Affiliations: [a] Dipartimento di Psicologia, Università degli Studi di Bologna, Italy | [b] Centro studi e ricerche in Neuroscienze Cognitive, Campus di Cesena, Cesena, Italy | [c] IRCCS Fondazione Santa Lucia, Roma, Italy | [d] Istituto di Riabilitazione Santo Stefano, Porto Potenza Picena, Macerata, Italy
Correspondence:
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Corresponding author: Elisabetta Làdavas, Centro studi e ricerche in Neuroscienze Cognitive, Viale Europa 980, 47123 Cesena, Italy. Tel.: +39 051 2091347; Fax: +39 051 2091844; E-mail: [email protected]
Correspondence:
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Corresponding author: Andrea Serino, Center for Neuroprosthetics, Ecole Polytechnique Fédérale de Lausanne, Station 19, CH-1015, Lausanne, Switzerland. Tel.: +41 21 69 30695; Fax: +41 21 69 31770; [email protected]
Note: [1] Present address: Center for Neuroprosthetics, Ecole Polytechnique Fédérale de Lausanne, Switzerland.
Abstract:
Background and objective: The aim of the study is to compare the effects of multiple sessions of cathodal (c-tDCS) or anodal tDCS (a-tDCS) in modulating the beneficial effects of prism adaptation (PA) treatment in neglect patients.
Methods: 30 neglect patients were submitted to 10 daily sessions of PA treatment. Patients were pseudo-randomly divided into 3 groups. In the c-tDCS-group, each PA session was coupled with 20 minutes of cathodal stimulation of the left, intact PPC; in the a-tDCS-group, anodal stimulation was applied to PPC of the damaged hemisphere; in the Sham group, sham stimulation was applied. Neglect was evaluated before and after treatment with the Behavioral Inattention Test.
Results: Combined tDCS-PA treatment induced stronger neglect improvement in the a-tDCS group as compared to the Sham group. No improvement was found in the c-tDCSgroup, with respect to that normally induced by PA and found in the Sham group.
Conclusions: c-tDCS abolished neglect amelioration after PA, possibly because stimulation affected the sensorimotor network controlling prism adaptation. Instead, a-tDCS PPC boosted neglect amelioration after PA probably thanks to increased excitability of residual tissue in the lesioned hemisphere, which in turn might reduce dysfunctional over-excitability of the intact hemisphere.
