IUBio

machine brains

Lisa Gardner lgardner at mbay.net
Thu Sep 18 14:29:13 EST 1997


[Posted and emailed to ray]

ray scanlon <rscanlon at wsg.net> wrote in article
<01bcc1c6$fbc972e0$LocalHost at asdf>...
[...]
> "What is thought except a movement that is not connected to a
> motor neuron."
>                               Attributed to Walle Nauta
[...]

Hi Ray...

First of all, let me explain that I am just an interested layman
and don't have any in-depth knowledge about the things that 
are being discussed here... so all I have to offer are my speculations.
My hope is that someone reading those speculations who is more
knowledgable than am I will be able to tell me and others whether 
or not my speculations are pure bullshit.

ray, when I first read the statement above I found it *extremely*
distasteful. Then I went to your web page and read some of
your ideas... as a schizoaffective myself, I began to think about how 
schizophrenia might fit in with your theory. What I came up with was 
this: you are saying, (basically) if I read you correctly, that there is a 
portion of the brain (call it _Part A_ for now, I can't remember what the 
proper name for it is ) which inhibits neural impulses going through the 
forebrain from being passed on to the portion of the brain which will 
pass them on as "movement signals". 

Might schizophrenia be partially a disorder of Part A? This
idea seems to be supported by the fact that schizophrenics who
are on a long-term course of heavy anti-psychotic drugs often
develop tardive dyskinesia (roughly, a disorder of movement- the
schizo makes repetitive, involuntary movements). If the
anti-psychotic drugs actually work by *acting on* Part A and
fiddling with its "potential to inhibit or not inhibit" pre-motor 
signals, *it makes sense* that the result of long term use of
these drugs might result in a movement disorder... ie, that 
Part A might begin *not* inhibiting signals that are "meant"
to be inhibited... and that these drugs might actually work
by inhibiting "runaway amplification" of chains of neural impulses
in the cortex and  basal ganglia that (you state) are normally
inhibited by local neurons there...

So your theory offers some interesting takes on schizophrenia,
IMHO, and research with that disease could possibly be used 
to support it (your theory)... have you looked at data on
schizophrenia?

I'm interested to know if anyone *has* done any research along
these lines- specifically research into the relation between 
schizophrenia and movement... if ray's ideas are correct in
some sense, might it be possible to "retrain" Part A somehow
into "recognizing" which signals "should" be associated with
movement-impulses and which should not? Or am I *really* 
simplifying things *way* too much here? I haven't really sat
down and went over ray's stuff with a fine-tooth comb yet...

Is everything I've suggested here just pure BS? :) Please let me 
know. If it's possible to do so in terms a layman can understand, 
please explain the BS-ness to me, if you would.

Ray, can I post the url to your web site in alt.support.schizophrenia?
Some psychiatrists read the group and I'd like to get their 
opinions on this... Thanks.

Lisa
-- 
landscapes, seascapes of mind... sometimes it frightens me




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