Tremor in Parkinson's disease patients can be induced by uncontrolled activation and uninhibited synchronization of alpha2-motoneuron firing to which alpha1-motoneuron firing synchronizes.
With the surface electromyography (sEMG) and the single nerve-fibre action potential recording method a mechanism is measured how rhythmic muscle contraction and tremor in Parkinson's disease patients is generated. With sEMG it could be shown that the tremor started when alpha2-motor units (FR-type) spontaneously began to fire synchronizedly oscillatory. Two possibilities of alpha2-motor unit synchronization were observed. In one case one alpha2-motor unit started to fire oscillatory and other alpha2-motor units started to fire oscillatory in synchronization with the first alpha2-motor unit. In a second case several alpha2-motor units fired oscillatory, but not in a synchronized manner. With the synchronization of the oscillatory firing alpha2-motor units again synchronizedly oscillatory firing of several alpha2-motor units appeared. When later on, several additional alpha1-motor units (FF-type) started to fire and in synchrony with the synchronizedly oscillatory firing alpha2-motor units (FR-type), rhythmic muscle contraction and tremor were observed. Visible muscle contraction and tremor stopped, when the alpha1-motor units stopped firing, which could a.o. be achieved by the patient concentrating on the tremor. The single nerve-fibre action potential recording method showed that alpha1 and alpha2-motoneurons in the cauda equine nerve roots fired oscillatory, that they could synchronize their firing and that these oscillatory firing motoneurons could build up an external loop to the periphery in the way that gamma-motoneurons and muscle spindle afferents were included in the rhythmic coordinated firing But the synchronization of oscillatory firing was only transient and the building up of an external loop to the periphery only occurred in non-Parkinson patients upon strong repetitive reflex stimulation. It is therefore concluded that in patients with Parkinson's disease there is firstly a lack of inhibition, so that motoneurons can start to fire oscillatory upon nearly no stimulation and there is secondly lack of mutual inhibition between oscillatory firing motoneurons, so that oscillatory firing motoneurons can synchronize their firing to give rise to rhythmic muscle contraction and tremor.
Schalow
Giselher
G
Institute of Exercise Biology and Physiotherapy, Centre of Behavioural and Health Sciences, University of Tartu, 5 Jakobi Street, Tartu 51014, Estonia.
D000200:Action Potentials / Q000502:physiology; D016022:Case-Control Studies; D004576:Electromyography; D006801:Humans; D009046:Motor Neurons / Q000502:physiology*; D018482:Muscle, Skeletal / Q000294:innervation / Q000503:physiopathology; D009412:Nerve Fibers / Q000502:physiology; D009469:Neuromuscular Junction / Q000503:physiopathology*; D010300:Parkinson Disease / Q000150:complications / Q000503:physiopathology*; D009435:Synaptic Transmission / Q000502:physiology*; D014202:Tremor / Q000209:etiology* / Q000503:physiopathology*