Abstract
In my series of experiments on poliomyelitis the average length of time elapsing between the intracerebral injection of the virus in the M. rhesus monkey and the onset of paralysis was from 5 to 10 days. The clinical effects of motor cell destruction were not noticed for some time, irrespective of the quantity (from 0.25 cc. to 2.0 cc.) and the concentration (from 1% to 10%) of the virus administered. When the motor areas of 2 monkeys were exposed at operation and from 0.25 cc. to 0.5 cc. of a 2% suspension of virus injected directly into their centers no paralysis developed immediately. When larger amounts (from 2.0 cc. to 2.5 cc. of a 2% suspension) were injected in 2 monkeys in the same area, some partial hemiparesis occurred following the recovery of the animals from the anesthetic. The hemiparesis that occurred was fleeting since the animals recovered within 24 hours. It was not due to the virus, but probably to local mechanical effects, since the same amount of homologous blood serum injected in the exact cortical motor area produced a similar slight immediate hemiparesis from which 2 monkeys recovered just as quickly. The quadriplegia which develops after the injection of the virus occurred only after the usual lag interval, i. e., days after the injection.
The cortical areas are very resistant or perhaps less susceptible than other areas of the central nervous system to the virus. The virus is considered to have a predilection for the motor cells of the lumbar enlargement.
What would follow the injection of the virus into the center of those very cells of the lumbar enlargement that are supposedly highly susceptible or least resistant to the virus?
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