'758 



IIWDHOllK lit' t'HYSIOI.IKJY 



NEUROPHYSIOLOGY III 



Thus, the increased cerebral vascular resistance 

 is not the result of permanent structural change. 

 Since ii is not released by stellate ganglion blockade 

 i j8), it is probably not sympathetic in origin. Al- 

 though some unidentified vasoconstrictor substance 

 circulating in the blood has often been postulated in 

 this disease, the sudden relaxation in response to a 

 fall in arterial pressure, however achieved, is not 

 easily explained in terms of a circulating humoral 

 agent. The observations generally give most support 

 to the hypothesis that the cerebral vasoconstriction is 

 a compensatory adjustment to the hypertension and 

 may be achieved by the homeostatic effects of the 

 local concentration of carbon dioxide on cerebral 

 vessels. 



A large number of diseases have been studied for 

 their relationship to cerebral blood flow. These in- 

 clude epilepsy (35), schizophrenia (58) and multiple 

 sclerosis (90). In none has there been a significant 

 change in cerebral blood flow from the normal or 

 expected value, so that it seems unlikely that a 

 generalized disturbance in cerebral circulation is 

 associated with any of these diseases. 



Concepts regarding the cerebral circulation have 

 thus progressed over the past century and a half from 



one which assumed this function to be fixed, to those 

 which recognized it as variable but entirely at the 

 command of the general circulation, to the most 

 recent ones which appreciate the importance of in- 

 trinsic factors in its regulation, making it more re- 

 sponsive to the local needs of the brain and in that 

 way belter serving the economy of the body. Much 

 has been learned in recent years concerning the circu- 

 lation of the brain in its highest state of development — 

 in conscious thinking man. Its fundamental impor- 

 tance to survival and to normal function has been 

 emphasized, but at the same time there has been an 

 opportunity to learn the inadequacies of certain 

 hypotheses which attributed to the cerebral circula- 

 tion an important role in the more complex and subtle 

 aspects of normal and disturbed mental function. 

 Many problems remain to be elucidated: the nature 

 and mechanism of the intrinsic control, the functions 

 of the nervous supply to cerebral vessels, the question 

 of vascular spasm in the brain, the relationship be- 

 tween regional circulation, metabolism and function 

 in the nervous system. These do not by any means 

 exhaust the list; they are merely an indication of some 

 of the questions to which more satisfactory answers 

 than are now available appear to be within reach. 



REFERENCES 



1. Alman, R. W., A. N. Bessman, G. J. Hayes and J. F. 



Fazekas. J. Lab. & Clin. Med. 39: 752, 1952. 

 _• Alman, R. VV., M. Rosenberg and J. F. Fazekas. 



.1. M. A. Arch. Xeurol. & Psychial. 67: 354, 1952. 

 i Ask-Ui-mark, E. Ada psychial. rl ncurol. Suppl. vi, 1935. 



4. Batson, O. V. Fed. Proc. 3: 139, 1944. 



5. Battey, L. L., A. Hevman and J. L. Patterson. J. A. M. 



1 '5 2 :6 > '953- 



>, I'.l KNSMEIER, A. AND K. SlEMONS. Arch. gtS. Physiol. 258: 



■49- "953 



7. Broman, T. Ada Path, el Microbiol. Scand. Suppl. 42, 1940. 



8. Campbell, A C P. .1 Res Nerv. & Mail. Dis., Proc. 18: 



69. '93 8 



9. Chute, A. L. and D. H. Smyth. Quart. J. Exper. Physiol. 



-'i 179. '939' 



10. Cobb, S. Cytology nn,l Cellular Pathology «/ thr Xervous 

 System. New York: Hoeber, 1932, p. 576. 



11. Cobb, S. and J. H. Talbott. '/; .1 Am. Physicians 42: 



, 1 1927 

 < RAion III 1 ' "'"/'. Neurol. 31: 429, 1920. 

 ij Denny-Brown, I) Vied Clin \ Imei 35: i4 r )7, 1 95 1 . 

 1 I Dumke, 1' K and C I Schmidi Am. I Physiol 138: 



I-' 1 '943- 

 15. Dunning, II S. \m> II G w J Comp. Neurol 6 



I33i "937 



I \- II II 1 . 1 . W I'n ki kinc and C. G. Rob. 



eta: 994, 1 954. 



17. Ecker, A. and P. A. Riemenschnfider. J. Xeurosurg. 8: 

 660, 1 95 1. 



18. Edwards, E. A. A.M. A. Arch. Neurol. & Psychial. 26: 801, 



'93'- 



19. Fazekas, J. F., R \\ Ai sun \mi A N. Bessman. Am. J. 

 M. Sc. 223: 245, 1952. 



20. Ferris, I. B I W .1. Arch. Neurol, & Psychial. 46: 377, 

 1941. 



21. Ferris, E. B., G. L. Encels, C. D. Stevens and M. 

 Logan. Am. J. Physiol. 147: 517, 194b. 



2a Finnertv, F A., L. Witkin and J. F. Fazekas. J. Clin. 

 Invest. 33 1227, 1954. 



23. Fisher, M. and D. G. Cameron. Neurology 3: 468, 1953. 



24. Forbes, H. S. A. Pes. Nerv. & Ment. Dis., Proc. 18: 92, 



'938. 



25. Forbes, H. S. .11/1 Arch. Neurol & Psychial. 43: 804, 



nit" 



16 Forbes, H S., K H. Finiiy and (;. I. Mason .1 1/ .1 

 Arch. Neurol. & Psychial. 30:957, 1933. 



27. Forbes, H. S. and H. G. \\ 1 11 1 1 I I/. I Arch, Neurol. & 

 Psychial. 19: 1057, 1928. 



28. Freyhan, F. A , K. I! \\ iford and S. S Ki iy. ./. 



v n Went. /'<> 1 1 ( 1 jm. 1951. 



.•11 Geiger. A \nd J Macnis Am. ./. Physiol. 149:517, 



'947 

 30. Gibbs, E. E. and F. A. Gibbs. Anal. Rec. 59: 419, 1934. 

 ji (iiiinv. I. 1.. \v (. Lennox \m> F. A Gibbs. Am. J. 



Psychial- 102 184, 1945. 



