Ties right into our look at other neurotransmitters in getting beyond the dopamine...

Unusual on two points:

First time an organophosphate based pesticide (widely used Malathion) has induced Parkinsonism and responded to levodopa therapy

First time an acute loss of acetylcholinesterase results in secondary Parkinsonism that is levodopa responsive. This means he had over expression of acetylcholine; why would taking levodopa help in a person who did not have low dopamine levels?

This raises questions on how perhaps a serious imbalance of one of the other catelochamines may be a trigger for Parkinson's. It is well documented that SSRI's trigger PD symptoms as well. So tipping the scales with merely one other neurotransmitter can induce Parkinsonism? In many cases the PD symptoms improve on their own but not in all.

BTW, clinically he was at stage V. How can this happen without a loss of dopamine?

Seems like we could learn from those who recover. How are our brains different or same? Can they look at something like this an animal model?

Laura