The doctor did my calf muscles again and this time we added the hamstrings too. Yup, it hurt... bad. I am hypersensitive to regular touch so imagine a needle... 8 of them (at least I stopped counting at 8).
As promissed from last time I took pictures, ok well, I didn't take them, my friend Janel did. I was busy trying not to scream... much.
Botox is purified form of the neurotoxin produced by an anaerobic (grows in the absence of oxygen) bacterium called Clostridium botulinum.
Although there are seven serotypes of botulinum neurotoxin, only A and B are currently approved for clinical use in the United States, and A is, by far, the most commonly used.
Botox (any serotype) works by blocking the release of acetylcholine.
To begin, it's important to understand what makes a muscle contract. In short (very, very short), an action potential is carried by axonal activity from the spine, down the nerve and to the linked muscles. At the neuromuscular junction, a measure of a chemical called acetylcholine is released into the very tiny space between the end of the axon and the muscle. Acetylcholine changes the electrical potential of the resting muscle fiber membrane and initiates a process that causes a contraction. (So, think of acetylcholine as working in a very similar manner as gasoline in a combustible engine. Gasoline is released in a small amount; it reacts (explodes), which sets about a chain of events that leads to motion (piston moving down, crankshaft turning... etc.).
Now, within the nerve ending itself are a series of proteins that are necessary to allow the synaptic vesicles to bind with the nerve endings and allow the release of the acetylcholine. One of these proteins is called SNAP-25, which is the one serotype A acts upon. So, basically, the botox cuts out a necessary protein in the chain of events leading up to the release of acetylcholine. The acetylcholine is never released, thus the action command is never communicated to the muscle.
Okay, here’s the cool part. The body recognizes that it is sending a signal to the treated muscle, telling it to react, but nothing is happening. The nerve terminals actually begin to sprout, sending those sprouts toward the muscle to form new synaptic contacts. Terminal nerve sprouting!!!
Scientists used to believe the treated nerve endings were permanently impaired and that the muscle returned to full functionality by receiving its messages from these new contacts. Recent tests are showing that the original contact heals, and once it becomes fully functional again, the sprouts retract.
What is NOT known, and what I find very interesting, is whether or not these sprouts retract on a newly innervating muscle.
My thanks to Mica (BPI Friends board) for writing this to explain how it works!
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