SPMLs & EtOH

One exception, ethanol, was block-ish, though it did not denervate (we biopsied muscle in cases when we had later reconstructions to do and easy access to muscle that had ethanol nerve ‘ block’ (= no significant denervation was seen). Ethanol failed as a ‘block’ making it a success as its function sparing treatment of reactivity spread. But, alone, it could not create movement that was not there nor remove very severe spasticity as an isolated method. Already aware that – at least in the spastic diplegia kids – we were seeing “spasticity in parallel” [but didn’t, back then, know why] we applied the ethanol dysmyelination (selective & focal) to those nerve branches that when stimulated made other things jump. With the anesthesia insights from our departed colleague we have watched and appended our lists of what and how much to do and how to test what to do. As new anesthesia agents are introduced this remains critical. Prime example is sevofluorane. One whiff and you are gone. Count backward from one… ‘wuh---’, out. Great for scared kids. But, it makes nerve finding impossible as it kills the reaction we are hunting. So, often, when the child is crazy scared… “Have you ever smelled this?” asleep – start IVs etc. mask the trachea to protect against vomiting – rare but can happen … and switch to other anesthetics (‘Sevo’ is gone almost as fast as it came in). Intubation , demanded by anesthesia in many academic places, is generally terrible as curare type drugs are paired with it and a deeper level of anesthesia is required to not get wild reaction to the tube. Deep anesthesia makes us blind to the reactivity we are looking for.