Origins of a repetitive and co-contractive pattern of muscle activation in Parkinson’s disease

<p>In studies of electromyographic (EMG) patterns during movements in Parkinson’s disease, often arepetitive and sometimes co-contractive pattern of antagonist muscle activation is observed. It has beensuggested that the origin of such patterns of muscle activation is a central one arising from impairmentsin the basal ganglia structures and/or the cortex, although afferent inputs can also modulate the voluntaryactivity. A neural network model of Parkinson’s disease, bradykinesia and rigidity, is extended toquantitatively study the conditions under which such a repetitive and co-contractive pattern of muscleactivation appears. Computer simulations show that an oscillatory disrupted globus pallidus internalsegment (GPi) response signal comprising at least two excitation–inhibition sequences as an input toa normally functioning cortico-spinal model of movement generation results in a repetitive, but not cocontractiveagonist–antagonist pattern of muscle activation. A repetitive and co-contractive pattern ofmuscle activation results when also dopamine is depleted in the cortex. Finally, additional dopaminedepletion in the spinal cord sites results in a reduction of the size, duration and rate of change of therepetitive and co-contractive EMG bursts. These results have important consequences in the developmentof Parkinson’s Disease therapies such as dopamine replacement in cortex and spinal cord, which canalleviate some of the impairments of Parkinson’s Disease such as slowness of movement (bradykinesia)and rigidity.</p>