Re: Nerves - burning tongue

[Guest guest]

Pam wrote:

> I starting noticing my first symptoms of achalasia after jaw surgery.

> ... I also started having symptoms of burning tongue syndrome.

>

There have been others in this support group that have stated that their

symptoms started after some kind of oral work done, such as the removal

of a tooth. Having things like that done is not that uncommon so in a

large enough group of people with a shared type of event in their lives

we can expect that some will have had that kind of thing done around the

time of that shared event. It could just be coincidence. In your case

the burning tongue could be related to the jaw surgery or to the

achalasia without the achalasia having to be connected to the jaw

surgery. A number of thing seem to able to start burning tongue. These

include: dry mouth, yeast infection, anxiety, depression, B vitamin

deficiencies, materials used in dentures, nerve damage to nerves that

control taste and pain in the tongue, allergies or reactions to foods,

reflux of stomach acid, certain medications, tongue thrusting, diabetes

and underactive thyroid, menopause, overbrushing of your tongue, overuse

of mouthwashes or having too many acidic drinks. It would seem that the

tongue can be sensitive to many things and it would not be unreasonable

to assume that the bodies response to the jaw surgery could explain the

burning. In that list are some things that can irritate the tongue but

could be similar to things that happen in achalasia. The yeast, reflux,

mouthwashes and acidic drinks, may be like the esophageal infections,

acid and other irritants caused by food fermenting in the esophagus. So

I can see where achalasia could also have caused it. Then there is the

nerve damage that is also listed. I don't see how the jaw surgery would

have done the damage that is usually seen in achalasia. If somehow there

was damage to the vagus nerve maybe it could have caused the problem but

you have to remember that the vagus also goes to many of your other

organs if they are functioning normal it would seem strange that the

damage just effected the esophagus. In primary achalasia the damage

seems to be the vagus connections to the esophagus (myenteric plexus,

postganglionic) for controlling the relaxation of the esophageal

muscles. The vagus connects to the myenteric plexus, which is like a net

of nerve cells around the esophagus. In this net are some bundles of

nerves cells called ganglions. Nerve fibers from the ganglions go into

the esophageal muscles to control them. Some of these fibers are used to

cause a relaxation to happen. The nerves for this are damaged or

destroyed in achalasia but not other nerves of the plexus or ganglions.

It is hard to imagine jaw surgery causing that specific damage to just

those nerves of the esophagus. In fact it is kind of tricky to figure

what could cause such specific damage while not damaging the other

nerves that are also part of the plexus. The nerves are not the only

thing that changes in the plexus. interstitial cells of Cajal (ICC) are

also effected. The act like pacemakers and interface the nerves with the

muscles. There is also something there happening with immune system

cells and mast cells. You can see that connecting the dots to anything,

not just jaw surgery, is going to be a problem, but there are some

ideas. (Later for that).

First this: As is so often the case with achalasia, there is more which

seems to conflict with what I have just told you. Take a look at:

Achalasia presenting after operative and nonoperative trauma

http://www.ncbi.nlm.nih.gov/pubmed/15628710

and

Chest trauma and aetiology of achalasia

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1856305/

In the first study motor vehicle accident and surgery trauma were found

to be more common in achalasia patients than in controls. In the second

and smaller study only motor vehicle and work accident trauma were found

in the achalasia patients and no trauma was found in the controls (the

study was probably to small).

These are interesting studies but they don't indicate what the trauma

did to cause the achalasia if it even did. One may jump to the

conclusion that the vagus nerve was injured in the trauma but it may not

have been and it could be that the body's response to the trauma, such

as the healing process, may have caused the achalasia. Then again maybe

it is damage to the vagus in these cases, but then why did the achalasia

not show up sooner in some of these cases? There are other studies like

these that show nerve damage outside of the esophagus can cause

achalasia but these kinds of damage are seldom seen in achalasia while

the nerve damage at the esophagus is often seen.

There is something I have been looking at that is a bit of jump from

this topic but it does relate. What if the damage to nerves is not the

initial cause of achalasia but part of the progression after it has

already started? Perhaps something blocks these nerve from activating

relaxation even before they are damaged. The damage to the nerves could

partly be due to the stretching of the esophagus when food accumulates

at the LES. Some nerves will only tolerate a limited amount of

stretching before they are damaged. If not the stretching perhaps

something else can damages the nerves when there is an obstruction in

the esophagus. Consider these animal studies:

Effect of incomplete obstruction on feline esophageal function with a

clinical correlation

http://www.ncbi.nlm.nih.gov/pubmed/3738763

" A Gore-Tex band, measuring 110% of resting esophageal circumference,

was placed about the esophagus at the gastroesophageal junction of 17

cats to produce incomplete obstruction by limiting the normal distention

that occurs with swallowing. ... Partial obstruction alters feline

esophageal body function and these achalasia-like changes are reversible

on relief of the obstruction and similar motility aberrations occur in

patients because of mechanical or functional distal obstruction; this

suggests that dysmotility can synergistically contribute to dysphagia. "

Electrical stimulation of the vagus nerve restores motility in an animal

model of achalasia

http://www.ncbi.nlm.nih.gov/pubmed/14592656

" Fifteen opossums were divided into three groups. ... In group 2 (n=6)

a loose Gore-Tex band (110% of the esophageal circumference) was placed

around the gastroesophageal junction to prevent relaxation of the lower

esophageal sphincter during swallowing. In group 3 (n=6) a relatively

tighter band (90% of the esophageal circumference) was used to further

elevate the lower esophageal sphincter pressure. ... Animals in group 2

demonstrated a vigorous variety of achalasia (high-amplitude,

simultaneous, repetitive contractions), moderate esophageal dilatation,

and degeneration of 40% to 60% of intramuscular nerve plexi. Animals in

group 3 developed amotile achalasia with typical low-amplitude

simultaneous (mirror image) contractions, severely dilated ( " bird beak " )

esophagus, and degeneration of 50% to 65% of nerve plexi. ...

peristaltic activity completely returned to normal only in the vigorous

(early) variety of achalasia. "

Enteric neuronal plasticity and a reduced number of interstitial cells

of Cajal in hypertrophic rat ileum

http://www.ncbi.nlm.nih.gov/pubmed/9691923

" Enteric neurones change their levels of expression of neuromessengers

in hypertrophic ileum. ICC are also affected "

Loss of interstitial cells of Cajal and development of electrical

dysfunction in murine small bowel obstruction

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2278884/

" ICC networks were disrupted oral to the obstruction, and this

disruption was accompanied by the loss of electrical slow waves and

responses to enteric nerve stimulation. These defects were not observed

aboral to the obstruction. ... " Removal of the obstruction led to the

redevelopment of ICC networks and recovery of slow wave activity within

30 days. Neural responses were partially restored in 30 days. "

These animal studies suggest that if an obstruction occurred at the LES

it would cause ICC, nerve and other tissue changes just above the LES.

It is interesting that there are nerves like those that are damaged in

achalasia elsewhere in the gut but those at the LES and lower esophagus

seem to be the target in achalasia. If they were just responding to an

obstruction at the LES it would be in line with these studies. There are

reports of gastric banding, gastric bypass, and fundoplication for GERD

that were too tight, leading to achalasia. In these studies the ICC were

able to repopulate but depending on the amount of damage and how long

the damage lasted the nerves sometimes did not recover. In achalasia the

damage has usually gone on much longer than in these animal studies.

Once the nerves are damaged the damage can cause the LES to fail to

relax. If this failure at the LES is often enough and complete enough,

it could act just like any other obstruction at the LES and continue the

tissue changes and damage to the nerves.

In some cases an immune system response may effect the ICC and nerves

creating the obstruction It may be that at least for some people the

initial obstruction was caused by an allergic reaction to something in

food or or environment, or something else that disturbed the ICC. In

time that resulted in nerve damage which then continues the ICC problem

and causes continued nerve damage. And so it progress, as long as the

obstruction at the LES is untreated. If you are interested in this idea

see my next post on " A progression and also Alcohol-Stasis. "

notan