The natural history of degenerative ataxia: a retrospective study in 466 patients.

The aim of the present study was (i) to compare disease progression and survival in different types of degenerative ataxia, and (ii) to identify variables that may modify the rate of disease progression. We included patients suffering from Friedreich's ataxia (FRDA, n = 83), early onset cerebellar ataxia (EOCA, n = 30), autosomal dominant cerebellar ataxia (ADCA) type I (ADCA-I, n = 273), ADCA-III (n = 13) and multiple system atrophy (MSA, n = 67). Molecular genetic testing allowed us to assign 202 ADCA-I patients to one of the following subgroups: spinocerebellar ataxia type I (SCAI, n = 36), SCA2 (n = 56) and SCA3 (n = 110). To assess disease progression we defined the following disease stages: stage 0 = no gait difficulties; stage 1 = disease onset, as defined by onset of gait difficulties; stage 2 = loss of independent gait; stage 3 = confinement to wheelchair; stage 4 = death. Disease progression was most rapid in MSA, intermediate in FRDA, ADCA-I and ADCA-III and slowest in EOCA. The rate of progression was similar in SCA1, SCA2 and SCA3. The CAG repeat length was a significant risk factor for faster progression in SCA2 and SCA3, but not in SCA1. In FRDA, the time until confinement to wheelchair was shorter in patients with earlier disease onset, suggesting that patients with long GAA repeats and early disease onset have a poor prognosis. Female gender increased the risk of becoming dependent on walking aids or a wheelchair, but it did not influence survival in FRDA, SCA3 and MSA. In SCA2, female gender was associated with shortened survival. In MSA, later age of onset increased the risk of rapid progression and death.

[1]  A. Harding Early onset cerebellar ataxia with retained tendon reflexes: a clinical and genetic study of a disorder distinct from Friedreich's ataxia. , 1981, Journal of neurology, neurosurgery, and psychiatry.

[2]  T. Klockgether,et al.  Repeat length and disease progression in spinocerebellar ataxia type 3 , 1996, The Lancet.

[3]  J. Bouchard,et al.  Clinical Description and Roentgenologic Evaluation of Patients with Friedreich's Ataxia , 1976, Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques.

[4]  David R. Cox,et al.  Regression models and life tables (with discussion , 1972 .

[5]  M. Skalej,et al.  Friedreich's ataxia with retained tendon reflexes , 1996, Neurology.

[6]  N. Quinn,et al.  Multiple system atrophy--the nature of the beast. , 1989, Journal of neurology, neurosurgery, and psychiatry.

[7]  N. Quinn,et al.  Survival of patients with pathologically proven multiple system atrophy , 1997, Neurology.

[8]  A. Harding CLASSIFICATION OF THE HEREDITARY ATAXIAS AND PARAPLEGIAS , 1983, The Lancet.

[9]  P. Lantos,et al.  Cellular pathology of multiple system atrophy: a review. , 1994, Journal of neurology, neurosurgery, and psychiatry.

[10]  S. Tsuji,et al.  A clinical and pathologic study of a large Japanese family with Machado‐ Joseph disease tightly linked to the DNA markers on chromosome 14q , 1994, Neurology.

[11]  Georg Auburger,et al.  Moderate expansion of a normally biallelic trinucleotide repeat in spinocerebellar ataxia type 2 , 1996, Nature Genetics.

[12]  N P Quinn,et al.  Clinical features and natural history of multiple system atrophy. An analysis of 100 cases. , 1994, Brain : a journal of neurology.

[13]  Alexandra Durr,et al.  Spinocerebellar ataxia 3 and machado‐joseph disease: Clinical, molecular, and neuropathological features , 1996, Annals of neurology.

[14]  P. Patel,et al.  Friedreich's Ataxia: Autosomal Recessive Disease Caused by an Intronic GAA Triplet Repeat Expansion , 1996, Science.

[15]  S. Tsuji,et al.  Identification of the spinocerebellar ataxia type 2 gene using a direct identification of repeat expansion and cloning technique, DIRECT , 1996, Nature Genetics.

[16]  A. Chiò,et al.  Reduced life expectancy in 40 cases of early onset cerebellar ataxia with retained tendon reflexes: a population‐based study , 1993, Acta neurologica Scandinavica.

[17]  Huda Y. Zoghbi,et al.  Expansion of an unstable trinucleotide CAG repeat in spinocerebellar ataxia type 1 , 1993, Nature Genetics.

[18]  F. Norris,et al.  Onset, natural history and outcome in idiopathic adult motor neuron disease , 1993, Journal of the Neurological Sciences.

[19]  D Petersen,et al.  Early onset cerebellar ataxia with retained tendon reflexes. Clinical, electrophysiological and MRI observations in comparison with Friedreich's ataxia. , 1991, Brain : a journal of neurology.

[20]  P. Preux,et al.  Survival prediction in sporadic amyotrophic lateral sclerosis. Age and clinical form at onset are independent risk factors. , 1996, Neuroepidemiology.

[21]  A. Harding Friedreich's ataxia: a clinical and genetic study of 90 families with an analysis of early diagnostic criteria and intrafamilial clustering of clinical features. , 1981, Brain : a journal of neurology.

[22]  G. De Michele,et al.  Age of onset, sex, and cardiomyopathy as predictors of disability and survival in Friedreich's disease , 1996, Neurology.

[23]  William B. Dobyns,et al.  Autosomal dominant cerebellar ataxia (SCA6) associated with small polyglutamine expansions in the α1A-voltage-dependent calcium channel , 1997, Nature Genetics.

[24]  A Dürr,et al.  Clinical and genetic abnormalities in patients with Friedreich's ataxia. , 1996, The New England journal of medicine.

[25]  J. Dichgans,et al.  Multiple system atrophy: natural history, MRI morphology, and dopamine receptor imaging with 123IBZM-SPECT. , 1994, Journal of neurology, neurosurgery, and psychiatry.

[26]  Shigenobu Nakamura,et al.  CAG expansions in a novel gene for Machado-Joseph disease at chromosome 14q32.1 , 1994, Nature Genetics.

[27]  A. Korczyn,et al.  Natural course of idiopathic torsion dystonia among Jews. , 1994, Neuroepidemiology.

[28]  X. Estivill,et al.  Clinical, neuropathologic, and genetic studies of a large spinocerebellar ataxia type 1 (SCA1) kindred , 1995, Neurology.

[29]  A. Harding The clinical features and classification of the late onset autosomal dominant cerebellar ataxias. A study of 11 families, including descendants of the 'the Drew family of Walworth'. , 1982, Brain : a journal of neurology.

[30]  Yves Agid,et al.  Cloning of the gene for spinocerebellar ataxia 2 reveals a locus with high sensitivity to expanded CAG/glutamine repeats , 1996, Nature Genetics.

[31]  Shirley Hansen,et al.  Dominantly inherited olivopontocerebellar atrophy from eastern Cuba Clinical, neuropathological, and biochemical findings , 1989, Journal of the Neurological Sciences.

[32]  J. Klein,et al.  Statistical Models Based On Counting Process , 1994 .

[33]  Michael Fetter,et al.  Late-onset Friedreich's ataxia. Molecular genetics, clinical neurophysiology, and magnetic resonance imaging. , 1993, Archives of neurology.

[34]  N. Mantel,et al.  Friedreich's disease , 1988, Neurology.