<p>Pain is among the most prevalent, disabling, and underrecognized non-motor symptoms of Parkinson’s disease (PD), affecting approximately 40–85% of patients across cohorts. It is heterogeneous, often multifactorial, and may occur at any stage of disease, including the prodromal phase. Pain in PD can reflect musculoskeletal strain, dystonia, neuropathic/radicular mechanisms, altered central nociceptive processing, or combinations thereof, and it frequently fluctuates with motor state, mood, sleep, and overall non-motor burden. Over time, the field has moved from purely clinical classifications toward mechanism-based systems, including the Parkinson’s Disease Pain Classification System, which may better guide individualized treatment. Management should therefore be multimodal rather than sequential, integrating optimization of dopaminergic therapy, targeted pharmacological and non-pharmacological interventions, rehabilitation, psychological support, and device-aided therapies where indicated. Botulinum toxin represents a shift from systemic pharmacological escalation to precision, mechanism-directed local therapy and may be a first line treatment choice in selected focal pain syndromes, especially painful dystonia and focal musculoskeletal pain and reduce polypharmacy burden and systemic adverse effects by replacing chronic oral symptomatic medications. This review summarizes the evolving classification of pain in PD, its clinical presentation across the disease continuum, and the rationale for an individualized, multidisciplinary, and mechanism-based treatment strategy, with special emphasis on botulinum toxin within multimodal care.</p>