ABSTRACT
OBJECTIVES: We aimed to disclose the relationship between restless leg syndrome (RLS) and antiparkinsonian treatment, and its effect on quality of life (QoL) in patients with Parkinson's disease (PD). BACKGROUND: Previous studies documented the prevalence of RLS among patients with PD to be higher than in the general population, but conclusions regarding the aetiology and impact were contradictory. METHODS: We examined 101 patients with idiopathic PD. All participants completed the five-dimension/five-level-EuroQoL questionnaire (EQ-5D-5L) and the International Restless-Legs-syndrome-study-group rating Scale (IRLS). RESULTS: The prevalence of RLS was 22.77 %. There were no statistically significant differences in levodopa or dopamine agonists (DA) doses between RLS-positive and negative participants. However, the use of levodopa as the last night-time medication was connected with a higher risk of RLS (OR=2.049, p=0.041). There was significantly lower prevalence of RLS in patients after surgical treatment for PD (p=0.024). Participants with RLS were at a greater risk for sleep disturbances (OR=3.866, p=0.023) and excessive daytime sleepiness (OR=7.202, p<0.001). Greater RLS symptoms were associated with worse QoL (higher IRLS score predicted higher EQ5D5L score, p=0.023). CONCLUSION: RLS is prevalent among PD patients and night-time dopaminergic over-excitation with levodopa plays an important role in its pathogenesis. Since the symptoms of RLS are associated with decreased QoL, early accurate diagnosis and appropriate adjustment of dopaminergic therapy can lead to immediate relief from RLS symptoms and to QoL improvement (Tab. 4, Fig. 1, Ref. 34).
Subject(s)
Parkinson Disease , Restless Legs Syndrome , Dopamine Agonists/adverse effects , Humans , Parkinson Disease/complications , Parkinson Disease/drug therapy , Parkinson Disease/epidemiology , Quality of Life , Restless Legs Syndrome/drug therapy , Restless Legs Syndrome/epidemiology , Surveys and QuestionnairesABSTRACT
Exercise can prevent the sedentary lifestyle-related risk of metabolic and cognitive decline, but mechanisms and mediators of exercise effects on human brain are relatively unexplored. We measured acute exercise-induced changes in adiponectin, insulin and other bioactive molecules in cerebrospinal fluid (CSF) and serum from young lean individuals. Samples of serum and CSF were obtained before and 1-h after the 90-min run (75-80% HRmax; maximal heart rate), additional serum was taken at finish-line. Body composition, physical fitness, metabolic rate, cognitive functions, food preference, glucose, insulin and albumin were measured. The spectrum of 174 cytokines was assessed by protein arrays, adiponectin was also determined by ELISA and immunoblotting. CSF adiponectin decreased post-exercise by 21.3% (arrays) and 25.8% (ELISA) (p < 0.009). Immunoblotting revealed reduction in a low-molecular-weight-adiponectin (p < 0.005). CSF adiponectin positively correlated with CSF/serum albumin ratio (p < 0.022), an indicator of blood-brain-barrier permeability. CSF and serum adiponectin were positively associated with memory and running-induced changes in insulinemia and CSF insulin. Additionally, running modulated CSF levels of 16 other cytokines. Acute running reduced CSF adiponectin and modulated insulin and albumin in CSF and serum. Associations of adiponectin with memory and metabolism indicate the potential role of this bioactive molecule in mediating exercise-induced adaptive response in human brain.
Subject(s)
Adiponectin/metabolism , Cytokines/metabolism , Insulin/metabolism , Running/physiology , Adiponectin/analysis , Adiponectin/cerebrospinal fluid , Adult , Blood Glucose/metabolism , Body Composition/physiology , Body Mass Index , Cytokines/analysis , Cytokines/cerebrospinal fluid , Exercise/physiology , Female , Healthy Volunteers , Humans , Insulin/analysis , Insulin/cerebrospinal fluid , Insulin Resistance/physiology , Male , Obesity/metabolism , Young AdultABSTRACT
BACKGROUND: Deep brain stimulation is an effective and safe technique. Displacement of the electrode relative to the optimal stimulation site can lead to insufficient effect and sometimes to the need of operative electrode re-position. OBJECTIVE: This study was aimed to analyse targeting accuracy of deep brain stimulation electrode implantation to subthalamic nucleus (STN) and globus pallidus internus (Gpi). It detected possible causes of inaccuracy and prevalent shift to certain direction. METHODS: Targeting accuracy was analysed in 47 patients with Parkinson´s disease (PD) and 11 patients with dystonia with bilateral implantation of deep brain stimulation electrodes between years 2009 and 2016. RESULTS: A shift of electrode to prevalent direction was observed on the left side to medial and posterior and on the right side to lateral direction. Greater shift was observed on the left side and in a higher angulation of trajectory laterally. Movement of the electrode, because of its traction in anchoring device, was identified as a possible factor for prevalent electrode shift. Calibration of stereotactic coordinates to correct prevalent shift was used. CONCLUSION: Targeting inaccuracy is the result of accumulation of errors in individual steps of electrode implantation. Direction of the shift can be random or it can be toward a prevalent direction. A correction of prevalent error can prevent a suboptimal electrode placement (Tab. 3, Fig. 11, Ref. 29).
