Background Cervical dystonia (CD) is characterized by involuntary contractions of the cervical muscles, leading to abnormal head, neck, or shoulder postures. While eye-tracking studies have shown saccadic abnormalities in CD, eye-movement dynamics during fixation remain understudied. Methods We examined fixation-related eye-movement dynamics during pro- and antisaccade tasks in 35 CD patients and 17 healthy controls, focusing on the 500-1500 ms interval during central fixation. Primary outcomes were maximal binocular angular speed, maximum 30-ms angular-speed variance, and maximal absolute left-right angular-speed difference. Results Primary clustered Wilcoxon analyses showed greater peak eye movement speed in CD (p = 0.002), greater short-term variability in speed (p=0.002), and a higher left-right angular-speed difference (p=0.02). These effects remained significant after medication-exclusion sensitivity analysis (p=0.002, p=0.002, and p=0.01, respectively). Conclusion Our preliminary findings indicate altered fixation-related eye-movement dynamics in CD and suggest that oculomotor abnormalities in CD may extend beyond saccadic control.
Objective We aimed to develop and validate a brief, self-administered questionnaire integrating motor and prodromal non-motor symptoms for screening Parkinson's disease (PD). Methods We conducted a three-phase study. Phase 1 used a prospectively registered systematic review of 107 studies to generate a 52-item draft. In Phase 2, the draft was refined in 205 participants (122 with early PD and 83 healthy controls) using item-level areas under the receiver operating characteristic curves (AUCs) and age- and sex-adjusted multivariable logistic regression. Phase 3 validated the 9-item Korean PD Screening Questionnaire (KPDSQ) in an independent cohort (n = 246; 122 PD, 45 essential tremor [ET], and 79 controls), and included a 4-week test-retest reassessment. Results The final 9-item KPDSQ comprises seven motor items (rest tremor, shuffling or short-step gait, slow daily activities, decreased arm swing, soft voice, masked face, and freezing of gait) and two non-motor items (hyposmia and dream-enactment behavior). At a cutoff of ≥2, sensitivity was 88.5% and specificity was 92.4% for distinguishing PD from controls (AUC = 0.970; 95% CI, 0.946-0.984; p < 0.001). At ≥3, the KPDSQ distinguished PD from ET (AUC = 0.774; 95% CI, 0.680-0.847; p < 0.001). Internal consistency was high (Cronbach's α = 0.800), test-retest reliability was excellent (ICC = 0.921), and scores correlated with MDS-UPDRS Part III scores in patients with PD (Spearman's ρ = 0.330; p < 0.001). Conclusions The 9-item KPDSQ is a reliable, clinically valid screening tool combining motor and prodromal non-motor features. Prospective community-based validation is warranted.
Cognitive impairment is a major nonmotor symptom of Parkinson’s disease (PD), yet effective strategies for preserving cognitive function remain limited. Although physical exercise may confer cognitive benefits, the biological pathways linking exercise to cognition in PD remain incompletely established. This narrative review presents a hypothesis-generating translational framework for 4 candidate mechanistic domains that may contribute to exercise-related cognitive effects in PD. First, exercise-responsive neurotrophic signaling, particularly through brain-derived neurotrophic factor–tropomyosin receptor kinase B, insulin-like growth factor 1, and vascular endothelial growth factor pathways, may support synaptic plasticity, neuronal survival, and neurovascular function. Second, exercise may modulate dopaminergic, cholinergic, and noradrenergic systems and influence corticostriatal plasticity relevant to cognitive function. Third, muscle-derived factors and exercise-induced metabolites may affect neurotrophic signaling, neuronal metabolism, and autophagy–lysosomal clearance of α-synuclein. Fourth, exercise may regulate systemic and central inflammatory responses through cytokine signaling, glial activation, inflammasome pathways, and complement-mediated synaptic remodeling. The evidence supporting these pathways is derived from basic, preclinical, observational, and exercise-intervention studies, but the strength of evidence varies considerably across stages of translation. Direct evidence that exercise-induced biological changes mediate cognitive improvement in patients with PD is lacking. These pathways should therefore be regarded as candidate mechanisms for hypothesis-driven investigation of the cognitive effects of exercise in PD.
