-- more info.....Re: spasms and vomiting

[Guest guest]

, I agree that your GI's perception of NCCP as an " atypical " symptom

for achalasia is pretty outdated, but unfortunately all too common. That

is sooooo frustrating!!!!

As far as anti-depressants being used to treat NCCPs associated with

achalasia, it's NOT so much the " stress relief " part of it, but rather the

neuromodulator/transmitter part of the drug. I don't know much about

treating other chronic pain syndromes with anti-depressants, but in this

instance it is generally a LOW DOSE anti-depressant (tricyclic or SSRI) --

the dose that is administered is BELOW the therapeutic level for treating

psychological symptoms. (I just wanted to clear this up b/c I didn't want

anyone to think that NCCPs are caused by " stress " and they would go away

if we'd just relax, etc. Many of us have been told that our dysphagia is

all in our heads, and I didn't want anyone to think that NCCPs are!)

The way it was explained by Dr. Clouse (who has done an amazing amount of

research on relationships between psychologic/psychiatric disorders,

gastrointestinal disorders, and medications) was that the brain interprets

" normal stimulus in an abnormal way " , and the anti-depressants help

modulate the reactions of that part of the brain that is " misinterpreting "

the signals. (For example, I will sometimes get a NCCP after sneezing...

in a normal person, a sneeze doesn't cause a pain-response from the brain,

but my brain " doesn't understand " what that stimulus was, so it reacts as

if it were painful.) The term " Visceral Hyperalgesia " is used in

describing this phenomenon; you may be familiar with that term.

I have several articles that discuss the correlation between various

anti-depressant medications, NCCP treatment, psychological treatment, etc.

I've pulled out certain quotes from some of them, but provided the link

for anyone who is interested in reading the whole thing with full context.

I'm anxious to see Dr. Clouse's latest article, which is expected to be

published within the next year. I'm having trouble finding the abstract,

though -- if anyone can find it for me, I'd be eternally grateful! It's

entitled: " Tricyclic antidepressants for chest pain from achalasia:

adjuvants to conventional therapy " by RE Clouse and PJ Lustman.

Anyway, here's a hodge podge of articles and quotes for your reading

pleasure!

Debbi in Michigan

http://www2.us.elsevierhealth.com/scripts/om.dll/serve?retrieve=/pii/S0016508501\

01352X & nav=full

Several investigators have observed an increased pain perception (visceral

hyperalgesia) in patients with angina-like pain following a variety of

stimuli (J Am Coll Cardiol 1990;16:1359–1366, 1994;24:329–335, Br Heart J

1992;68:282–285, Circulation 1994;90:50–60). The precise origin or

intimate mechanism involved in the generation of this visceral

hyperalgesia remains to be defined. Triycyclic antidepressants improve

chronic pain of somatic and visceral origin. At low doses, these

pharmacologic agents have documented beneficial effects in the treatment

of diverse types of chronic pain syndromes (Scand J Gastroenterol

1984;19:835–843). The mechanism of action of these compounds is not known,

although it is likely that the analgesic effect of these agents is not

dependent on mood altering virtues. Two previous trials have shown

beneficial effects of trazodone (Gastroenterology 1987;92:1027–1036) and

imipramine (N Engl J Med 1994;330:1411–1417) in the treatment of chest

pain. In the most recent trial, Cannon et al. found that the response to

imipramine was not dependent on the results of cardiac, esophageal, or

psychiatric testing. However, repeat assessment of cardiac sensitivity

while on treatment showed significant improvement afforded by imipramine

(N Engl J Med 1994;330:1411–1417). This latter observation suggests that

the improvement induced by imipramine likely is caused by a visceral

analgesic effect. This hypothesis is also supported by the recent work of

Peghini et al. in healthy subjects (Gut 1998;42:807–813).

The study by Varia et al. is important for several reasons (Am Heart J

2000;140:367–372). First, the findings shed light into the potential

mechanism involved in chest pain. The chest pain–reducing effects of an

SSRI underscore the potential role of serotonin as neurotransmitter in

patients with chest pain. Second, their observations that sertraline

improves chest pain regardless of a concomitant improvement in

psychological scores confirms parallel observations obtained with

psychotropic compounds such as imipramine and trazodone during earlier

trials (N Engl J Med 1994;330:1411–1417, Gastroenterology

1987;92:1027–1036). Third, their findings expand the therapeutic choices

for the treatment of these challenging patients. This is particularly

important because the traditionally available agents imipramine and

trazodone can produce undesirable effects that limit their use, such as

anticholinergic reactions, antiarrhythmic activity, and sedating effects.

Furthermore, trazodone can induce priapism in male patients.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve & db=pubmed & dopt=Abstra\

ct & list_uids=10630484

Antidepressants are of demonstrated value in short-term treatment of

functional chest pain, but long-term outcome data are unavailable.

Follow-up information over a median of 2.7 years (0.8-8.6 years) was

systematically obtained from 21 outpatients treated with tricyclic

antidepressants after incomplete response to antireflux therapy. Initial

treatment produced at least moderate symptom reduction or remission in 17

subjects (81.0%). Of these, 7 (41.2%) were successfully treated

continuously or for symptom relapses over an average of 2.6 years; 5

(29.4%) discontinued successful treatment after >0.5 years with sustained

benefits; and 5 (29.4%) eventually discontinued treatment because of side

effects or for uncertain reasons (1 having a sustained remission).

Low-dose tricyclic antidepressants were considered the most effective

long-term chest pain treatment significantly more often than were

antireflux medications or calcium-channel blockers in this selected

patient group (P<0.05 for each). We conclude from this retrospective

review that fully three fourths of subjects with functional chest pain who

initially respond to open-label treatment with low-dose tricyclic

antidepressants will use them continuously or for symptom relapses over at

least the next two to three years and consider them the most effective

treatment for their symptoms.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve & db=pubmed & dopt=Abstra\

ct & list_uids=1595754

-- Psychoactive medications have been used to manage chest pain of

presumed esophageal origin, especially in syndromes associated with

esophageal motor dysfunction. The rationale for their use is based on (a)

the high prevalence of psychiatric disorders reported in patient groups

with esophageal symptoms and minor motor dysfunction, ( recognized

psychophysiologic effects on esophageal motor activity, © the potential

benefits that nerve-modulating drugs may have on the pathogenesis of the

syndromes (independent of psychiatric factors), and (d) observations from

treatment trials for chronic pain--including irritable bowel syndrome, a

disorder that shares some clinical features with functional esophageal

chest pain. Although psychiatric factors may have interactive effects on

the presentation and course of reflux disease, the use of psychoactive

drugs in reflux disease has not been tested. The effects of psychoactive

drugs have been systematically explored and documented in only one study.

At present, the mechanisms of esophageal symptom reduction resulting from

psychopharmacologic treatments are not clear, but reduced sensitivity to

visceral stimuli remains one possibility.

http://www.pulsus.com/Gastro/12_06/pate_ed.htm

Tricyclic antidepressant (eg, amitriptyline in doses of 25 to 100 mg/day)

should be used in patients with nonspecific abnormalities on diagnostic

tests but a suspected esophageal source. These drugs are particularly

indicated in patients with documented visceral hyperalgesia.

http://www2.gastrojournal.org/scripts/om.dll/serve?action=searchDB & searchDBfor=a\

rt & artType=abs & id=pm3549420 & nav=abs & special=hilite & query=%5Bcontribs%5D%28clouse\

%2C%29

Low-dose trazodone for symptomatic patients with esophageal contraction

abnormalities. A double-blind, placebo-controlled trial

We conclude that low-dose trazodone therapy can be of benefit in the

management of symptomatic patients with esophageal contraction

abnormalities. In addition, our findings support recent observations that

manometric abnormalities characterizing this patient group may not be

solely responsible for symptoms.

http://www2.gastrojournal.org/scripts/om.dll/serve?action=searchDB & searchDBfor=a\

rt & artType=abs & id=pm6862161 & nav=abs

Nine patients with intermittent chest pain thought clinically to be

secondary to esophageal " spasms " developed typical pain while being

studied with an intraluminal transducer probe placed in the distal

esophagus. Manometric changes from control periods were examined preceding

and during pain episodes. No significant difference in distal esophageal

wave duration or amplitude or in frequency of abnormal peristalsis was

observed preceding or during pain episodes when compared with nonpain

periods over a mean monitoring time of 227 min. No change from the nonpain

periods in esophageal baseline pressure occurred during pain episodes, nor

was there any other obvious manometric change by gross inspection of the

tracings. We conclude that patients clinically suspected of having

esophageal " spasms " as the source of chest pain frequently do not,

regardless of the presence or absence of motility abnormalities on

conventional esophageal manometric studies. (Gastroenterology 1983

Aug;85(2):395-402)

http://www2.gastrojournal.org/scripts/om.dll/serve?action=searchDB & searchDBfor=a\

rt & artType=fullfree & id=a0020100495 & special=hilite & query=%5Barticletitle%5D%28che\

st+pain%2C%29

Treatment of patients with noncardiac chest pain (NCCP) is a major

clinical dilemma. Imipramine has been found beneficial in the management

of this condition (N Engl J Med 1994;330:1411–1417). However, the

mechanism involved in chest pain improvement is unknown. Imipramine has

several potential actions including anticholinergic, antihistamine

activity, norepinephrine, and serotonin reuptake blockade.

http://www.emedicine.com/med/topic743.htm

Tricyclic antidepressants -- These agents, specifically imipramine, have

been shown to decrease chest pain with no apparent cause on angiogram.

Studies specifically evaluating nutcracker esophagus are not yet

available. The mechanism of action of imipramine is not known.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve & db=pubmed & dopt=Abstra\

ct & list_uids=10957931

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve & db=pubmed & dopt=Abstra\

ct & list_uids=11096564

http://www2.gastrojournal.org/scripts/om.dll/serve?action=searchDB & searchDBfor=a\

rt & artType=abs & id=a0020200290 & nav=abs

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve & db=pubmed & dopt=Abstra\

ct & list_uids=9285856

Pharmacotherapy of altered brain-gut interactions in functional

gastrointestinal disorders.

> Debbi,

>

> I recently went to a new Gastroenterologist to get scoped cause I'm old

> enough now to start the regular check ups. Since statistically we

> achalasians have a higher risk of e cancer, I'll probably get scoped every

> few years. Anyway, the point is, when I told him about my spasms, fairly

> infrequent these days compared to my history, his take was this was

> " atypical symptomology " ! Based on the posts on this board, I don't think

> we're all " atypical " !

>

> Regarding antidepressants, I've not read the literature on NCCP's but I am

> familiar with the use of Selective Serotonin Reuptake Inhibitor (SSRI's)

> antidepressants with chronic pain patients. Pain increases the stress

> response in the body (increased cortisol levels, etc.) and the presence of

> chronic pain can be depressing psychologically. The SSRI's seem to help

> in both regards, reducing the biological stress response and easing

> depression / anxiety. We know that depression and anxiety increase the

> perception of pain, so conversely, reducing them will reduce the

> perception of pain. Another way of saying this, is that it doesn't

> eliminate the pain, but does help us to deal with it more effectively. I

> think Notan has posted on this issue at some length.

>

>

>

> Warm aloha,

>

>