Autonomic dysfunctions in idiopathic Parkinson's disease

Jost, Wolfgang H.

doi:10.1007/s00415-003-1105-z

Cited by 80 publications

(78 citation statements)

References 11 publications

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“…The estimated prevalence of autonomic dysfunction in PD ranges between 14% and 80%. 754 A recent study of 123 patients with PD and 96 agematched controls using a newly validated nonmotor questionnaire for PD (NMSQuest) reported that autonomic symptoms were significantly more common in all stages of the disease than in controls. 343 Another study evaluated autonomic symptoms in patients with PD using the SCOPA-AUT, and found that autonomic symptoms were more common in patients with PD than controls and increased in association with increasing age, disease severity, and medication use.…”

Section: Impulse Dyscontrol and Dopamine Dysregulation Disordersmentioning

confidence: 99%

“…Autonomic dysfunction, including constipation, nocturia, and orthostatic hypotension, can be disabling for some patients with PD and have a significant effect on their quality of life. 754 Autonomic dysfunction in PD is attributed to pathologic involvement of central and peripheral autonomic neurons. The ventrolateral medulla, nucleus tractus solitarius, periaqueductal gray matter in the midbrain, descending sympathetic and parasympathetic pathways, and peripheral autonomic neurons and ganglia have all been reported to have Lewy bodies and to be involved in the PD neurodegenerative process.…”

Section: Impulse Dyscontrol and Dopamine Dysregulation Disordersmentioning

confidence: 99%

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The scientific and clinical basis for the treatment of Parkinson disease (2009)

Olanow¹,

Stern²,

Sethi³

2009

Neurology

771

658

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Parkinson disease (PD) is an age-related neurodegenerative disorder that affects as many as 1-2% of persons aged 60 years and older. With the aging of the population, the frequency of PD is expected to increase dramatically in the coming decades. Current therapy is largely based on a dopamine replacement strategy, primarily using the dopamine precursor levodopa. However, chronic treatment is associated with the development of motor complications, and the disease is inexorably progressive. Further, advancing disease is associated with the emergence of features such as freezing, falling, and dementia which are not adequately controlled with dopaminergic therapies. Indeed, it is now appreciated that these nondopaminergic features are common and the major source of disability for patients with advanced disease. Many different therapeutic agents and treatment strategies have been evaluated over the past several years to try and address these unmet medical needs, and many promising approaches are currently being tested in the laboratory and in the clinic. As a result, there are now many new therapies and strategic approaches available for the treatment of the different stages of PD, with which the treating physician must be familiar in order to provide patients with optimal care. This monograph provides an overview of the management of PD patients, with an emphasis on pathophysiology, and the results of recent clinical trials. It is intended to provide physicians with an understanding of the different treatment options that are available for managing the different stages of the disease and the scientific rationale of the different approaches. 1 PD is the second most common neurodegenerative disorder, with an average age at onset of about 60 years. An estimated 5 million people throughout the world have PD, with 1 million individuals each in the United States and in Europe with the disorder. PD affects approximately 0.3% of the population and 1% to 2% of those older than 60 years.2 With the aging of the population and the substantial increase in the number of at-risk individuals older than 60 years, it is anticipated that the prevalence of PD will increase dramatically in the coming decades.

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Section: Impulse Dyscontrol and Dopamine Dysregulation Disordersmentioning

confidence: 99%

Section: Impulse Dyscontrol and Dopamine Dysregulation Disordersmentioning

confidence: 99%

The scientific and clinical basis for the treatment of Parkinson disease (2009)

Olanow¹,

Stern²,

Sethi³

2009

Neurology

771

658

View full text Add to dashboard Cite

show abstract

“…For example, disturbances of gastrointestinal function observed in those patients, such as constipation and delayed gastric emptying, detract immensely from www.fhc.viamedica.pl quality of life, even though do not pose an imminent life-threatening situation. Epidemiological evidence has shown that gut dysfunctions even predate well-defined motor symptoms [4][5][6][7]. Braak et al proposed that the pathological staging of the disease should be directly linked to its clinical progression.…”

Section: Introductionmentioning

confidence: 99%

Neuropathic alterations of the myenteric plexus neurons following subacute intraperitoneal administration of salsolinol

Kurnik

Gil

Gajda

et al. 2015

Folia Histochem Cytobiol.

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Introduction. Impairment of the enteric nervous system has been suggested to occur within the pathogenesis of neurodegenerative diseases. Thus, in the current study, we consider salsolinol (1-methyl-6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline, SAL) as a substance that can potentially induce myenteric neurodegeneration. Material and methods. Male Wistar rats were subjected to continuous intraperitoneal dosing of salsolinol (200 mg/kg in total) with osmotic mini-pumps for either two or four weeks. An equivalent group of rats served as the control. Jejunal myenteric neurons were subjected to immunofluorescence staining to detect neuron specific protein -protein gene product (pan-neuronal marker, PGP 9.5), nitric oxide synthase (NOS), choline acetyltransferase (ChAT), Bax-protein and alpha-synuclein. In search of any functional impairment within the gastrointestinal tract, gut motility was assessed by determining the residual solid food contents in the stomach and the small and large intestine transit. Results. The myenteric neuron count, the mean size of the neuron body, the area of ganglia and the diameter of nerve strands were decreased in both of the salsolinol-treated groups compared with the controls. The number of NOS-positive cells was lower in the salsolinol-treated groups, while the number of ChAT-positive cells remained unchanged in comparison with the controls. Neurons expressing the pro-apoptotic Bax protein and alpha-synuclein deposits were observed among the myenteric neurons of the salsolinol-treated rats. Conclusions. Salsolinol evokes enteric neuronal cell death via initiation of apoptosis and leads to the formation of pathological aggregates of alpha-synuclein. Impairment of myenteric neurons, mainly the inhibitory motor neurons, might be responsible for the abnormal intestinal transit. Thus, salsolinol might be regarded as a suitable compound for inducing experimental enteric neurodegeneration in rats.

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“…Распространенность вегетативных нарушений у пациентов с БП варьирует от 14 до 80% в зависимо-сти от стадии заболевания [89]. При ортостатиче-ской и постпрандиальной гипотензии помимо наи-более частых жалоб на рассеянность внимания, не-четкость зрения, головокружение, обмороки и пред-обморочные состояния пациенты также могут предъявлять жалобы на ДС [90].…”

Section: дс как маска ортостатической и постпрандиальной гипотензииunclassified

Heterogeneity of excessive daytime sleepiness in Parkinson’s disease

2016

Z. nevrol. psikhiatr. im. S.S. Korsakova

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Autonomic dysfunctions in idiopathic Parkinson's disease

Cited by 80 publications

References 11 publications

The scientific and clinical basis for the treatment of Parkinson disease (2009)

The scientific and clinical basis for the treatment of Parkinson disease (2009)

Neuropathic alterations of the myenteric plexus neurons following subacute intraperitoneal administration of salsolinol

Heterogeneity of excessive daytime sleepiness in Parkinson’s disease

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