Loxoprofen overdose without toxicity: pharmacokinetics of loxoprofen and metabolites analysed by liquid chromatography-mass spectrometry: a case report.

Parkinson's disease (PD) is a neurodegenerative disorder primarily affecting the basal ganglia-thalamo-cortical circuitry, and abnormally hypersynchronous oscillations in the beta frequency range (13–30 Hz) within the cortical-subcortical motor network represent a pathophysiological hallmark of the disease. Local field potentials (LFP) and electroencephalography recordings have consistently demonstrated their presence in deep brain stimulation (DBS) target structures (including the globus pallidus internus (GPi)) as well as in the coherence between basal ganglia (BG) and sensorimotor cortex (SMC). Importantly, hypersynchronous beta activity correlates with motor symptom severity and is suppressed by both dopaminergic medication and DBS, making it a valuable biomarker that has been recently translated into novel adaptive DBS systems. However, the source of pathological beta activity in PD remains debated. While early evidence suggested that abnormal beta oscillations originate in the BG and secondarily spread to the SMC, subsequent studies proposed the opposite hypothesis. Indeed, functional connectivity analyses between cortex and BG provided a higher likelihood for cortical beta driving into the BG rather than the opposite. Accordingly, enhancing beta oscillations at the SMC through non-invasive brain stimulation worsened bradykinesia severity in PD patients.