First, although I most-often focus upon
experience, doing so because the pendulum
has swung too-far in favor of 'genetics', I
=do not= discount Genetics.
It's just that, given a 'normal' nervous sys-
tem, any of the conditions that are supposed
to 'be genetically-founded' can be reproduced
through the sole function of external experiential
I emphasize this in an effort to reach folks with
respect to that which anyone and everyone can
do. It doesn't have to be 'ceded' to Professionals.
The other thing in your post that I disagree with
is your repetitive assertion that the "same" condi-
tion can be evoked via any of multiple lesions.
This's not True.
What happens is that subtlties go unrecognized -
like back when the cerebellum and basal ganglia
were treated as 'motor' subsystems - because the
most-prominent features of cerebellar and basal
ganglia dysfunction are observable in motor dyn-
Part of the problem has been that folks've 'cleaned-
up' their data in order to be able to point to a 'con-
cise' set of things, in order to get Published. They
'discard' the subtlties - sort of in a way that has a
'band-wagon' mentality with respect to Publication.
["Say anything, as long as one knows it's what the
Reviewers already believe."]
The other, other thing in your post that I disagree
with is your assertion that it's difficult to sort-out
It's arduous, but only because there's a lot that
has to be sorted-out - not because it's inherently
hard-to-do [not because there's 'mysterious'
stuff going on within nervous systems].
All one has to do is analyze in terms of directionality
within the "special topological homeomorphism",
knowing that everything in-there 'normally' seeks
to climb the energy-gradient that is WDB2T.
Why it's of first-importance to comprehend the
primacy of experience is be-cause groupwise be-
havior literally creates the external experiential
environment, and that results in the fact that the
external experiential environment can be =any-
thing=, and, as long as it's recurring enough to
become 'familiar' [TD E/I-minimized], the nervous
systems involved will experience it as 'being normal'.
Then, individuals from such acultured external
experiential environments encounter one another,
and the one 'thinks' the other is 'abnormal'.
Which is False.
What's Sorrowfully 'hilarious' is that any society
is comprised of a hierarchy of groups, with the
group that holds 'power' seeing only that with
which =it= is 'familiar' as 'being normal'.
Which is False.
But the 'powerful' folks steam-roller anything
that's not-self, anyway.
Where it really gets 'hilarious' is when the 'power-
ful' folks are, supposedly, in the business of
seeking-Truth, but one comes to them with-Truth,
and, because it's relatively-'unfamiliar' within the
'powerful' folks' in-group-sustained external ex-
periential environments, Truth itself is treated as
'being abnormal' :-]
Anyway, I disagree with what you've discussed
for reasons stated above.
ken [k. p. collins]
"NMF" <neil.fournier at sympatico.ca> wrote in message
news:EyFSb.68029$Kg6.842363 at news20.bellglobal.com...
> Very intriguing concept, Ken. I agree with you 110% percent!!! However,
> wouldn't go as far to say that "panic disorder" can never have genetic
> factors that contribute to some aspect of the source of variance. (But I
> would rather say that it is situational specific).
>> I think one of the major problems that has emerged in the pursuit of
> brain-behavioral correlates has been through the use of traditional
> bivariate approaches to understanding brain functioning. This method has
> been traditionally employed using single-lesion methods by which a single
> structure or an aggregate of spatially adjacent structures is destroyed.
> The total elimination of a behavior or its converse (the emergence of a
> novel or unique behavior) is considered optimal. A good portion of what
> know regarding the neuronal correlates of behavior have been derived
> such approaches. (Unfortunately, many researchers do not considered the
> innate limitations regarding such approaches). This bivariate
> satisfies the beliefs: 1) of scientific parsimony, and 2) that the nominal
> presence or absence of an event is totally associated with the nominal
> presence or absence of a cause. In the real world, brain research never
> adheres to such strictly "serial approaches" in functioning. For example,
> Cohen showed that destruction of all three of the separate neuroanatomical
> pathways mediating learned cardioaccleration in pigeons was required
> conditioned response was eliminated. Single lesion studies do not
> necessarily allow one to discern the source(s) regarding the mechanism
> involved with producing a behavior. Only by considering the complex
> of neuronal interactions (or your concept of "biological mass") and their
> accompanied time-varying neurophysiological processes, can we begin to
> delineate any real understanding of brain functioning. (I admittedly
> that such multivariate approaches to brain functioning are extremely
> difficult). However, many are beginning to take the view that global
> functioning and dynamics are important for investigating the emergence of
>> Certain combinations of behaviors are placed under the umbrella of "panic
> disorder". In this case the output of the system can be produced by a
> variety of different factors. These factors will all produce the same
> output and would all be used in the diagnostic and classification schemes
> disorder. (As measured through psychological assessment,
> approaches, etc). (A classification which can be quite vague and ambiguous
> depending on the context. Hence, the ambiguity and limitation of clinical
> assessment and the labeling of behavior).
>> The same qualitative "behavior" can be generated through a variety of
> complex interactions involving many different convergent (and even
> divergent) systems. The problem is that a variety of different causes and
> changes in neuronal functioning could be responsible for producing the
> output and thence would be considered in the etiological basis of the
> disorder (in this case panic disorder). This is analogous to the saying,
> "All roads lead to Rome", where a variety of seemingly qualitatively and
> even quantitatively different routes will lead to the same goal or
> destination. From a neuronal perspective, a variety of different complex
> interactions among multifocal neuronal aggregates could be responsible for
> producing the same output or behavioral profile of the system, however,
> component would be considered qualitatively (and even quantitatively)
> different. Hence, a variety factors (including in some cases genetic)
> lead to a seemingly similar production of behavior. (This is similar to
> another disorder, schizophrenia, where there really is no such thing as
> "schizophrenia" but instead "schizophrenias").