Somatosensory evoked potentials correlate with genetics in Huntington's disease

Sándor Beniczky, S. Kéri, Andrea Antal, Katalin Jakab, Helga Nagy, G. Benedek, Z. Janka, L. Vécsei

Research output: Contribution to journalArticle

10 Citations (Scopus)

Abstract

Abnormalities of somatosensory evoked potentials (SEPs) have been reported in Huntington's disease, a neuropsychiatric disorder caused by the expansion of a CAG trinucleotide repeat. The aim of our study was to determine the relationship between these electrophysiological changes and the length of the nucleotide repeat. We found a striking correlation between the decrease in the early component amplitudes (N20 and N30) of the median nerve SEP and the repeat length, suggesting that these SEP alterations are indeed related to the genetically determined pathological process. The cortical components of the tibial nerve SEP exhibited a dramatic alteration in the patient group and were the only SEP changes found in the group of asymptomatic carriers of the mutation, being more sensitive than the median nerve SEPs.

Original languageEnglish
Pages (from-to)2295-2298
Number of pages4
JournalNeuroReport
Volume13
Issue number17
DOIs
Publication statusPublished - Dec 3 2002

Fingerprint

Somatosensory Evoked Potentials
Huntington Disease
Median Nerve
Trinucleotide Repeats
Tibial Nerve
Pathologic Processes
Nucleotides
Mutation

Keywords

  • CAG nucleotide repeat
  • Huntington's disease
  • Somatosensory evoked potentials

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Somatosensory evoked potentials correlate with genetics in Huntington's disease. / Beniczky, Sándor; Kéri, S.; Antal, Andrea; Jakab, Katalin; Nagy, Helga; Benedek, G.; Janka, Z.; Vécsei, L.

In: NeuroReport, Vol. 13, No. 17, 03.12.2002, p. 2295-2298.

Research output: Contribution to journalArticle

Beniczky, Sándor ; Kéri, S. ; Antal, Andrea ; Jakab, Katalin ; Nagy, Helga ; Benedek, G. ; Janka, Z. ; Vécsei, L. / Somatosensory evoked potentials correlate with genetics in Huntington's disease. In: NeuroReport. 2002 ; Vol. 13, No. 17. pp. 2295-2298.
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