A MATHEMATICAL-MODEL OF PATHOGENESIS IN IDIOPATHIC PARKINSONISM

We used our observations relating clinical deficits in idiopathic park insonism (IP) to age and to disease duration (Lee et al, Brain 1994; 1 17: 501-7), to develop a mathematical model of the temporal profile of neurodegeneration in IP, We also examined other sets of relevant publ ished observations and applied three additional assumptions which perm itted the formulation of this model. Our model indicates that accelera ting or decelerating processes should be excluded as the driving force s behind neuronal death in IP. Mechanisms in accord with the model inc lude: (i) an event that kills some neurons and damages others in such a way that their life expectation is reduced; or (ii) an event that st arts a process which is continuously killing healthy neurons at a cons tant rate. The model enables us to extrapolate back to estimate when t he causal event occurred. It also explains why IP proceeds more rapidl y in older patients. The model has potential relevance to other neurod egenerative disorders, such as Alzheimer's disease and amyotophic late ral sclerosis.