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In 1916, Guillain, Barre and Strohl 1 described a previously unrecognized type of polyneuritis characterized by definite changes in the cerebrospinal fluid. The essentials of the disease were widespread flaccid paralysis, loss of tendon reflexes, preservation of cutaneous reflexes, conservation of idiomuscular contraction on percussion, minimal changes in the electrical reactions of the muscles and nerves, occasional involvement of cranial nerves, muscle tenderness, paresthesias with little disturbance of objective sensibility and, most specifically, increase in the protein content of the cerebrospinal fluid which was not accompanied by a proportionate degree of pleocytosis. The paralysis was often of the ascending variety and of rapid onset, but recovery was also usually rapid and was complete, with no residual atrophy. The authors expressed the belief that the disease was the result of a concomitant attack on the nerve roots, peripheral nerves and muscles, probably by an infectious or toxic agent, and they termed
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Russell N. De Jong (1940) studied this question.
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