Abstract
BACKGROUND: Deep brain stimulation (DBS) is an established treatment for motor complications in Parkinson's disease. While appendicular motor symptoms often improve, gait and balance frequently deteriorate over time, contributing substantially to disability and falls. The mechanisms underlying this deterioration remain debated and include stimulation-related effects, interactions with dopaminergic therapy, and disease progression. OBJECTIVE: To re-examine gait and balance deterioration after DBS in Parkinson's disease using a counterfactual interpretive approach that distinguishes stimulation-related effects from medication interactions and time-dependent progression. METHODS: A structured narrative review was conducted following PRISMA reporting principles. Studies evaluating gait and balance outcomes after DBS were synthesized using clinically relevant counterfactual contrasts, including stimulation ON versus OFF, medication ON versus OFF, and early versus late postoperative time points. Eligibility criteria were expanded to specify inclusion of original observational, experimental, and programming studies that reported gait or balance outcomes under interpretable stimulation, medication, or temporal conditions. RESULTS: Gait and balance deterioration after DBS reflects multiple, non-exclusive mechanisms. Acute or early postoperative worsening may occur in association with stimulation activation or electrode implantation and can be partially reversible with stimulation adjustment. Several studies demonstrate non-additive and sometimes opposing effects of DBS and dopaminergic medication on gait and balance. In contrast, longitudinal studies consistently show progressive gait and balance decline over extended follow-up despite sustained improvement in appendicular motor symptoms, supporting a prominent role for time-dependent disease progression. Balance outcomes, particularly dynamic postural control, appear more consistently affected than gait measures. CONCLUSIONS: Gait and balance deterioration after DBS in Parkinson's disease cannot be attributed to a single mechanism. Interpreting outcomes through counterfactual contrasts clarifies the relative contributions of stimulation effects, medication interactions, and disease progression, and provides a clinically grounded framework for understanding postoperative deterioration. This framework supports more precise clinical attribution of postoperative gait decline and may inform individualized programming, medication adjustment, and patient counseling.