The objective of the study is to investigate the correlation between bilirubin and uric acid (UA) concentrations and symptoms of Parkinson's disease (PD) in Chinese population. A total of 425 PD patients and 460 controls were included in the current study. Patients were diagnosed by a neurologist and assessed using the Hoehn & Yahr (H&Y) scale. Venous blood samples were collected, and bilirubin and UA concentrations were analyzed. Compared to controls, indirect bilirubin (IBIL) and UA concentrations were lower in PD patients (P IBIL = 0.015, P UA = 0.000). Serum IBIL in different age subgroups and H&Y stage subgroups were also lower compared to the control group (P IBIL = 0.000, P UA = 0.000) but were not significantly different among these subgroups. Females in the control group had significantly lower serum IBIL and UA concentrations than males (P IBIL = 0.000, P UA = 0.000) and the PD group (P IBIL = 0.027, P UA = 0.000). In early PD (patients with <2-year medical history and no treatment), serum IBIL and UA concentrations were also lower than the controls (P IBIL = 0.013, P UA = 0.000). Although IBIL concentration was positively correlated with UA concentration in controls (R IBIL = 0.229, P IBIL = 0.004), this positive association was not observed in the PD group (R IBIL = -0.032, P IBIL = 0.724). Decreased levels of serum IBIL and UA were observed in PD patients. It is possible that individuals with decreased serum bilirubin and UA concentrations lack the endogenous defense system to prevent peroxynitrite and other free radicals from damaging and destroying dopaminergic cells in the substantia nigra. Our results provide a basis for further investigation into the role of bilirubin in PD.

Movement disorders are a recognized complication of stroke. Here we present a case of hemichorea-hemiballism (HCHB) after stroke. Basal ganglia and thalamus are typically recognized as sites responsible for HCHB. The MRI scan showed acute infarction which was unexpectedly present in both sides of corona radiate and cortex, but not in basal ganglia. This cortical HCHB could have evolved due to hypoperfusion of basal ganglia undetectable at the MRI scan or due to interruption of excitatory connections from the cerebral cortex to basal ganglia.

Background and Objective: The effects of the combination of naloxone and edaravone on acute cerebral infarction (ACI), a severe cerebrovascular disease, have seldom been referred. This study aimed to assess the therapeutic effects of naloxone combined with edaravone on elderly ACI patients. Materials and Methods: A total of 176 ACI patients were randomly divided into control and experimental groups (n = 88) to be administered with edaravone and naloxone combined with edaravone, respectively for 2 weeks. Neurological function was evaluated by the National Institute of Health Stroke Scale (NIHSS) score. Living ability was assessed with the Barthel score. The levels of serum inflammatory factors and related markers were measured. Results: The total effective rate of the experimental group (92.05%) exceeded that of the control group (72.73%) (p<0.05). Two weeks after treatment, cerebral infarction volume and NIHSS score significantly declined and Barthel score rose in both groups, especially in the experimental group (p<0.05). Interleukin-6 (IL-6), IL-8, tumor necrosis factor-", C-reactive protein, matrix metalloproteinase-9, neuron-specific enolase, S100B, ubiquitin carboxy-terminal hydrolase L1, homocysteine, Fibulin-5, thromboxane B2 and 6-keto-prostaglandin F1" levels reduced in both groups, being lower in the experimental group (p<0.05). Superoxide dismutase and vascular endothelial growth factor levels increased in both groups, which were higher in the experimental group (p<0.05). Conclusion: Naloxone combined with edaravone exerts obvious therapeutic effects on ACI by inhibiting inflammatory cascade and platelet aggregation, reducing cerebral infarction volume, endothelial cell adhesion and blood viscosity, promoting angiogenesis and improving neurological function and daily living ability.