Journal articles: 'Atypical Parkinsonian Disorders'

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Portera-Cailliau, Carlos, and Yvette Bordelon. "Atypical Parkinsonian Disorders." Seminars in Neurology 34, no. 02 (June 25, 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 (June 2004): 42–64. http://dx.doi.org/10.1212/01.con.0000293567.17705.8e.

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Wenning, Gregor K., and 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, and Marisol Gallardo. "Caribbean parkinsonism and other atypical Parkinsonian disorders." Parkinsonism & Related Disorders 10 (May 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, and Gregor K. Wenning. "Gait and postural disorders in parkinsonism: a clinical approach." Journal of Neurology 267, no. 11 (May 22, 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, and N. Pyatigorskaya. "Neuroimaging in Atypical Parkinsonian Disorders." Neurographics 8, no. 3 (June 1, 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, and Carlo Colosimo. "Dystonia in atypical parkinsonian disorders." Parkinsonism & Related Disorders 66 (September 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 (August 2007): 434–37. http://dx.doi.org/10.1097/wco.0b013e32823ecfa7.

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Bhidayasiri, Roongroj, Onanong Jitkritsadakul, and 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, and Giovanni Fabbrini. "Neuropsychiatric disturbances in atypical parkinsonian disorders." Neuropsychiatric Disease and Treatment Volume 14 (October 2018): 2643–56. http://dx.doi.org/10.2147/ndt.s178263.

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Litvan, Irene. "Recent advances in atypical parkinsonian disorders." Current Opinion in Neurology 12, no. 4 (August 1999): 441–46. http://dx.doi.org/10.1097/00019052-199908000-00011.

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Clark, Mary, Daniel Geschwind, and Brent Fogel. "The Neurogenetics of Atypical Parkinsonian Disorders." Seminars in Neurology 34, no. 02 (June 25, 2014): 217–24. http://dx.doi.org/10.1055/s-0034-1381738.

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Jellinger, K. A. "Atypical Parkinsonian Disorders - Clinical and Research Aspects." European Journal of Neurology 12, no. 11 (November 2005): 918. http://dx.doi.org/10.1111/j.1468-1331.2005.01228.x.

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Coakeley, Sarah, and Antonio P. Strafella. "Imaging pathological tau in atypical parkinsonian disorders." Current Opinion in Neurology 28, no. 4 (August 2015): 447–52. http://dx.doi.org/10.1097/wco.0000000000000210.

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Chen, L., and B. S. Zhang. "P1.109 Clinical features of atypical Parkinsonian disorders." Parkinsonism & Related Disorders 15 (December 2009): S57. http://dx.doi.org/10.1016/s1353-8020(09)70231-7.

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Hammerstad, J. "Atypical Parkinsonian Disorders: Clinical and Research Aspects." Neurology 67, no. 9 (November 13, 2006): 1726–27. http://dx.doi.org/10.1212/01.wnl.0000244410.30371.83.

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Petsani, Chrysi, Athina-Maria Aloizou, Vasileios Siokas, Lambros Messinis, Eleni Peristeri, Christos Bakirtzis, Grigorios Nasios, and Efthimios Dardiotis. "Therapeutic Application of rTMS in Atypical Parkinsonian Disorders." Behavioural Neurology 2021 (December 23, 2021): 1–12. http://dx.doi.org/10.1155/2021/3419907.

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The terms atypical parkinsonian disorders (APDs) and Parkinson plus syndromes are mainly used to describe the four major entities of sporadic neuronal multisystem degeneration: progressive supranuclear palsy (PSP), corticobasal degeneration (CBD), multiple system atrophy (MSA), and dementia with Lewy bodies (LBD). APDs are characterized by a variety of symptoms and a lack of disease modifying therapies; their treatment thus remains mainly symptomatic. Brain stimulation via repetitive transcranial magnetic stimulation (rTMS) is a safe and noninvasive intervention using a magnetic coil, and it is considered an alternative therapy in various neuropsychiatric pathologies. In this paper, we review the available studies that investigate the efficacy of rTMS in the treatment of these APDs and Parkinson plus syndromes. Τhe majority of the studies have shown beneficial effects on motor and nonmotor symptoms, but research is still at a preliminary phase, with large, double-blind studies lacking in the literature.

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Macleod, Angus, and Carl Counsell. "MORTALITY IN PARKINSON'S DISEASE AND ATYPICAL PARKINSONIAN DISORDERS." Journal of Neurology, Neurosurgery & Psychiatry 86, no. 11 (October 14, 2015): e4.88-e4. http://dx.doi.org/10.1136/jnnp-2015-312379.178.

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BackgroundWe evaluated the mortality associated with Parkinson's disease (PD), Lewy body dementia (LBD), progressive supranuclear palsy (PSP), multiple system atrophy (MSA), and vascular parkinsonism (VP) using a community-based incident cohort.MethodsAll incident parkinsonism cases identified over 4.5 years (2002-4, 2006-9) were tagged to the NHS central register for regular death notifications. Kaplan-Meier survival probabilities were plotted. Standardised mortality ratios (SMRs) and life expectancy, adjusted for age, sex and calendar year, were calculated using regional mortality data.ResultsUntil June 2014, 90 deaths occurred in 198 PD patients, and 107 deaths in 117 patients with other syndromes. Median survival in PD, LBD, PSP, MSA, and VP was 7.8 (6.7–9.4), 3.3 (2.3–4.1), 2.6 (1.1–3.8), 5.1 (1.3–NA), 2.1 (1.5–3.4) years, respectively. SMRs were 1.5 (1.2–1.9), 4.2 (3.0–5.9), 3.8 (2.6–5.5), 1.8 (0.9–3.4), 4.2 (3.0–6.0) respectively. In PD, median survival was lower than life expectancy, but more so in under 65s.ConclusionsMortality in PD was increased by 50% over expected population mortality. Younger patients have proportionally more to lose. Survival was much poorer in other syndromes.

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Raccagni, Cecilia, Heiko Gaßner, Sabine Eschlboeck, Sylvia Boesch, Florian Krismer, Klaus Seppi, Werner Poewe, et al. "Sensor-based gait analysis in atypical parkinsonian disorders." Brain and Behavior 8, no. 6 (May 7, 2018): e00977. http://dx.doi.org/10.1002/brb3.977.

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Almeida, Leonardo, Bilal Ahmed, Roger Walz, Sol De Jesus, Addie Patterson, Daniel Martinez-Ramirez, David Vaillancourt, et al. "Depressive Symptoms are Frequent in Atypical Parkinsonian Disorders." Movement Disorders Clinical Practice 4, no. 2 (June 24, 2016): 191–97. http://dx.doi.org/10.1002/mdc3.12382.

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Panyakaew, Pattamon, Chanawat Anan, and Roongroj Bhidayasiri. "Posturographic abnormalities in ambulatory atypical parkinsonian disorders: Differentiating characteristics." Parkinsonism & Related Disorders 66 (September 2019): 94–99. http://dx.doi.org/10.1016/j.parkreldis.2019.07.016.

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Potashkin, Judith A., Jose A. Santiago, Bernard M. Ravina, Arthur Watts, and Alexey A. Leontovich. "Biosignatures for Parkinson’s Disease and Atypical Parkinsonian Disorders Patients." PLoS ONE 7, no. 8 (August 27, 2012): e43595. http://dx.doi.org/10.1371/journal.pone.0043595.

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Köllensperger, Martin, and Gregor K. Wenning. "Assessing disease progression with MRI in atypical parkinsonian disorders." Movement Disorders 24, S2 (2009): S699—S702. http://dx.doi.org/10.1002/mds.22582.

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Seki, Morinobu, Klaus Seppi, Christoph Mueller, Thomas Potrusil, Georg Goebel, Eva Reiter, Michael Nocker, et al. "Diagnostic Potential of Multimodal MRI Markers in Atypical Parkinsonian Disorders." Journal of Parkinson's Disease 9, no. 4 (October 11, 2019): 681–91. http://dx.doi.org/10.3233/jpd-181568.

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Pal, PramodKumar, Pooja Mailankody, and M. Netravathi. "Review of tremor in Parkinson's disease and atypical parkinsonian disorders." Neurology India 65, no. 5 (2017): 1083. http://dx.doi.org/10.4103/neuroindia.ni_880_16.

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Botsford, Edward, Jayan George, and Ellen Buckley. "Parkinson’s Disease and Metal Storage Disorders: A Systematic Review." Brain Sciences 8, no. 11 (October 31, 2018): 194. http://dx.doi.org/10.3390/brainsci8110194.

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Metal storage disorders (MSDs) are a set of rare inherited conditions with variable clinical pictures including neurological dysfunction. The objective of this study was, through a systematic review, to identify the prevalence of Parkinsonism in patients with MSDs in order to uncover novel pathways implemented in Parkinson’s disease. Human studies describing patients of any age with an MSD diagnosis were analysed. Foreign language publications as well as animal and cellular studies were excluded. Searches were conducted through PubMed and Ovid between April and September 2018. A total of 53 publications were identified including 43 case reports, nine cross-sectional studies, and one cohort study. The publication year ranged from 1981 to 2018. The most frequently identified MSDs were Pantothenate kinase-associated neurodegeneration (PKAN) with 11 papers describing Parkinsonism, Hereditary hemochromatosis (HH) (7 papers), and Wilson’s disease (6 papers). The mean ages of onset of Parkinsonism for these MSDs were 33, 53, and 48 years old, respectively. The Parkinsonian features described in the PKAN and HH patients were invariably atypical while the majority (4/6) of the Wilson’s disease papers had a typical picture. This paper has highlighted a relationship between MSDs and Parkinsonism. However, due to the low-level evidence identified, further research is required to better define what the relationship is.

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Federico, Francesco, Isabella L. Simone, Vincenzo Lucivero, Giovanni Iliceto, Michele de Mari, Paolo Giannini, Domenico M. Mezzapesa, Alfredo Tarantino, and Paolo Lamberti. "Proton magnetic resonance spectroscopy in parkinson's disease and atypical parkinsonian disorders." Movement Disorders 12, no. 6 (November 1997): 903–9. http://dx.doi.org/10.1002/mds.870120611.

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Coakeley, Sarah, Sang Soo Cho, Yuko Koshimori, Pablo Rusjan, Madeleine Harris, Christine Ghadery, Jinhee Kim, et al. "Positron emission tomography imaging of tau pathology in progressive supranuclear palsy." Journal of Cerebral Blood Flow & Metabolism 37, no. 9 (December 22, 2016): 3150–60. http://dx.doi.org/10.1177/0271678x16683695.

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Progressive supranuclear palsy is a rare form of atypical Parkinsonism that differs neuropathologically from other parkinsonian disorders. While many parkinsonian disorders such as Parkinson’s disease, Lewy body dementia, and multiple system atrophy are classified as synucleinopathies, progressive supranuclear palsy is coined a tauopathy due to the aggregation of pathological tau in the brain. [18F]AV-1451 (also known as [18F]-T807) is a positron emission tomography radiotracer that binds to paired helical filaments of tau in Alzheimer’s disease. We investigated whether [18F]AV-1451 could be used as biomarker for the diagnosis and disease progression monitoring in progressive supranuclear palsy. Six progressive supranuclear palsy, six Parkinson’s disease, and 10 age-matched healthy controls were recruited. An anatomical MRI and a 90-min PET scan, using [18F]AV-1451, were acquired from all participants. The standardized uptake value ratio from 60 to 90 min post-injection was calculated in each region of interest, using the cerebellar cortex as a reference region. No significant differences in standardized uptake value ratios were detected in our progressive supranuclear palsy group compared to the two control groups. [18F]AV-1451 may bind selectivity to the paired helical filaments in Alzheimer’s disease, which differ from the straight conformation of tau filaments in progressive supranuclear palsy.

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Brooks, David J. "Imaging Familial and Sporadic Neurodegenerative Disorders Associated with Parkinsonism." Neurotherapeutics 18, no. 2 (January 11, 2021): 753–71. http://dx.doi.org/10.1007/s13311-020-00994-4.

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AbstractIn this paper, the structural and functional imaging changes associated with sporadic and genetic Parkinson’s disease and atypical Parkinsonian variants are reviewed. The role of imaging for supporting diagnosis and detecting subclinical disease is discussed, and the potential use and drawbacks of using imaging biomarkers for monitoring disease progression is debated. Imaging changes associated with nonmotor complications of PD are presented. The similarities and differences in imaging findings in Lewy body dementia, Parkinson’s disease dementia, and Alzheimer’s disease are discussed.

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Bougea, Anastasia. "MicroRNA as Candidate Biomarkers in Atypical Parkinsonian Syndromes: Systematic Literature Review." Medicina 58, no. 4 (March 26, 2022): 483. http://dx.doi.org/10.3390/medicina58040483.

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Background and Objectives: Multiple system atrophy (MSA) and progressive supranuclear palsy (PSP) are rare atypical parkinsonian syndromes, characterized by motor and cognitive symptoms. Their clinical diagnosis is challenging because there are no established biomarkers. Dysregulation of microRNAs (miRNAs/miRs) has been reported to serve an important role in neurodegenerative diseases. However, the miRNA profiles of MSA and PSP patients are rarely reported. The aim of this study was to critically review the role of miRNAs as diagnostic biomarkers to differentiate these atypical parkinsonian disorders and their role in disease pathogenesis. Materials and Methods: A systematic literature search of PubMed was conducted up to February 2022 according the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. Results: A total of 15 studies were analyzed. Three studies have shown that miR-9-3p, miR-19a, miR-19b, and miR-24 are potential biomarkers for MSA. In two studies, miR-132 was downregulated, whereas miR-147a and miR-518e were upregulated in the brain tissue of PSP patients. Conclusions: The potential of miRNA is still uncertain as a potential differential diagnostic marker to identify these disorders. Pre-analytical and analytical factors of included studies were important limitations to justify the introduction of miRNAs into clinical practice.

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Maloney, Eimer M., Atbin Djamshidian, and Sean S. O'Sullivan. "Phenomenology and epidemiology of impulsive-compulsive behaviours in Parkinson's disease, atypical Parkinsonian disorders and non-Parkinsonian populations." Journal of the Neurological Sciences 374 (March 2017): 47–52. http://dx.doi.org/10.1016/j.jns.2016.12.058.

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Klingelhoefer, Lisa, Elisaveta Sokolov, and K. Ray Chaudhuri. "Therapeutic options for nocturnal problems in Parkinson’s disease and atypical parkinsonian disorders." Journal of Neural Transmission 121, S1 (April 3, 2014): 25–31. http://dx.doi.org/10.1007/s00702-014-1202-6.

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Müller, J., G. K. Wenning, J. Wissel, K. Seppi, and W. Poewe. "Botulinum toxin treatment in atypical parkinsonian disorders associated with disabling focal dystonia." Journal of Neurology 249, no. 3 (March 1, 2002): 300–304. http://dx.doi.org/10.1007/s004150200009.

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Pathan, Meerakhan, Junfang Wu, Hans-Åke Lakso, Lars Forsgren, and Anders Öhman. "Plasma Metabolite Markers of Parkinson’s Disease and Atypical Parkinsonism." Metabolites 11, no. 12 (December 9, 2021): 860. http://dx.doi.org/10.3390/metabo11120860.

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Differentiating between Parkinson’s disease (PD) and the atypical Parkinsonian disorders of multiple system atrophy (MSA) and progressive supranuclear palsy (PSP) is difficult clinically due to overlapping symptomatology, especially at early disease stages. Consequently, there is a need to identify metabolic markers for these diseases and to develop them into viable biomarkers. In the present investigation, solution nuclear magnetic resonance and mass spectrometry metabolomics were used to quantitatively characterize the plasma metabolomes (a total of 167 metabolites) of a cohort of 94 individuals comprising 34 PD, 12 MSA, and 17 PSP patients, as well as 31 control subjects. The distinct and statistically significant differences observed in the metabolite concentrations of the different disease and control groups enabled the identification of potential plasma metabolite markers of each disorder and enabled the differentiation between the disorders. These group-specific differences further implicate disturbances in specific metabolic pathways. The two metabolites, formic acid and succinate, were altered similarly in all three disease groups when compared to the control group, where a reduced level of formic acid suggested an effect on pyruvate metabolism, methane metabolism, and/or the kynurenine pathway, and an increased succinate level suggested an effect on the citric acid cycle and mitochondrial dysfunction.

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Bhidayasiri, Roongroj, Jirada Sringean, Stephen G. Reich, and Carlo Colosimo. "Red flags phenotyping: A systematic review on clinical features in atypical parkinsonian disorders." Parkinsonism & Related Disorders 59 (February 2019): 82–92. http://dx.doi.org/10.1016/j.parkreldis.2018.10.009.

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Allali, Gilles, Valentina Garibotto, Ismini C. Mainta, Stephane Armand, Richard Camicioli, Osman Ratib, Habib Zaidi, Francois R. Herrmann, and Frederic Assal. "Dopaminergic denervation is not necessary to induce gait disorders in atypical parkinsonian syndrome." Journal of the Neurological Sciences 351, no. 1-2 (April 2015): 127–32. http://dx.doi.org/10.1016/j.jns.2015.02.051.

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Savoiardo, M. "Differential diagnosis of Parkinson's disease and atypical parkinsonian disorders by magnetic resonance imaging." Neurological Sciences 24 (May 1, 2003): s35—s37. http://dx.doi.org/10.1007/s100720300036.

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Ko, Ji Hyun, Chong Sik Lee, and David Eidelberg. "Metabolic network expression in parkinsonism: Clinical and dopaminergic correlations." Journal of Cerebral Blood Flow & Metabolism 37, no. 2 (July 21, 2016): 683–93. http://dx.doi.org/10.1177/0271678x16637880.

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Little is known of the precise relationship between the expression of disease-related metabolic patterns and nigrostriatal dopaminergic dysfunction in parkinsonism. We studied 51 subjects with Parkinson's disease (PD) (18 non-demented, 24 demented, and 9 dementia with Lewy bodies) and 127 with atypical parkinsonian syndromes (47 multiple system atrophy (MSA), 38 progressive supranuclear palsy (PSP), and 42 corticobasal syndrome (CBS)) with 18F-fluorodeoxyglucose PET to quantify the expression of previously validated disease-related patterns for PD, MSA, PSP, and CBS and 18F-fluoropropyl-β-CIT PET to quantify caudate and putamen dopamine transporter (DAT) binding. The patients in each group exhibited significant elevations in the expression of the corresponding disease-related pattern ( p < 0.001), relative to 16 healthy subjects. With the exception of cerebellar MSA (MSA-C), all groups displayed significant reductions in putamen DAT binding relative to healthy subjects ( p < 0.05). Correlations between the dopaminergic and metabolic measures were significant in PD and CBS but not in MSA and PSP. In all patient groups with the exception of MSA-C and CBS, pattern expression values and DAT binding correlated with disease duration and severity measures. The findings suggest that in these parkinsonian disorders, metabolic network expression and DAT binding provide complementary information regarding the underlying disease process.

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Poznic-Jesic, Milana, Aleksandar Jesic, Jasmina Babovic-Filipovic, and Olga Zivanovic. "Extrapyramidal syndromes caused by antipsychotics." Medical review 65, no. 11-12 (2012): 521–26. http://dx.doi.org/10.2298/mpns1212521p.

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Introduction. Extrapyramidal syndromes are significant side effects of antipsychotic therapy due to their severity, frequent occurrence and complications. This paper gives a brief summary of the literature with the emphasis on epidemiology, etiology, diagnosis and differential diagnosis, as well as the treatment of extrapyramidal disorders induced by antipsychotics. Dystonia. Sustained muscle contractions cause twisting and repetitive movements or abnormal postures. It may appear either as an acute or delayed, i.e. tardive sign. The incidence of dystonia is 2-3% among the patients treated with antipsychotics, and 50% among the ones cured with conventional antipsychotics. Akathisia. The main feature of this curious adverse effect is the psychomotor restlessness and the inability to remain motionless. Although akathisia is not very frequent, its incidence and prevalence ranges from 5 to 50% among the treated patients. It is most probably a result of the blockage of dopaminergic receptors. Parkinsonism. The most frequent secondary Parkinsonism is the one caused by drugs. The characteristic parkinsonian signs regress 4 to 16 weeks after the discontinuation of antipsychotic therapy. In the era of atypical antipsychotics this adverse effect appears less frequently. Tardive dyskinesia. Involuntary choreatic movements may appear days and months after the introduction of continuous use of antipsychotics. The individual susceptibility may play the major role in the development of this side effect. Conclusion. Numerous studies have compared conventional and atypical antipsychotics as well as atypical ones with one another in order to decrease the risk of development of extrapyramical side effects as well as to prevent their occurrence and improve their treatment.

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Mondello, Stefania, Radu Constantinescu, Henrik Zetterberg, Ulf Andreasson, Björn Holmberg, and Andreas Jeromin. "CSF α-synuclein and UCH-L1 levels in Parkinson's disease and atypical parkinsonian disorders." Parkinsonism & Related Disorders 20, no. 4 (April 2014): 382–87. http://dx.doi.org/10.1016/j.parkreldis.2014.01.011.

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Lucivero, V., L. Simone, M. De Mari, I. G. Iliceto, D. M. Mezzapesa, S. Lamberti, and F. Federico. "5-30-04 Proton magnetic resonance spectroscopy in Parkinson's disease and atypical parkinsonian disorders." Journal of the Neurological Sciences 150 (September 1997): S316. http://dx.doi.org/10.1016/s0022-510x(97)86443-x.

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Tohanean, Nicoleta, and Lacramioara Perju Dumbrava. "Transcranial ultrasonography in Parkinson's disease and other movement disorders." Romanian Journal of Neurology 8, no. 4 (December 31, 2009): 160–63. http://dx.doi.org/10.37897/rjn.2009.4.2.

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In recent years, transcranial ultrasonography (TCS) has become widely used for the visualization of the brainstem. With this method, changes of the echotexture – increased echogenicity – of the substantia nigra (SN) in about 90% of patients with Parkinson’s disease (PD). In contrast, increased SN echogenicity is rarely found in patients with atypical or symptomatic Parkinsonian syndromes, providing a valuable tool for differential diagnosis. Interestingly, increased SN echogenicity can also be found in about 8 to 10% of healthy subjects. The studies showed that the ultrasound signal does not change in the course of the disease and this hyperechogenicity of the SN is present in the early stages of the disease, also in the presymptomatic patients. So, TCS may represent a biomarker for vulnerability of the nigrostriatal system and this method may even be helpful for the preclinical identification of people at risk for PD.

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Magdalinou, N. K., R. W. Paterson, J. M. Schott, N. C. Fox, C. Mummery, K. Blennow, K. Bhatia, et al. "A panel of nine cerebrospinal fluid biomarkers may identify patients with atypical parkinsonian syndromes." Journal of Neurology, Neurosurgery & Psychiatry 86, no. 11 (January 14, 2015): 1240–47. http://dx.doi.org/10.1136/jnnp-2014-309562.

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BackgroundPatients presenting with parkinsonian syndromes share many clinical features, which can make diagnosis difficult. This is important as atypical parkinsonian syndromes (APSs) such as progressive supranuclear palsy (PSP), multiple system atrophy (MSA) and corticobasal syndrome (CBS) carry a poor prognosis, compared with patients with Parkinson's disease (PD). In addition, there is overlap between APS and dementia diseases, such as Alzheimer's disease (AD) and frontotemporal dementia (FTD).ObjectiveTo use a panel of cerebrospinal fluid (CSF) biomarkers to differentiate patients with APS from PD and dementia.MethodsA prospective cohort of 160 patients and 30 control participants were recruited from a single specialist centre. Patients were clinically diagnosed according to current consensus criteria. CSF samples were obtained from patients with clinical diagnoses of PD (n=31), PSP (n=33), CBS (n=14), MSA (n=31), AD (n=26) and FTD (n=16). Healthy, elderly participants (n=30) were included as controls. Total τ (t-τ), phosphorylated τ (p-τ), β-amyloid 1–42 (Aβ42), neurofilament light chain (NFL), α-synuclein (α-syn), amyloid precursor protein soluble metabolites α and β (soluble amyloid precursor protein (sAPP)α, sAPPβ) and two neuroinflammatory markers (monocyte chemoattractant protein-1 and YKL-40) were measured in CSF. A reverse stepwise regression analysis and the false discovery rate procedure were used.ResultsCSF NFL (p<0.001), sAPPα (p<0.001) and a-syn (p=0.003) independently predicted diagnosis of PD versus APS. Together, these nine biomarkers could differentiate patients with PD from APS with an area under the curve of 0.95 and subtypes of APS from one another. There was good discriminatory power between parkinsonian groups, dementia disorders and healthy controls.ConclusionsA panel of nine CSF biomarkers was able to differentiate APS from patients with PD and dementia. This may have important clinical utility in improving diagnostic accuracy, allowing better prognostication and earlier access to potential disease-modifying therapies.

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Jaimini, Abhinav, Madhavi Tripathi, Maria M. D’Souza, Puja Panwar, Rajnish Sharma, Saloni Mehta, Santosh Pandey, et al. "Utility of intrastriatal ratios of FDOPA to differentiate idiopathic Parkinson’s disease from atypical parkinsonian disorders." Nuclear Medicine Communications 34, no. 5 (May 2013): 426–31. http://dx.doi.org/10.1097/mnm.0b013e32835fcd7f.

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Chang, Kuo-Hsuan, Guan-Chiun Lee, Chin-Chang Huang, Hung-Chou Kuo, Chiung-Mei Chen, Ya-Chin Hsiao, Hsuan-Chu Hsu, et al. "Genetic and functional characters of GRN p.T487I mutation in Taiwanese patients with atypical parkinsonian disorders." Parkinsonism & Related Disorders 51 (June 2018): 61–66. http://dx.doi.org/10.1016/j.parkreldis.2018.02.045.

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Hall, Sara, Shorena Janelidze, Yulia Surova, Håkan Widner, Henrik Zetterberg, and Oskar Hansson. "P3-270: CEREBROSPINAL FLUID CONCENTRATIONS OF INFLAMMATORY MARKERS IN PARKINSON'S DISEASE AND ATYPICAL PARKINSONIAN DISORDERS." Alzheimer's & Dementia 14, no. 7S_Part_22 (July 1, 2006): P1180. http://dx.doi.org/10.1016/j.jalz.2018.06.1630.

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Mitchell, Steven D., Roger L. Albin, William T. Dauer, John L. Goudreau, and Christos Sidiropoulos. "Heterozygous VPS13A and PARK2 Mutations in a Patient with Parkinsonism and Seizures." Case Reports in Neurology 13, no. 2 (June 11, 2021): 341–46. http://dx.doi.org/10.1159/000515805.

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Neuroacanthocytosis (NA) is a diverse group of disorders in which nervous system abnormalities co-occur with irregularly shaped red blood cells called acanthocytes. Chorea-acanthocytosis is the most common of these syndromes and is an autosomal recessive disease caused by mutations in the <i>vacuolar protein sorting 13A</i> (VPS13A) gene. We report a case of early onset parkinsonism and seizures in a 43-year-old male with a family history of NA. Neurologic examinations showed cognitive impairment and marked parkinsonian signs. MRI showed bilateral basal ganglia gliosis. He was found to have a novel heterozygous mutation in the VPS13A gene, in addition a heterozygous mutation in the PARK2 gene. His clinical picture was atypical for typical chorea-acanthocytosis (ChAc). The compound heterozygous mutations of VPS13A and PARK2 provide the most plausible explanation for this patient’s clinical symptoms. This case adds to the phenotypic diversity of ChAc. More research is needed to fully understand the roles of epistatic interactions on phenotypic expression of neurodegenerative diseases.

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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.

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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.

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Jabbari, Edwin, John Woodside, Tong Guo, Nadia K. Magdalinou, Viorica Chelban, Dilan Athauda, Andrew J. Lees, et al. "Proximity extension assay testing reveals novel diagnostic biomarkers of atypical parkinsonian syndromes." Journal of Neurology, Neurosurgery & Psychiatry 90, no. 7 (March 13, 2019): 768–73. http://dx.doi.org/10.1136/jnnp-2018-320151.

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ObjectiveThe high degree of clinical overlap between atypical parkinsonian syndromes (APS) and Parkinson’s disease (PD) makes diagnosis challenging. We aimed to identify novel diagnostic protein biomarkers of APS using multiplex proximity extension assay (PEA) testing.MethodsCerebrospinal fluid (CSF) samples from two independent cohorts, each consisting of APS and PD cases, and controls, were analysed for neurofilament light chain (NF-L) and Olink Neurology and Inflammation PEA biomarker panels. Whole-cohort comparisons of biomarker concentrations were made between APS (n=114), PD (n=37) and control (n=34) groups using logistic regression analyses that included gender, age and disease duration as covariates.ResultsAPS versus controls analyses revealed 11 CSF markers with significantly different levels in cases and controls (p<0.002). Four of these markers also reached significance (p<0.05) in APS versus PD analyses. Disease-specific analyses revealed lower group levels of FGF-5, FGF-19 and SPOCK1 in multiple system atrophy compared with progressive supranuclear palsy and corticobasal syndrome. Receiver operating characteristic curve analyses suggested that the diagnostic accuracy of NF-L was superior to the significant PEA biomarkers in distinguishing APS, PD and controls. The biological processes regulated by the significant proteins include cell differentiation and immune cell migration. Delta and notch-like epidermal growth factor-related receptor (DNER) had the strongest effect size in APS versus controls and APS versus PD analyses. DNER is highly expressed in substantia nigra and is an activator of the NOTCH1 pathway which has been implicated in the aetiology of other neurodegenerative disorders including Alzheimer’s disease.ConclusionsPEA testing has identified potential novel diagnostic biomarkers of APS.

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Marsili, Luca, Jennifer Sharma, Tiago Fleming Outeiro, and Carlo Colosimo. "Stem Cell Therapies in Movement Disorders: Lessons from Clinical Trials." Biomedicines 11, no. 2 (February 9, 2023): 505. http://dx.doi.org/10.3390/biomedicines11020505.

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Stem cell-based therapies (SCT) to treat neurodegenerative disorders have promise but clinical trials have only recently begun, and results are not expected for several years. While most SCTs largely lead to a symptomatic therapeutic effect by replacing lost cell types, there may also be disease-modifying therapeutic effects. In fact, SCT may complement a multi-drug, subtype-specific therapeutic approach, consistent with the idea of precision medicine, which matches molecular therapies to biological subtypes of disease. In this narrative review, we examine published and ongoing trials in SCT in Parkinson’s Disease, atypical parkinsonian disorders, Huntington’s disease, amyotrophic lateral sclerosis, and spinocerebellar ataxia in humans. We discuss the benefits and pitfalls of using this treatment approach within the spectrum of disease-modification efforts in neurodegenerative diseases. SCT may hold greater promise in the treatment of neurodegenerative disorders, but much research is required to determine the feasibility, safety, and efficacy of these complementary aims of therapeutic efforts.

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Journal articles on the topic 'Atypical Parkinsonian Disorders'

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