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DOI 10.1016/j.clinph.2009.07.001

Медицинская библиотека · Clinical neurophysiology : official journal of the International Federation of Clinical Neurophysiology · 2009

Ulnar nerve impairment at the wrist does not contribute to extramedian sensory symptoms in carpal tunnel syndrome.

Tamburin Stefano, Cacciatori Carlo, Praitano Maria Luigia, Marani Silvia, Zanette Giampietro

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Аннотация

OBJECTIVE

Extramedian spread of sensory symptoms is frequent in carpal tunnel syndrome (CTS) but its mechanisms are unclear. We explored the possible role of subtle ulnar nerve abnormalities in the pathogenesis of extramedian symptoms.

METHODS

We recruited 350 CTS patients. After selection, 143 patients (225 hands) were included. The hand symptoms distribution was graded with a diagram into median (MED) and extramedian (EXTRAMED) pattern. We tested the correlation of ulnar nerve conduction measures with the distribution and the severity of symptoms involving the ulnar territory. The clinical significance of ulnar nerve conduction findings was explored with quantitative sensory testing (QST).

RESULTS

EXTRAMED distribution was found in 38.7% of hands. The ulnar neurographic measures were within normal values. Ulnar nerve sensory measures were significantly better in EXTRAMED vs MED hands and not significantly correlated to ulnar symptoms severity. Ulnar and median nerve sensory measures were significantly correlated. QST showed normal function of ulnar nerve alphabeta-fibers.

CONCLUSIONS

Ulnar nerve sensory abnormalities do not contribute to the spread of sensory symptoms into the ulnar territory.

SIGNIFICANCE: Our data favour the hypothesis that spinal and supraspinal neuroplastic changes may underlie extramedian spread of symptoms in CTS.

Для цитирования: Tamburin Stefano, Cacciatori Carlo, Praitano Maria Luigia, Marani Silvia, Zanette Giampietro. Ulnar nerve impairment at the wrist does not contribute to extramedian sensory symptoms in carpal tunnel syndrome.. Clinical neurophysiology : official journal of the International Federation of Clinical Neurophysiology. 2009. DOI: 10.1016/j.clinph.2009.07.001.

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