Description

Parkinson's disease (PD) commonly presents with gait slowing, reduced step length, balance impairment and freezing of gait, leading to falls and loss of independence. The supplementary motor area (SMA) is a key hub for internally generated movement, sequencing, and gait initiation. Anodal transcranial direct current stimulation (tDCS) over SMA can increase cortical excitability and modulate cortico-basal ganglia networks. Nordic Walking (NW) is a task-specific, cue-rich gait training method that promotes rhythmic arm-leg coupling, stride elongation, and postural control. Delivering SMA-targeted tDCS concurrently with NW is expected to leverage state-dependent plasticity, priming motor networks while patients practice the target skill, thereby enhancing the functional yield of training.

Objectives and hypotheses: The primary objective is to determine whether anodal SMA tDCS given during NW improves walking speed more than sham tDCS during the same NW program. We hypothesize superiority of the active condition on gait speed (10-Meter Walk Test) at post-intervention, with maintenance at 1-month follow-up. Secondary objectives include effects on balance, motor signs, and disease-specific quality of life, and documentation of safety/tolerability.

Design and setting: Single-center, parallel-group, randomized, double-blind, sham-controlled clinical trial conducted at a university outpatient neurorehabilitation facility in Brazil. Participants are randomized 1:1 using a computer-generated sequence (permuted blocks) by an investigator not involved in enrollment or assessments. Allocation is concealed using sequentially numbered, opaque, sealed envelopes stored in a secure location accessible only to the randomization custodian. Masking and fidelity: Participants, treating therapists, and outcome assessors remain blinded. The stimulator is pre-programmed under coded modes; device indicators and procedures are identical across groups. The sham program includes brief current ramp-in/out to mimic sensations, then no sustained current. Intervention fidelity is supported by standardized checklists, session logs, and periodic supervision of therapists not involved in outcome assessment. Participants: Adults with idiopathic PD on stable antiparkinsonian medication who can follow simple commands. The sample targets a slow-gait phenotype to maximize clinical relevance. Exclusion criteria address contraindications to tDCS (e.g., implanted cranial/brain devices, non-intact scalp at electrode sites), unsafe exercise participation, cognitive impairment incompatible with consent/testing, and concurrent neuromodulation trials. Assessments are scheduled in a standardized medication state (e.g., "on" medication) to reduce variability. Interventions: Active tDCS + NW - Anodal tDCS over SMA (midline, approximately FCz) using saline-soaked sponge electrodes (5×7 cm); cathode supraorbital contralateral. Intensity 2.0 mA for 20 minutes with 30-s ramp-in/out, three sessions/week for 4 weeks (12 sessions). Stimulation is delivered concurrently with NW. The NW session lasts 30 minutes (5-min warm-up; 20-min continuous walking with poles at moderate effort monitored by perceived exertion; 5-min cool-down), supervised by trained staff with standardized instruction on pole technique and cadence. Sham tDCS + NW - Identical setup, timing, and NW protocol; sham involves brief ramping then zero current for the remainder of the stimulation window. Other therapies and exercises are not allowed during the trial. Outcomes and assessment schedule: The primary outcome is gait speed (m/s) on the 10-Meter Walk Test at post-intervention and 1-month follow-up, referenced to baseline. Secondary outcomes include Timed Up and Go, Berg Balance Scale, Freezing of Gait Questionnaire, MDS-UPDRS Part III, and PDQ-39; adverse events are recorded each session using a structured checklist. Assessments occur at baseline, post-intervention, and 1-month follow-up under standardized conditions and assessor training. Sample size and statistical analysis: The trial is powered to detect a between-group difference in gait speed consistent with a minimally important change in PD, allowing for attrition. The primary analysis uses ANCOVA with post-intervention gait speed as the dependent variable, group as fixed effect, and baseline gait speed as covariate; corresponding estimates with 95% confidence intervals and effect sizes are reported. Sensitivity analyses include linear mixed-effects models across baseline, post, and follow-up time points. Analyses follow the intention-to-treat principle with appropriate handling of missing data (e.g., maximum likelihood/multiple imputation); a per-protocol analysis is planned as supportive. Responder analyses (e.g., proportion achieving ≥0.10 m/s improvement) and exploratory subgroup analyses (e.g., disease severity, baseline freezing status) are prespecified. Safety and monitoring: Vital signs (heart rate, blood pressure, SpO₂) are checked pre/post sessions; skin under electrodes is inspected before/after stimulation. Common tDCS sensations (tingling, itching, mild erythema) and exercise-related symptoms are systematically queried. Predefined criteria permit pausing or discontinuation (e.g., severe headache, dizziness, hypertensive response, arrhythmia, significant skin irritation). Serious adverse events are reported promptly to the ethics board per institutional policy. Data management and dissemination: De-identified data are stored on secure, access-controlled servers with audit trails; only authorized study personnel can access the linkage file. Results will be disseminated through peer-reviewed publications and scientific meetings. Individual-participant data sharing will adhere to the plan stated in the IPD section of this record.