JHarper33(AT)aol.com wrote:
>
> My understanding is that the differences are caused
> by where on the spine the tm occurred and how severely...
I believe there is another dimension, namely the
underlying cause of the inflammation. Last week I
asked my neuro what caused mine. He replied that
it was an infarction [blocked artery] at T9-10.
This had been the original diagnosis in the out
of state location where it had happened, but I
had not believed it. Down deep I believed I had
had a marginally tight spot caused by arthritis
with the irritation and consequent inflammation
kept under control by the oral prednisone I have
been on for decades. I had just recently started
an inhaled topical steroid for my lungs, and
three days before the incident I had reduced the
oral steroid by 25%. I might have lost my
[supposed] protection. It seemed to me that if
the [supposed] irritation had been exacerbated by
the twelve hour drive that day, then the cord
could swell, get even more squeezed, and swell
more, etc. So I challenged his diagnosis.
He replied that the description of and later
recovery from the incident was consistent with a
stroke of the spinal cord. The onset was rapid,
taking about a half hour or less to result in
paralysis. Before I lost motor control, I had
severe pain on the lower legs and then really
extreme pain in the lower back.
He said that when a viral infection is the cause,
the onset is much slower.
Still unconvinced [my wife would say “pig
headed”,] I said, “But they gave me massive doses
of steroids, and I got better.” He replied that I
would have recovered the same without the
steroids. Besides, the MRI showed there was no
constriction. He went on to explain as follows
[but in my own words/interpretation and as best
as I remember]:
Where my injury occurred, the cord has four
sections, the entirety being supplied by four
arteries with considerable, but incomplete,
overlap. If one of these arteries has a complete
and sudden blockage at the cord, then the region
without a redundant supply will start to die.
This necrosis cannot be seen in an MRI. The
necrosis can spread or be contained. [I suppose
the dead tissue puts a stress on the nearby
tissue.] “That is why no one will give a firm
prognosis in the early days.”
Motor control is vital for [animal] survival, so
there are redundant paths in the cord. Once these
other sections recover from the incident, the
redundancy yields recovery in function. Likewise
touch. Pin prick pain sensation is not vital and
is almost certainly not going to ever recover.
---------------------------
Notice when reading the TM’er stories that some
onsets were very rapid (e.g. Parker, Sandy, Cole,
Habib, Rittenhouse, Pearce, and Phil), and some
took days.
So we have at least two dimensions to TM --- the
level of the injury and the underlying cause. I
don’t know if the recovery likelihood is related
to the cause, but I’d not be surprised. He
indicated that in the case of an infarction, the
recovery will be significant or nil, depending
upon the necrosis.
Alton, who did think this made sense