Effects of deep brain stimulation and medication on bradykinesia and muscle activation in Parkinson's disease

Abstract

Deep brain stimulation (DBS) of the subthalamic nucleus (STN) and antiparkinsonian medication (Meds) have proved to be effective therapies for treating bradykinesia in Parkinson's disease. However, it is not currently known how or to what extent STN stimulation alters the control signals to agonist and antagonist muscles to change movement speed. Our objective was to investigate movement speed along with the amplitude and temporal features of EMG activity to determine how and to what extent these parameters are changed by DBS and medication. Nine patients with Parkinson's disease were studied following neurosurgery that implanted high-frequency stimulating electrodes in the STN. The experiments for the patients were performed in each of four treatment conditions: (i) OFF treatment; (ii) STN DBS; (iii) Meds; and (iv) Meds plus STN DBS. Also, a group of age- and gender-matched control subjects were examined. Medication and DBS had similar effects in that both treatments increased movement speed, increased the amplitude of the first agonist burst, increased burst duration, reduced the number of agonist bursts, reduced cocontraction, increased the size of the antagonist EMG, and reduced the centroid time of the antagonist EMG. When DBS and medication were combined, only temporal measures of burst duration and the number of agonist bursts were different from the medication alone condition. There was a positive association between the level of bradykinesia OFF treatment and the level of bradykinesia following DBS and medication. The movement speed of neurologically normal control subjects' was over 40% higher during both flexion and extension movements when compared with the patients during Meds plus STN DBS. The changes in the muscle activation patterns provide a mechanism of action for the pharmacological and surgical interventions used to treat bradykinesia in Parkinson's disease. However, despite the success of medication and DBS at improving bradykinesia in patients with Parkinson's disease, patients' movement speed was not restored to normal due to limitations in the amplitude and temporal scaling of the agonist and antagonist bursting pattern. These findings suggest a link between basal ganglia function in scaling both the amplitude and temporal parameters of the input to the motor neuron pool.

Signal features of surface electromyography in advanced Parkinson’s disease during different settings of deep brain stimulation

“…The medication on-state may have affected the results by decreasing differences between different DBS setting -states in some patients. It has been noticed earlier that both medication and DBS affect the surface EMG signals in PD but neither one of them is able to normalize the signals and muscle activation patterns (Sturman et al, 2004(Sturman et al, , 2007Vaillancourt et al, 2004Vaillancourt et al, , 2006Robichaud et al, 2002). It has been noticed that even with medication on, the DBS affects the agonist EMG burst characteristics during movement .…”

Role of hyperactive cerebellum and motor cortex in Parkinson's disease

“…The model predicts that bradykinesia would occur in PD, in that reducing the excitatory inputs to the motor cortex would slow movements. The model also predicts that levodopa and deep brain stimulation can alleviate bradykinesia (Brown et al, 1999;Vaillancourt et al, 2004). However, the model does not explain hyperactivation in the motor cortex or how changing the task demands could alter the correlation between the motor cortex and different signs of PD.…”

Effects of STN DBS on Rigidity in Parkinson's Disease

“…As the disease progresses, the efficacy of L-dopa decreases and the incidence and severity of the side effects increase [2]. Deep brain stimulation (DBS) of the subthalamic nucleus (STN) has been shown to modify several of the neurophysiological parameters associated with tremor and bradykinesia better than medication alone [3], [4]. STN DBS has also been shown to improve clinical measures of rigidity [2], [5]- [8].…”