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Changes in the thalamocortical component of high frequency oscillations following botulinum toxin treatment in cervical dystonia

Cruciani, Alessandro; Anzini, Gaia; Magliozzi, Alessandro; Musumeci, Gabriella; Corp, Daniel T.; Altavista, Maria Concetta; Di Lazzaro, Vincenzo; Marano, Massimo

Changes in the thalamocortical component of high frequency oscillations following botulinum toxin treatment in cervical dystonia

Cruciani, Alessandro
Anzini, Gaia
Magliozzi, Alessandro
Musumeci, Gabriella
Corp, Daniel T.
Altavista, Maria Concetta
Di Lazzaro, Vincenzo
Marano, Massimo
Katso/Avaa
1-s2.0-S1388245725005619-main.pdf (1.231Mb)
Lataukset: 

Elsevier BV
doi:10.1016/j.clinph.2025.03.048
URI
https://doi.org/10.1016/j.clinph.2025.03.048
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Julkaisun pysyvä osoite on:
https://urn.fi/URN:NBN:fi-fe2025082790542
Tiivistelmä

OBJECTIVE

This study aims to investigate the central effects of Botulinum toxin type A (BoNT-A) on the somatosensory system in patients with cervical dystonia (CD), focusing on the thalamocortical pathway using high-frequency oscillations (HFOs) and short-latency afferent inhibition (SAI).

METHODS

An observational longitudinal study was conducted on 10CD patients and 10 healthy controls (HC). HFOs and SAI were assessed for CD and HC at baseline (T0; the day before BoNT-A treatment). Then only for CD patients, SAI and HFOs were assessed again 30 days after (T1) BoNT-A treatment. Changes in SAI values and HFO early and late area between T0 and T1 in CD patients were evaluated with the Wilcoxon signed-rank test.

RESULTS

At T0, CD patients exhibited significantly reduced early HFOs compared to HC, with no significant differences in late HFOs or SAI values. After BoNT-A treatment, a significant increase in early HFOs was observed in CD patients at T1, while late HFOs and SAI values remained unchanged.

CONCLUSION

The findings suggest that BoNT-A treatment may have central effects on thalamocortical activity, as evidenced by changes of early HFOs in CD patients following injections.

SIGNIFICANCE

This study provides neurophysiological evidence supporting the central effects of BoNT-A on the somatosensory system and corroborates the idea of a somatosensory involvement in CD pathogenesis. This funding could pave the way for future integrated treatment approaches.

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