This thesis describes the construction of a model that duplicates the global dynamics of the induction of unconsciousness in humans due to cerebral ischemia produced by linear acceleration stress (G-LOC). It is an attempt to provide a theory that can both replicate historical human acceleration tolerance data and present possible underlying mechanisms. The mathematical tools for the creation of the model were provided by the emerging science of Complexity theory which suggests ways to synthesize and analyze systems that (among other qualities) have many degrees of freedom, are non-linear, spatially extended, and have long-range order that is induced by the interplay among local dynamical systems. Complexity theory holds that even though specific physical details of the local systems may not be available, a satisfactory model of global behavior can be constructed by making reasonable assumptions about the dynamical interplay of these local systems. The inspiration for the characteristics of the locally interacting elements was provided by the physiologic mechanism of arousal (the all-or-nothing aspect of consciousness), the utilization of oxygen in neural tissue during ischemia, and the response of neural cells to metabolic threats. The new theory of acceleration tolerance presented here views unconsciousness as an active protective mechanism that is triggered by a metabolic threat which in this case is acceleration induced ischemia. The interplay among the local systems is determined by using a percolation network which models the connectivity of the arousal mechanism (the reticular activating system). When normal neuronal function is suppressed due to local cerebral ischemia, the corresponding node is removed from the percolation network. The configuration of the percolation network varies as a function of time. When the network is no longer able to support arousal, unconsciousness results. The model was able to simulate a wide range of human data with a high degree of fidelity. By successfully duplicating the observed global behavior of humans, this model may provide insight into some (currently) unobservable local dynamics of the central nervous system. The existence of a neurologic protective mechanism has implications that extend beyond aerospace medicine into the areas of anesthesiology and early stroke intervention.
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Title
A dynamic percolation model of the central nervous system under acceleration (+Gz) induced ischemic/hypoxic insult
Creators
Joseph P. Cammarota Jr.
Contributors
Leonid Hrebien (Advisor)
Awarding Institution
Drexel University
Degree Awarded
Doctor of Philosophy (Ph.D.)
Publisher
Drexel University; Philadelphia, Pennsylvania
Number of pages
xii, 205 pages
Resource Type
Dissertation
Language
English
Academic Unit
College of Engineering (1970-2026); Electrical (and Computer) Engineering [Historical]; Drexel University