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2 results

  • Can total electrical energy (TEED) after subthalamic DBS alter verbal fluency in Parkinson’s disease patients? A preliminary evidence

  • Fabiana Ruggiero, Francesca Mameli, Edoardo Nicolò Aiello, Eleonora Zirone, Filippo Cogiamanian, Linda Borellini, Elena Pirola, Antonella Ampollini, Barbara Poletti, Angelica De Sandi, Marco Prenassi, Sara Marceglia, Nicola Ticozzi, Vincenzo Silani, Marco Locatelli, Giordano D’Urso, Sergio Barbieri, Alberto Priori, Roberta Ferrucci
  • Journal:
    CNS Spectrums / Volume 29 / Issue 5 / October 2024
    Published online by Cambridge University Press:
    28 October 2024, pp. 412-415
    • Article
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      • Open access
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  • Objective

    Deep brain stimulation (DBS) of the subthalamic nucleus (STN) improves motor outcomes in Parkinson’s disease (PD) but may have adverse long-term effects on specific cognitive domains. The aim of this study was to investigate the association between total electrical energy (TEED) delivered by DBS and postoperative changes in verbal fluency.

    Methods

    Seventeen PD patients undergoing bilateral STN-DBS were assessed with the Alternate Verbal Fluency Battery (AVFB), which includes phonemic (PVF), semantic (SVF), and alternate verbal fluency (AVF) tests, before surgery (T0) and after 6 (T1) and 12 months (T2). Bilateral TEED and average TEEDM were recorded at T1 and T2. For each AVFB measurement, changes from T0 to T1 (Δ-01) and from T0 to T2 (Δ-02) were calculated.

    Results

    At T1, PVF (p = 0.007) and SVF scores (p = 0.003) decreased significantly. TEED measures at T1 and T2 were unrelated to Δ-01 and Δ-02 scores, respectively. However, an inverse, marginally significant association was detected between the TEEDM and Δ-01 scores for the AVF (p = 0.041, against an αadjusted = 0.025).

    Conclusions

    In conclusion, the present reports provide preliminary evidence that TEED may not be responsible or only slightly responsible for the decline in VF performance after STN-DBS in PD.

  • Chapter 11 - Imaging Genetic and Epigenetic Markers in Mood Disorders

  • from Section 4 - Novel Approaches in Brain Imaging
  • Edited by Sudhakar Selvaraj, Paolo Brambilla, Università degli Studi di Milano, Jair C. Soares
  • Book:
    Mood Disorders
    Published online:
    12 January 2021
    Print publication:
    07 January 2021, pp 135-150

  • Summary

    Genetics explain 60–85% and 31–50% of the risk to develop, respectively, bipolar disorder (BD) (1, 2) and major depressive disorder (MDD) (3, 4). Thus, hereditability has emerged as a crucial factor in the pathophysiology of mood disorders. Early genetics studies focused their attention on specific single-nucleotide polymorphism (SNP), preselected on prior evidence for their functional role in coding products that may influence relevant features of the disorders, also known as candidate gene approach. In these studies, we define risk allele, genetic variants associated with the disorder or worse clinical features such as reduced response to therapeutics, early onset, and higher recurrence.