Taming the Fractious Belladonnoids

Like the bucket-carrying brooms in Fantasia, once BZ molecules began to flow into the body no one, in 1961, seemed to know how to turn them off. They moved easily into the brain, largely unimpeded by the blood-brain barrier that blocks out many unwanted substances. Their high degree of relative central potency enabled them to gain access to nerve cells in the gray matter. 

Once they reach acetylcholine receptors, BZ molecules hang on for dear life. So tenacious is their grip that they take hit after hit from the weaker acetylcholine molecules. For tens of hours acetylcholine is unable to exert command and control of mental activities. Like sugar in a gas tank, BZ gums up the transmission. The result is incapacitation. 

In 1961, we understood how BZ delirium was turned on , but none of us knew how to stop the flow. All we could do was sit and watch the fanciful drama just described, and take detailed notes. 

Surprisingly, it appeared that there had been hardly any therapeutic progress in the management of belladonna poisoning since the 19 century, when opium was the most commonly used treatment. The first six decades of the 20 century spawned many new drugs, but no one seemed to have reported anything good for atropine delirium in mainstream medical journals. 

Encouraged, we decided to try physostigmine again. We were delighted when it dramatically restored NF scores of clearly incapacitated volunteers to near normal levels. The first time this happened, I could not help feeling a little 

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