Relevant bibliographies by topics / Parkinson's disease

Academic literature on the topic 'Parkinson's disease'

Author: Grafiati
Published: 4 June 2021
Last updated: 30 July 2024

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Contents

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Parkinson's disease.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Journal articles on the topic "Parkinson's disease"

1

Búřil, Jiří, Petra Búřilová, Andrea Pokorná, Ingrid Kováčová, and Marek Baláž. "Representation of Parkinson's disease and atypical Parkinson's syndromes in the Czech Republic—A nationwide retrospective study." PLOS ONE 16, no. 2 (February 2, 2021): e0246342. http://dx.doi.org/10.1371/journal.pone.0246342.

Full text
Abstract:
Background Parkinson's disease is a progressive neurodegenerative disease which causes health problem that affects more patients in the past few years. To be able to offer appropriate care, epidemiological analyses are crucial at the national level and its comparison with the international situation. Aim The demographic description of reported patients with parkinsonism (including Parkinson's disease and atypical parkinsonian syndromes) according to the International Classification of Diseases (ICD-10) from the national health registries. Methods Retrospective analysis of data available from the National Health Information System–NHIS and the National Registry of Reimbursed Health Services (NRRHS). Analyzed epidemiological data are intending to determine the regional and specific prevalence of Parkinsonism in the Czech Republic. The International Classification of Diseases diagnoses (ICD-10) of G20 (Parkinson’s disease—PD) and G23.1, G23.2, G23.3 (other degenerative disorders of basal ganglia), and G31.8 (another degenerative disease of basal ganglia) from the period of 2012 to 2018 were included into the analysis. Results We identified 78 453 unique patients from national registries in the period 2012 to 2018. Diagnoses of G20, G23.1, G23.2, and G31.8 were registered as the principal diagnoses in 76.6% of all individual patients. Conclusion We have found a growing number of patients coded with ICD-10 of dg. G20, G23.1, G23.2, G23.3, or G31.8 (N = 27 891 in 2012, and N = 30 612 in 2018). We have proven regional differences in the prevalence of Parkinson´s diagnoses. Therefore we assume most likely also differences in the care of patients with PD based on the availability of specialty care centers.
APA, Harvard, Vancouver, ISO, and other styles
2

Alonso, Ma Elisa, Enrique Otero, Rosalinda D'Regules, and Hector Hugo Figueroa. "Parkinson's Disease: A Genetic Study." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 13, no. 3 (August 1986): 248–51. http://dx.doi.org/10.1017/s0317167100036362.

Full text
Abstract:
ABSTRACT:A sample of 122 patients with Parkinson's Disease was studied for the purpose of investigating if the frequency of relatives affected with Parkinson in this group was higher than in a control group and to see if the genetic load was more important in some of the subtypes of Parkinson described by Barbeau and Pourcher (1982).7 In our 122 patients, we found that 1.7% were post-encephalic parkinsonian, 12.3% were symptomatic cases and 86% of the idiopathic variety. There were 16.1% early onset patients in the idiopathic group and among these we found 23.5% with a positive family history of Parkinson in the first-degree relatives. In 6 cases with the tremor onset form of the disease, the family history was positive and 5 patients, 4.7% had familial essential tremor-related Parkinsonism. Our results support Barbeau's hypothesis7.19 that Parkinson is a heterogeneous disease in which some subtypes (such as early onset Parkinson) have an important genetic subceptibility component.
APA, Harvard, Vancouver, ISO, and other styles
3

Blonder, Lee X., and John T. Slevin. "Emotional Dysfunction in Parkinson’s Disease." Behavioural Neurology 24, no. 3 (2011): 201–17. http://dx.doi.org/10.1155/2011/143857.

Full text
Abstract:
In addition to motor symptomatology, idiopathic Parkinson’s disease is characterized by emotional dysfunction. Depression affects some 30 to 40 percent of Parkinson patients and other psychiatric co-morbidities include anxiety and apathy. Neuropsychological and neuroimaging studies of emotional dysfunction in Parkinson patients suggest abnormalities involving mesolimbic and mesocortical dopaminergic pathways. There is also evidence suggesting that the interaction between serotonin and dopamine systems is important in the understanding and treatment of mood disorders in Parkinson’s disease. In this review we discuss the neuropsychiatric abnormalities that accompany Parkinson's disease and describe their neuropsychological, neuropharmacologic, and neuroimaging concomitants.
APA, Harvard, Vancouver, ISO, and other styles
4

Hayes, Michael T. "Parkinson's Disease and Parkinsonism." American Journal of Medicine 132, no. 7 (July 2019): 802–7. http://dx.doi.org/10.1016/j.amjmed.2019.03.001.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Agid, Y. "Parkinson's disease or Parkinson's diseases?" Biomedicine & Pharmacotherapy 53, no. 7 (August 1999): 301–2. http://dx.doi.org/10.1016/s0753-3322(00)88499-1.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Ellis, Harold. "James Parkinson: Parkinson's Disease." Journal of Perioperative Practice 23, no. 11 (November 2013): 262–63. http://dx.doi.org/10.1177/175045891302301106.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Taggart, Chris, and Chantal Simon. "Parkinson's Disease." InnovAiT: Education and inspiration for general practice 2, no. 4 (April 2009): 222–28. http://dx.doi.org/10.1093/innovait/inn164.

Full text
Abstract:
James Parkinson was born in Hoxton Square, London, in 1755. His most important medical work was ‘An Essay on the Shaking Palsy’ (1817). In this short essay, Parkinson gave the classic, albeit in modern terms limited, clinical description of the illness later termed ‘Parkinson's disease’: ‘Involuntary tremulous motion, with lessened muscular power, in parts not in action and even when supported; with a propensity to bend the trunk forwards, and to pass from a walking to a running pace: the senses and intellect being uninjured’.
APA, Harvard, Vancouver, ISO, and other styles
8

Whitlock, F. A. "The Psychiatric Complications of Parkinson's Disease." Australian & New Zealand Journal of Psychiatry 20, no. 2 (June 1986): 114–21. http://dx.doi.org/10.3109/00048678609161325.

Full text
Abstract:
Although James Parkinson in 1817 excluded mental symptoms from his original description of paralysis agitans, it has become clear that a wide range of psychiatric disorders can develop in patients with this disease. The principal conditions of dementia, depression and confusional syndromes, many of which are precipitated by drugs used in the treatment of parkinsonism, are reviewed. Particular attention is given to the frequency of dementia and its likely pathogenesis, to the nature of depression in Parkinson's disease and to the effects of different drugs, notably levodopa. A number of rare disorders characterised by parkinsonian and psychiatric symptoms are also discussed.
APA, Harvard, Vancouver, ISO, and other styles
9

Dickson, D. W. "Parkinson's Disease and Parkinsonism: Neuropathology." Cold Spring Harbor Perspectives in Medicine 2, no. 8 (June 20, 2012): a009258. http://dx.doi.org/10.1101/cshperspect.a009258.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Nicita-Mauro, V., G. Basile, A. Mento, A. Epifanio, G. Martino, and L. Morgante. "Parkinson's disease, Parkinsonism and aging." Archives of Gerontology and Geriatrics 35 (January 2002): 225–38. http://dx.doi.org/10.1016/s0167-4943(02)00138-3.

Full text
APA, Harvard, Vancouver, ISO, and other styles
More sources

Dissertations / Theses on the topic "Parkinson's disease"

1

Archibald, Neil Kenneth. "Visual symptoms in Parkinson's disease and Parkinson's disease dementia." Thesis, University of Newcastle Upon Tyne, 2011. http://hdl.handle.net/10443/1177.

Full text
Abstract:
Non-motor symptoms such as dementia and visual hallucinations are key determinants of long-term outcome and quality of life in Parkinson’s disease (PD). Attempting to understand these issues better was the motivation behind this thesis. A major aim of the study was to characterise the visual symptoms experienced by patients with PD and PD dementia, focussing not just on complex visual hallucinations, whose prognostic implications are already well-described, but also on a range of other visual symptoms including illusory misperceptions, sensations of passage and presence and double vision. A major objective was to define key measures of visual exploration strategy during visuocognitive assessment and examine the link between strategy, cognition and visual and motor symptoms. We also set out to examine the utility of retina-specific visual assessment techniques to define the potential role of retinal dysfunction in visual impairment and symptomatology. A major finding of this study was that not all visual symptoms share a common pathophysiological basis. Our results argue in favour of splitting hallucinations into separate phenomenological groups in order to better define causation and predictive value in future longitudinal studies. In addition, exploration strategy on a variety of visual tasks was demonstrated to be significantly less efficient in subjects with perceptual difficulties, providing insight into the interaction between cognition and eye movements in PD. Retinal structure, as assessed by optical coherence tomography, was not significantly altered in PD and our results would caution against the use of this technique as a disease biomarker until more is known about the limitations of this method. Finally, our neurophysiological assessment hints at the retina as the site of diminished visual acuity in PD despite there being no striking differences in central and peripheral retinal responses between control and PD subjects.
APA, Harvard, Vancouver, ISO, and other styles
2

Quinn, Niall. "Young onset of Parkinson's disease and juvenile parkinsonism." Thesis, University of Cambridge, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.283845.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Ng, Khuen Yen Prince of Wales Medical Research Institute Faculty of Medicine UNSW. "Isoprenoids in Parkinson's disease." Awarded by:University of New South Wales. Prince of Wales Medical Research Institute, 2009. http://handle.unsw.edu.au/1959.4/44827.

Full text
Abstract:
Parkinson???s disease (PD) is a progressive neurodegenerative disease characterised pathologically by the selective death of the dopaminergic neurons of the substantia nigra and the appearance of abnormal inclusions in some surviving neurons. A body of evidence from epidemiological, in vitro and in vivo studies suggest that isoprenoids, a lipid family which includes cholesterol, dolichol and ubiquinone, may play a role in PD, although to date the data has been conflicting with little consensus regarding the type or direction of change in isoprenoids in PD. The current study investigated isoprenoids in PD by quantifying a range of isoprenoids in blood sera, brain homogenates and olfactory mucosa derived from PD patients and controls. Further, isoprenoid synthesis pathways were investigated by comparing the activitites and amount of the rate-limiting enzyme for isoprenoid synthesis, HMG CoA reductase, in olfactory mucosal cultures from individuals with sporadic PD and leucine-rich repeat kinase 2 (LRRK2)-PD with those from healthy individuals. Serum levels of total cholesterol, LDL cholesterol, HDL cholesterol, triglycerides and dolichol were unchanged in patients with PD compared with controls. Similarly, total tissue cholesterol was unchanged in degenerating and non-degenerating regions of the PD brain, but tissue dolichol was significantly decreased in the substantia nigra in the PD brain, possibly reflecting a change in the neuron/glia ratio in this brain region. In olfactory mucosa, a significant decrease in cellular cholesterol content was identified in patients with LRRK2-PD compared with patients with sporadic PD or controls. The reduction in cholesterol was similar in two different LRRK2 mutations but was not associated with a change in either the amount or activity of HMG CoA reductase. This study suggests that decreased cholesterol is associated with LRRK2-PD but not with sporadic PD. As cholesterol levels in cells with different LRRK2 mutations were reduced to a similar extent, it is suggested that mutations in this gene result in a loss-of-function of LRRK2 protein. Further it suggests a role for LRRK2 in cholesterol homeostasis independent of HMG-CoA reductase-associated pathways. Recent data has suggested a functional role of LRRK2 in autophagy, a mechanism which may explain the reduction in cholesterol observed in LRRK2-PD.
APA, Harvard, Vancouver, ISO, and other styles
4

Silveira, Moriyama L. "Olfaction in Parkinson's Disease." Thesis, University College London (University of London), 2009. http://discovery.ucl.ac.uk/18728/.

Full text
Abstract:
This thesis examines the clinical and pathological involvement of the olfactory system in Parkinson’s Disease (PD). The main aim is to investigate the practical use of smell identification tests (SITs) in parkinsonism and tremor. A secondary objective is to investigate the pathological involvement of the rhinencephalon. Commercially available SITs were used to differentiate PD patients from control subjects in the UK, Brazil and Sri Lanka, showing SITs have combinations of sensitivity and specificity greater than 80%. Based on the data obtained a traffic light ruler was devised to determine the likelihood of a patient having PD at the time of the initial consultation. This was then used to interpret SITs in 34 patients with possible parkinsonism, showing 86.4% sensitivity and 80.0% specificity of SITs when compared to dopamine transporter imaging using single photon emission computed tomography (SPECT) as the gold-standard for detecting nigrostriatal dopamine denervation. Olfaction was shown to be severely impaired in parkinsonism related to LRRK2 mutations, moderately impaired in subjects with pure autonomic failure, multiple system atrophy and progressive supranuclear palsy (PSP) and normal in patients with essential tremor, dystonia and in subjects who had been diagnosed as having PD, but were found to have normal scans. This indicates that SITs will be more useful in differentiating PD from non-degenerative tremors than from atypical parkinsonism. Neuropathological changes were investigated in the rhinencephalon and it was demonstrated that α-synuclein accumulation in the primary olfactory cortex is heterogeneous, being more severe in the temporal subdivision of the piriform cortex. The piriform cortex had Lewy body pathology in all 10 PD cases studied, as well as in 7 control cases who presented incidental Lewy body pathology and four cases of LRRK2 related parkinsonism. The piriform cortex had abnormal tau accumulation in 6 PSP patients, suggesting tauopathy in the rhinencephalon is a possible substrate for hyposmia in PSP.
APA, Harvard, Vancouver, ISO, and other styles
5

Kass-Iliyya, Lewis. "Pain in Parkinson's disease." Thesis, University of Manchester, 2017. https://www.research.manchester.ac.uk/portal/en/theses/pain-in-parkinsons-disease(2c746ce7-5ff0-4852-9a55-851ef0f5543c).html.

Full text
Abstract:
Background: Pain is a very common symptom in Parkinson’s disease (PD). The underlying mechanism of pain in PD is poorly understood. Compared to PD, the characteristics of pain in other parkinsonian disorders such as Multiple System Atrophy (MSA) and Progressive Supranuclear Palsy (PSP) have not been studied. Musculoskeletal factors have been implicated in the generation of pain in PD. However, studies in PD have shown impaired central processing of nociceptive inputs. Recently, small fibre neuropathy has also been found to be common in PD with significantly reduced C-fibres density compared to controls. A subclass of C-fibres known as C tactile afferents (CT) mediate the pleasant sensation associated with gentle skin stroking (affective touch). CT afferents have recently been shown to have pain-inhibiting properties. These findings may implicate central sensitisation in pain generation in PD. Objectives: 1) To better understand the mechanisms of pain in PD and study the characteristics of pain in MSA and PSP compared to PD. 2) To quantify small fibre neuropathy in PD and explore its relation to pain utilising a novel diagnostic technique: corneal confocal microscopy (CCM). 3) To assess the perception of affective touch in PD and its relationship to pain. Methods: Four studies were conducted: Study 1: A cross sectional study of pain characteristics in PD, MSA and PSP. Study 2: A descriptive study of pain characteristics in a large cohort of early PD (disease duration < 3 years, n=1763). Study 3: A cross sectional study to quantify small fibre density in PD (n=26) compared to control subjects (n=26) using CCM and skin biopsies. Nerve density was correlated with non-motor symptoms in PD including pain. Study 4: A study to assess the CT-mediated perception of affective touch in PD and correlate it with clinical symptoms such as pain. Results: Study 1: Pain prevalence and intensity was significantly higher in MSA and PD compared to PSP, p < 0.05. Female sex and motor fluctuations but not motor severity were predictors for pain intensity in PD. Study 2: Pain was common in early PD (84.2%). Only a minority of PD patients (19.7%) reported that their pain improved with Levodopa therapy of their motor symptoms. Study 3: PD patients had significantly reduced small fiber nerve density on both CCM and skin biopsies compared to controls. Denervation correlated with autonomic symptoms but not with pain intensity. Study 4: Perception of pleasantness followed a linear relationship with nerve density and was abnormally enhanced in PD compared to control and correlated with pain at a very slow stroking velocity. Conclusions: Pain is common in early PD, does not respond to levodopa treatment and correlates with motor complications but not motor severity favouring central sensitisation. Pain is significantly less common in PSP compared to PD and MSA. Small fibre neuropathy does not appear to be an important cause of pain in PD but small fibre nerve density correlates with affective touch perception, which is enhanced in PD despite peripheral denervation. Corneal confocal microscopy identifies corneal denervation in PD offering a novel non-invasive way of assessing PD pathology.
APA, Harvard, Vancouver, ISO, and other styles
6

Marinus, Johan. "Clinimetrics in Parkinson's disease /." Leiden : Marinus, 2003. http://catalogue.bnf.fr/ark:/12148/cb402330919.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Valdinocci, Dario. "Exploring Mechanisms of Alpha-Synuclein Spread in Parkinson's and Atypical Parkinson's Diseases." Thesis, Griffith University, 2020. http://hdl.handle.net/10072/393604.

Full text
Abstract:
The development of neurodegenerative diseases is an ever increasing risk faced by modern society as aging populations rise globally. For complex diseases such as Alzheimer‟s Disease (AD) or Parkinson‟s Disease (PD) the prospect of finding a cure within the immediate future is unlikely. These complexities arise primarily from the interactions of the protein of interest each of the diseases, which in the case of typical and atypical PD is α-synuclein (α-syn). Thought to be involved in neuronal vesicle recycling in its monomeric α-helical state, change to a β-sheet conformation allows α-syn to misfold, creating oligomers and eventually aggregates which form the initial bedrock for inclusion bodies. One of the more fascinating features of pathological α-syn is the difference in inclusion body composition and cell type affected in typical and atypical PD variants. For instance within Multiple System Atrophy (MSA), an atypical PD variant, α-syn aggregates form Glial Cytoplasmic Inclusions (GCIs) the composition of which differs from the Lewy Bodies (LB) formed in PD, and are largely found in oligodendrocytes. Unlike neurons, oligodendrocytes normally express only minimal amounts of α-syn which does not alter even after GCIs are formed, indicating acquisition of α-syn from an external source. How oligodendrocytes acquire pathological α-syn and the mechanisms by which the protein is able to spread within the central nervous system (CNS) are topics currently with more questions than answers. Thus the primary focus of the thesis is to investigate potential models of α-syn spread in order to develop future novel targets to slow disease progression. The investigations within Chapters 2 and 3 focus on exploring microglial cells as a potential vehicle for α-syn migration within the CNS. Along with the presence of α-syn inclusion bodies, part of the degeneration taking place within MSA is due to the chronic inflammatory activation and actions of the CNS resident immune cell, the microglia. Whilst microglial inflammatory responses play a role in PD, the severity of inflammation is greater in MSA. Microglia possess many traits which contribute to their ability to become a potential transporter of α-syn, including the lack of ability to degrade internalised pathological α-syn variants such as oligomers and aggregates. Post-mortem human MSA brain tissues were examined for evidence of microglial interactions with GCI-affected oligodendrocytes. Not only were interactions between these cells noted in a variety of different tissue regions and patients, but qualitative evidence of microglial migration with internalised α-syn distal from GCI-affected cells was obtained. Whilst these findings suggest that microglia could play a potential role in α-syn spread within the CNS and α-syn occurrence within oligodendrocytes, post-mortem examination is limited to detailing what may occur following the observed interactions. An in vitro assay was developed to investigate α-syn uptake and mobilisation by cells from a point source of immobilized protein. In this assay, monomeric and aggregated α-syn uptake and migration were assessed when exposured to THP-1 monocytes and microglial-like differentiated THP-1 cells. Microglial-like differentiated THP-1 cells were found to show uptake and migration with internalised aggregate α-syn to distal regions, not observed with undifferentiated THP-1 monocytes or monomeric protein. This result indicates that microglia/microglial-like cells are more likely to internalise pathological α-syn such as aggregates than the normal, monomeric form. The greater numbers of differentiated THP-1 with internalised aggregated α-syn indicates that once the protein has been taken up by microglia, then it becomes a transported to distal brain regions. The inability of microglia to degrade aggregated α-syn, similar to microglia within the CNS, likely contributes microglial-mediated α-syn spread. Further testing using highly aggressive proliferating immortalised (HAPI) cells, a rat microglial cell line, was conducted which corroborated the previous findings, indicating that microglia take up the pathological variant of α-syn, mobilizing the protein rather than degrading it. Utilising the same α-syn mobilization assay, inhibition of microtubule instability through the use of the microtubule stabilising agent Epothilone D (EpoD) proved successful in lowering both uptake and mobilization of aggregated α-syn, showing promise as a novel therapy against α-syn spread. Inhibition of the microglial inflammatory response through TAK-242 treatment, a Toll-like Receptor 4 (TLR4) inhibitor, was also trialled to investigate if TLR4 plays a significant role with regards to α-syn uptake and mobilisation. However, unlike EpoD, TAK-242 proved ineffective. For Chapter 4 experimentation focussed on investigating the role of intercellular mitochondrial transfer through tunnelling nanotubes (TnTs) as a potential means of α-syn spread. Pathological α-syn species have been described to bind to intercellularly migrating organelles such as lysosomes for spread to adjacent sites. The role of mitochondria in typical and atypical PD has predominantly focussed on their role in degeneration and as such gaps exist as to mitochondrial function in relation to α-syn propagation. Utilising Stimulated Emission Depletion (STED) super resolution microscopy, SH-SY5Y, 1321N1 and differentiated THP-1 monocultures, as models of neurons, astrocytes and microglia, were each inoculated with aggregated α-syn to examine transfer to adjacent cells via TnTs whilst bound to mitochondria. Under each cell culture condition, the formation of TnT-like structures was observed between adjacent cells, each containing migrating mitochondria with α-syn aggregates bound to the outer mitochondrial membrane. Further exploration of this result through 1321N1 / differentiated THP-1 co-culture showed that this mechanism of α-syn spread is not limited to monoculture conditions and may be a potential mechanism relevant to typical and atypical PD. Knockdown of Miro1, a critical protein bridging mitochondria to the motor adaptor complex for intercellular migration, was performed in order to ascertain if its role is significant in the α-syn spread process and a potential therapeutic target. Miro1 silencing however proved qualitatively ineffective in the prevention of α-syn spread mediated by mitochondria, indicating other factors in addition to Miro1 may be involved in bridging mitochondria to intercellular motor complexes. Taken together these results illustrate the great complexity of mechanisms of α-syn spread and the inherent difficulties associated with attempting to combat them.
Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Medical Science
Griffith Health
Full Text
APA, Harvard, Vancouver, ISO, and other styles
8

Hillman, Anne M. "Perceived control in the everyday occupational roles of people with Parkinson's disease and their partners." Connect to full text, 2006. http://hdl.handle.net/2123/1621.

Full text
Abstract:
Thesis (Ph. D.)--University of Sydney, 2006.
Title from title screen (viewed May 1, 2007). Submitted in fulfilment of the requirements for the degree of Doctor of Philosophy to the School of Occupation and Leisure Sciences. Includes bibliographical references. Also issued in print.
APA, Harvard, Vancouver, ISO, and other styles
9

Michell, Andrew William. "Parkinson's disease : α-synuclein and disease markers." Thesis, University of Cambridge, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.613821.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Gu, Mei. "Mitochondrial function in Parkinson's disease and other neurodegenerative diseases." Thesis, University College London (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.322371.

Full text
APA, Harvard, Vancouver, ISO, and other styles
More sources

Books on the topic "Parkinson's disease"

1

Inc, ebrary, ed. Parkinson's disease. London: Manson, 2009.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
2

Mouradian, M. Maral. Parkinson's Disease. New Jersey: Humana Press, 2001. http://dx.doi.org/10.1385/1592591426.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Olanow, C. Warren, Fabrizio Stocchi, and Anthony E. Lang, eds. Parkinson's Disease. Oxford, UK: Blackwell Publishing Ltd., 2011. http://dx.doi.org/10.1002/9781444397970.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Galvez-Jimenez, Nestor, Hubert H. Fernandez, Alberto J. Espay, and Susan H. Fox, eds. Parkinson's Disease. Cambridge: Cambridge University Press, 2016. http://dx.doi.org/10.1017/cbo9781107284210.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

West, Richard. Parkinson's disease. London: Office of Health Economics, 1991.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
6

1917-, Yahr Melvin D., Bergmann Kenneth J, International Federation of Parkinson's Disease Foundations., and International Symposium on Parkinson's Disease (8th : 1985 : New York, N.Y.), eds. Parkinson's disease. New York: Raven Press, 1987.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
7

S, Ebadi Manuchair, and Pfeiffer Ronald, eds. Parkinson's disease. Boca Raton: CRC Press, 2005.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
8

Anthony, Kilmister C. A., and Parkinson's Disease Society, eds. Parkinson's disease. London: Macdonald Optima, 1991.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
9

P, Hammerstad John, and Gancher S. T, eds. Parkinson's disease. St. Louis: Mosby Year Book, 1992.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
10

P, Hammerstad John, and Gancher Stephen T, eds. Parkinson's disease. London: Edward Arnold, 1992.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
More sources

Book chapters on the topic "Parkinson's disease"

1

Tröster, Alexander I. "Parkinson's disease and parkinsonism." In APA handbook of neuropsychology, Volume 1: Neurobehavioral disorders and conditions: Accepted science and open questions (Vol. 1)., 499–528. Washington: American Psychological Association, 2023. http://dx.doi.org/10.1037/0000307-024.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Stocchi, Fabrizio, Margherita Torti, Giovanni Palleschi, and Antonio Carbone. "Bladder Dysfunction in Parkinson's Disease and Other Parkinsonism." In Parkinson's Disease, 274–83. Oxford, UK: Blackwell Publishing Ltd., 2011. http://dx.doi.org/10.1002/9781444397970.ch25.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Romero-Ramos, Marina, Matthew Maingay, and Deniz Kirik. "Parkinson's Disease." In Neuroprotection, 31–50. Weinheim, FRG: Wiley-VCH Verlag GmbH & Co. KGaA, 2005. http://dx.doi.org/10.1002/3527603867.ch2.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Truong, Daniel D., and Roongroj Bhidayasiri. "Parkinson's Disease." In International Neurology, 159–65. Oxford, UK: Wiley-Blackwell, 2010. http://dx.doi.org/10.1002/9781444317008.ch43.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Jellinger, Kurt A. "Parkinson's Disease." In Neurodegeneration: The Molecular Pathology of Dementia and Movement Disorders, 194–223. Oxford, UK: Wiley-Blackwell, 2011. http://dx.doi.org/10.1002/9781444341256.ch21.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Truong, Daniel, and Roongroj Bhidayasiri. "Parkinson's disease." In International Neurology, 188–96. Chichester, UK: John Wiley & Sons, Ltd, 2016. http://dx.doi.org/10.1002/9781118777329.ch50.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Berg, D., R. Krüger, O. Rieß, and P. Riederer. "Parkinson's Disease." In Handbook of Neurochemistry and Molecular Neurobiology, 1–19. Boston, MA: Springer US, 2007. http://dx.doi.org/10.1007/978-0-387-30377-2_1.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Belmin, Joël. "Parkinson's Disease." In Pathy's Principles and Practice of Geriatric Medicine, 731–37. Chichester, UK: John Wiley & Sons, Ltd, 2012. http://dx.doi.org/10.1002/9781119952930.ch63.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Coelho, Miguel, Joaquim Ferreira, and Cristina Sampaio. "Parkinson's Disease." In Evidence-based Neurology: Management of Neurological Disorders, 199–220. Oxford, UK: Blackwell Publishing Ltd, 2007. http://dx.doi.org/10.1002/9780470988350.ch20.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Hughes, Graham R. V. "Parkinson's Disease……" In Understanding Hughes Syndrome, 28. London: Springer London, 2009. http://dx.doi.org/10.1007/978-1-84800-376-7_15.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Conference papers on the topic "Parkinson's disease"

1

Thomas, Jerry K., and R. Syama. "Comparison Study of Different Classifiers for Detecting Parkinson Disease using Machine Learning Language." In 2nd International Conference on Modern Trends in Engineering Technology and Management. AIJR Publisher, 2023. http://dx.doi.org/10.21467/proceedings.160.23.

Full text
Abstract:
In Parkinson's disease, dopamine-producing neurons in the brain are disrupted. Communication between brain cells is enabled by it. Dopamine is responsible for the control, adaption and easiness of movements. This disease occurs mainly in aged persons, but in this current scenario Parkinson’s disease symptoms showing after age 35. So researchers try to find more ways to recognize the symptoms of Parkinson’s disease as early as possible. The purpose of this paper is to present different classifiers that use machine learning to diagnose Parkinson's disease. Here I use 3 different classifiers-SVM, KNN and XGBoost. I will build a model for all 3 classifiers and calculate their accuracy of detecting the Parkinson’s disease by giving the same dataset input. From the 3 classifiers I select the more accuracy one. This paper propose select the XGBoost classifiers to detect the Parkinson’s disease person. XGBoost gives 94.7.
APA, Harvard, Vancouver, ISO, and other styles
2

Kuosmanen, Elina, Valerii Kan, Julio Vega, Aku Visuri, Yuuki Nishiyama, Anind K. Dey, Simon Harper, and Denzil Ferreira. "Challenges of Parkinson's Disease." In MobileHCI '19: 21st International Conference on Human-Computer Interaction with Mobile Devices and Services. New York, NY, USA: ACM, 2019. http://dx.doi.org/10.1145/3338286.3340133.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Wei, Yunyue, Bingquan Zhu, Chen Hou, Chen Zhang, and Yanan Sui. "Interactive Video Acquisition and Learning System for Motor Assessment of Parkinson's Disease." In Thirtieth International Joint Conference on Artificial Intelligence {IJCAI-21}. California: International Joint Conferences on Artificial Intelligence Organization, 2021. http://dx.doi.org/10.24963/ijcai.2021/718.

Full text
Abstract:
Diagnosis and treatment for Parkinson's disease rely on the evaluation of motor functions, which is expensive and time consuming when performing at clinics. It is also difficult for patients to record correct movements at home without the guidance from experienced physicians. To help patients with Parkinson’s disease get better evaluation from in-home recorded movement videos, we developed an interactive video acquisition and learning system for clinical motor assessments. The system provides real-time guidance with multi-level body keypoint tracking and analysis to patients, which guarantees correct understanding and performing of clinical tasks. We tested its effectiveness on healthy subjects, and the efficiency and usability on patient groups. Experiments showed that our system enabled high quality video recordings following clinical standards, benefiting both patients and physicians. Our system provides a novel learning-based telemedicine approach for the care of patients with Parkinson’s disease.
APA, Harvard, Vancouver, ISO, and other styles
4

Elcin, Huseyn. "PARKINSON'S DISEASE MEDICAL REHABILITATION METHODS." In International Trends in Science and Technology. RS Global Sp. z O.O., 2021. http://dx.doi.org/10.31435/rsglobal_conf/30062021/7623.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Graca, Ricardo, Rui Sarmento e Castro, and Joao Cevada. "ParkDetect: Early diagnosing Parkinson's Disease." In 2014 IEEE International Symposium on Medical Measurements and Applications (MeMeA). IEEE, 2014. http://dx.doi.org/10.1109/memea.2014.6860027.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Torres, R., M. Huerta, R. Gonzalez, R. Clotet, J. Bermeo, and G. Vayas. "Sensors for Parkinson's disease evaluation." In 2017 International Caribbean Conference on Devices, Circuits and Systems (ICCDCS). IEEE, 2017. http://dx.doi.org/10.1109/iccdcs.2017.7959715.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Tang, Shih-Tsang, Chi-Fen Chang, Chun-Hwei Tai, Kang-Ping Lin, and Yueh-Fang Huang. "Speech Rehabilitation Platform for Parkinson's Disease." In Biomedical Engineering / Robotics Applications. Calgary,AB,Canada: ACTAPRESS, 2014. http://dx.doi.org/10.2316/p.2014.818-060.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Akbari, Shirin, Emad Fatemizadeh, and Mohammad Reza Deevband. "Functional Brain Networks in Parkinson's Disease." In 2017 24th National and 2nd International Iranian Conference on Biomedical Engineering (ICBME). IEEE, 2017. http://dx.doi.org/10.1109/icbme.2017.8430243.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Kuosmanen, Elina, Valerii Kan, Aku Visuri, Julio Vega, Yuuki Nishiyama, Anind K. Dey, Simon Harper, and Denzil Ferreira. "Mobile-based Monitoring of Parkinson's Disease." In MUM 2018: 17th International Conference on Mobile and Ubiquitous Multimedia. New York, NY, USA: ACM, 2018. http://dx.doi.org/10.1145/3282894.3289737.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Anthoniraj, S., A. Naresh Kumar, Galiveeti Hemakumar Reddy, Sadhan Gope, and More Raju. "Parkinson's Disease Detection Using Machine Learning." In 2022 International Conference on Smart and Sustainable Technologies in Energy and Power Sectors (SSTEPS). IEEE, 2022. http://dx.doi.org/10.1109/ssteps57475.2022.00070.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Reports on the topic "Parkinson's disease"

1

Singh, Ruchi, Akhiya Nail, and Nirendra Kumar Rai. Effectiveness of Vitamin B12 Supplementation on cognitive, motor & mood instability of Parkinson’s disease patients on levodopa treatment :A Systematic review. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, February 2023. http://dx.doi.org/10.37766/inplasy2023.2.0066.

Full text
Abstract:
Review question / Objective: The treatment of choice for patients of Parkinson's disease is levodopa. However, levodopa has been suggested to decrease Vit B12 level in these patients. Thus, the research question for this systematic review is whether vit B 12 supplementation in Parkinson's disease(PD) patients on treatment with levodopa improves vit B12 level effecting the Cognition, Motor functions and Mood instability among them in comparison to PD patients on levodopa treatment who are not supplemented with Vit B12. Condition being studied: Parkinson disease is the progressive degeneration of dopaminergic neurons present within the substantia nigra that can lead to altered movements along with the prevalence of cognitive and mood instability as a result of dopamine(neurotransmitter) deficiency. The most effective treatment for the Parkinson's disease is the administration of levodopa, a dopamine precursor . Long term treatment with levodopa causes an increase in homocysteine levels and tissue deficiency of vitamin B12 and folate may occur. Vitamin B12 supplementation is administered as after management regime, in Parkinson patient on levodopa treatment . This study aims to conduct a systematic review, of studies , randomized control trials investigating the ability of vitamin B12 supplementation to enhances the recovery/reduce the decline, if any, of the symptoms of cognitive, motor, mood impairments associated with Parkinson's disease patient on levodopa treatment.
APA, Harvard, Vancouver, ISO, and other styles
2

Trimble, Brian A. Alaska Native Parkinson's Disease Registry. Fort Belvoir, VA: Defense Technical Information Center, November 2008. http://dx.doi.org/10.21236/ada493391.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Katz, Edward. Biomechanical Assessment of Parkinson's Disease. Portland State University Library, January 2000. http://dx.doi.org/10.15760/etd.83.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Beal, M. F. Oxidative Damage in Parkinson's Disease. Fort Belvoir, VA: Defense Technical Information Center, January 2005. http://dx.doi.org/10.21236/ada434051.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Tanner, Caroline M. Alaska Native Parkinson's Disease Registry. Fort Belvoir, VA: Defense Technical Information Center, July 2013. http://dx.doi.org/10.21236/ada609026.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Trimble, Brian A. Alaska Native Parkinson's Disease Registry. Fort Belvoir, VA: Defense Technical Information Center, June 2011. http://dx.doi.org/10.21236/ada609150.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Trimble, Brian A. Alaska Native Parkinson's Disease Registry. Fort Belvoir, VA: Defense Technical Information Center, November 2010. http://dx.doi.org/10.21236/ada609645.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Seroogy, Kim B., and David M. Yurek. Neuregulins, Neuroprotection and Parkinson's Disease. Fort Belvoir, VA: Defense Technical Information Center, December 2002. http://dx.doi.org/10.21236/ada415998.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Beal, M. F. Oxidative Damage in Parkinson's Disease. Fort Belvoir, VA: Defense Technical Information Center, October 2001. http://dx.doi.org/10.21236/ada416957.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Trimble, Brian A. Alaska Native Parkinson's Disease Registry. Fort Belvoir, VA: Defense Technical Information Center, November 2009. http://dx.doi.org/10.21236/ada511588.

Full text
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the extended bibliographies on the topic 'Parkinson's disease' for particular source types:
Journal articles Dissertations / Theses Books
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

To the bibliography