460 GENERAL DISCUSSION 



are certain because they are in connection with the cell; of course, it is not always 

 easy to be sure it is not an accident. I would say there is no question at all that 

 there are nerve fibers and dendrites within the lesion. What are they due to? This 

 is an open question. Some people may say that these are preserved fibers. No 

 doubt, with a light lesion some fibers may be preserved, but there are many more 

 fibers which appear. So, even if you wish to assume that there are no fibers at all 

 regenerating, we still have to account for an apparent large increase of the fibers. 

 The argument does not rest on the fact that the fibers first degenerate, even though 

 there is evidence that they do. There is positive evidence of sprouting fibers, we 

 believe. Whether this is regeneration or, as we think, a perfectly normal growth 

 which only becomes apparent with light irradiation remains to be determined. 



Law^rence Kruger (University of California, Los Angeles, California): Having 

 switched teams, oceans, and cyclotrons, it is a particular pleasure for me 

 to be able to say that with lesions of the same size as we had with the Brookhaven 

 series, in another species, the rat, and in another laboratory — Dr. Tobias' laboratory 

 at Berkeley — Dr. Clemente and I have had excellent correspondence of dosage. 

 It occurred to me, however, in listening to Dr. Haymaker, that there was a slight 

 discrepance — perhaps an unimportant one. The lowest dosage in the series of Dr. 

 Haymaker and his co-workers appears lower than the first animals we irradiated 

 in Berkeley which were treated with smaller dosage. We had one animal with 

 4,000 rad at 28 days without a lesion, and yet these animals were irradiated on 

 the same run. It would seem reasonable to suggest that the size of the lesion could 

 explain the discrepancy, since this is the only likely difference in the conditions 

 of both sets of experiments. Size is probably important, because Dr. Tobias did 

 show an excellent slide of dosage times volume as being an important variable. 

 This is also important in discussing the vascular problem in relation to a neuronal 

 lesion. Dr. Sourander stated that, with a slit of 1.5 mm and 10 mm, the dosage for 

 neuron damage was still 20,000 rad although the appearance was different. I 

 wonder whether he would care to comment upon the difference in a general way 

 to explain the nature of the dosage volume relationship. Some of the discrepancies 

 that might have been apparent at first must be solved in this way. As for species 

 difference, it is remarkable that we have a good correspondence now for line 

 lesions of the same size for rat, rabbit, and cat. This is now true for independent 

 cyclotrons, too. This good agreement in different species does not appear to exist 

 for vascular damage, suggesting that neuronal and capillary damage might be 

 independent variables. How reasonable is it to assume that the destruction of 

 neurons is concerned with the destruction of capillary circulation? I should like 

 to join the Drs. Bailey in stating that it does not seem reasonable to say that all 

 neuron destruction is the result of capillary damage. To me, the most convincing 

 argument is probably the appearance of a line lesion. The sharpness of the lesion 

 would in itself discourage the interpretation that this is vascular. However, this 

 is certainly not a proof. The collateral circulation might be extensive, and here 

 is where the dose-volume problem might solve the question to some extent. A 

 recent observation that Dr. Clemente and I have made is that the gross observation 

 of capillaries would appear to indicate that the time relationship of the vascular 

 change and the neuronal changes in an India ink injected preparation are vastly 



