In 1926,1 one of us (Dr. Killian) and his associate reported that spinal fluid from cases of meningitis showed unusually high values for lactic acid and low ones for sugar. The source of the increased lactic acid appeared to lie in the metabolic activity of the leukocytes. These studies were continued, and in 1928 2 we came to the conclusion that the changes in lactic acid concentration were a better index of the progress of the infection than the changes in the sugar content. In meningitis the lactic acid of the spinal fluid was greater than that of the blood, but the sugar of the spinal fluid was less than that of the blood. Furthermore, the lactic acid of the spinal fluid may fluctuate within a wide range, although the amount of sugar remains normal. Since our first observations, similar studies have been reported by others.3 In the recent paper by Wright, Herr and Paul 4 on the spinal fluid in suppurative meningitis, an excellent review on this subject is found, and it is therefore unnecessary to repeat such a summary here.In the present report we wish to add further evidence to support the original conclusions and to enlarge on their significance. An intensive study of the sugar, lactic acid and cell count of the spinal fluid in various types of meningitis was made in order to determine whether the lactic acid varies with the cell count and whether it may be utilized as an index of the progress of the infection or of the From the
The difficulties attendant to making a diagnosis of acute infectious polyneuritis during an epidemic of poliomyelitis were emphasized in a recent minor epidemic of poliomyelitis. Acute infectious polyneuritis was first described in 1908 by Laurens.1 The original article of Guillain, Barr\l=e'\and Strohl 2 in 1916 defined the syndrome as one characterized by a slowly ascending paralysis, a normal cell count with increased protein of the cerebrospinal fluid and a favorable prognosis.The condition has most often been called Guillain\x=req-\ Barr\l=e'\'s syndrome. Casamajor 3 emphasized the nominal usage because of the inadequacy of the various descriptive names applied to the condition. Yet, because of our reluctance to use proper names, we shall continue to call it acute infectious polyneuritis.The necessity for differentiating between acute infectious polyneuritis and acute anterior poliomyelitis is more than an academic consideration. The all important question of prognosis is always uppermost in both the physician's and the parent's mind during an attack of either of these diseases. The prognosis of polio¬ myelitis in the presence of any degree of paralysis is always in doubt for a prolonged period. It is impossible for the physician to prognosticate as to the amount of residual paralysis that will be present when the final stages of the disease have been reached. On the other hand, as suggested by Guillain and Barré in 1916, a favorable prognosis can be made in infectious poly¬ neuritis, predicting the absence of any residual paralysis after a period of months to one or two years.A great deal of doubt has been cast on this license to present a favorable prognosis by Forster, Brown and Merritt.4 They present 26 cases of polyneuritis with facial diplegia and show a mortality of 42 per cent. In this group there were 3 cases that might be included in a pédiatrie series. The range in ages was from 2 to 15 years. Two of these patients died and 1 evidently recovered completely. The highest spinal fluid cell count among the 3 cases was 11 cells per cubic milli¬ meter, certainly within the normal range. The spinal fluid protein determinations are more controversial. In the 2 fatal cases the spinal fluid proteins were 68 mg.per hundred cubic centimeters and 9 mg. per hundred cubic centimeters ; the former is only a slight rise (10 to 47 is normal)5 and the latter is low, if anything. On the other hand, the 2 year old child who recovered showed a definitely increased protein to 363 mg. per hundred cubic centimeters.Forster is justified in including these 2 fatal cases in his group presenting polyneuritis with facial diplegia. Viets e and Taylor and McDonald 7 use this terminology and describe similar cases, but if we are to accept Guillain's criterion of a "noteworthy hyperalbuminosis of the cerebrospinal fluid in the absence of cytological reaction" as diagnostic of infectious polyneuritis it is difficult to classify the first 2 cases in this discussion, while the third case, in which recovery evidently occurred, ...
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