A study on ADHD

I am going to be doing a study on ADHD in the Spring 1997. I would like
to design it from a PCT perspective. My interest is in the use of
Neurofeedback as a nondrug treatment for ADHD. The people in the study
will be children in the age range of 8 to 12 years old who have been on
drug therapy for ADHD. I would like to know if Neurofeedback can help
these children come off the drug.

Before saying what I have in mind for the study, I would be interested
in and appreciate some brainstorming by my fellow listmates. The whole
discussion we have been having on research design in general has been
interesting. Perhaps a concrete example would take us a little further.

Rick's idea of using a tape of an interview with each child in the study
could be one idea. The child might be quite different before and after
the Neurofeedback treatment; on the drug or off the drug.

···

From: David M. Goldstein, Ph.D.
Subject: A study on ADHD
Date: 11/29/97

[From Rick Marken (971130.1000)]

David M. Goldstein (971129) --

I am going to be doing a study on ADHD in the Spring 1997.

What is ADHD, David?

Before saying what I have in mind for the study, I would be
interested in and appreciate some brainstorming by my fellow
listmates.

Great idea. I'll try to storm as soon as I know what ADHD is.
And Neurofeedback too, for that matter.

Best

Rick

···

--

Richard S. Marken Phone or Fax: 310 474-0313
Life Learning Associates e-mail: rmarken@earthlink.net
http://home.earthlink.net/~rmarken/

Hi David,
I'm delighted to hear you will be doing this study with an interest in the PCT approach. I hope your request will also be answered by those more fluent with PCT than I. What I'd like to throw in is my own view of the mislabelling aspect in ADHD. I've worked in schools a lot and did some programme evaluation work with kindergarten failures. My conclusion: anxiety is the issue. One outcome of anxiety seems to be a need to overprocess everything that is happening in one's environment ..... danger may be lurking anywhere. In PCT terms, perhaps, it represents the addition of many controlled variables once one walks into the chaos of a classroom.

Unfortunately, labelling it as anxiety just shifts one over to a different framework of explanatory dynamics. Good luck ..... the field is a mess with most concerned happy to label it all a neurological deficit for which no one is responsible. I think that explanation is patently nonsensical. With many years of neurophysiology research and reading behind me, I feel some sense of confidence in opposing the DRUG THE KIDS solution.

Could you say more about neurofeedback?

best wishes,

David Wolsk
Victoria, BC Canada

···

at 07:35 30/11/97 David Wolsk wrote:

At 09:38 29/11/97 -0500, David wrote:

I am going to be doing a study on ADHD in the Spring 1997. I would like
to design it from a PCT perspective. My interest is in the use of
Neurofeedback as a nondrug treatment for ADHD. The people in the study
will be children in the age range of 8 to 12 years old who have been on
drug therapy for ADHD. I would like to know if Neurofeedback can help
these children come off the drug.

Rick Marken asks " What is ADHD? " The letters stand for Attention
Deficit Hyperactivity Disorder. It is discussed and defined in the
DSM-IV manual on pages 78 through 85.

My way of initially selecting children for the study is that: (a) they
have been identified by their doctor, parent and teacher as displaying
the characteristics of ADHD, and (b) they have been given medication
(usually a stimulant) and have responded in a way that the doctor,
parent, and teacher consider to be a clinically significant reduction in
ADHD symptoms.

Rick Marken and David Wolsk both ask: What is Neurofeedback?
Neurofeedback is EEG biofeedback which is designed to alter a person's
brainwaves in a certain way. In the case of ADHD, the desired change
is to decrease theta and increase beta waves at frontal locations. This
has been found to be equally as effective as stimulant drugs in one
study as a means of reducing ADHD symptoms.

Thanks for the questions.

Richard Marken wrote:

···

From: David Goldstein, Ph.D.
Subject: Re: A study on ADHD
Date: 11/30/97

[From Rick Marken (971130.1000)]

David M. Goldstein (971129) --

> I am going to be doing a study on ADHD in the Spring 1997.

What is ADHD, David?

> Before saying what I have in mind for the study, I would be
> interested in and appreciate some brainstorming by my fellow
> listmates.

Great idea. I'll try to storm as soon as I know what ADHD is.
And Neurofeedback too, for that matter.

Best

Rick
--

Richard S. Marken Phone or Fax: 310 474-0313
Life Learning Associates e-mail: rmarken@earthlink.net
http://home.earthlink.net/~rmarken/

David,

As an I/O psychologist, ADHD is not an area in which I regularly read.
However, I have long thought that at least for some, ADHD provides a very
nice example of PCT and the counterintuitive intervention one might use
given the PCT understanding. My theory, and I use the term in the sense of
a guess about the nature of the particular control system(s) involved, is
that for some (an important qualifier as ADHD seems a catchall given its
focus on behaviors) ADHD is the result of a relatively low perception of
stimulation within the system. Specifically, the hypothesized central
control system in this "disorder" is an intrinsic system that is monitoring
(and has a set point for) the amount of stimulation in the system. Due to
biological differences (although the exact cause is open for debate, nor
does the initial cause preclude non-biological interventions) some
individuals tend to reduce or dampen stimuli as it moves from the receptors
to higher centers. Others augment it. These terms are relative. That is,
a given amount of stimuli is reduced or augmented relative to others. The
same stimuli results in different amounts of neural activity for different
individuals. The result is that a given environment (a classroom) will
have different phenomenological effects on the individuals in the
environment. Most who talk about it this way (at least back when I was
looking at this literature 10 years ago) seem to assume the stimulation set
point (reference signal) is the same for all individuals. Thus, individual
differences in behavior related to this system are the result of
differences in the perception and this augmenting/reducing mechanism and
not to the level of the set point. When the set point is not reached, the
output function is to increase the arousal level of the individual. If
this all is true, the reason stimulants work is that they cause the amount
of stimulation to reach the set point more readily and more like the rest
of the individuals in that environment. Thus, giving "speed" to
hyperactive kids actually decreases hyperactive because they reach their
stimulation set point more readily. Very counter-intuitive for non-PCT
thinkers.
        Much of what I describe has been talked about in the literature (mostly
stemming from Eysenck's stimulation set point work and his extroversion
concept). However, it does not (at least when I was looking at it) fully
describe the potential loop involved. If that were the case, other ideas
for treatment might surface. For instance, providing additional stimuli to
these kids that does not interfere with learning or encouraging a
reorganization of output functions that use the increased arousal in
positive (from an external point of view) ways. Indeed, the I/O
psychologist in me has wanted to look at this individual difference
variable as a predictor of performance in certain kinds of settings. That
is, the reducer might make a good air traffic controller in busy airports
but a bad one in non-busy airports.
        I am not sure what the neurofeedback training is all about, but it seems
like it would focus on the environmental variable (note that because this
is an intrinsic loop, the environment relates to the functioning with the
human system) such that the dampened stimuli is bounced around in the brain
enough to get to the desired level of stimulation. Or it is about
redirecting the error signal to more "effective" subsystems (i.e.,
reorganizing the output function)?
        Is any of this making any sense or what you are looking for?

From: David M. Goldstein, Ph.D.
Subject: A study on ADHD
Date: 11/29/97

I am going to be doing a study on ADHD in the Spring 1997. I would like
to design it from a PCT perspective. My interest is in the use of
Neurofeedback as a nondrug treatment for ADHD. The people in the study
will be children in the age range of 8 to 12 years old who have been on
drug therapy for ADHD. I would like to know if Neurofeedback can help
these children come off the drug.

Before saying what I have in mind for the study, I would be interested
in and appreciate some brainstorming by my fellow listmates. The whole
discussion we have been having on research design in general has been
interesting. Perhaps a concrete example would take us a little further.

Rick's idea of using a tape of an interview with each child in the study
could be one idea. The child might be quite different before and after
the Neurofeedback treatment; on the drug or off the drug.

Jeffrey B. Vancouver
Department of Psychology
Ohio University
Athens, OH 45701
phone: 614-593-1071
fax: 614-593-0579
vancouve@oak.cats.ohiou.edu

···

At 09:38 AM 11/29/1997 -0500, you wrote:

[From Bill Powers (971201.0914 MST)]

Jeff Vancouver (971130) --

My theory, and I use the term in the sense of
a guess about the nature of the particular control system(s) involved, is
that for some (an important qualifier as ADHD seems a catchall given its
focus on behaviors) ADHD is the result of a relatively low perception of
stimulation within the system.

...

Due to
biological differences (although the exact cause is open for debate, nor
does the initial cause preclude non-biological interventions) some
individuals tend to reduce or dampen stimuli as it moves from the receptors
to higher centers. Others augment it. These terms are relative. That is,
a given amount of stimuli is reduced or augmented relative to others. The
same stimuli results in different amounts of neural activity for different
individuals.

In general I like your approach; it does explain, for example, why
hyperactive children calm down when given substances that speed other
people up. Your picture of what is happening in the perceptual system,
however, is a little confused in my view. Why not just say that the
sensitivity of perceptual input functions varies? A "stimulus" is usually
defined as an event at the sensory interface -- stimuli do not move up
through the nervous system. Signals produced by stimuli do that. And what
happens to those signals as they pass upward depends on the forms of the
neural computations that handle them.

If
this all is true, the reason stimulants work is that they cause the amount
of stimulation to reach the set point more readily and more like the rest
of the individuals in that environment. Thus, giving "speed" to
hyperactive kids actually decreases hyperactive because they reach their
stimulation set point more readily. Very counter-intuitive for non-PCT
thinkers.

Good PCT reasoning. I would still substitute "signals" for "stimuli" to
avoid confusion. The stimulus -- the actual physical effect received by
sensory endings -- is not changed. The response of the nervous system
changes in terms of how much signal is generated for a given amount of
stimulation.

Best,

Bill P.

THAT biofeedback! My confusion came from thinking about biofeedback in a classroom situation. I've been fascinated by the biofeedback research since James G. Miller (I believe) at Yale got rats to selectively increase the blood flow to one ear or the other by "rewarding" them, I think, with electrical stimulation in the area of the brain that James Olds discovered is "rewarding." More recently, my wife Ingrid did a series of sessions at the Biofeedback Clinic in Seattle to help her with migraine pain. Her feedback signal was based on raising the surface temperature of her hands.

  It sounds to me like your EEG feedback is related to relaxation. And, I would guess that if your students learn to relax in the class, they will certainly be way way ahead. Maybe you should also try it with the teachers. Can you imagine learning to read when your attention span doesn't last the length of a sentence? Please keep us informed of your progress.
best wishes,
David Wolsk
Victoria, BC Canada

···

at 07:15 01/12/97 David Wolsk wrote

At 20:11 30/11/97 -0500, David Goldstein wrote:

Rick Marken and David Wolsk both ask: What is Neurofeedback?
Neurofeedback is EEG biofeedback which is designed to alter a person's
brainwaves in a certain way. In the case of ADHD, the desired change
is to decrease theta and increase beta waves at frontal locations. This
has been found to be equally as effective as stimulant drugs in one
study as a means of reducing ADHD symptoms.

[Jeff Vancouver 971202.0940 EST]

Some thoughts on Bill's response to my post.

[From Bill Powers (971201.0914 MST)]

Jeff Vancouver (971130) --

My theory, and I use the term in the sense of
a guess about the nature of the particular control system(s) involved, is
that for some (an important qualifier as ADHD seems a catchall given its
focus on behaviors) ADHD is the result of a relatively low perception of
stimulation within the system.

...

Due to
biological differences (although the exact cause is open for debate, nor
does the initial cause preclude non-biological interventions) some
individuals tend to reduce or dampen stimuli as it moves from the receptors
to higher centers. Others augment it. These terms are relative. That is,
a given amount of stimuli is reduced or augmented relative to others. The
same stimuli results in different amounts of neural activity for different
individuals.

In general I like your approach; it does explain, for example, why
hyperactive children calm down when given substances that speed other
people up. Your picture of what is happening in the perceptual system,
however, is a little confused in my view. Why not just say that the
sensitivity of perceptual input functions varies? A "stimulus" is usually
defined as an event at the sensory interface -- stimuli do not move up
through the nervous system. Signals produced by stimuli do that. And what
happens to those signals as they pass upward depends on the forms of the
neural computations that handle them.

I agree there is a problem with terminology here. It does seem that it
would be more accurate to substitute the word signals for the first two
instances in which I use the word stimuli in my paragraph above. However,
for the last instance, I think that stimuli is a better term. Part of the
confusion is that I am using the word stimulus to refer to both the
information impinging on the system's receptors _and_ the information
impinging on the focal control unit's input function. Stimuli is the
general term I use to refer to the information hitting the input functions
of control units at the system/environment boundary (in most models the
word feedback is used, but this implies that the only influence on the
environmental variable is via the system's output and not anything from
disturbances). Anyway, as we move our point-of-view to intrinsic units,
the system's internal environment becomes the focal unit's environment, and
thus information impinging on that unit's sensors is stimuli. In this case
that stimuli is the (amount of) signals in the perceptual hierarchy.

However, I would say that my above comments are a poor defence. The true
source of the problem is that I am borrowing Esyenck's description of the
control unit as one that is controlling stimulation on the system. This is
only indirectly true. It is (hypothetically) controlling the amount of
signaling in the brain. The amount of signaling is presumably a function
of the stimulation reaching the system's receptors. Thus, we would be
better served talking about a signal set point. Good call Bill.

Nonetheless, I did have a problem with your placement of the individual
difference in the input function of the (newly named) "signal control
unit." Interestingly, when I originally wrote the post, this is what I
said, that it was differences in the input functions. However, upon
further reflection I revised myself. I realized that the concept had a
failing. Specifically, the source of the individual difference, if my
hypothesis is correct, is that the amount of signaling going on in the
system differs for different individuals due to the dampening/augmenting
effect. That is, the actually environmental variable from the
point-of-view of the focal control unit is what is different, not the input
function designed to measure it. Perhaps this is a subtle point, but it
makes more sense. Otherwise, we have to understand how the drug changes
the input function.

If
this all is true, the reason stimulants work is that they cause the amount
of stimulation to reach the set point more readily and more like the rest
of the individuals in that environment. Thus, giving "speed" to
hyperactive kids actually decreases hyperactive because they reach their
stimulation set point more readily. Very counter-intuitive for non-PCT
thinkers.

Good PCT reasoning. I would still substitute "signals" for "stimuli" to
avoid confusion. The stimulus -- the actual physical effect received by
sensory endings -- is not changed. The response of the nervous system
changes in terms of how much signal is generated for a given amount of
stimulation.

Yes, your use of the word "stimulus" in the above paragraph makes sense and
my point more clear.

Jeffrey B. Vancouver
Department of Psychology
Ohio University
Athens, OH 45701
phone: 614-593-1071
fax: 614-593-0579
vancouve@oak.cats.ohiou.edu

···

At 09:23 AM 12/1/1997 -0700, you wrote:

Bill Powers said to Jeff Vancouver:

"Why not just say that the
sensitivity of perceptual input functions varies?"

Bill, how would you go about measuring this, say in a pursuit tracking
task?

The discussion on the proprosed ADHD study seems to have maxed out.
Perhaps this is because many of the people on the net are not familiar
enough with ADHD to feel comfortable to make suggestions.

Russell Barclay, who has a reputation as an expert on ADHD, has
published a new book in which he advances the theme that ADHD is a
problem of self control. This idea connects with the idea that ADHD is
a result of frontal lobe functioning deficits. The frontal lobes are
commonly described as playing a major role in goal directed activity.

As a PCT fan, this means to me that PCT should have something valuable
to say about ADHD. What follows is one possible experiment.

A person diagnosed with ADHD could be given one or more, say two, of
Bill Power's tracking tasks which has two model parameters, delay and
sensitivity. This could be done on and off medication. We could look
at, probably make a good guess about how the person's parameters change
on versus off the medication.

Then the person could be given Neurofeedback training. After which,
the person could be regiven the tracking tasks. The person, after
Neurofeedback, should show model parameters which resemble the on drug
pre-training performance more than the off drug performance. The child
could be posttested on and off the drugs. After Neurofeedback
training, there would be little or no difference between the on versus
off drug conditions.

I would repeat the above procedure with several children, say 10. I
would look for a consistent result in 100% of the children.

Reactions?

···

From: David M. Goldstein
Subject: [From Bill Powers (971201.0914 MST)]
Date: 12/4/97

[From Bill Powers (971204.0307 MST)]

From: David M. Goldstein
Subject: [From Bill Powers (971201.0914 MST)]
Date: 12/4/97

Bill Powers said to Jeff Vancouver:

"Why not just say that the
sensitivity of perceptual input functions varies?"

Bill, how would you go about measuring this, say in a pursuit tracking
task?

I don't know. It's not an easy problem because there are too many free
variables. From external observations, you can deduce the loop gain and
find what part of it is due to the processes between input and output of
the organism, but figuring out how much of that gain is in the input
function and how much in the output functions seems impossible to me. You'd
have to have some independent way of measuring the reference signal, to
figure out the basic scaling factors between perceptions and their external
counterparts. Now that you raise the question, I'm not so sure about my
suggestion to Jeff Vancouver. It still makes sense to me, but I don't see
how anyone could ever prove it without direct neurological investigation.

The discussion on the proprosed ADHD study seems to have maxed out.
Perhaps this is because many of the people on the net are not familiar
enough with ADHD to feel comfortable to make suggestions.

For me, the problem is that I can think of too many explanations for ADHD
that would drop the two "D's" -- it may not be either a deficit or a
disorder, at least not in the children. If I'm explaining something vitally
interesting to me to someone else, and see that his attention is wandering,
I can say either that this person has an attention deficit, or that I'm
boring the socks off him. If I coop a bunch of healthy and energetic kids
up in a stuffy classroom and subject them to hour after hour of dull
monotonous snail's-pace "teaching," I can blame their restlessness on them,
or I can ask myself what _I_ am doing that they're trying to escape from.
I'm quite sure that when I was in grade school, I would have instantly been
classed as ADHD had the diagnostic category existed 60 or so years ago. And
I shudder to think how my life would have turned out if I had been drugged
into conformity. Do you think PCT would exist? Well, maybe, but I wouldn't
have had anything to do with it.

You've convinced me in past conversations that there are cases in which
drugs can knock the edges off some really desperate situations, and give a
person some chance of reorganizing at a reasonable pace before total chaos
sets in. And of course I accept that there are physiological disorders,
defects in the machinery, that drugs can help to manage. There are hardware
problems as well as software problems.

But I just can't believe that millions upon millions of children have a
medical disorder -- "frontal lobe deficits" -- that requires drug treatment
by a doctor. The vast numbers of children diagnosed as ADHD, it seems to
me, amount to a diagnosis of the system under which we're trying to raise
them. ADHD is a consequence of something we're doing to the children;
there's nothing wrong with most of them. That's my strong suspicion.

This is why I'm less than enthusiastic about aiding and abetting any
research program that assumes from the start that there is something wrong
that needs fixing in all "ADHD children". The problem hasn' been examined
honestly, with ALL possible causes being considered. And simply by treating
a child as if he or she is defective, you help to destroy confidence and
self-respect -- a crime, if you happen to be wrong.

Best,

Bill P.

David,

Your ADHD study appears to involve two perceptions you wish to control.
One is the development of a non-drug therapy for ADHD, the other is a test
of PCT (leading to greater acceptance). These control systems might
dovetail nicely, but they might not. You need to address the following
questions. How will neurofeedback change a parameter in the control systems
that lead to ADHD? And what parameter exactly? Bill and I seem to
disagree about what might be the underlying source of ADHD (is it
differences in the environmental variable or differences in the input
function). On the other hand, in PCT the source of the variance is not
necessarily critical. Changes to the input function, reference level,
output function, or environmental variable are all possible means for
intervention. But which are you suggesting? Without that
discussion/theorizing you are simply suggesting that biofeedback can result
in a change in a distinguishing factor of ADHD (the amount of beta v. alpha
brain waves). This is hardly a compelling test of PCT if you have no PCT
explanation for the cause of the distinguishing factor much less the reason
the neurofeedback impacts that cause. Thus you will probably have no
effect on the second perception you (and I) wish to control. Further, your
use of Bill's tracking tasks do not, in my opinion, help in controlling
that second perception.

To control that second perception you a) need to theorize a PCT explanation
and b) describe why your intervention validates that explanation and
invalidates other, competing, explanations. If no other explanations exist

But I just can't believe that millions upon millions of children have a
medical disorder -- "frontal lobe deficits" -- that requires drug treatment
by a doctor. The vast numbers of children diagnosed as ADHD, it seems to
me, amount to a diagnosis of the system under which we're trying to raise
them. ADHD is a consequence of something we're doing to the children;
there's nothing wrong with most of them. That's my strong suspicion.

I am sympathetic with this argument. However, not with this argument:

And simply by treating
a child as if he or she is defective, you help to destroy confidence and
self-respect -- a crime, if you happen to be wrong.

Some subset of children diagnosed with ADHD would appreciate the means for
dealing with the "boring" situations that confront them. Such a means
would increase confidence and self-respect. It seems that the first
perception that I am suggesting that you are trying to control (a non-drug
therapy) is laudable for this reason (although I have no problem with drugs
per se). Particularly if your therapy was not designed to change the
variance in the environmental variable (amount of signalling), but in the
output function (channel the desire for stimulation in useful ways).
However, my guess is that at least for the extreme cases, short of
dampening gain, changes to the output function will not be sufficient (this
statement assumes gain is a part of the output function).

Nonetheless, Bill's argument is one reason I am interested in matching
individuals to the environments that would best suit them. We need
augmenters working on vigilance tasks and reducers working on high
stimulation tasks (or in high stimulation environments). If the variance
in stimulations in classrooms do not
match the variance in stimulations in the adult world, than part of what
ADHD is about is claiming humans should be more homogeneous than is
justified in the real world.

Food for thought,

From: David M. Goldstein
Subject: [From Bill Powers (971201.0914 MST)]
Date: 12/4/97

Bill Powers said to Jeff Vancouver:

"Why not just say that the
sensitivity of perceptual input functions varies?"

Bill, how would you go about measuring this, say in a pursuit tracking
task?

The discussion on the proprosed ADHD study seems to have maxed out.
Perhaps this is because many of the people on the net are not familiar
enough with ADHD to feel comfortable to make suggestions.

Russell Barclay, who has a reputation as an expert on ADHD, has
published a new book in which he advances the theme that ADHD is a
problem of self control. This idea connects with the idea that ADHD is
a result of frontal lobe functioning deficits. The frontal lobes are
commonly described as playing a major role in goal directed activity.

As a PCT fan, this means to me that PCT should have something valuable
to say about ADHD. What follows is one possible experiment.

A person diagnosed with ADHD could be given one or more, say two, of
Bill Power's tracking tasks which has two model parameters, delay and
sensitivity. This could be done on and off medication. We could look
at, probably make a good guess about how the person's parameters change
on versus off the medication.

Then the person could be given Neurofeedback training. After which,
the person could be regiven the tracking tasks. The person, after
Neurofeedback, should show model parameters which resemble the on drug
pre-training performance more than the off drug performance. The child
could be posttested on and off the drugs. After Neurofeedback
training, there would be little or no difference between the on versus
off drug conditions.

I would repeat the above procedure with several children, say 10. I
would look for a consistent result in 100% of the children.

Reactions?

Jeffrey B. Vancouver
Department of Psychology
Ohio University
Athens, OH 45701
phone: 614-593-1071
fax: 614-593-0579
vancouve@oak.cats.ohiou.edu

···

at the level of PCT (i.e., the functional mechanisms) you will have to settle for "a." Perhaps you have such an explanation in mind that you have not shared with us, I would love to hear it. In terms of Bill's (971204.0307 MST) post, he said:
At 02:20 AM 12/4/1997 -0500, you wrote:

[From Tim Carey (971205.0610)]

Hi Bill,

This post really struck a chord with me, particularly ...

But I just can't believe that millions upon millions of children have a
medical disorder -- "frontal lobe deficits" -- that requires drug

treatment

by a doctor. The vast numbers of children diagnosed as ADHD, it seems to
me, amount to a diagnosis of the system under which we're trying to raise
them. ADHD is a consequence of something we're doing to the children;
there's nothing wrong with most of them. That's my strong suspicion.

I've worked as a behaviour intervention specialist for a number of years
and for about four years I worked with adolescents attending state
secondary schools. Many of the students I had the opportunity to work with
were diagnosed as ADHD and were being medicated to some degree.

In a most unscientific was I like to apply the "Supernintendo test" with
ADHD kids, and guess what? These kids could easily sit for an hour or more
playing these games. They would even play it with friends and take turns
and share and do all sorts of social things. But when it was time to do
school work again, whoops, back would come the ADHD :wink: I always found it
curious that someone with a physical deficit (such as frontal lobe deficit)
was so fortunate (or unfortunate depending on your perspective) that it
never activated and caused them problems while they were doing stuff they
liked. I'm sure people with epilepsy would love to have the same measure of
control.

I actually had the opportunity to ask one student about his ADHD. Most
students weren't interested in it they just knew they had it; this
particular student, however, was very interested in it and when I told him
I didn't know anything about it (and you'll probably deduce that's true
from the above paragraph ;-)) he explained to me what was happening to his
neurotransmitters. He also explained that the disease just meant that he
couldn't listen to teachers. He'd try really hard but before too long, he'd
just find himself tuning out and thinking about other things and he
couldn't help it.

On a slightly different note, I find it curious that as professionals we
medicate children from an early age when _we_ perceive they have a problem
and then when they get to adolescence and start to self medicate (with
drugs of their own choosing) when _they_ perceive they have a problem ...
we complain!!

It seems to me that the diagnosis of ADHD is based entirely on the kid's
scribble (from the knot and dot activity) would simple research that just
tried to identify some controlled variables be out of the question?

Just some rambling,

Tim

[From Bruce Gregory (971204.1715)]

Tim Carey (971205.0610)

Just some rambling,

Very thoughtful rambling. Thanks.

Bruce