Parkinson's disease (PD) is a progressive neurodegenerative disease characterized by rigidity, bradykinesia, resting tremor, and postural instability. Rigidity, defined as an increased resistance to passive movement of a joint, progresses faster than other motor signs in PD. Rigidity is attributable to both exaggerated neural reflex and altered muscle mechanical properties. However, little is known about the contributions of individual components to rigidity. Further, there is no evidence regarding the effects of dopaminergic medication on individual components. Objectives of this study were to quantify the contributions of neural reflexes and intrinsic muscle properties to rigidity and investigate the effects of medication on each contributing component. Joint torque and muscle activities of the wrist in 14 patients and 14 controls were measured during externally induced movements. Each subject with PD was tested in Off- and On-medication states. A system identification technique was applied to differentiate and quantify the neural reflex and intrinsic mechanical components. A mixed model of ANOVA was performed to compare the differences between the two components of rigidity for both groups, and to compare between the Off- and On-medication states for patients. The results showed that reflex and intrinsic components are comparable (p >0.05), and both are enhanced in subjects with PD than in the controls (p < 0.05). Medication decreased the reflex component of rigidity (p < 0.01). It is concluded that both reflex and intrinsic factors are responsible for rigidity. Present findings are clinically significant as they may provide guidance in development of effective therapeutic interventions.