and quality of life. Vision impairment leads to difficulties in many common activities including reading, ambulating, and driving. Falls and injuries, made more likely because of impaired vision, result in an early loss of independence. Awareness of the problem, patient education, ophthalmologic care, selected therapeutics, physical therapy, and occupational therapy are crucial to maximizing quality of life in these patients.

A. E. Lang - One of the best experts on this subject based on the ideXlab platform.

  • pharmacological treatment of Parkinson Disease a review
    JAMA, 2014
    Co-Authors: Barbara S Connolly, A. E. Lang
    Abstract:

    Importance Parkinson Disease is the second most common neurodegenerative Disease worldwide. Although no available therapies alter the underlying neurodegenerative process, symptomatic therapies can improve patient quality of life. Objective To provide an evidence-based review of the initial pharmacological management of the classic motor symptoms of Parkinson Disease; describe management of medication-related motor complications (such as motor fluctuations and dyskinesia), and other medication adverse effects (nausea, psychosis, and impulse control disorders and related behaviors); and discuss the management of selected nonmotor symptoms of Parkinson Disease, including rapid eye movement sleep behavior disorder, cognitive impairment, depression, orthostatic hypotension, and sialorrhea. Evidence Review References were identified using searches of PubMed between January 1985 and February 2014 for English-language human studies and the full database of the Cochrane Library. The classification of studies by quality (classes I-IV) was assessed using the levels of evidence guidelines from the American Academy of Neurology and the highest-quality data for each topic. Results Although levodopa is the most effective medication available for treating the motor symptoms of Parkinson Disease, in certain instances (eg, mild symptoms, tremor as the only or most prominent symptom, aged Conclusions and Relevance Strong evidence supports using levodopa and dopamine agonists for motor symptoms at all stages of Parkinson Disease. Dopamine agonists and drugs that block dopamine metabolism are effective for motor fluctuations and clozapine is effective for hallucinations. Cholinesterase inhibitors may improve symptoms of dementia and antidepressants and pramipexole may improve depression. Evidence supporting other therapies for motor and nonmotor features is less well established.

  • Pharmacological treatment of Parkinson Disease: a review.
    2014
    Co-Authors: Barbara S Connolly, A. E. Lang
    Abstract:

    IMPORTANCE: Parkinson Disease is the second most common neurodegenerative Disease worldwide. Although no available therapies alter the underlying neurodegenerative process, symptomatic therapies can improve patient quality of life. OBJECTIVE: To provide an evidence-based review of the initial pharmacological management of the classic motor symptoms of Parkinson Disease; describe management of medication-related motor complications (such as motor fluctuations and dyskinesia), and other medication adverse effects (nausea, psychosis, and impulse control disorders and related behaviors); and discuss the management of selected nonmotor symptoms of Parkinson Disease, including rapid eye movement sleep behavior disorder, cognitive impairment, depression, orthostatic hypotension, and sialorrhea. EVIDENCE REVIEW: References were identified using searches of PubMed between January 1985 and February 2014 for English-language human studies and the full database of the Cochrane Library. The classification of studies by quality (classes I-IV) was assessed using the levels of evidence guidelines from the American Academy of Neurology and the highest-quality data for each topic. RESULTS: Although levodopa is the most effective medication available for treating the motor symptoms of Parkinson Disease, in certain instances (eg, mild symptoms, tremor as the only or most prominent symptom, aged

Yehonatan Sharabi - One of the best experts on this subject based on the ideXlab platform.

  • cardiac sympathetic denervation preceding motor signs in Parkinson Disease
    Cleveland Clinic Journal of Medicine, 2009
    Co-Authors: David S Goldstein, Ahmed Saleem, Yehonatan Sharabi, Barbara I Karp, Oladi Bentho, Karel Pacak, Graeme Eisenhofer
    Abstract:

    There is substantial interest in identifying biomarkers to detect early Parkinson Disease (PD). Cardiac noradrenergic denervation and attenuated baroreflex-cardiovagal function occur in de novo PD, but whether these abnormalities can precede PD has been unknown. Here we report the case of a patient who had profoundly decreased left ventricular myocardial 6-[18F]fluorodopamine-derived radioactivity and low baroreflex-cardiovagal gain, 4 years before the onset of symptoms and signs of PD. The results lead us to hypothesize that cardiac noradrenergic denervation and decreased baroreflex-cardiovagal function may occur early in the pathogenesis of PD.

  • neurocirculatory abnormalities in Parkinson Disease with orthostatic hypotension independence from levodopa treatment
    Hypertension, 2005
    Co-Authors: David S Goldstein, C Holmes, Basil A Eldadah, Sandra Pechnik, Jeffrey Moak, Ahmed Saleem, Yehonatan Sharabi
    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 F]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.