J Stroke.  2024 Sep;26(3):458-462. 10.5853/jos.2024.01529.

Neuroprotective Effects of Pulsed Electromagnetic Fields in Acute Stroke

Affiliations
  • 1Department of Medicine and Surgery, Unit of Neurology, Neurophysiology, Neurobiology and Psychiatry, Università Campus Bio-Medico di Roma, Roma, Italy
  • 2Fondazione Policlinico Universitario Campus Bio-Medico, Roma, Italy
  • 3IRCCS Istituto delle Scienze Neurologiche di Bologna, Department of Neurology and Stroke Center, Maggiore Hospital, Bologna, Italy
  • 4Neurology Unit, Neuromotor & Rehabilitation Department, Azienda USL-IRCCS di Reggio Emilia, Reggio Emilia, Italy
  • 5Stroke Unit, Tor Vergata Polyclinic Hospital, Tor Vergata University, Roma, Italy
  • 6Department of Neuroscience and Rehabilitation, Division of Neurology, University Hospital of Ferrara, Ferrara, Italy
  • 7University Vita-Salute San Raffaele, Milan, Italy
  • 8Experimental Neurophysiology Unit, Institute of Experimental Neurology, Scientific Institute San Raffaele, Milan, Italy
  • 9Department of Neurorehabilitation Sciences, Casa di Cura Igea, Milan, Italy
  • 10Department of Information Engineering, Electronics and Telecommunications (DIET), Sapienza University of Rome, Roma, Italy
  • 11Medical Division, IGEA, Carpi, Italy


Figure

  • Figure 1. CONSORT study flow diagram. CONSORT, Consolidated Standards of Reporting Trials; FU, follow-up; MRI, magnetic resonance imaging. *Of the 16 patients in the active group, 14 were available for analysis at the 7-day FU: two patients were excluded from the analysis because they did not meet the inclusion criteria “2” and “3” (Supplementary Methods); 11 patients were available for analysis at the 45-day and 90-day FUs: three patients did not return for follow-up visit during the COVID-19 pandemic, but when interviewed by telephone, they were in good health and did not mention any negative effect related to the treatment; †Of the 21 patients in the placebo group, 20 were available for analysis at the 7-day FU: one patient was excluded from the analysis because he did not meet the inclusion criteria “3” (Supplementary Methods), 19 patients were available for analysis at the 45-day and 90-day FUs: one patient died from causes unrelated to the treatment.

  • Figure 2. Primary and secondary outcomes. (A) Line graph showing mean lesion volumes (±SE) at baseline, 7 days, and 45 days in the placebo and active groups. (B) Normalized MRI volume reduction (mean±SE). (C) Distribution of scores on the mRS at 90 days. (D) BI over time in the active and placebo groups (mean±SE). (E) NIHSS over time in the active and placebo groups (mean±SE). SE, standard error; MRI, magnetic resonance imaging; mRS, modified Rankin Scale; BI, Barthel Index; NIHSS, National Institutes of Health Stroke Scale. *P<0.05; **P<0.01; †P=nonsignificant (vs. baseline).

  • Figure 3. Subgroup analysis. (A) Line graph showing mean lesion volumes (±SE) at baseline, 7 days, and 45 days in the placebo and active groups. (B) NIHSS score (means±SE) over time in the active and placebo. NIHSS score significantly improved over baseline in both groups. (C) Distribution of scores on the mRS at 90 days. Excellent outcome at 90 days was achieved in 85.7% of patients in the active group and in 63.6% of patients in the placebo group (P=0.634). (D) BI score (means±SE) over time in the active and placebo groups. The BI score improved from 42.5±30.9 at baseline to 92.9±16.8 (PP<0.01) at 90 days in the active group; whilst in the placebo group, BI increased from 54.2±37.2 at baseline to 82.7±37.2 (P=0.100) at 90 days. SE, standard error; NIHSS, National Institutes of Health Stroke Scale; mRS, modified Rankin Scale; BI, Barthel Index. *P<0.05; **P<0.01; †P=nonsignificant (vs. baseline).


Reference

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