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Studies have shown that bladder dysfunction significantly influences quality\u2010of\u2010life (QOL) measures, early institutionalisation, and health economics. We review the pathophysiology of bladder dysfunction in PD, lower urinary tract symptoms (LUTS), objective assessment, and treatment options. In patients with PD, disruption of the dopamine D1\u2010GABAergic direct pathway may lead to LUTS. Overactive bladder (OAB) is the most common LUT symptom in PD patients, and an objective assessment using urodynamics commonly shows detrusor overactivity (DO) in these patients. The post\u2010void residual (PVR) volume is minimal in PD, which differs significantly from multiple system atrophy (MSA) patients who have a more progressive disease that leads to urinary retention. However, subclinical detrusor weakness during voiding may also occur in PD. Regarding bladder management, there are no large, double\u2010blind, prospective studies in this area. It is well recognised that dopaminergic drugs can improve or worsen LUTS in PD patients. Therefore, an add\u2010on therapy with anticholinergics is required. Beta\u20103 adrenergic agonists are a potential treatment option because there are little to no central cognitive events. Newer interventions, such as deep brain stimulation (DBS), are expected to improve bladder dysfunction in PD. Botulinum toxin injections can be used to treat intractable urinary incontinence in PD. Transurethral resection of the prostate gland (TURP) for comorbid BPH in PD is now recognised to be not contraindicated if MSA is excluded. Collaboration of urologists with neurologists is highly recommended to maximise a patients' bladder\u2010associated QOL.<jats:italic>Neurourol. 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