Onset features and time to diagnosis in Friedreich’s Ataxia

Background In rare disorders diagnosis may be delayed due to limited awareness and unspecific presenting symptoms. Herein, we address the issue of diagnostic delay in Friedreich’s Ataxia (FRDA), a genetic disorder usually caused by homozygous GAA-repeat expansions. Methods Six hundred eleven genetic...

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Vydané v:Orphanet journal of rare diseases Ročník 15; číslo 1; s. 198 - 8
Hlavní autori: Indelicato, Elisabetta, Nachbauer, Wolfgang, Eigentler, Andreas, Amprosi, Matthias, Matteucci Gothe, Raffaella, Giunti, Paola, Mariotti, Caterina, Arpa, Javier, Durr, Alexandra, Klopstock, Thomas, Schöls, Ludger, Giordano, Ilaria, Bürk, Katrin, Pandolfo, Massimo, Didszdun, Claire, Schulz, Jörg B., Boesch, Sylvia
Médium: Journal Article
Jazyk:English
Vydavateľské údaje: London BioMed Central 03.08.2020
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Springer Nature B.V
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ISSN:1750-1172, 1750-1172
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Abstract Background In rare disorders diagnosis may be delayed due to limited awareness and unspecific presenting symptoms. Herein, we address the issue of diagnostic delay in Friedreich’s Ataxia (FRDA), a genetic disorder usually caused by homozygous GAA-repeat expansions. Methods Six hundred eleven genetically confirmed FRDA patients were recruited within a multicentric natural history study conducted by the EFACTS (European FRDA Consortium for Translational Studies, ClinicalTrials.gov -Identifier NCT02069509). Age at first symptoms as well as age at first suspicion of FRDA by a physician were collected retrospectively at the baseline visit. Results In 554 of cases (90.7%), disease presented with gait or coordination disturbances. In the others ( n  = 57, 9.3%), non-neurological features such as scoliosis or cardiomyopathy predated ataxia. Before the discovery of the causal mutation in 1996, median time to diagnosis was 4(IQR = 2–9) years and it improved significantly after the introduction of genetic testing (2(IQR = 1–5) years, p  < 0.001). Still, after 1996, time to diagnosis was longer in patients with a) non-neurological presentation (mean 6.7, 95%CI [5.5,7.9] vs 4.5, [4.2,5] years in those with neurological presentation, p  = 0.001) as well as in b) patients with late-onset (3(IQR = 1–7) vs 2(IQR = 1–5) years compared to typical onset < 25 years of age, p  = 0.03). Age at onset significantly correlated with the length of the shorter GAA repeat (GAA1) in case of neurological onset (r = − 0,6; p  < 0,0001), but not in patients with non-neurological presentation (r = − 0,1; p  = 0,4). Across 54 siblings’ pairs, differences in age at onset did not correlate with differences in GAA-repeat length (r = − 0,14, p  = 0,3). Conclusions In the genetic era, presentation with non-neurological features or in the adulthood still leads to a significant diagnostic delay in FRDA. Well-known correlations between GAA1 repeat length and disease milestones are not valid in case of atypical presentations or positive family history.
AbstractList Background In rare disorders diagnosis may be delayed due to limited awareness and unspecific presenting symptoms. Herein, we address the issue of diagnostic delay in Friedreich’s Ataxia (FRDA), a genetic disorder usually caused by homozygous GAA-repeat expansions. Methods Six hundred eleven genetically confirmed FRDA patients were recruited within a multicentric natural history study conducted by the EFACTS (European FRDA Consortium for Translational Studies, ClinicalTrials.gov-Identifier NCT02069509). Age at first symptoms as well as age at first suspicion of FRDA by a physician were collected retrospectively at the baseline visit. Results In 554 of cases (90.7%), disease presented with gait or coordination disturbances. In the others (n = 57, 9.3%), non-neurological features such as scoliosis or cardiomyopathy predated ataxia. Before the discovery of the causal mutation in 1996, median time to diagnosis was 4(IQR = 2–9) years and it improved significantly after the introduction of genetic testing (2(IQR = 1–5) years, p < 0.001). Still, after 1996, time to diagnosis was longer in patients with a) non-neurological presentation (mean 6.7, 95%CI [5.5,7.9] vs 4.5, [4.2,5] years in those with neurological presentation, p = 0.001) as well as in b) patients with late-onset (3(IQR = 1–7) vs 2(IQR = 1–5) years compared to typical onset < 25 years of age, p = 0.03). Age at onset significantly correlated with the length of the shorter GAA repeat (GAA1) in case of neurological onset (r = − 0,6; p < 0,0001), but not in patients with non-neurological presentation (r = − 0,1; p = 0,4). Across 54 siblings’ pairs, differences in age at onset did not correlate with differences in GAA-repeat length (r = − 0,14, p = 0,3). Conclusions In the genetic era, presentation with non-neurological features or in the adulthood still leads to a significant diagnostic delay in FRDA. Well-known correlations between GAA1 repeat length and disease milestones are not valid in case of atypical presentations or positive family history.
Abstract Background In rare disorders diagnosis may be delayed due to limited awareness and unspecific presenting symptoms. Herein, we address the issue of diagnostic delay in Friedreich’s Ataxia (FRDA), a genetic disorder usually caused by homozygous GAA-repeat expansions. Methods Six hundred eleven genetically confirmed FRDA patients were recruited within a multicentric natural history study conducted by the EFACTS (European FRDA Consortium for Translational Studies, ClinicalTrials.gov -Identifier NCT02069509). Age at first symptoms as well as age at first suspicion of FRDA by a physician were collected retrospectively at the baseline visit. Results In 554 of cases (90.7%), disease presented with gait or coordination disturbances. In the others (n = 57, 9.3%), non-neurological features such as scoliosis or cardiomyopathy predated ataxia. Before the discovery of the causal mutation in 1996, median time to diagnosis was 4(IQR = 2–9) years and it improved significantly after the introduction of genetic testing (2(IQR = 1–5) years, p < 0.001). Still, after 1996, time to diagnosis was longer in patients with a) non-neurological presentation (mean 6.7, 95%CI [5.5,7.9] vs 4.5, [4.2,5] years in those with neurological presentation, p = 0.001) as well as in b) patients with late-onset (3(IQR = 1–7) vs 2(IQR = 1–5) years compared to typical onset < 25 years of age, p = 0.03). Age at onset significantly correlated with the length of the shorter GAA repeat (GAA1) in case of neurological onset (r = − 0,6; p < 0,0001), but not in patients with non-neurological presentation (r = − 0,1; p = 0,4). Across 54 siblings’ pairs, differences in age at onset did not correlate with differences in GAA-repeat length (r = − 0,14, p = 0,3). Conclusions In the genetic era, presentation with non-neurological features or in the adulthood still leads to a significant diagnostic delay in FRDA. Well-known correlations between GAA1 repeat length and disease milestones are not valid in case of atypical presentations or positive family history.
In rare disorders diagnosis may be delayed due to limited awareness and unspecific presenting symptoms. Herein, we address the issue of diagnostic delay in Friedreich's Ataxia (FRDA), a genetic disorder usually caused by homozygous GAA-repeat expansions. Six hundred eleven genetically confirmed FRDA patients were recruited within a multicentric natural history study conducted by the EFACTS (European FRDA Consortium for Translational Studies, ClinicalTrials.gov-Identifier NCT02069509). Age at first symptoms as well as age at first suspicion of FRDA by a physician were collected retrospectively at the baseline visit. In 554 of cases (90.7%), disease presented with gait or coordination disturbances. In the others (n = 57, 9.3%), non-neurological features such as scoliosis or cardiomyopathy predated ataxia. Before the discovery of the causal mutation in 1996, median time to diagnosis was 4(IQR = 2-9) years and it improved significantly after the introduction of genetic testing (2(IQR = 1-5) years, p < 0.001). Still, after 1996, time to diagnosis was longer in patients with a) non-neurological presentation (mean 6.7, 95%CI [5.5,7.9] vs 4.5, [4.2,5] years in those with neurological presentation, p = 0.001) as well as in b) patients with late-onset (3(IQR = 1-7) vs 2(IQR = 1-5) years compared to typical onset < 25 years of age, p = 0.03). In the genetic era, presentation with non-neurological features or in the adulthood still leads to a significant diagnostic delay in FRDA. Well-known correlations between GAA1 repeat length and disease milestones are not valid in case of atypical presentations or positive family history.
In rare disorders diagnosis may be delayed due to limited awareness and unspecific presenting symptoms. Herein, we address the issue of diagnostic delay in Friedreich's Ataxia (FRDA), a genetic disorder usually caused by homozygous GAA-repeat expansions.BACKGROUNDIn rare disorders diagnosis may be delayed due to limited awareness and unspecific presenting symptoms. Herein, we address the issue of diagnostic delay in Friedreich's Ataxia (FRDA), a genetic disorder usually caused by homozygous GAA-repeat expansions.Six hundred eleven genetically confirmed FRDA patients were recruited within a multicentric natural history study conducted by the EFACTS (European FRDA Consortium for Translational Studies, ClinicalTrials.gov -Identifier NCT02069509). Age at first symptoms as well as age at first suspicion of FRDA by a physician were collected retrospectively at the baseline visit.METHODSSix hundred eleven genetically confirmed FRDA patients were recruited within a multicentric natural history study conducted by the EFACTS (European FRDA Consortium for Translational Studies, ClinicalTrials.gov -Identifier NCT02069509). Age at first symptoms as well as age at first suspicion of FRDA by a physician were collected retrospectively at the baseline visit.In 554 of cases (90.7%), disease presented with gait or coordination disturbances. In the others (n = 57, 9.3%), non-neurological features such as scoliosis or cardiomyopathy predated ataxia. Before the discovery of the causal mutation in 1996, median time to diagnosis was 4(IQR = 2-9) years and it improved significantly after the introduction of genetic testing (2(IQR = 1-5) years, p < 0.001). Still, after 1996, time to diagnosis was longer in patients with a) non-neurological presentation (mean 6.7, 95%CI [5.5,7.9] vs 4.5, [4.2,5] years in those with neurological presentation, p = 0.001) as well as in b) patients with late-onset (3(IQR = 1-7) vs 2(IQR = 1-5) years compared to typical onset < 25 years of age, p = 0.03). Age at onset significantly correlated with the length of the shorter GAA repeat (GAA1) in case of neurological onset (r = - 0,6; p < 0,0001), but not in patients with non-neurological presentation (r = - 0,1; p = 0,4). Across 54 siblings' pairs, differences in age at onset did not correlate with differences in GAA-repeat length (r = - 0,14, p = 0,3).RESULTSIn 554 of cases (90.7%), disease presented with gait or coordination disturbances. In the others (n = 57, 9.3%), non-neurological features such as scoliosis or cardiomyopathy predated ataxia. Before the discovery of the causal mutation in 1996, median time to diagnosis was 4(IQR = 2-9) years and it improved significantly after the introduction of genetic testing (2(IQR = 1-5) years, p < 0.001). Still, after 1996, time to diagnosis was longer in patients with a) non-neurological presentation (mean 6.7, 95%CI [5.5,7.9] vs 4.5, [4.2,5] years in those with neurological presentation, p = 0.001) as well as in b) patients with late-onset (3(IQR = 1-7) vs 2(IQR = 1-5) years compared to typical onset < 25 years of age, p = 0.03). Age at onset significantly correlated with the length of the shorter GAA repeat (GAA1) in case of neurological onset (r = - 0,6; p < 0,0001), but not in patients with non-neurological presentation (r = - 0,1; p = 0,4). Across 54 siblings' pairs, differences in age at onset did not correlate with differences in GAA-repeat length (r = - 0,14, p = 0,3).In the genetic era, presentation with non-neurological features or in the adulthood still leads to a significant diagnostic delay in FRDA. Well-known correlations between GAA1 repeat length and disease milestones are not valid in case of atypical presentations or positive family history.CONCLUSIONSIn the genetic era, presentation with non-neurological features or in the adulthood still leads to a significant diagnostic delay in FRDA. Well-known correlations between GAA1 repeat length and disease milestones are not valid in case of atypical presentations or positive family history.
Background In rare disorders diagnosis may be delayed due to limited awareness and unspecific presenting symptoms. Herein, we address the issue of diagnostic delay in Friedreich’s Ataxia (FRDA), a genetic disorder usually caused by homozygous GAA-repeat expansions. Methods Six hundred eleven genetically confirmed FRDA patients were recruited within a multicentric natural history study conducted by the EFACTS (European FRDA Consortium for Translational Studies, ClinicalTrials.gov -Identifier NCT02069509). Age at first symptoms as well as age at first suspicion of FRDA by a physician were collected retrospectively at the baseline visit. Results In 554 of cases (90.7%), disease presented with gait or coordination disturbances. In the others ( n  = 57, 9.3%), non-neurological features such as scoliosis or cardiomyopathy predated ataxia. Before the discovery of the causal mutation in 1996, median time to diagnosis was 4(IQR = 2–9) years and it improved significantly after the introduction of genetic testing (2(IQR = 1–5) years, p  < 0.001). Still, after 1996, time to diagnosis was longer in patients with a) non-neurological presentation (mean 6.7, 95%CI [5.5,7.9] vs 4.5, [4.2,5] years in those with neurological presentation, p  = 0.001) as well as in b) patients with late-onset (3(IQR = 1–7) vs 2(IQR = 1–5) years compared to typical onset < 25 years of age, p  = 0.03). Age at onset significantly correlated with the length of the shorter GAA repeat (GAA1) in case of neurological onset (r = − 0,6; p  < 0,0001), but not in patients with non-neurological presentation (r = − 0,1; p  = 0,4). Across 54 siblings’ pairs, differences in age at onset did not correlate with differences in GAA-repeat length (r = − 0,14, p  = 0,3). Conclusions In the genetic era, presentation with non-neurological features or in the adulthood still leads to a significant diagnostic delay in FRDA. Well-known correlations between GAA1 repeat length and disease milestones are not valid in case of atypical presentations or positive family history.
In rare disorders diagnosis may be delayed due to limited awareness and unspecific presenting symptoms. Herein, we address the issue of diagnostic delay in Friedreich's Ataxia (FRDA), a genetic disorder usually caused by homozygous GAA-repeat expansions. Six hundred eleven genetically confirmed FRDA patients were recruited within a multicentric natural history study conducted by the EFACTS (European FRDA Consortium for Translational Studies, ClinicalTrials.gov -Identifier NCT02069509). Age at first symptoms as well as age at first suspicion of FRDA by a physician were collected retrospectively at the baseline visit. In 554 of cases (90.7%), disease presented with gait or coordination disturbances. In the others (n = 57, 9.3%), non-neurological features such as scoliosis or cardiomyopathy predated ataxia. Before the discovery of the causal mutation in 1996, median time to diagnosis was 4(IQR = 2-9) years and it improved significantly after the introduction of genetic testing (2(IQR = 1-5) years, p < 0.001). Still, after 1996, time to diagnosis was longer in patients with a) non-neurological presentation (mean 6.7, 95%CI [5.5,7.9] vs 4.5, [4.2,5] years in those with neurological presentation, p = 0.001) as well as in b) patients with late-onset (3(IQR = 1-7) vs 2(IQR = 1-5) years compared to typical onset < 25 years of age, p = 0.03). Age at onset significantly correlated with the length of the shorter GAA repeat (GAA1) in case of neurological onset (r = - 0,6; p < 0,0001), but not in patients with non-neurological presentation (r = - 0,1; p = 0,4). Across 54 siblings' pairs, differences in age at onset did not correlate with differences in GAA-repeat length (r = - 0,14, p = 0,3). In the genetic era, presentation with non-neurological features or in the adulthood still leads to a significant diagnostic delay in FRDA. Well-known correlations between GAA1 repeat length and disease milestones are not valid in case of atypical presentations or positive family history.
Background In rare disorders diagnosis may be delayed due to limited awareness and unspecific presenting symptoms. Herein, we address the issue of diagnostic delay in Friedreich's Ataxia (FRDA), a genetic disorder usually caused by homozygous GAA-repeat expansions. Methods Six hundred eleven genetically confirmed FRDA patients were recruited within a multicentric natural history study conducted by the EFACTS (European FRDA Consortium for Translational Studies, ClinicalTrials.gov-Identifier NCT02069509). Age at first symptoms as well as age at first suspicion of FRDA by a physician were collected retrospectively at the baseline visit. Results In 554 of cases (90.7%), disease presented with gait or coordination disturbances. In the others (n = 57, 9.3%), non-neurological features such as scoliosis or cardiomyopathy predated ataxia. Before the discovery of the causal mutation in 1996, median time to diagnosis was 4(IQR = 2-9) years and it improved significantly after the introduction of genetic testing (2(IQR = 1-5) years, p < 0.001). Still, after 1996, time to diagnosis was longer in patients with a) non-neurological presentation (mean 6.7, 95%CI [5.5,7.9] vs 4.5, [4.2,5] years in those with neurological presentation, p = 0.001) as well as in b) patients with late-onset (3(IQR = 1-7) vs 2(IQR = 1-5) years compared to typical onset < 25 years of age, p = 0.03). Age at onset significantly correlated with the length of the shorter GAA repeat (GAA1) in case of neurological onset (r = - 0,6; p < 0,0001), but not in patients with non-neurological presentation (r = - 0,1; p = 0,4). Across 54 siblings' pairs, differences in age at onset did not correlate with differences in GAA-repeat length (r = - 0,14, p = 0,3). Conclusions In the genetic era, presentation with non-neurological features or in the adulthood still leads to a significant diagnostic delay in FRDA. Well-known correlations between GAA1 repeat length and disease milestones are not valid in case of atypical presentations or positive family history. Keywords: Friedreich's Ataxia, Age at onset, Genetic testing, Diagnostic delay, Natural history study
ArticleNumber 198
Audience Academic
Author Pandolfo, Massimo
Amprosi, Matthias
Boesch, Sylvia
Eigentler, Andreas
Mariotti, Caterina
Giunti, Paola
Giordano, Ilaria
Didszdun, Claire
Matteucci Gothe, Raffaella
Schulz, Jörg B.
Klopstock, Thomas
Indelicato, Elisabetta
Schöls, Ludger
Durr, Alexandra
Nachbauer, Wolfgang
Arpa, Javier
Bürk, Katrin
Author_xml – sequence: 1
  givenname: Elisabetta
  surname: Indelicato
  fullname: Indelicato, Elisabetta
  organization: Department of Neurology, Medical University of Innsbruck
– sequence: 2
  givenname: Wolfgang
  surname: Nachbauer
  fullname: Nachbauer, Wolfgang
  organization: Department of Neurology, Medical University of Innsbruck
– sequence: 3
  givenname: Andreas
  surname: Eigentler
  fullname: Eigentler, Andreas
  organization: Department of Neurology, Medical University of Innsbruck
– sequence: 4
  givenname: Matthias
  surname: Amprosi
  fullname: Amprosi, Matthias
  organization: Department of Neurology, Medical University of Innsbruck
– sequence: 5
  givenname: Raffaella
  surname: Matteucci Gothe
  fullname: Matteucci Gothe, Raffaella
  organization: Department of Public Health, Health Services Research and Health Technology Assessment, UMIT - University of Health Sciences, Medical Informatics and Technology
– sequence: 6
  givenname: Paola
  surname: Giunti
  fullname: Giunti, Paola
  organization: Department of Molecular Neuroscience, UCL Institute of Neurology
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  givenname: Caterina
  surname: Mariotti
  fullname: Mariotti, Caterina
  organization: Unit of Genetics of Neurodegenerative and Metabolic Diseases, Fondazione IRCCS Istituto Neurologico Carlo Besta
– sequence: 8
  givenname: Javier
  surname: Arpa
  fullname: Arpa, Javier
  organization: Reference Unit of Hereditary Ataxias and Paraplegias, Department of Neurology, IdiPAZ, Hospital Universitario La Paz
– sequence: 9
  givenname: Alexandra
  surname: Durr
  fullname: Durr, Alexandra
  organization: Sorbonne Université, Institut du Cerveau et de la Moelle épinière (ICM), AP-HP, Inserm U 1127, CNRS UMR 7225, University Hospital Pitié-Salpêtrière
– sequence: 10
  givenname: Thomas
  surname: Klopstock
  fullname: Klopstock, Thomas
  organization: Department of Neurology with Friedrich-Baur-Institute, University of Munich, German Center for Neurodegenerative Diseases (DZNE)
– sequence: 11
  givenname: Ludger
  surname: Schöls
  fullname: Schöls, Ludger
  organization: Department of Neurodegenerative Diseases, Hertie-Institute for Clinical Brain Research, University of Tübingen, German Center for Neurodegenerative Diseases (DZNE)
– sequence: 12
  givenname: Ilaria
  surname: Giordano
  fullname: Giordano, Ilaria
  organization: Department of Neurology, University Hospital of Bonn, German Center for Neurodegenerative Diseases (DZNE)
– sequence: 13
  givenname: Katrin
  surname: Bürk
  fullname: Bürk, Katrin
  organization: Department of Neurology, Philipps University of Marburg
– sequence: 14
  givenname: Massimo
  surname: Pandolfo
  fullname: Pandolfo, Massimo
  organization: Laboratory of Experimental Neurology, Université Libre de Bruxelles
– sequence: 15
  givenname: Claire
  surname: Didszdun
  fullname: Didszdun, Claire
  organization: Department of Neurology, RWTH Aachen University, JARA-BRAIN Institute of Molecular Neuroscience and Neuroimaging, Forschungszentrum Jülich GmbH and RWTH Aachen University
– sequence: 16
  givenname: Jörg B.
  surname: Schulz
  fullname: Schulz, Jörg B.
  organization: Department of Neurology, RWTH Aachen University, JARA-BRAIN Institute of Molecular Neuroscience and Neuroimaging, Forschungszentrum Jülich GmbH and RWTH Aachen University
– sequence: 17
  givenname: Sylvia
  orcidid: 0000-0003-1657-7368
  surname: Boesch
  fullname: Boesch, Sylvia
  email: sylvia.boesch@i-med.ac.at
  organization: Department of Neurology, Medical University of Innsbruck
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Cites_doi 10.1126/science.271.5254.1423
10.1371/journal.pone.0189990
10.1016/j.nmd.2010.02.019
10.1016/B978-0-444-64189-2.00005-6
10.1016/S1474-4422(07)70054-6
10.1111/jnc.12215
10.1016/S1474-4422(16)30287-3
10.1002/ana.24595
10.1136/adc.84.2.167
10.1093/eurheartj/ehu284
10.1056/NEJM199610173351601
10.1037/0021-843X.110.1.40
10.1007/s11832-012-0457-4
10.1002/1531-8249(199902)45:2<200::AID-ANA10>3.0.CO;2-U
10.1016/S0022-510X(01)00681-5
10.1111/jnc.12317
10.1007/s004150050362
10.1212/WNL.0000000000006121
10.1093/jnen/nlx087
10.1016/S1474-4422(14)70321-7
10.1038/nrneurol.2009.26
10.1002/mus.880100604
10.1001/archneur.62.12.1865
10.1002/mds.26382
10.1002/ana.25084
10.1007/BF00315657
ContentType Journal Article
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Issue 1
Keywords Natural history study
Age at onset
Genetic testing
Friedreich’s Ataxia
Diagnostic delay
Friedreich's Ataxia
Language English
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References AH Koeppen (1475_CR28) 2017; 76
P Vankan (1475_CR1) 2013; 126
K Reetz (1475_CR10) 2015; 14
J Berciano (1475_CR19) 2002; 194
BL Fogel (1475_CR24) 2007; 6
JB Schulz (1475_CR14) 2009; 5
GA Miller (1475_CR21) 2001; 110
M Cossee (1475_CR4) 1999; 45
A Filla (1475_CR5) 1990; 237
H Leonard (1475_CR16) 2001; 84
MR Konieczny (1475_CR22) 2013; 7
1475_CR30
CA Galea (1475_CR9) 2016; 79
1475_CR12
1475_CR13
M Synofzik (1475_CR26) 2018; 155
C Lecocq (1475_CR18) 2016; 31
R Bhidayasiri (1475_CR17) 2005; 62
G Caruso (1475_CR3) 1987; 10
A Durr (1475_CR6) 1996; 335
AH Koeppen (1475_CR29) 2017; 76
A Long (1475_CR27) 2017; 12
K Reetz (1475_CR7) 2018; 91
K Reetz (1475_CR11) 2016; 15
M Renaud (1475_CR25) 2017; 82
PM Elliott (1475_CR23) 2014; 35
N Quercia (1475_CR15) 2010; 20
V Campuzano (1475_CR8) 1996; 271
MH Parkinson (1475_CR2) 2013; 126
G Coppola (1475_CR20) 1999; 246
References_xml – volume: 271
  start-page: 1423
  issue: 5254
  year: 1996
  ident: 1475_CR8
  publication-title: Science.
  doi: 10.1126/science.271.5254.1423
– volume: 12
  issue: 12
  year: 2017
  ident: 1475_CR27
  publication-title: PLoS One
  doi: 10.1371/journal.pone.0189990
– volume: 20
  start-page: 340
  issue: 5
  year: 2010
  ident: 1475_CR15
  publication-title: Neuromuscul Disord
  doi: 10.1016/j.nmd.2010.02.019
– volume: 155
  start-page: 73
  year: 2018
  ident: 1475_CR26
  publication-title: Handb Clin Neurol
  doi: 10.1016/B978-0-444-64189-2.00005-6
– volume: 76
  start-page: 101
  issue: 2
  year: 2017
  ident: 1475_CR29
  publication-title: J Neuropathol Exp Neurol
– volume: 6
  start-page: 245
  issue: 3
  year: 2007
  ident: 1475_CR24
  publication-title: Lancet Neurol
  doi: 10.1016/S1474-4422(07)70054-6
– volume: 126
  start-page: 11
  issue: Suppl 1
  year: 2013
  ident: 1475_CR1
  publication-title: J Neurochem
  doi: 10.1111/jnc.12215
– volume: 15
  start-page: 1346
  issue: 13
  year: 2016
  ident: 1475_CR11
  publication-title: Lancet Neurol
  doi: 10.1016/S1474-4422(16)30287-3
– ident: 1475_CR12
– volume: 79
  start-page: 485
  issue: 3
  year: 2016
  ident: 1475_CR9
  publication-title: Ann Neurol
  doi: 10.1002/ana.24595
– volume: 84
  start-page: 167
  issue: 2
  year: 2001
  ident: 1475_CR16
  publication-title: Arch Dis Child
  doi: 10.1136/adc.84.2.167
– volume: 35
  start-page: 2733
  issue: 39
  year: 2014
  ident: 1475_CR23
  publication-title: Eur Heart J
  doi: 10.1093/eurheartj/ehu284
– ident: 1475_CR30
– volume: 335
  start-page: 1169
  issue: 16
  year: 1996
  ident: 1475_CR6
  publication-title: N Engl J Med
  doi: 10.1056/NEJM199610173351601
– volume: 110
  start-page: 40
  issue: 1
  year: 2001
  ident: 1475_CR21
  publication-title: J Abnorm Psychol
  doi: 10.1037/0021-843X.110.1.40
– volume: 7
  start-page: 3
  issue: 1
  year: 2013
  ident: 1475_CR22
  publication-title: J Child Orthop
  doi: 10.1007/s11832-012-0457-4
– volume: 45
  start-page: 200
  issue: 2
  year: 1999
  ident: 1475_CR4
  publication-title: Ann Neurol
  doi: 10.1002/1531-8249(199902)45:2<200::AID-ANA10>3.0.CO;2-U
– volume: 194
  start-page: 75
  issue: 1
  year: 2002
  ident: 1475_CR19
  publication-title: J Neurol Sci
  doi: 10.1016/S0022-510X(01)00681-5
– volume: 126
  start-page: 103
  issue: Suppl 1
  year: 2013
  ident: 1475_CR2
  publication-title: J Neurochem
  doi: 10.1111/jnc.12317
– volume: 246
  start-page: 353
  issue: 5
  year: 1999
  ident: 1475_CR20
  publication-title: J Neurol
  doi: 10.1007/s004150050362
– ident: 1475_CR13
– volume: 91
  start-page: e917
  issue: 10
  year: 2018
  ident: 1475_CR7
  publication-title: Neurology
  doi: 10.1212/WNL.0000000000006121
– volume: 76
  start-page: 969
  issue: 11
  year: 2017
  ident: 1475_CR28
  publication-title: J Neuropathol Exp Neurol
  doi: 10.1093/jnen/nlx087
– volume: 14
  start-page: 174
  issue: 2
  year: 2015
  ident: 1475_CR10
  publication-title: Lancet Neurol
  doi: 10.1016/S1474-4422(14)70321-7
– volume: 5
  start-page: 222
  issue: 4
  year: 2009
  ident: 1475_CR14
  publication-title: Nat Rev Neurol
  doi: 10.1038/nrneurol.2009.26
– volume: 10
  start-page: 503
  issue: 6
  year: 1987
  ident: 1475_CR3
  publication-title: Muscle Nerve
  doi: 10.1002/mus.880100604
– volume: 62
  start-page: 1865
  issue: 12
  year: 2005
  ident: 1475_CR17
  publication-title: Arch Neurol
  doi: 10.1001/archneur.62.12.1865
– volume: 31
  start-page: 62
  issue: 1
  year: 2016
  ident: 1475_CR18
  publication-title: Mov Disord
  doi: 10.1002/mds.26382
– volume: 82
  start-page: 892
  issue: 6
  year: 2017
  ident: 1475_CR25
  publication-title: Ann Neurol
  doi: 10.1002/ana.25084
– volume: 237
  start-page: 345
  issue: 6
  year: 1990
  ident: 1475_CR5
  publication-title: J Neurol
  doi: 10.1007/BF00315657
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Snippet Background In rare disorders diagnosis may be delayed due to limited awareness and unspecific presenting symptoms. Herein, we address the issue of diagnostic...
In rare disorders diagnosis may be delayed due to limited awareness and unspecific presenting symptoms. Herein, we address the issue of diagnostic delay in...
Background In rare disorders diagnosis may be delayed due to limited awareness and unspecific presenting symptoms. Herein, we address the issue of diagnostic...
Background: In rare disorders diagnosis may be delayed due to limited awareness and unspecific presenting symptoms. Herein, we address the issue of diagnostic...
Abstract Background In rare disorders diagnosis may be delayed due to limited awareness and unspecific presenting symptoms. Herein, we address the issue of...
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StartPage 198
SubjectTerms Adult
Age
Age at onset
Ataxia
Cardiomyopathy
Cardiovascular disease
Clinical genetics and genomics
Delayed Diagnosis
Development and progression
Diagnosis
Diagnostic delay
Dysarthria
Friedreich Ataxia - diagnosis
Friedreich Ataxia - genetics
Friedreich’s Ataxia
Gait
Genetic aspects
Genetic disorders
Genetic screening
Genetic testing
Homozygote
Human Genetics
Humans
Life Sciences
Medical diagnosis
Medical research
Medicine
Medicine & Public Health
Mutation
Natural history study
Neurons and Cognition
Pharmacology/Toxicology
Rare diseases
Retrospective Studies
Scoliosis
Statistical analysis
Studies
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Title Onset features and time to diagnosis in Friedreich’s Ataxia
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