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Previous Volume 336:1021-1023 April 3, 1997 Number 14 Next

	Since this article has no abstract, we have provided an extract of the first 100 words of the full text and any section headings.

	Full Text Add to Personal Archive Add to Citation Manager Notify a Friend E-mail When Cited Related Article by Rosenberg, R. N. Related Article by Rosenberg, R. N. Related Article by Dürr, A. PubMed Citation

To the Editor: Dürr and colleagues (Oct. 17 issue)¹ correlated the phenotypic features of Friedreich's ataxia and the size of an intronic GAA-triplet repeat in the gene that causes the disease, X25, and concluded that "the clinical spectrum of Friedreich's ataxia is broader than previously recognized" and that "the direct molecular test for the GAA expansion on chromosome 9 is useful for diagnosis, determination of prognosis, and genetic counseling." We disagree with these conclusions.

For many years the diagnosis of Friedreich's ataxia has been based on clinical criteria. According to these criteria, 103 of their patients had typical Friedreich's ataxia, . . . [Full Text of this Article]

References

This article has been cited by other articles:

• Delatycki, M. B, Williamson, R., Forrest, S. M (2000). Friedreich ataxia: an overview. J. Med. Genet. 37: 1-8 [Abstract] [Full Text]  
• Santoro, L, De Michele, G, Perretti, A, Crisci, C, Cocozza, S, Cavalcanti, F, Ragno, M, Monticelli, A, Filla, A, Caruso, G (1999). Relation between trinucleotide GAA repeat length and sensory neuropathy in Friedreich's ataxia. J. Neurol. Neurosurg. Psychiatry 66: 93-96 [Abstract] [Full Text]