 |
 |
janet marie paterson posted an abstract that contained: > ... The olfactory vector hypothesis suggests that the causative agent for > IPD enters the brain via the nasal route ... > > It is proposed that the initial causative event in IPD may start in > the rhinencephalon (olfactory brain) prior to damage in the basal > ganglia. Little attention has been devoted to research of the olfactory aspect of PD. If the above hypothesis of where PD begins is true, then the initial causal factor could be some toxin in the air, such as a pesticide or an industrial pollutant, or, as has been claimed in some cases, carbon monoxide. The olfactory system might then be the place at which to direct treatments in early PD. The spread of PD from the olfactory bulb to other parts of the nervous system -- to the brain stem and to the autonomic nervous system as well -- would also need to be researched and prevented. The effects of PD on movement have been regarded as primary because they are so disabling. This has determined the main focus of research, even the definition of PD itself. It would be a different story if, like other mammals, the sense of smell were a vital faculty. But to develop means of prevention, early detection, and early intervention, I would think that research needs to confirm just where in the nervous system PD begins, regardless of whether the early symptoms are of negligible importance, and focus its efforts there. Phil Tompkins Hoboken NJ age 62/dx 1990