Alcohol / Ethanol chemoneurolysis

Alcohol  Blocks

Obturator Nerve Blocks




Alcohol is a chemical class as well as a discrete substance name. In chemistry, a hydroxyl group ( -OH ) added to a molecule of carbon structure is called an 'alcohol'. So add  an -OH to a benzene ring and get phenol. Drink that and you die quickly. Phenol is really what is used when people think formaldehyde is being used.  It is an alcohol but it isn't "alcohol". Alcohol, a term standing alone without something else modifying it means booze - Ethyl alcohol. Eth means two carbons.

CH2           This is 'alcohol', short for ethyl alcohol.

Ethyl alcohol makes you silly. All the others make you goobered. As ethyl alcohol has access to the citrate cycle, the main metabolic engine of our cells, it can be gobbled up into something else or turned into energy. But it does still have certain effects before it gets consumed in the citrate energy cycle. It can affect neurotransmission such that we crash our cars, or slow neuron migration such that embryo brains don't get all the circuits they need.


G-Protein Coupled Receptors are made of a long pipe curl of amino acids folded into 7 parallel segments that form a cylinder with a central passage - a pipe.  It penetrates and lives in the cell membrane as a pore - a grommet.  Parts stick out outside the cell and inside the cell. The outside bit flairs out like a mushroom with pock holes. Those pock holes attract or at least attach weakly certain substances. The important substance is Gamma-Amino-Butyric-Acid or GABA. When GABA latches on the pipe curls twist a bit and alter the way chloride passes through. That is what this thing does, it passes chloride and in doing so quiets the nerve membrane excitability. Opened wider or longer quiets the nerve by disallowing a 'potential' (electrical gradient) to form that can then go fire off willy nilly.

Valium adheres to one spot and makes the pipe open longer before it shoo's it away.  Ethanol (shown floating in the extracellular space) does something similar but attaches to another spot on that set of 7 pipe curls. Barbiturates also attach causing the pore to stay open longer once it opens. . .  ONCE IT OPENS  See? These drugs don't open the pore, they affect how wide or for how long it will open when GABA opens it. They affect what GABA does either by how fast it can recycle (how frequently it opens) or how long it stays open each time. Neurosteroids also glom on to this thing. G-Protein Coupled Receptors are like the funnel cake concession at the world fair, very popular hang out.

Sometimes - not always nor all places - but a lot of these pipes have a Gprotein complex that can grab on. The complex has three main pieces  called (nope, not 1,2,3) alpha, beta, gamma. In response to something attaching to the outside portion, the change that produces allow these inner portions to become active. This is aside from passing anything through the pipe. So these things act as locks that unlock cell processes. What gets unlocked depends on what that mechanism feeds with energy. This G-proten complex let's loose a barrage of  energy stuff (GTP and or ATP) and the like.

So THAT's how alcohol is used to do nerve blocks?

NO!        But that was sure interesting, wasn't it? It isn't used as a neuro transmission pore interacting thingy for alcohol blocks.

Alcohol is a good chemical defatting agent . Rub it on your hands and see how chafed they get. That last feature is what we use alcohol for. Fat removal. It is used in window cleaning agents for that chemical trait.

Nerves come in two main sorts, those with fat envelopes and those without. The fat insulation speeds up the nerve transmission chemistry by insulating it from the general circulating milieu, the part with chloride and sodium and potassium and calcium ions just itching to pour through neural pores. Fat covered nerves conduct faster by controlling that conduction specific milieu and focusing the ion current to receptive nodes.

If there is a nerve that, innocent as it may be, is carrying way too much data as inappropriate bursts of spastic overly repetitive pulses, then placing a speed bump on that nerve can reduce the ill of that overactivity.

Alcohol injected right on the nerve directly, strips off the fat from that location and slows  conduction there. Multiple speeding impulses pile up and come through as one single impulse. So a stream of impulses such as :


comes through the block area as:

go-----go-----go-----go-----           Engineers call this a low pass filter.

When a muscle gets hit with a single "go" it responds. When it gets hit with a barrage of gogogogogogogogog it gets thrown into tetany, a rigid hard to undo contractile state. Worse, it screams for help over  feed back circuits which (in spasticity) are mistakenly linked into the motor circuits by reflex spinal pathways.

Slowing certain nerves in the loop can drop the recruitment of the reflex mechanisms which get drawn into the fray from further and further away in the spinal pathways as the recruitment gets worse.

The result of aborting that run away reflex recruitment of far away muscles is not just less overactivity of the muscles supplied by the nerve but more precision. Precision? Yes. Often a child cannot just activate a single muscle without getting a smorgasbord of other stuff at the same time. Indeed, the youngster may not even know that there is such a thing as just that muscle.

Imagine if you flip a switch in your house and every single time the toilet flushes, the TV goes on, the garbage disposal comes alive and a light goes on. Do you call that a light switch? Only if you can peel off the unwanted stuff, then yes.

This has impact on learning. Children can't learn what does what when no matter what they do - everything happens. Much of the motor learning delay that we see is from kids trying to figure what to suppress in order to just get the one thing they want. They learn oddball secondary acts which seem to inhibit the unwanted actions.

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<= Here is a good before example of an alcohol block (to the obturator nerves which serve the hip adductors and parts of the hamstrings). In this youngster, any attempt to manually separate the knees reflexly elicited adductor and hamstring activity in both legs. This caused an inability to continue walking without extreme support measures. You see the examiner trying to pull the knees apart as the youngster just sits still. The bouncing box bar graphs measure electrical activity in each adductor set (left and right). They ought to be quiet and flat for passive motion.

<= With the volume of crossed reflex muscle stimulus reduced by way of the alcohol nerve block filter, the youngster can now open and close the legs at will. There is not only movement, but controlled movement. Following the alcohol block, the ability to walk without support and play adaptive tennis proceeded. Interestingly, the effects of alcohol blocks have few drawbacks in the patient groups with the most unpredictable natures - ataxia, athetosis, and dystonia. This youngster had athetoid cerebral palsy. Such children can go from doing well to suddenly doing something strange and disabling. Surgical procedures may outlive the oddities and wind up as additional problems.

In athetoid patients, we can do surgical procedures but must be certain that we are only surgically dealing with a spastic subset of what is ongoing. That is, is there is a very specific spastic component sitting there, was there always, always the same, then we can deal with it. Otherwise blocks are better.


The Block:

It is fairly easy in concept. Mix ethyl alcohol (NOT PHENOL) with some water in a syringe and inject it with a needle that is plastic coated. The needle has an electrode built in that goes to a special box that helps find the nerve.

We do NOT just inject blindly where we think a nerve ought to be. The nerve is the needle in a hay stack. Our injection must touch that nerve.

You have to have the right tools. The reasons are
1) if we miss we fail
2) if we inject alcohol onto the wrong nerves other things will happen
3) if we just push larger volumes of alcohol to get a better "hit" percentage then we also have alcohol tracking along the nerve (it tracks rather well) and will find its way to the root and main divisions which carry sensory components which will cause "burning".

A spastic child with burning will react to the burning and that reaction will be troublesome in itself. The child may refuse to put the foot down, etc. Certain drugs can treat the burning, however, should it occur.

Certain nerves are best suited to blocks, others less so. Those that are heavily mixed with sensory and motor nerves do less well and are best avoided. Some nerves branch before or after entering the muscles they enervate. If before, we may be fooled into thinking we got the whole thing and only have one branch.

Advantages of alcohol over Botox include low toxicity and long duration of effect to many muscles at one time. A single inject may well last 18 months to 2 years and not require repetition.

Disadvantages include the need to anesthetize as no kid will sit still as the region of the nerve is being probed and stimulated electrically. Certain muscles do not have nerves of the type which can be alcohol blocked without sensory disturbance.


Obturatoretc. Nerve Blocks

Alcohol, as ethanol, can be used to  defat a portion of any nerve. But those which have little overt sensory components (ie, won't 'burn') are ideal. So certain ones are favored as they have little in the way of after burn called dysaesthesia. Branches to the pectoral muscles, the obturators, and hard to isolate but very useful the nerve branches to tibialis posterior and to rectus femoris are the main locations. Every once in a while the branch to the hip abductors running alongside the ilium is a most useful way to treat excessive hip aBduction caused by spasticity (yeah, it can go that way at times). Typically this last one arises as a cause apparent of lumbar scoliosis. Pulling the legs into like hikes the pelvis instead.


Phenol deserves special mention as to what it isn't. Many years ago, attempts to reduce muscle activity utilized injections of phenol into muscle areas where the nerve endings tend to enter the muscle fibers. That phenol was often referred to as an alcohol - as technically - in chemistry terms it is. But in plain language it is embalming fluid. It kills tissue. Its job was to chemically fry a portion of nerve endings at the muscle site.

It had nasty effects if it tracked through the injection site along the needle as chemical burns, but it did its job well - kill tissue. It is still used when tissue needs killing - certain warts etc. But when you kill the nerve to a muscle, after about 18 months to 2 years, if that nerve does not recover and return, the muscle itself dies and turns to scar. That scar simply does not grow. In a growing child denervated muscle scar causes contractures worse than spasticity and are harder to undo. We do not use phenol. If we do, we call it phenol, not alcohol. Life is confusing enough!


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