Bibliographies thématiques / Atypical Parkinsonian Disorders

Littérature scientifique sur le sujet « Atypical Parkinsonian Disorders »

Auteur : Grafiati
Publié le 10 mars 2023

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Articles de revues sur le sujet "Atypical Parkinsonian Disorders"

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Portera-Cailliau, Carlos, et Yvette Bordelon. « Atypical Parkinsonian Disorders ». Seminars in Neurology 34, no 02 (25 juin 2014) : 119–20. http://dx.doi.org/10.1055/s-0034-1381731.

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Litvan, Irene. « ATYPICAL PARKINSONIAN DISORDERS ». CONTINUUM : Lifelong Learning in Neurology 10 (juin 2004) : 42–64. http://dx.doi.org/10.1212/01.con.0000293567.17705.8e.

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Wenning, Gregor K., et Werner Poewe. « Atypical parkinsonian disorders ». Movement Disorders 20, S12 (2005) : S1. http://dx.doi.org/10.1002/mds.20554.

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Tolosa, Eduardo, Daniela Calandrella et Marisol Gallardo. « Caribbean parkinsonism and other atypical Parkinsonian disorders ». Parkinsonism & ; Related Disorders 10 (mai 2004) : S19—S26. http://dx.doi.org/10.1016/j.parkreldis.2004.02.003.

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Raccagni, Cecilia, Jorik Nonnekes, Bastiaan R. Bloem, Marina Peball, Christian Boehme, Klaus Seppi et Gregor K. Wenning. « Gait and postural disorders in parkinsonism : a clinical approach ». Journal of Neurology 267, no 11 (22 mai 2019) : 3169–76. http://dx.doi.org/10.1007/s00415-019-09382-1.

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Abstract Disturbances of balance, gait and posture are a hallmark of parkinsonian syndromes. Recognition of these axial features can provide important and often early clues to the nature of the underlying disorder, and, therefore, help to disentangle Parkinson’s disease from vascular parkinsonism and various forms of atypical parkinsonism, including multiple system atrophy, progressive supranuclear palsy, and corticobasal syndrome. Careful assessment of axial features is also essential for initiating appropriate treatment strategies and for documenting the outcome of such interventions. In this article, we provide an overview of balance, gait and postural impairment in parkinsonian disorders, focusing on differential diagnostic aspects.
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Ollivier, M., D. Leclercq, M. O. Habert, D. Dormont, B. Law-ye, S. Lehericy et N. Pyatigorskaya. « Neuroimaging in Atypical Parkinsonian Disorders ». Neurographics 8, no 3 (1 juin 2018) : 154–66. http://dx.doi.org/10.3174/ng.1700054.

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Marsili, Luca, Matteo Bologna, Maja Kojovic, Alfredo Berardelli, Alberto J. Espay et Carlo Colosimo. « Dystonia in atypical parkinsonian disorders ». Parkinsonism & ; Related Disorders 66 (septembre 2019) : 25–33. http://dx.doi.org/10.1016/j.parkreldis.2019.07.030.

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Litvan, Irene. « Update of atypical parkinsonian disorders ». Current Opinion in Neurology 20, no 4 (août 2007) : 434–37. http://dx.doi.org/10.1097/wco.0b013e32823ecfa7.

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Bhidayasiri, Roongroj, Onanong Jitkritsadakul et Carlo Colosimo. « Nocturnal Manifestations of Atypical Parkinsonian Disorders ». Journal of Parkinson's Disease 4, no 2 (2014) : 223–36. http://dx.doi.org/10.3233/jpd-130280.

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Belvisi, Daniele, Isabella Berardelli, Antonio Suppa, Andrea Fabbrini, Massimo Pasquini, Maurizio Pompili et Giovanni Fabbrini. « Neuropsychiatric disturbances in atypical parkinsonian disorders ». Neuropsychiatric Disease and Treatment Volume 14 (octobre 2018) : 2643–56. http://dx.doi.org/10.2147/ndt.s178263.

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Thèses sur le sujet "Atypical Parkinsonian Disorders"

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Rosini, Francesca. « The role of Ocular Movement Analysis in the differential diagnosis of Atypical Parkinsonian Disorders : a study on Multiple System Atrophy, Progressive Supranuclear Palsy and Corticobasal Degeneration ». Doctoral thesis, 2019. http://hdl.handle.net/2158/1155497.

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Atypical Parkinsonian Disorders (APD) are a group of neurodegenerative diseases characterized by progressive extrapyramidal symptoms and signs, unresponsive to levo-dopa and associated with a wide range of distinctive clinical features. According to the neuropathological substrate, APD may be classified in two broad categories of pathologies related to the accumulation of abnormal aggregates of proteins: the Alpha-synucleinopathies (Multiple-System Atrophy type C and P – MSA-C and MSA-P) and the Taupathies (Progressive Supranuclear Palsy - PSP and Corticobasal Degeneration - CBD). Due to the presence of overlapping clinical features, their differential diagnosis may often be challenging. Various oculomotor abnormalities, such as saccade dysmetria, increased latency, saccadic intrusions, nystagmus and vertical gaze palsy are often described in APDs with inconstant specificity. My aim was to determine peculiar changes in oculomotor profile that may help in distinguishing these disorders. I examined the eye movements of eleven patients with MSA-C, eight with MSA-P, twelve with PSP and six with CBD. Mean age of MSA-C patients was 58 (mean disease duration 3,7 years); in MSA-P, mean age was 65 (mean disease duration 3,7 years); in PSP group, mean age was 68 (mean disease duration 2 years); in CBD group, mean age was 67 (mean disease duration 2 years). Eye movement recording was obtained through an eye-tracker device (Applied Science Laboratories, Bedford, MA, USA); the visual target was a red dot on a black screen. Horizontal (±10°and 18°) and vertical (up/down 8°) visually-guided saccades, horizontal voluntary saccades (antisaccades) and fixation task were tested and statistically compared with EVAlab’s normative data obtained by healthy controls. As for saccades. standard saccadic parameters (latency, peak velocity, duration, gain and accuracy) were evaluated; moreover, presence of multistep saccades (i.e. saccades constitutes by two or more steps to reach the tardet) was assessed. For antisaccades, number of antisaccade errors with relative corrections, latency and gain of correct antisaccades, latency and gain of prosaccades erroneously directed toward the target and latency of corrective antisaccades were determined. Finally, eventual fixation changes (saccadic intrusions, nystagmus) were evaluated. MSA-C showed slight increased latency in reflexive and voluntary eye movements, with good performance in antisaccade task (low errors rate, high corrections rate). Velocity appeared to be preserved, whereas mild hypometria, with no more than two steps to reach the target, and poor accuracy, defined the saccadic profile. They had a lower number of SWJs in respect to PSP and MSA-P groups, but exhibited diverse forms of central nystagmus. MSA-P patients showed normal latency of reflexive eye movements, and prolonged latency of voluntary, associated to moderate to high range of errors and low percentage of corrections in the antisaccades. Hypometria with high frequency of multistep saccades, characterized by two or more steps to reach the target, and normal velocity defined the dynamic profile. Fixation appeared to be interrupted by SWJs, characterized by small amplitude and high frequency similar to PSP patients, but no nystagmus. Patients with PSP showed saccade slowing both in the horizontal and, more evidently, in the vertical plane, associated with prominent saccadic hypometria with very high range of multistep saccade (usually three of four), analogously defined by slow velocity. Vertical supranuclear palsy was common, so that some patients could not be recorded in the vertical plane. Latency was prolonged in both reflexive and voluntary tasks. Very high number of errors, with equally high number of corrections, characterized the antisaccade performance. Furthermore, PSP showed the highest rate of SWJs, peculiarly characterized by large amplitude and prolonged intersaccadic latency. CBD group made hypometric saccades with high frequency of multistep with two or more steps, and presented a mild saccade slowing. No supranuclear palsy was observable. Furthermore, they showed prominent increased latency in both reflexive and voluntary tasks; they were virtually incapable to perform antisaccade task, and exhibited the highest rate of errors and a very low rate of corrections. Finally, SWJs frequency was the lowest among groups. My findings substantiate peculiar changes of saccade dynamics in APDs, related to specific neuroanatomical substrate. Slowing and fragmentation of all ocular movements is the major finding in PSP patients, due to prominent atrophy of pons and, to a lesser extent, basal ganglia involvement. Saccades are of normal velocity but inaccurate in MSA, particularly MSA-C. MSA-P patients are more hypometric (lower gain and higher number of steps) than MSA-C, suggesting a greater basal ganglia involvement in the former, and a greater cerebellar impairment in the latter, also explaining the MSA-C low accuracy (dispersion of fixation around target) and the presence of central nystagmus. Latency and voluntary saccades performance are more impaired in PSP and particularly in CBD group than both MSA, suggesting a greater cortical impairment (particularly frontal and parietal cortex) in CBD. Saccadic intrusions are mostly typical of MSA-P and PSP, but they differed for the diverse amplitude (greater in PSP than MSA-P) and the intersaccadic latency (the latency between the first and second saccade of the intrusions, greater in PSP than MSA-P). Taken together, these abnormalities may help in configuring a peculiar disease “profile”. Qualitative and quantitative oculomotor profile examination may therefore be considered as a useful tool helping in differentiating ADPs with overlapping clinical features.
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Livres sur le sujet "Atypical Parkinsonian Disorders"

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Litvan, Irene, dir. Atypical Parkinsonian Disorders. Totowa, NJ : Humana Press, 2005. http://dx.doi.org/10.1385/159259834x.

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Irene, Litvan, dir. Atypical Parkinsonian disorders. Totowa, N.J : Humana Press, 2004.

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Handbook of atypical parkinsonism. Cambridge : Cambridge University Press, 2011.

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Litvan, Irene. Atypical Parkinsonian Disorders. Humana Press Inc.,U.S., 2004.

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Colosimo, Carlo, David E. Riley et Gregor K. Wenning. Handbook of Atypical Parkinsonism. Cambridge University Press, 2011.

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Colosimo, Carlo, David E. Riley et Gregor K. Wenning. Handbook of Atypical Parkinsonism. Cambridge University Press, 2011.

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Colosimo, Carlo, David E. Riley et Gregor K. Wenning. Handbook of Atypical Parkinsonism. Cambridge University Press, 2011.

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Colosimo, Carlo, David E. Riley et Gregor K. Wenning. Handbook of Atypical Parkinsonism. Cambridge University Press, 2011.

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Litvan, Irene. Atypical Parkinsonian Disorders : Clinical and Research Aspects (Current Clinical Neurology). Humana Press, 2005.

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Politis, Marios. Imaging in Movement Disorders : Imaging in Atypical Parkinsonism and Familial Movement Disorders. Elsevier Science & Technology, 2018.

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Chapitres de livres sur le sujet "Atypical Parkinsonian Disorders"

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Duyckaerts, Charles. « Atypical Parkinsonian Disorders ». Dans Atypical Parkinsonian Disorders, 111–38. Totowa, NJ : Humana Press, 2005. http://dx.doi.org/10.1385/1-59259-834-x:111.

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Lees, Andrew. « Atypical Parkinsonism ». Dans Atypical Parkinsonian Disorders, 495–501. Totowa, NJ : Humana Press, 2005. http://dx.doi.org/10.1385/1-59259-834-x:495.

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Thomas, Madhavi, et Joseph Jankovic. « Clinical Diagnosis of Vascular Parkinsonism and Nondegenerative Atypical Parkinsonian Disorders ». Dans Atypical Parkinsonian Disorders, 393–408. Totowa, NJ : Humana Press, 2005. http://dx.doi.org/10.1385/1-59259-834-x:393.

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Litvan, Irene. « What is an Atypical Parkinsonian Disorder ? » Dans Atypical Parkinsonian Disorders, 1–9. Totowa, NJ : Humana Press, 2005. http://dx.doi.org/10.1385/1-59259-834-x:001.

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Goetz, Christopher G. « Historical Issues and Atypical Parkinsonian Disorders ». Dans Atypical Parkinsonian Disorders, 11–21. Totowa, NJ : Humana Press, 2005. http://dx.doi.org/10.1385/1-59259-834-x:011.

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Zermansky, Adam, et Yoav Ben-Shlomo. « Epidemiology of Progessive Supranuclear Palsy and Multiple System Atrophy ». Dans Atypical Parkinsonian Disorders, 23–31. Totowa, NJ : Humana Press, 2005. http://dx.doi.org/10.1385/1-59259-834-x:023.

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Mackenzie, Ian R. A. « Neuropathology of Atypical Parkinsonian Disorders ». Dans Atypical Parkinsonian Disorders, 33–63. Totowa, NJ : Humana Press, 2005. http://dx.doi.org/10.1385/1-59259-834-x:033.

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Lewis, Jada, et Michael Hutton. « Animal Models of Tauopathies ». Dans Atypical Parkinsonian Disorders, 65–76. Totowa, NJ : Humana Press, 2005. http://dx.doi.org/10.1385/1-59259-834-x:065.

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Goedert, Michel, et Maria Grazia Spillantini. « Neurodegenerative α-Synucleinopathies ». Dans Atypical Parkinsonian Disorders, 77–94. Totowa, NJ : Humana Press, 2005. http://dx.doi.org/10.1385/1-59259-834-x:077.

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Contreras-Vidal, José Luis. « Computer Modeling in Basal Ganglia Disorders ». Dans Atypical Parkinsonian Disorders, 95–109. Totowa, NJ : Humana Press, 2005. http://dx.doi.org/10.1385/1-59259-834-x:095.

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Actes de conférences sur le sujet "Atypical Parkinsonian Disorders"

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Mikael, Luana de Rezende, Coralia Gabrielle Vieira Silveira, Camilla Duarte Ribeiro, Daniel Damiani, Pedro Henrique de Lara Leite, Helton Benevides Santana de Oliveira, Danilo Donizete de Faria, Roberta Arb Saba Rodrigues Pinto et Sonia Maria Cesar de Azevedo Silva. « Fahr’s syndrome as a differential diagnosis amid parkinsonian syndromes : a case report ». Dans XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.465.

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Context: Parkinsonian syndromes are routinely identified by neurologists. However, the differential diagnosis among probable etiologies can be challenging and complex. In Fahr’s syndrome, calcifications of the basal ganglia secondary to disorders of calcium metabolism are observed. A possible clinical presentation associated with this entity is the presence of a parkinsonian syndrome. Case report: A 54-years-old female patient presented with a progressive tremor in the right upper and lower limbs associated with bradykinesia. Seizures were observed during the course of the disease. After extensive clinical workup, primary hypoparathyroidism was diagnosticated along with the recognition of a mutation in the calcium activator gene. Computed tomography and magnetic resonance imaging of the head showed bilateral coarse calcifications in thalami and basal ganglia compatible with Fahr’s syndrome. We began treatment for control of the underlying disease, as well as for symptomatic control of parkinsonism. Conclusions: Different pathologies could justify the parkinsonian syndrome observed initially in the case described. Among them: Iidiopathic Parkinson’s Disease, Multiple System Atrophy, Progressive Supranuclear Palsy. In our patient, the atypical evolution in a young woman led to the research of possible secondary treatable causes. A diagnosis of Fahr’s syndrome related to hypoparathyroidism was unveiled. The differential diagnosis of Parkinson’s Syndrome is broad and difficult. We must be aware of the possible atypical presentations due to the possibility of a secondary condition whose etiology could be effectively treated.
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Souto, Emília Correia, Carolina Maria Marin, Gustavo Carvalho Costa, Igor Braga Farias, Bruno de Mattos Lombardi Badia, Icaro França Navarro Pinto, Roberta Ismael Lacerda Machado, Paulo Victor Sgobbi de Souza, Wladimir Bocca Vieira de Rezende Pinto et Acary Souza Bulle Oliveira. « Family with atypical Parkinsonism due to CHCHD10 gene mutation ». Dans XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.502.

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Introduction: Parkinson’s disease - PD is the second most common agerelated neurodegenerative disorder. Characterized by a variety of motor and non-motor symptoms that relate to the loss of dopaminergic neurons in the midbrain black substance. Although most cases of PD are sporadic, 5–10% of patients have monogenetic mutations with a description of more than 20 genes for the familial form. Mitochondrial mutation in CHCHD10 has also been reported to be associated with a wide spectrum of neurodegenerative disorders, including PD. Objectives: Description of a rare recently described genetic cause of autosomal dominant parkinsonism. Methodology: Describe the case of a Brazilian woman with atypical parkinsonism due to CHCHD10 pathogenic variant that was followed up in our service. Result: Female, 64 years old. “. He started episodes of imbalance about 5 years ago, with falls, in addition to limb stiffness, worse on the left. 4 years ago, he started myalgia to great efforts with low subsequent tolerance to light effort. 1 year ago with urinary incontinence and choking past of poor performance in physical activities without pre-motor symptoms FAMILY: mother with clinical picture of possible dementia syndrome at age 60, history in the maternal family of myalgia, intolerance to physical exercise and hearing loss in adulthood. EXOMA: presence of variant c.146C > T (p.Ala49Val) in simple heterozygosity without CHCHD10 gene. MRI with thigh muscle hypotrophy in anterior and posterior thigh compartments; slight muscle edema in the legs. Conclusion: Pathogenic variants in the CHCHD10 gene should be considered in cases of atypical parkinsonism, especially in cases of positive familial history of mitochondrial myopathy or dementia.
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