TABLE OF CONTENTS of this chain:
21/ AMS <* THIS PANEL *>
22/ Babies and Kids
23/ A bit of song (like camp songs)
24/ What is natural?
25/ A romantic notion of high-tech employment
26/ Other news groups of related interest, networking
27/ Films/cinema references
28/ References (written)
1/ DISCLAIMER
2/ Ethics
3/ Learning I
4/ learning II (lists, "Ten Essentials," Chouinard comments)
5/ Summary of past topics
6/ Non-wisdom: fire-arms topic circular discussion
7/ Phone / address lists
8/ Fletcher's Law of Inverse Appreciation / Rachel Carson / Foreman and
Hayduke
9/ Water Filter wisdom
10/ Volunteer Work
11/ S**** bite
12/ Netiquette
13/ Questions on conditions and travel
14/ Dedication to Aldo Leopold
15/ Leopold's lot.
16/ Morbid backcountry
17/ Information about bears
18/ Poison ivy, frequently ask, under question
19/ Lyme disease, frequently ask, under question
20/ "Telling questions" backcountry Turing test (under construction)
AMS (acute mountain sickness) -- UNDER CONSTRUCTION
A recurring topic of discussion is altitude sickness and treatment.
AMS (acute mountain sickness)
Time and a distinct lack of resources can quickly elevate the
dangers of a medical emergency. High Altitude Pulmonary Edema (HAPE),
High Altitude Cerebral Edema (HACE), and retinal hemorrhaging
are all problems which can take place in some individuals as low
as 5-8,000 feet. You can read references, but you have a responsibility
to be in reasonable physical shape, drinking plenty of fluids.
But the im****tant thing to realize is that you have a MARGIN of safety
that you are cutting.
You should consult YOUR physician about YOUR special needs.
Diamox or Previtin should not be taken lightly.
[Do you understand the concept of body/drug interactions?]
Reactions to other drugs (even aspirin), allergries can differ at
higher elevations. See a physician.
Another topic where urban thinking can harm you.
Drug treatment is not a substitute for descending.
[Do you understand the concept of body/drug interactions?]
Gamow bags have been discussed as an expensive measure (perhaps most
useful for high altitude expeditions). Bottled LO2 is also a possibility.
The medical definition of what constitutes a high altitude starts at 8,000
ft.
This is the elevation where the PO2 is .75 that of a standard atmopshere.
14,000 ft. is .666 (2/3) a ATM, and 18,000 ft. is 1/2 an ATM. This is
clearly
non-linear [check your linear thinking at the door]. So the problem
ranges
are:
8,000-14,000 ft.
14,000-18,000 ft.
Above 18,000 ft.
Bibliography:
1 Ferreira and Grundy, _Dexamethasone in the Treatment of Acute Mountain
Sickness_, NEJM, VOl. 312, No 21, page 1390, 23 May 1985.
2 Oelz, Oswald, _A Case of High-Altitude Pulmonary Edema Treated with
Nifedipine_, JAMA, Vol 257, No 6, page 780, 13 Feb 1987.
"Medicine for Mountaineering: Third Edition" edited by James A. Wilkerson,
M.D., 1985, The Mountaineers, ISBN 0-89886-086-5.
"Medicine for the Outdoors" by Paul S. Auerbach, M.D., 1986, Little,
Brown and Company, ISBN 0-316-05928-5 (hc) 0-316-05929-3 (pbk).
"Wilderness Medicine" by William Forgey, M.D., 1987, ICS Books, Inc.,
ISBN 0-934802-37-8
"Mountain Sickness"
by Charles S. Houston
Scientific American, October 1992, page 58.
Synopsis at top of the article says:
"The varied and subtle symptoms of this potentially lethal disorder
humble many who scale the summit. But the problem is often
preventable."
Jim West's book.
"NOLS Wilderness First Aid" by Tod Schimelpfenig and Linda Lindsey, 1991,
National Outdoor Leader****p School and Stackpole Books, ISBN 0-8117-3084-0
%X Just finished the book. Excellent. Too repetitive at some points
is my only real criticism.
Excerpt from the Physician's Desk Reference, 1993
Diamox is a potent carbonic anhydrase inhibitor, effective
in the control of fluid secretion (e.g. some types of glaucoma),
in the treatment of certain convulsive disorders (e.g. epilepsy),
and in the promotion of diuresis in instances of abnormal
fluid retention (e.g. cardiac edema).
Diamox is an enzyme inhibitor that acts specifically on ...
the hydration of carbon dioxide and the dehydration of
carbonic acid. In the eye, this inhibitory action decreases
the secretion of aqueous humor and results in a drop in
intraocular pressure, a reaction considered desirable in
cases of claucoma. ... The diuretic effect of Diamox is due
to its action in the kidney on the reversible reaction
involving hydration of carbon dioxide and dehydration of
carbonic acid. The result is renal loss of HCO3 ion, which
carries out sodium, water, and potassium.
Diamox Sequels sustained-release capsules provide prolonged
action to inhibit aqueous humor secretion for 18 to 24
hours after each dose, whereas tablets act for only 8 to 12
hours. ... Blood concentrations of Diamox peak between 3 to 6
hours after administration of Sequels, compared to 1 to 4
hours with tablets.
Placebo-controlled clinical trials have shown that prophylactic
administration of Diamox at a dose of 250mg every 8 to 12 hours
(or 500mg Sequels once daily) before and during rapid ascent
to altitude results in fewer and/or less severe symptoms (such
as headache, nausea, shortness of breath, dizziness, drowsiness,
and fatigue) of acute mountain sickness (AMS). Pulmonary
function is greater in the Diamox treated group, both in
subjects with AMS and asymptomatic subjects. The Diamox
treated climbers also had less difficulty in sleeping.
....
Diamox therapy is contraindicated in situations in which sodium
and/or potassium blod serum levels are depressed, in cases of
marked kidney and liver disease, in suprarenal gland failure,
and in hyperchloremic acidosis. It is contraindicated in
patients with cirrhosis because of the risk of development
of hepatic encephalopathy.
....
Fatalities have occurred, although rarely, due to severe
reactions to sulfonamides including Stevens-Johnson syndrome,
toxic epidermal necrolysis, fulminant hepatic necrosis,
agranulocytosis, aplastic anemia, and other blood dyscrasias.
.... Caution is advised for patients receiving concomitant
high-dose aspirin and Diamox, as anorexia, tachypnea,
lethargy, coma, and death have been re****ted.
Increasing the dose does not increase the diuresis, and may
increase the incidence of drowsiness and/or paresthesia.
Increasing the dose often results in a decrease in diuresis.
....
Gradual ascent is desirable to try to avoid acute mountain
sickness. If rapid ascent is undertaken and Diamox is used,
it should be noted that such use does not obviate the need
for prompt descent if severe forms of high altitude sickness
occur, i.e. pulmonary edema or cerebral edema.
....
Long term studies in animals to evaluate the carcinogenic
potential of Diamox have not been conducted. In a bacterial
mutagenicity assay, EE was not mutagenic when evaluated
with and without metabolic activation.
The drug had no effect on fertility when administered in the
diet to male and female rats at a daily intake of up to four
times the maximum recommended human dose. Diamox has been shown
to produce birth defects of the limbs in mice, rats, hamsters,
and rabbits. There are no adequate and well-controlled studies
in pregnant women. EE should be used in pregnancy only if the
potential benefit justifies the potential risk to the fetus.
Because of the potential for serious adverse reactions in nursing
infants from EE, a decision should be made whether to discontinue
nursing or to discontinue the drug, taking into account the
im****tance of the drug to the mother.
The safety and effectiveness of Diamox in children have
not been established.
Adverse reactions, occurring most often early in therapy,
include a "tingling" feeling in the extremities, hearing
dysfunction or tinnitus, loss of appetite, taste alteration
and gastrointestinal disturbances such as nausea, vomiting,
diarrhea, and occasional instances of drowsiness and confusion.
....
No data are available regarding Diamox overdosage in humans as
no cases of acute poisoning with this drug have been re****ted.
Animal data suggest that Diamox is remarkably non-toxic. No
specific antidote is known. Treatment should be symptomatic
and sup****tive. Electrolyte imbalance, development of an
acidotic state, and central nervous system effects might be
expected to occur.
....
Dosage is 500mg to 1000mg daily, in divided doses using tablets
or Sequels as appropriate. In cir***stances of rapid ascent,
such as in rescue or military operations, the higher dose level
of 1000mg is recommended. It is preferable to initiate dosing
24 to 48 hours before ascent and to continue for 48 hours while
at high altitude, or longer as necessary to control symptoms.
Store at controlled room temperature (59 to 86 deg F).
http://205.162.195.3/hra/brochure.html
http://205.162.195.3/hra/AMS-clinguide.html
-----tage line-----
From: faustina@[EMAIL PROTECTED]
(ANDREA FAUSTINA)
Newsgroups: rec.skiing.alpine
Subject: Re: altitude sickness
As written in the PharmAssist:
Drug Class & Use:
This drug is a Carbonic anhydrase inhibitor used to treat insomnia, fluid
retention, glaucoma, epileptic seizures, and shortness of breath.
Related Generic Names:
Acetazolamide
Dichlorphenamide
Methazolamide
Related Brand Names:
Acetazolam
Ak-Zol
Apo-Acetazolamide
Daranide
Dazamide
Diamox
Diamox Sequels
Neptazane
General Information:
Addiction Potential? No
Prescription Required? Yes
Available in generic form? Yes
Decreases fluid retention (and internal eye pressure) by preventing the
action of carbonic anhydrase.
Time Required To Take Effect:
Allow approximately 2 hours for this drug to take effect.
What to do if a Dose is Missed:
Retake as soon as you remember, then continue based on the original
schedule.
Possible Adverse Effects:
Life threatening can include convulsions. If this occurs contact
Emergency Medical Help Immediately. On rare occasion some may experience
ringing ears, irregular or weak heartbeat, fever, back pain, headache,
hives, nausea, vomiting, blood in urine, mood changes, confusion,
hoarseness, trembling, and difficulty breathing. If this occurs cease
taking this drug and consult with your doctor as soon as possible.
Possible Drug Interactions:
1. May increase the effect of Amphetamines, Tricyclic Antidepressants,
Quinidine and Sympathomimetics.
2. May diminish the effect of Aspirin, Lithium and Methenamine.
3. May result in toxicity when used with Digitalis preparations and
Salicylates.
4. May increase the loss of potassium when used with oral Antidiabetics,
Cortisone drugs and Diuretics.
5. May result in a loss of bone minerals when used with Anticonvulsants.
Caution/Alert:
1. This drug should not be used if you have kidney disease, diabetes,
adrenal grand failure, or are allergic to any carbonic anhydrase
inhibitor.
2. Before using this drug consult with your doctor if you have lupus,
gout, are allergic to any Sulfa drug, or will be having surgery
(including dental) within the next 2 months requiring either spinal or
general anesthesia.
3. If pregnant or breast-feeding consult with your doctor before using
this drug.
4. People over 60 years of age should consult with your doctor before
using this drug.
5. This drug should not be given to children under 12 years of age.
6. Extended use of this drug may result in jaundice, kidney stones,
weight loss, vision changes, and a possible loss of both taste and smell.
Overdose Symptoms:
Overdose symptoms can include a numbing sensation in the hands and feet,
confusion, nausea, vomiting, drowsiness, excitability and coma. If you
suspect an overdose contact medical help and area Poison Control Center
immediately.
Andrea
From: pbgogo@[EMAIL PROTECTED]
(Prospero Barquero Gogo)
Newsgroups: rec.skiing.alpine
Subject: Altitude sickness
Date: 2 Nov 1994 18:30:52 -0500
Organization: The George Wa****ngton University School of Medicine
There is really not much one can do for mountain sickness. In the August
Journal of Wilderness Medicine, they reviewed the origins and attempted
treatments for altitude sickness. To sum it up: (1) physical fitness has
no effect on altitude sickness (although all the test subjects were in
relatively good shape); (2) people are unpredictably susceptible to acute
mountain sickness (AMS) (3) AMS and the often associated high-altitude
pulmonary edema (when water leaks into your lungs; HAPE) happen less
often in people who (a) subconsciously increase their breathing (even
while asleep) and (b) respond to high altitude (greater than 8000 feet)
by concentrating their blood oxygen carrying component (by diuresis --
that is, peeing alot). (4) AMS can be prevented in the short run by
taking a diuretic (this is technical but, one of the carbonic annhydrase
inhibitor class). It prevents AMS by making you pee, and causes you to
breathe more by decreasing the pH of your blood (breathing brings the pH
back to normal). (5) the reason one needs to "acclimate" to high
altitude is that it takes the body some time to manufacture new red blood
cells, which carry oxygen to your tissues, among other physiologic
changes. (6) diuretic therapy in the long run is controversial because it
decreases the body's response of making new red blood cells. (7)
hyperbaric chambers (where one is surrounded by sea level atmosphere
pressure) are effective treatments for severe AMS and HAPE
As someone has already posted, drinking lots of water is beneficial when
going to high altitude. This prevents dehydration, and it also improves
your body's chances of responding by diuresis. The diuretic mentioned
earlier can only be obtained from your doctor in the USA, and be aware
that it may have side effects, as any drug. Usually, take the diuretic
only if you've had problems with high altitude before, or if you're going
to very high altitudes (>13000 feet).
I'll try to answer any other questions if I get them via email.
Perky Gogo
pbgogo@[EMAIL PROTECTED]
rec.climbing
From: beall@[EMAIL PROTECTED]
(Jim Beall)
Subject: RE: AMS and Tums/Rolaids/etc
Regarding recent posts wondering about the reputed benefits of taking Tums
or Rolaids to reduce the effects of altitude sickness:
Here is a brief quote from
Peter Hackett, M.D.'s 1984 book
"Mountain Sickness: Prevention, Recognition and Treatment" (ISBN 0 930410
10 6)
"Aluminum hydroxide sodium carbonate (Roliads) has been suggested as a
prophylaxis for acute mountain sickness (Penberthy, 1977). It is
incor****ated into a four-point prevention program designed for Mt. Rainier
climbers which includes:
1) adequate hydration,
2) high carbohydrate intake while climbing,
3) Rolaids to maintain urine pH at 5.5 to 6.5 (slightly acid), and
4) regulating climbing pace to keep the heart rate
(pulse) below two-thirds of maximum.
It is the opinion of this writer [Dr. Hackett] that such a program on
Mount Rainier is of obvious value in preventing acute mountain sickness,
even without the use of Rolaids. There has not, as of this writing,
been a controlled study on the use of Rolaids and although there are
no noted harmful side effects in the dosages recommended,
we do not recommend its use as mountain sickness prophylaxis."
Granted it's a ten year old reference, but the story's been around for
much longer.
Another gem from Hackett's little book: "Local Sherpa wisdom dictates
never to get drunk the first night at altitude"!
From: tom@[EMAIL PROTECTED]
(Tom Bunch)
Newsgroups: rec.climbing
Subject: Re: altitude sickness FYI
Date: 4 Jan 1995 03:39:43 GMT
In my original post I omitted the side effects of Diamox. I did this
because I didn't really understand how they worked, and I didn't want
to spread still more misinformation on the whole topic, but in
retrospect, I'm afraid people might assume I've told the whole story.
Fortunately, Allen Sanderson (allen@[EMAIL PROTECTED]
) took the time
to fill in the blanks for me, and point out one or two other things.
I will include the relevant bits of his letter (with permission).
Also I remember reading a post here about an alternative drug in
testing, but I couldn't remember any specifics. The post turns out to
have been by Denzil Boradhurst regarding bnezolomide, and I will
append it as well. This info may never, sadly, become useful since,
as Denzil points out, it does not seem to have a profitable market and
so probably won't be produced.
-Tom
--
From: Allen Sanderson
Diamox is a trademark name for acetazolamide.
You are almost correct in what an acetazolamide does. It is an
ihibitor, but not quite everywhere you mention in the chemical
reation. [I'm sure this is what he meant, but actually it inhibits
production of the enzyme that catalyzes the reaction, which amounts
to the same thing. -Tom]
Bicarbonate reduces down to hydronium and carbonite acid. Carbonic
anhydrase comes into play in breaking down the carbonic acid into
water and carbon dioxide which is expelled through your renal system
(kidneys) and repitory system (lungs), respectively.
You kinda implied that cardonic anhydrase helps break down bicarbonate
which it does not - it only affects the second reaction. [This
contradicts what was told to me by a physician, but Allen may be
right -- this physician emphasized that he was not current on this
stuff. -Tom]
Now when you take acetazolamide it inhibits the break down of carbonic
acid into water and carbon dioxide. Thus it makes your blood acidic
(ie brings on acidosis) because there is too much carbonic acid in the
blood. Your body reacts in two ways. First, it tries to bring in
more oxygen so a pH balance is maintianed between oxygen and the
carbonic acid which is what we want. But at the same time your body
tries to dump the extra carbonic acid (and other good elecrolytes and
water that you really want to keep) through the renal system, not what
we want.
So you end up breathing more, slight hyperventilation, and you piss
like a race horse. So as you can see it does help but at a price.
--
From: denzil_b@[EMAIL PROTECTED]
(Denzil Broadhurst)
Date: Wed, 26 Oct 94 10:14:54 GMT
Just returned from the British Medical Expedition to Everest - great time,
though I wasn't one of the people climbing Everest, just some of the
trekking peaks (20,000-21,000 ft).
One of the medical trials was a double blind test on Benzolomide to see if
it
had the same effects for acclimatisation as Acetazolomide (Diamox).
Provisional
results show it to be just as effective, and with fewer side effects. You
still get the tingles in extremities, (including one area where the ladies
wouldn't suffer from!) but it doesn't seem to affect the mental
state like Diamox.
Now for the bad news! The drug was manufactured in the 60's as a possible
replacement for Diamox in treatment of Glaucoma - but it didn't work. No
more
has been made and we've just used up the world stocks in the trial!
Anyone out there working for a drugs company prepared to make some more
(and
put it through the necessary safety trials - shouldn't cost more than a
couple
of million!)?
The doctor in charge of the trial will be publi****ng his finding and
talking
to various Pharmaceutical companies, but if its only application is AMS it
is
likely that there wouldn't be sufficient demand to justify the investment.
Shame really, one of the guys with me had problems 15 years back with AMS
when
he went to Everest base camp, this time on the trial he got up to 21,000
ft
with no problems.
From: tom@[EMAIL PROTECTED]
(Tom Bunch)
Newsgroups: rec.climbing
Subject: Re: altitude sickness FYI
Date: 31 Dec 1994 03:09:06 GMT
In article <3dg5pc$bk6@[EMAIL PROTECTED]
>,
BillOldMan <billoldman@[EMAIL PROTECTED]
> wrote:
>Just a little more on using tums to avert mild AMS; The hypothsis is that
>overbreathing at altitude, from exertion or other causes, results in loss
>of CO2, which results in loss of carbonic acid (H2CO3) which normally
>causes the acid ****ft in blood that stimulates nerves in the central
>nervous system which stimulate breathing, but the body needs O2 and
begins
>to compensate for the loss of CO3 by providing CO3 ions from other
>sources, and runs low, short term, so tums help balance things out, short
>term. Seems as though low carbonic acid should result in alkalosis, and
>that adding an antacid should make things worse, but it's the carbonate
>ions that are lost and that are replaced by tums. I think dehydration is
a
>bigger threat, but I've never run into serious problems, being a more or
>less a moderate mountaineer.
That's the hypothesis, more or less, but it's been been pretty
conclusively debunked. Another im****tant part of the theory is that
the phenomnae noted above trigger vasodilation in the brain (maybe
elsewhere too -- I'm a lay person) which can lead to hypoxic brain
damage.
I decided it was silly to live with all the misinformation on the
Rolaids thing, so I gave Tom Hornbein a buzz, since his office is
quite near mine. Dr. Hornbein was interviewed in the most recent in
R&I in the article by Alan Fitch. He's one of the foremost researches
on all this rot. Any errors this post may (is likely to) contain are
mine. Anything particuarly clever is probably his.
The skinny is this: the Rolaids idea came from Larry Penberthy, then
owner and president of MSR. This was his new idea, after his
suggestion of superdoses of the watersoluble vitamins fell from favor.
Rob Roach, who was at the time a grad student at Evergreen (here in
Wa****ngton state) did a controlled study of aluminum hydroxide sodium
carbonate versus (Rolaids) on Mt. Rainier and found, as a majority of
respectable scientists predicted, no benefit. Hornbein wrote a
critique of Penberthy's unconventional interpretation of the
scientific method, and Penberthy wrote irate letters to the Dean of
the medical school and the President of U. Wa****ngton, then Charles
Oderguard. The critique was published in one of the climbing rags,
maybe _Summit_ or _Climbing_. I wish I could tell you more specifically,
but I can't. Doc Hornbein had considered this history more or less
successfully repressed until I brought it up. He was openly shocked
at the idea that anyone was still recommending Rolaids to stave off
AMS. After Larry Penberthy gave up on all this, he made an abortive
bid for U.S. Senate, which is, I suppose, totally irrelevant.
Now I'm going to go farther out on a limb and try to describe what
Diamox is all about. Diamox is a carbonic anhydrase inhibitor.
Carbonic anhydrase (henceforth C.A.) is an enzyme carried around
mostly by red blood cells which aids carbon-dioxide trans****t from the
tissues and its release from the blood in the lungs by catalyzing the
reversible hydration of carbon dioxide to carbonic acid. Vastly
simplified, the body produces lots of h2co3 (bicarbonate) when sugars
are used, and C.A. is a catalyst as it goes to h+ and hco3- (hydronium
ion and carbonic acid) and from there to h20 and c02. Inhibitting
C.A. merely slows down this reaction. I'm still a little mystified by
the intricacies of it -- intuitively, how can you correct an imbalance
by inhibitting the enzyme the body uses to readjust that balance? But
my understanding is that hyperventilation causes you to blow off an
excess of co2, resulting in acidosis which can lead to cerebral edema.
But if co2 is not so readily available to be blown off, it's just
retained as carbonic acid or bicarbonate. Apparently, loading up with
that dross doesn't inhibit absorbtion of o2. Bicarbonate, by the way,
is the most im****tant PH buffering agent in our bodies. Also, bear in
mind that some of this stuff is still just theory. For example, it's
still debatable that acidosis -> vasoconstriction in the brain ->
hypoxic brain damage and cerebral edema. Another thing Dr. Hornbein
went into was that inhibitting C.A. raised the difference in partial
pressure of CO2 between, I think, arteries and capillaries, which in
turn keeps the CO2 out in the tissue instead of in the blood where it
will have to be dealt with. My understanding of this last bit is
minimal, and I didn't want to keep him busy too long answering dopey
questions.
Anyway, given all the above, it's not surprising that people might
think Rolaids might help -- it's full of carbonate. The fact is, it
only helps with indigestion and such.
One controlled study (again, I can't cite it specifically) got results
something like this with Diamox:
incidence of headache
patients with nothing 70%
patients with placebo 50%
patients on Diamox 7%
This was on a two day climb of Mt. Rainier (14,410 ft). It's
generally accepted that headaches and nausea are at one end of the
spectrum that leads to cerebral edema. Whether the mechanisms are
approximately the same for pulminary edema is a matter of less
concensus.
An alternative drug is Decadon (sp?), a steroid. There has been no
comparing study between the two so far as Dr. Hornbein knows. I
should think, given the prevalence of Diamox, that Decadron is only of
interest to patients for whom Diamox is contraindicated, such as those
with acute narrow angle glaucoma (rare form of glaucoma).
Effectiveness of Diamox has been shown to vary quite significantly
between individuals. Basically, you want to ask your doctor about it,
but most prescribe 250mg two or three times per day. Many believe
that once per day is enough, but once you've found what works, you
tend to stick with it. If you take what is, for you, a large dose,
you will get tingly sensations in your extremities. If it's not
uncomfortable, fine. But it can apparently make you feel "really
weird". If so, you should (again, ask the prescribing doctor) be ok
to cut your dosage in half.
I tried to look up a few specific citations just now, but apparently
the database is down. Isn't it great having computers to blame for
things?
-Tom Bunch
P.S. If we're lucky T.H. himself may come around and clarify this
further for us -- I pointed him in the general direction of
rec.climbing. Now, if he can suffer all the slings and arrows,
perhaps we'll see his face here.
Article 34948 of rec.climbing:
From: dunwiddt@[EMAIL PROTECTED]
(Tom Dunwiddie)
Subject: Re: Neurological effects of high altitude
Well, here's a few to get you started... not complete agreement,
but most of them do seem to suggest that there are some problems
following climbing at high elevation. Now if they could just figure
out what's wrong with our brains to make us climb to begin with. 8^)
Tom Dunwiddie
-----------
AU - Cavaletti G
AU - Tredici G
TI - Long-lasting neuropsychological changes after a single high altitude
climb.
AB - Acute neuropsychological changes due to high altitude climbing
without supplementary oxygen are well known. However, many climbers
re****t vague symptoms of brain dysfunction after return to sea level
suggesting that long-lasting neuropsychological impairment may ensue
even after a single ascent. In this study we evaluated a series of
neuropsychological functions in a group of 11 climbers who ascended
over 5000 m. Besides memory, also reaction time and concentration
were less efficient when the climbers were evaluated 75 days after
their return to sea level, confirming that even a single high
altitude climb may be harmful for central nervous system functions.
SO - Acta Neurol Scand 1993 Feb;87(2):103-5
AU - Regard M
AU - Landis T
AU - Casey J
AU - Maggiorini M
AU - Bartsch P
AU - Oelz O
TI - Cognitive changes at high altitude in healthy climbers and in
climbers developing acute mountain sickness.
AB - We re****t the cognitive functions of 17 non-acclimatized
mountaineers
who ascended from low lands to an altitude of 4,559 m in 24 h and
were studied there within 6 h. We found that this rapid ascent to
high altitude had small, but differential effects upon cognitive
performance depending upon the later development of acute mountain
sickness (AMS). Subjects who developed AMS within a 24-48-h stay at
high altitude were mildly impaired in short term memory, but
improved
in conceptual tasks, while subjects who remained healthy had a
better
short term memory performance but no improvement in cognitive
flexibility. Possible explanations for these unexpected effects of
high altitude are discussed.
SO - Aviat Space Environ Med 1991 Apr;62(4):291-5
AU - White AJ
TI - Cognitive impairment of acute mountain sickness and acetazolamide.
AB - In a trial to *****s the cognitive impairment attributable to benign
acute mountain sickness (AMS) and to acetazolamide, six women and
five men, 20-35 years old, ascended from sea-level to 3600 m in 36 h
and were *****sed for deterioration in performance on psychological
tests. Of five ***-matched pairs with a mean age difference of 3.4
years (S.D. +/- 4.4 years), one member took slow-release
acetazolamide 500 mg daily and one placebo on a double-blind basis
during the ascent and again for an identical course at low altitude
32-38 d later. The unmatched woman took placebo during ascent.
Before, during, and after each drug course each subject performed an
Environmental Symptom Questionnaire (ESQ) and a psychological test
battery consisting of trail-making, paced auditory serial addition
test (PASAT), letter-digit code, dual-task cancellation and
subtraction, and memory subtests. On ascent, ESQ score deteriorated
by an average of 62 points in placebo subjects compared with 32 in
acetazolamide subjects (p = 0.055). Deterioration in the
psychological test battery was only significant in the PASAT (p less
than 0.05) and memory (p less than 0.01) subtests of subjects taking
placebo. For those taking acetazolamide, no test showed significant
impairment, suggesting it had no detectable cognitive impairment at
this dose.
SO - Aviat Space Environ Med 1984 Jul;55(7):598-603
AU - Jason GW
AU - Pajurkova EM
AU - Lee RG
TI - High-altitude mountaineering and brain function: neuropsychological
testing of members of a Mount Everest expedition.
AB - Concern has been raised regarding the possibility that hypoxic
conditions encountered during high-altitude mountaineering may have
lasting harmful effects on the human brain. Members of an expedition
to Mount Everest completed a series of neuropsychological tests
before and after the expedition. Exposure to altitudes above 7,200 m
was limited to a maximum of four consecutive nights, separated by
rest periods at lower altitudes. No significant decline in
performance was observed on any test. The subjects also completed a
short series of tests at different altitudes during the expedition.
No significant deterioration was observed at altitudes up to 7,500
m.
There do not appear to be lasting harmful effects on brain function
under these conditions.
SO - Aviat Space Environ Med 1989 Feb;60(2):170-3
AU - Cavaletti G
AU - Garavaglia P
AU - Arrigoni G
AU - Tredici G
TI - Persistent memory impairment after high altitude climbing.
AB - High altitude climbing without supplementary oxygen is a common
s****ting practice and athletes have been extensively evaluated with
respect to possible brain functional impairment during its
performance. Little is known on the contrary about long-term effects
of hypoxia on the central nervous system. We evaluated, at sea
level,
a group of 10 high-altitude climbers with a battery of
neuropsychological tests before and 75 days after the ascent. Our
results suggest the occurrence of an impairment of memory
performance
after return to sea-level at least in some subjects, while speech
and
certain practical abilities were unchanged.
SO - Int J S****ts Med 1990 Jun;11(3):176-8
AU - Hornbein TF
TI - Long term effects of high altitude on brain function.
AB - Absence of oxygen to the brain for even a very few minutes results
in
loss of consciousness and can cause permanent injury. Can the
wanderer to the limits of earth-bound hypoxia suffer similar harm
from more prolonged exposure to milder hypoxia that does not cause
loss of consciousness? I shall review the results from studies where
neurobehavioral function has been compared in mountaineers before
and
after return from great heights and in individuals with chronic
pulmonary disease before and after prolonged, continuous oxygen
therapy. Many (although not all) of these studies re****t mild
impairment of neurobehavioral function after fairly prolonged
hypoxic
exposure. Impairment was manifest by deficits in memory storage and
recall, aphasia, concentration, and finger tapping speed; the last
deficit was still detectable a year later in one group of
mountaineers. Limited evidence suggests that climbers with a high
ventilatory response to hypoxia (HVR) may be more susceptible to
impairment than those with a lower HVR.
SO - Int J S****ts Med 1992 Oct;13 Suppl 1:S43-5
AU - Hornbein TF
AU - Townes BD
AU - Schoene RB
AU - Sutton JR
AU - Houston CS
TI - The cost to the central nervous system of climbing to extremely high
altitude.
AB - To *****s the possibility that climbing to extremely high altitude
may result in hypoxic injury to the brain, we performed
neuropsychological and physiologic testing on 35 mountaineers before
and 1 to 30 days after ascent to altitudes between 5488 and 8848 m,
and on 6 subjects before and after simulation in an altitude chamber
of a 40-day ascent to 8848 m. Neuropsychological testing revealed a
decline in visual long-term memory after ascent as compared with
before; of 14 visual items of information on the Wechsler Memory
Scale, fewer were recalled after ascent by both the simulated-ascent
group (a mean [+/- SD] of 10.14 +/- 1.68 items before, as compared
with 7.00 +/- 3.35 items after; P less than 0.05) and the
mountaineers (12.33 +/- 1.96 as compared with 11.36 +/- 1.88; P less
than 0.05). Verbal long-term memory was also affected, but only in
the simulated-ascent group; of a total of 10 words, an average of
8.14 +/- 1.86 were recalled before simulated ascent, but only 6.83
+/-
1.47 afterward (P less than 0.05). On the aphasia screening test, on
which normal persons make an average of less than one error in
verbal
expression, the mountaineers made twice as many aphasic errors after
ascent (1.03 +/- 1.10) as before (0.52 +/- 0.80; P less than 0.05).
A
higher ventilatory response to hypoxia correlated with a reduction
in
verbal learning (r = -0.88, P less than 0.05) and with poor
long-term
verbal memory (r = -0.99, P less than 0.01) after ascent. An
increase
in the number of aphasic errors on the aphasia screening test also
correlated with a higher ventilatory response to hypoxia in both the
simulated-ascent group (r = 0.94, P less than 0.01) and a subgroup
of
11 mountaineers (r = 0.59, P less than 0.05). We conclude that
persons with a more vigorous ventilatory response to hypoxia have
more residual neurobehavioral impairment after returning to lower
elevations. This finding may be explained by poorer oxygenation of
the brain despite greater ventilation, perhaps because of a decrease
in cerebral blood flow caused by hypocapnia that more than offsets
the increase in arterial oxygen saturation.
SO - N Engl J Med 1989 Dec 21;321(25):1714-9
AU - Regard M
AU - Oelz O
AU - Brugger P
AU - Landis T
TI - Persistent cognitive impairment in climbers after repeated exposure
to extreme altitude.
AB - We performed neuropsychological testing in eight world class
climbers
who had reached summits higher than 8,500 meters without
supplementary oxygen. Five had mildly impaired concentration, short-
term memory, and ability to ****ft concepts and control errors. There
were no defects in perception or other cognitive activities. The
pattern of impairment suggests malfunctioning of bifronto-tem****o-
limbic structures. Repeated extreme-altitude exposure can cause mild
but persistent cognitive impairment.
SO - Neurology 1989 Feb;39(2 Pt 1):210-
From: Jeff turbo Deifik <turbo@[EMAIL PROTECTED]
>
> > Acetazolamide (AMS)
> > Methylprednisolone (HACE)
>
> I spoke with Dr William Forgey about a year ago about HAPE.
> Among other wilderness medicine books, he wrote
> "Wilderness Medicine 4th Edition"
>
> Since I have gotten HAPE, at only 11.2k feet, the subject is im****tant
to
> me. I have tried diamox and dexamethasone. They didn't help once
symptoms developed.
> I hiked down, starting at 1am, for about 6 miles.
>
> Forgey said the drug of choice is Procardia (nifediprine) 20 mg every 8
hours during
> ascent, and for 3 additional days at altitude. This is relativly new
information. The
> book was published 3/95. I haven't had a chance to try procardia. It
works by relaxing
> the pulminary artery, which is what is belived to cause HAPE.
Jeff turbo Deifik jdeifik@[EMAIL PROTECTED]
turbo@[EMAIL PROTECTED]
..
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