Somatosensory evoked potentials correlate with genetics in Huntington's disease

Neuroreport. 2002 Dec 3;13(17):2295-8. doi: 10.1097/00001756-200212030-00025.

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adolescent
  • Adult
  • Afferent Pathways / physiopathology*
  • Age Factors
  • Aged
  • Aged, 80 and over
  • Electric Stimulation
  • Evoked Potentials, Somatosensory / genetics*
  • Female
  • Humans
  • Huntington Disease / genetics*
  • Huntington Disease / pathology
  • Huntington Disease / physiopathology*
  • Male
  • Median Nerve / physiopathology
  • Middle Aged
  • Neural Conduction / genetics*
  • Peripheral Nerves / physiopathology*
  • Sex Characteristics
  • Somatosensory Cortex / physiopathology*
  • Tibial Nerve / physiopathology
  • Trinucleotide Repeat Expansion / genetics