an ALS Hypothesis - extended to all 'abnormal' neural atrophy

dag.stenberg at dag.stenberg at
Wed Feb 2 03:48:26 EST 2000

kenneth Collins <kpaulc at> wrote:
> > > >> the Hypothesis:
> > I had not earlier been able to find this among the over-long lines.
> my fault, as explained at the top of this post. i apologize for the
> unnecessary difficulty my failure imposed upon you.

No worries about the difficulty, but the fact was that I never saw that
there was a hypothesis, because the entire message consisted of three
or four superlines...

> one must put-things-together. the lesion alters cerebellar function,
> which results in abnormal motor-system dynamics, 

Please, do not even try to explain the pathology in ALS through the
cerebellum. It does not work, lower motor symptoms could NOT occur that

> because, the
> interminable TD E/I(up) condition that the lesion interjects prevents
> normal achievment of 'type II synchronization" (as evidences in ALS
> fasciculations and fibrilations.

Can't see that. The fasciculations and fibrillations are not due to
disturbed coordination, but to denervation, which dissolves the motor
units plus induces muscle membrane hypersensitivity. The spasticity is
another thing altogether.

> the late onset of respiratory functionality ...

The pathology seems to ascend in a rostral direction. Your explanation
is too complicated, and all of it, illustrated by the citation below,
seems totally hopelessly untrue.

> in other words, the demise of the motor neurons results in an =actual=
> 're-engineering of the neural topology of the brain stem, and, as a
> result, the relationship between the respiratory nucs of the brain stem
> with respect to TD E/I-minimization becomes rewired, and what remains of
> the supersystem 'blindly' 'seeks-out', and 'attacks' the 'normal'
> respiratory functionality as a TD E/I(up)-condition, which results in
> the aberrant 'shutting-down of respiratory functionality.

> > How would you diagnose the disease 35+ years before outbreak?

> =iff= there's anything to the hypothesis that i've been discussing,
> contemporary 'scanning' methods would disclose the aberrant TD
> E/I-minimization 'struggle', through which, what has been considered to
> be the disease condition, is generated (precipitated). and sensitive
> versions of those scanning methods should be able disclose the TD
> E/I(up)-generating 'lesion' location. of course, all such work can only
> occur with respect to deviations from a background database that tracks
> 'normal' (average) activation 'states'. building this
> background-comparison database would, itself, be a major undertaking,
> but would definitely, itself, become o font of useful insight.

Yeah, you earlier asked for a scanning method do discriminate excitatory
from inhibitory activity. We are not there yet. Actually imaging
techniques do not seem to be moving in that direction at all. I have
been impressed lately by proton imaging of lactic acid accumulation, but
even that does not take us anywhere in a TD I/E direction. 

> so, in it, i've kept my word about advancing the Science.

Er - I think that is still a very premature conclusion, sorry. 
As I mentioned some time last year, I had a boss who had a all-encompassing
'neurodarwinist' theory (not Edelman, who also proposed another neurodarwinist
theory). Unfortunately, all my former boss's theorizing has never advanced
science at all, whereas actual measuring has during the same decades
advanced neuroscience hugely.

Dag Stenberg

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