Scott,  I hope someone can give you helpful ideas, but I would tell you
to give up "trying to convince him" because he is incapable of
responding to reason or logic due to the disease process.  Controlling
or manipulating his environment are your options.  If you think of the
process as reversing of childhood developmental milestones-he is
responding at an automatic, reflex kind of level....probably with little
cognitive input.  I was happy to hear that the feeding tube restored his
weight--we don't hear that much for dementia.
Best wishes-it's hard.
Beth

Scott-

So sorry you, your family and your father are suffering so. How does one
respond to your post  without sounding as cruel & heartless as the
feeding regimen you described.

Knowing only what you have given,...

Take off the gloves, vest, etc.  Hopefully, your father will remove the
feeding tube himself ..  allowing some dignity to return to all... feed
him as best you can, and should he still be unable to take water &
sustenance---
allow nature to take its' course or "God's will be done"..

Dear Scott,

I hope you don't think me callous, but I don't believe in the use of feeding
tubes, unless it is in someone who has an expectation of recovery.

Meanwhile, I hope you find a way to cope with your situation.

<snip>

If I am ever in that situation my instructions are that someone pulls the
plug on me.
What is the point of the life you describe?

sounds like a difficult situation for everyone :(

what's the worst that caan happen if he does chew on something? IE why CAN'T
he have a teether or chew toy or pacifier for that matter?

Visual facial grasp.

Riestra AR, Heilman KM.

Department of Neurology of the Mexican Institute of Neurosciences,
Huixquilucan Estado de Mexico, Mexico.
alonso_riestra@intramedios.com.mx

Some patients with degenerative neurological diseases have a release of
the vestibular-ocular reflex (VOR), as detected by passive head
movement during visual fixation on a moving target ("doll's
eyes"maneuver). However, a positive doll's eyes sign might be induced
by other defects and the purpose of this article is to describe a new
ocular sign of cortical dysfunction, the visual facial grasp. We
observed three patients, one with progressive supranuclear palsy (PSP),
another with probable Alzheimer's disease (AD) and a third with
cortico-basal degeneration (CBD) all of whom appeared to demonstrate a
release of the vestibulo-ocular reflex (VOR) with passive head
movements. Whereas the patient with PSP, who was unable to inhibit the
VOR regardless of the visual target used probably had a true release of
the VOR, the patients with AD and CBD were able to inhibit this reflex
when the visual target was the examiner's moving face. These two
patients also exhibited spontaneous preference for visual fixation on
the examiner's face and improvement in smooth pursuit when the
examiner's face was the visual target. This clinical observation
suggests that the deficits in these two patients with AD and CBD were
related to the emergence of a primitive stimulus-bound behavior, the
visual facial grasp.

Verbal learning and visuomotor attention in Alzheimer's disease and
geriatric depression.

Strang JM, Donnelly KZ, Grohman K, Kleiner J.

We compared the verbal learning and visuomotor attention of 34
Alzheimer's patients and 18 depressive patients. Verbal learning was
assessed using The Hopkins Verbal Learning Test--Revised (HVLT--R);
visuomotor attention was assessed using the Trail Making Test (TMT).
The Alzheimer's patients had significantly lower scores on immediate
and delayed recall of a word list. There was a nonsignificant trend in
this group toward a fewer number of true positives and a greater number
of false positives. Alzheimer's patients were significantly slower on
Trails A, with a nonsignificant trend toward slower performance on
Trails B. No difference was observed in accuracy of attentional
processing. The results are discussed in terms of other factors, such
as stage of cognitive decline, which might have influenced the findings.

Visuospatial deficits due to impaired visual attention: investigation
of two cases of slowly progressive visuospatial impairment.

Suzuki K, Otsuka Y, Endo K, Ejima A, Saito H, Fujii T, Yamadori A.

Division of Neuropsychology, Department of Disability Medicine, Tohoku
University Graduate School of Medicine, Sendai, Japan.
kyon@mail.cc.tohoku.ac.jp

Two patients with slowly progressive visuospatial impairment
demonstrated a peculiar type of visuoconstructive deficit. The most
prominent manifestation appeared when handling kanji (logogram)
characters and other figurative patterns. The patients showed pure
agraphia for complex kanji but not for kana (syllabogram) or Arabic
numerals. Their abilities to read and understand kanji characters and
to orally describe the structure of a kanji character were preserved.
They could not draw or copy figures or symbols except for single lines
or simple symbols, although they could identify and name the targets
easily. They also performed poorly in such visuoconstructive tasks as
the block design subtest and matching to sample tests that require the
ability to simultaneously attend to multiple saliencies. When asked to
copy multiple kana characters scattered on a sheet of paper, they could
correctly describe the location of a particular character in relation
to the others, but actually wrote each character in grossly mislocated
positions. These findings suggest that when the patients start
particular tasks, which require detailed visual analysis, their range
of visual attention becomes extremely narrow. This task-dependent
narrowing and fixation of visual attention might explain some of the
visuoconstructive symptoms described in patients with slowly
progressive visuospatial impairment.

Consistent immunohistochemical detection of intracellular
beta-amyloid42 in pyramidal neurons of Alzheimer's disease entorhinal
cortex.

D'Andrea MR, Nagele RG, Wang HY, Lee DH.

Johnson and Johnson Pharmaceutical Research and Development, Spring
House, PA 19477, USA.

We compared the effects of three pretreatment immunohistochemical
techniques (no pretreatment, pepsin predigestion and heat pretreatment
(HEAT)) for detecting intracellular beta-amyloid42 (Abeta42) in
pyramidal neurons of formalin-fixed Alzheimer's disease (AD) cortices
(n = 25). Although all three protocols immunostained Abeta42 in amyloid
plaques using four commercially-obtained Abeta42 specific antibodies,
only the HEAT protocol consistently detected prominent intracellular
Abeta42 in pyramidal neurons. This suggests that the Abeta42 present in
amyloid plaques may be structurally distinct from that located within
the neurons perhaps due to differential binding proteins coupling or a
consequence of formalin fixation. Detection of an abundant
intracellular Abeta42 in neurons may provide alternate explanations for
the origin of dense-core amyloid plaques in AD cortices other than the
conventional chronic extracellular Abeta42 deposition hypothesis.
Copyright 2002 Elsevier Science Ireland Ltd.

Neither major depression nor glucocorticoid treatment affects the
cellular integrity of the human hippocampus.

Muller MB, Lucassen PJ, Yassouridis A, Hoogendijk WJ, Holsboer F, Swaab
DF.

Max Planck Institute of Psychiatry, Kraepelinstrasse 2-10, 80804
Munich, Germany. muellerm@mpipsykl.mpg.de

In major depression, decreased hippocampal volume has been attributed
to hypercortisolemia, a frequent sign of the disorder, because in
animals an excess of corticosteroids has led to dendritic atrophy,
astrogliosis and loss of neurons in this brain region. The present
study is the first to investigate the structural integrity of the human
hippocampus in major depression and following glucocorticoid treatment.
Post-mortem hippocampal tissue from 15 patients who had had major
depression or bipolar affective disorder, 10 patients who had been
treated with glucocorticoids and 16 controls was assessed using
haematoxylin-eosin, Nissl and Bodian staining. The patterns of reactive
astrogliosis (glial fibrillary acidic protein, GFAP), synaptic density
(synaptophysin), synaptic reorganization (growth-associated protein
B-50) and early signs of Alzheimer's disease (Alz-50) were examined
immunocytochemically. Multivariate analysis, with the patients' age,
tissue fixation time and postmortem delay as covariates, was performed.
There was no evidence of neuronal cell loss or other major
morphological alterations in any of the groups, nor was there a
significant change in the distribution pattern of synaptophysin or
Alz-50. Changes in B-50 and GFAP staining were observed in the
steroid-treated and depressed patients in areas CA1 and CA2 only. The
human hippocampus in major depression and after glucocorticoid
treatment does not reveal any major morphological changes or signs of
neuronal cell death, but does show subtle alterations in B-50 and GFAP
expression in selected parts of the pyramidal cell layer.

Optimization of techniques for the maximal detection and quantification
of Alzheimer's-related neuropathology with digital imaging.

Cummings BJ, Mason AJ, Kim RC, Sheu PC, Anderson AJ.

Institute for Brain Aging, University of California, Irvine, CA
92697-4540, USA.

Prior to undertaking quantitative neuropathological studies of
Alzheimer's disease, methods for detecting plaques and tangles must be
optimized. While suitable antibodies have been developed with great
sensitivity, specificity, and reliability, there is no standard
pre-treatment protocol for key AD-related pathology. It is well known
that formic acid treatment enhances the detection of beta-amyloid. But
what concentration of formic acid is best; can similar methods enhance
the detection of tau-related pathology? This study compared multiple
antigen retrieval techniques (e.g. boiling in citrate or glycine
buffer, microwaves, formic acid concentrations), to develop an optimal,
standardized protocol for quantitative digital microscopy.
Free-floating (40 microm) and paraffin-embedded (12 microm) sections of
formalin fixed frontal cortex from mild, moderate, and severe AD cases
(n = 18) were pretreated with fifteen different protocols and stained
with each of the following antibodies: beta42, PHF-1, MC-1 and AT8.
Random fields were digitally captured and images were thresholded to
select for positively stained areas versus background (e.g. "load"). As
previously reported, high concentrations of formic acid were extremely
effective in enhancing the detection of beta-amyloid; as much as a
2-fold enhancement in Abeta "load" values were observed. Surprisingly,
tau-related pathology detection also increased significantly following
pretreatment. Depending on the antibody, between a 3-fold and 6-fold
enhancement was possible relative to no pretreatment. Comparable
results were found in paraffin-embedded sections. Similar enhancements
in the detection of pathology were obtained following 99% formic acid
exposure, microwaving in citrate buffer (pH 9.0) or exposure to 99%
formic acid then boiling in citrate buffer (pH 6.0). Because the latter
treatments were often harsh on the tissue and more difficult to
control, we recommend a standard tissue pretreatment of 99% formic acid
for seven minutes for both beta-amyloid and tau-related pathology.

Dynamic allocation of attention in aging and Alzheimer disease:
uncoupling of the eye and mind.

Mapstone M, Rosler A, Hays A, Gitelman DR, Weintraub S.

Cognitive Neurology and Alzheimer's Disease Center, Northwestern
University Medical School, 320 E Superior St, Chicago, IL 60611.

CONTEXT: Visual attention can be distributed focally, in the direction
of gaze, or globally, throughout the extrapersonal space. Aging, and
especially Alzheimer disease (AD), may influence global attention,
resulting in shifts of gaze to attend to the global workspace.
OBJECTIVE: To determine if subjects who have AD and cognitively intact
older subjects shift their gaze more often than young subjects while
viewing a dynamic stimulus that emphasizes global attention. DESIGN:
Experimental study of eye fixation patterns in response to a simulated
driving scene with stationary and moving distractors. SETTING: Urban,
medical school, National Institute on Aging-funded Alzheimer's Disease
Center. PARTICIPANTS: Thirteen subjects with mild probable AD, 13
age-comparable cognitively intact older control subjects, and 11 young
control subjects. MAIN OUTCOME MEASURE: Proportion of eye fixations
within and outside of a central region of interest encompassing the
"road" surface. RESULTS: Young controls made significantly more eye
fixations (mean number of eye fixations, 47.5) than either of the other
2 groups (older controls mean, 33.2; patients with AD mean, 32.2).
However, 76% of their fixations remained within the central region of
interest. Older controls and subjects with AD made proportionately
fewer fixations within this region (48% and 49%, respectively) than
young controls and moved their eyes more often to the periphery but did
not differ from one another. CONCLUSIONS: Young controls maintain
central eye position regardless of peripheral distraction. Older
controls move their eyes to the periphery, presumably to widen the
window of attention. Subjects with mild AD did not experience an
additional disadvantage beyond that associated with aging.

Scott,I don't have any answer for you on this;but onething that jumped
out at me from your post and concerned me greatly was where you said
your Dad sometimes puts his hearing aids in his mouth and chews on them!
It seems that would ruin his hearing aids;but more importantly I'm
thinking of what might happen if he swallowed a hearing aid battery. I
could be wrong on this;but it seems I've read somewhere that swallowing
such a battery could make a person very ill or even kill them? So y'all
surely need to talk to your Dad's doctor or someone knowledgeable about
that.

Pardon me for asking, and I don't want to sound critical, but why
in the world would anyone install a gastric feeding tube for
someone with a fatal dementia?  Why didn't you just let nature
take its course when he could no longer swallow food?  Why are
you torturing this poor man by feeding him through a tube when he
obviously doesn't like it?  Is your family keeping him alive so
that he can die slowly from declining brain function?  Is it
being done FOR him or TO him?

This is why I have a living will that instructs my doctor and
other caregivers that I DO NOT want to be fed through a tube.  To
me, it sounds like slow torture.

And no, I can't offer any advice because in my family we all
agree that we would never want to be treated like that.  My
mother simply stopped eating several weeks before she died, and
we acted in accordance with her living will and her expressed
wish that she be allowed to die with dignity and without invasive
medical intervention.

  To those who have responded so far to my query:

    I wish to thank all of you who have already responded to my
posting.  I especially would like to thank those who have added
helpful suggestions.  A number of opinions were tendered, and not all
of them do I fully agree with, but I thank all of you for the
suggestions nonetheless.

    I perhaps failed to describe the situation as fully as might
have been necessary.  The situation is much more complex than I have
described.  As well, I am not the primary caregiver involved in this.
As such, I am not the one making the decisions involving my father's
care at this time--that role falls to my mother, who is still quite
competent.  Some time ago, a consensus was reached that when the time
comes that my father is fully failing, then we would place him in the
appropriate assisted living environment, and no excessive (unnecessary
and painful) treatment measures would be resorted to then... at that
point, then, 'nature will be allowed to run its course'... However, as
long as there was still some quality of life present for my father,
then care and treatment would continue.  At this time, he is not
capable of swallowing, and requires a GI tube. Insertion of a GI tube
is not considered an extraordinary measure at this time, though; in
fact, it is not an uncommon treatment at all at this point in the
progression of Alzheimer's disease.  He may be incapable of swallowing
now; however, he is still capable of talking, answering simple
questions (his answers are limited pretty much to 'yes' and 'no' now),
walking (sometimes long walks, in excess of a half a mile or even a
mile).  He still understands some of the things we say to him, but we
have discovered that the processing time has been greatly lengthened.
He can also read passages from a book (with guidance), with assistance
he still recognizes some of us, and he is capable of writing out
sentences, etc., (again with guidance), watching TV/movies, playing
catch with a ball, etc.  We understand that he is not fully aware of
his environment, and that this is an ultimately fatal condition, but
the consensus was that it is not yet time to cease assistance on our
part.  Some of you might disagree with this decision, and that is all
well and good--you are certainly entitled to your opinion.

    I took some time and thought long and hard about whether I
should respond or not, but decided in the end that I should.  Some of
you might disagree with what I say in the following, but my intention
is not to be personal or critical.  Again I thank everyone who
responded, and I still hope to hear of any other
experiences/advice/web links which might be pertinent.

    Beth: I perhaps misspoke when I asked for something that would
'dissuade' him from continued chewing. I certainly didn't mean to
'convince' in an intellectual sense.  My father is well passed that
now.  I meant more of a physical dissuasion, as for example, a bitter
taste when chewing on something.  Since I posted, I was informed that
bitter taste might not even be a sufficient deterence, as the taste
sensation in his mouth, and his reaction to 'bitterness' might not be
functioning either.  Also, such deterence doesn't work if there is not
association or learning, and that might be the case here.  I want to
thank you as well for your support regarding the GI feeding tube and
my father's weight gain.  

    Lee: I will look into the 'chew toy' or 'teething device' or
pacifier option.  I had not thought of that, and I will relay the
information on to my mother.  Thank you for your suggestion.

    Ronnie:  I thank you for your support as well, and
particularly your input regarding the battery issue.  I will inform my
mother of this promptly.

    J:   Thank you, too.

    Dr. Harmon:  Thank you for whatever advice you gave me in all
those posted article abstracts.  But I don't believe that 'visual
facial grasp' is at issue with the behavior I described at this point.
I think it's more simply a case of chewing, and 'getting at' the
gloves / mittens which are on his hands (which he must find
distressing at some level), as well as other things...

    Evelyn:  I thank you for your reply, and no, I don't believe
what you said was callous.  I don't happen to fully agree with it, but
I appreciate your input anyway.  At that point a year ago or so, a
consensus was reached to go with the GI tube implant.  I understand
that there is no expectation of recovery, but that fact alone does not
and should not necessarily preclude any and all treatment.  He still
has some good time left in him--how much longer though, we don't know.

    Tumbleweed:  I thank you as well for your input.  However,
there was no 'plug' involved, and thus no need to pull anything... I
don't have an answer to your question, other than to say that the
decision was made to prolong his life as long as there was still some
good time left in him, and after that to not take extraordinary
measures.  Again, I appreciate your response to my query--but you
didn't answer the question I asked...

    Dennis:    I wish to thank you as well for your response.  At
the time when he was losing his ability to swallow, it was quite
evident that my father was in great distress; he obviously didn't like
the fact that he was starving...  And so, the decision was made to
have a GI tube inserted--again, a not uncommon decision at all made
for patients who have reached this point in their disease.  Since
then, he has regained his old weight, and is still engaging
life--albeit at an inexorably declining rate.
    I hope you forgive what I am going to say now, as it will be
blunt.  I don't mean to be personal, but I feel it is necessary to say
this.
    I appreciate that you have an opinion on this matter--I
imagine it is certainly better than not having one.  However, I do not
fully agree with your take on it.  Moreover, you (and a few others)
did not answer the question I asked; you answered what you wanted to
hear--in other words, the question you wanted to have been asked.
Ultimately, that is entirely self-serving and of little help to the
person asking for help.
    Obviously, this is a necessarily fatal dementia, and we are
quite well aware of that.  Every question that you posed is one that
our family has struggled with for a very long time as well.  It is
arrogant to assume that others haven't considered these issues, or to
assume that treatment such as a GI tube insertion must be tantamount
to torture.  That is an opinion and nothing more.  There are a great
many things which can cause distress to those who suffer dementia. One
example of this would be scratching at itches to the point that
lesions form.  It is reasonable to restrain a patient in such
situations (by use of mittens, etc) so as not to worsen the lesions.
That a patient suffers from an inevitably fatal disease of dementia
should not preclude reasonable efforts taken, then, to ameliorate any
other threat, even if the treatment itself (GI tube) causes distress
as well. Following the sort of logic you advocate to the extreme, one
would be fully justified in allowing a victim of, say, a terminal
cancer to die from a minor infection when you have the means to cure
it, or in shutting off the breathing apparatus for a quadriplegic
suffering progressively worsening paralysis--even while both still
have some quality time left.  After all, the patient is just going to
die in the end anyway, right?
    Not everyone necessarily agrees with you, and not everyone
defines quality of life the same way.  Suffice it to say, different
people arrive at different conclusions and make different decisions;
perhaps it is best that each decision be given the respect it
deserves.  And as well, just to reiterate, the situation is much more
complex, and I am not the decisionmaker.
    Finally, I appreciate that this is a strong moral position
that you and your family have taken regarding living wills and dying
with dignity, and I respect your courage and foresight in having done
so.  But our parents did not make the same decision, and neither have
we, their children--at least not yet.  In hijacking an honest request
for assistance and turning it into an opportunity for personal
fulmination, one defeats the whole purpose of a forum such as this,
which is to share information, experience, advice, etc, and to answer
questions in an environment free of acrimony, judgement, or
incivility.  Turning a request for assistance into a private soapbox
is pretentious and rude.

    Again, I thank all of you for the advice you have given me so
far.  I appreciate your help, and look forward to any other
information or web links anyone can give me.

Scott