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(2)

hands in warm water, would have set up a violent convulsion with
opisthotonos, muscular twitchings etc.

During all of this time Mrs. Stanford was either standing or
sitting, not very characteristic of strychnine poisoning. And now
after this very a-typical interval for strychnine poisoning comes
the only spasm noted by witnesses and we would expect to see in a
convulsion sufficiently strong to cause death, twitchings of
individual muscles follwed by violent tetanic convulsions, with
opisthotonos (curving backward in an arch) abdominal muscles hard
as a board, chest fixed, face livid, eye balls staring, risus
sardonicus, and, when there is a slight let up, a slight stimulus
setting up a still more violent convulusive seizure. Instead of this
strinking picture we find that Mrs. Stanford continues sitting in a
chair, the body is not thrown forward, the kees remain flexed,
the neck does not become rigid as Miss Berner states who was
standing behind her at the time. But Mrs. Stanford simply grips
Miss Berner's hands more tightly, and the muscles of her calf
stiffen, and her feet turn in somewhat towards the vessel which is
between them into which Mrs. Stanford has attempted to vomit. Then
she says "Oh! Oh! Oh!" (no contraction around the mouth) and finally
Mrs. Stanford's head falls to the side just as Miss Berner
disengages one hand to hold Mrs. Stanford's head from falling.
Her muscles gradually stiffen but not with the sudden muscular
jerking of strychnine poisoning. This is the picture of many
deaths which take place in a sitting posture. The very fact that
the patient could remain sitting on an ordianry stiff-backed chair
would almost rule out a convulsion from strychnine poisoning.

The whole history of the case, so far as can be told from the
evidence, lacks entirely the exaggerated reflexes and muscular
excitability which is so striking a feature of strychnine poisoning
during and between the attacks. Of the fact that this undue
sensibility of the sensory and organs sending up a the least
stimulus and impulse to the cord and a tremendously exaggerated
impulse down to a muscle, being the most characteristic, and par
excellence the distinguishing feature of strychnine poisoning,
there is no doubt, not only from clinical experience, (the sligh-
test external stimulus setting the patient off into the most
marked muscular contractions) but it is also shown by experiments
on the lower animals. For instance, Poulsen found that a frog
dipped into cocaine solution underwent no convulsion after inject-
ing strychnine, the cocaine used being sufficient to paralize[sic] the
cord. Claud Bernard showed this, even more conclusively, by
dividing all the posterior (sensory) roots of the spinal nerves
of the frog, and then injecting strychnine, when no convulsions
occurred except when the proximal ends of the divided nerves were
stimulated. Now in Mrs. Stanford's case external stimulation
seemed to have just the opposite effect prior to the last, and
probably only true spasm, and the whole picture in this spasm
looks very much more as though it originated from something other
that an external stimulation, as is the case in strychnine poison-
ing.

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