Modern aspects of management of craniocerebral injury

MODERN ASPECTS OF MANAGEMENT OF CRANIOCEREBRAL INJURY ALBERT

S. CRAWFORD,

M.D.

Surgeon-in-Charge, Division of NeuroIogicaI Surgery, Henry Ford Hospital DETROIT, MICHIGAN

I

N spite of nation-wide organized efforts to prevent accidents in our country, the number of injuries and deaths by this means stiI1 remains aIarmingIy high. AIthough accurate statistics are not yet avaiIabIe for the whoIe nation, it is estimated that at Ieast IOO,OOOcases of craniocerebra1 injury are cared for each year. AIthough probabIy most of these are being cared for in the 2,030 hospitaIs which have been approved for surgery by the American CoIIege of Surgeons, undoubtedIy many are being treated in smaIIer hospitals and some at home by genera1 practitioners. Statistica studies of Iarge series of cases are of definite value and heIp in the genera1 progress being made in management. But instead of attempting to report our experiences from a study of over 1200 cases of craniocerebra1 injuries treated in this hospita1, we have pIanned to limit the scope of this paper to enumerating some practica1 points in management with special reference to some of its newer aspects. We hope that this may stimuIate those who are not speciaIists to acquire for themseIves from the Iiterature a broader working knowledge, which shouId make for more satisfaction in the care of these cases and bring about better immediate and end resuIts. As evidence of an increasing genera1 interest in this probIem, over 700 articIes were Iisted in the Cumulative Index of the American MedicaI Association for the Iast three years. An increasing number were experimenta work deaIing with the chemica1 and physioIogic aspects. We shah not concern ourseIves here with the average case, IabeIIed as concussion, in which IittIe or no serious brain damage has occurred and where usuaIIy a good organic recovery resuIts. But we are extremeIy 477

interested in the 20 per cent that have in the past been caIIed contusions, Iacerations and hemorrhage. And we wouId Iike to see a further reduction in the death rate which averages from IO to 18 per cent. There are three types in this Iatter fata group, which chaIIenges us to improved methods of care: (I) those patients who are dying from IocaIized removable cIots or encysted Auid which are not being diagnosed and operated upon earIy enough; (2) those dying from anoxia because unfavorabIe ceIIuIar changes are permitted to deveIop from a recoverabIe to a hopeIess state through misconceptions or ignorance of ceIIuIar physioIogy; and (3) those dying from the secondary effects of meduIIary and vasomotor shock which might be prevented if treated promptIy and effectively. A subject worthy of more emphasis than is possibIe here is a review of the anatomy and physiology of the brain and its circuIation. One can better anticipate probable resuIts of fractures of the skuI1 if one remembers such points as : (I) the thinner more brittIe inner tabIe of the vault; (2) the cIoseIy adherent, rigid-waIIed, easiIy tom, bIood sinuses at the base; (3) the half bony and haIf dura1 cana for the lower part of the middIe meningea1 artery just after it enters the skuI1 through the foramen spinosum, as it is here that the artery is commonIy torn across in skuI1 fractures; (4) that venous stasis is an easiIy produced compIication of brain sweIIing because of the roundabout, antigravity Aow in veins and sinuses; (5) that destruction of brain ceIIs is made easier because the arterial bIood is carried by end vesseIs with IittIe or no coIIatera1 circuIation; and (6) that the norma circuIation of the cerebrospina1 Auid is easiIy interfered with because of

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Iimited reserve space and the easiIy obstructed connecting aqueduct of SyIvius and foramina of Majendi and Luschka. Physiopathologic facts also to be borne in mind are: (I) that aside from direct damage to, or cutting off of, the vita1 centers by tissue destruction, the most important disturbance that results from cerebra1 trauma is that affecting the circmation to and from the brain cells; (2) that shock, sweIIing of tissue, anemia, hyperthermia and depression by hypnotic and sedative drugs are apt to set up vicious cycIes which may resuIt in one or more forms of anoxia of sufficient severity frequentIy to produce characteristic destruction of brain tissue; (3) that brain ceIIs are much more vuInerabIe to oxygen deprivation than other body ceIIs and are destroyed if the oxygen is compIeteIy excIuded for five to ten minutes; and (4) that apparentIy there is no regeneration of the important ceIIs thus destroyed. Fracture of the skuI1 still seems to be heId in the mind of the average layman, and particularly in a jury, as the important index of seriousness of head injuries. It has been brought out in many papers, apparentIy without enough genera1 knowledge as yet, that the skull fracture of itself is important onIy in the foIIowing: (I) as an indication that the trauma has been at least fairIy severe; (2) when the fracture is compound and thereby may have permitted foreign materia1 to penetrate to the brain; (3) when the fracture has gone more or Iess horizontaIIy across the Iower part of the tempora1 bone and severed the middIe meningeal artery as it Iies in the cana which is part bone and part dura, thus resuIting in the rapidIy forming and potentiahy fatal extradura1 cIot; (4) when the fracture has torn across a basal blood sinus, with its usua1 resuIting fata hemorrhage; (5) when the fracture extends across the petrous bone or the ethmoids, or into the fronta air ceIIs, resulting in cerebrospina rhinorrhea, with its risk of subsequent meningitis; and (6) if the fracture is depressed. Otherwise the type, location and

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resuIts of the brain damage are the important factors. In earIier years the chief emphasis in management of brain trauma was the contro1 of so caIIed “compression.” Surgica1 intervention was common. Death rates were high. During the Iast two or three decades more conservatism has been the rule and the non-surgica1 decompression of edema has been accompIished by Iumbar punctures and dehydration. The amount of operating has been reduced. The mortaIity rates have been decidedIy Iess than before. But of Iate it has become apparent to many that stiI1 further improvements in results are possibIe. As they have in the past, so they wiI1 in the future depend upon the scientific advance in physiology and chemistry. The destructive effect of cerebra1 trauma upon brain tissue and cerebra1 circuIation has Iong been known and throughout the years considerabIe vaIuabIe experimenta work has been done upon the various probIems such as edema, anemia and hemorrhage. There has been accumuIating more and more vaIuabIe information from experiments in the field of ceIIuIar physioIogy using biochemica1 and electrica methods. This is forcing a change in many of our oId conceptions and is bringing about a graduaI transition in some of the principies of management, with apparent benefit. We shaI1 not attempt to give a comprehensive List of the many contributions, but wiI1 mention a few which are pointing the way to further progress. After his exceIIent monograph with Randlm6 on cell changes from fata cerebral trauma, CourviIIe revived interest in the problem of cerebral anoxia.798 Since then much work has been done by a number of investigators on the effects upon brain ceIIs of oxygen deprivation, sedative and hypnotic drugs with resuIts which compare with his findings. Schreiber and Gates9 and Iater Schreiber’O reported studies made upon over 500 chiIdren, where apnea at the time of birth had been present in over 70 per cent of the infants. The study reIated the anaIgesics

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given to the mothers at dehvery, the apnea of the infants at birth, the Iater deveIopment of signs and symptoms of anoxia, and the subsequent objective evidences of ceIIuIar destruction. Hartmanl’ summarized the important data upon cerebra1 anoxia. The combined materia1 in this and his previous reports, aIone12 and with Majo convincingIy show that destructive ceI1 changes, conforming to the pattern characteristic of anoxia, can occur from hyperthermia, narcotics and hypnotics, acute aIcohoIism, cerebra1 injury, and acute shock. CeII deprivation of oxygen seems to be common to a11 these conditions and it is reasonabIe to conclude that it is the important factor. The effect of anemia upon brain ceIIs was restudied by GiIdea and Cobb’* on cats. They corroborated the previous findings and concIuded that ten minutes of compIete cutting off of arteria1 bIood is sufficient to produce permanent ceIIuIar destruction characteristic of anoxia. The earIier teachings had given the Iimit as five minutes. The probIem of anoxia is, of course, compIex. CeIIuIar deprivation of oxygen is intimateIy reIated to tissue and blood oxygen tension, sugar and other chemical constituents in the bIood, and is definiteIy affected by sedative and hypnotic drugs and hyperthermia. Gerard,16 in an exceIIent summary of anoxia and neura1 metaboIism, stated that the brain is thirty times as sensitive to oxygen deprivation as muscIe or nerve tissue and that oxygen tension controIs the utiIization of sugar. GeIIhorn, Ingraham, and MaIdavskylg studied the influence of hypogIycemia on the sensitivity of the central nervous system to oxygen want. They found that the oxidative processes of the ceIIs are diminished by the hypoglycemic state. Cheyne-Stokes respiration, present during experiments with low sugar content and reduced oxygen, could be aboIished by increasing the bIood sugar towards normaI. McCIure, Hartman, Schnedorf, and SchiIIing2b found cIinicaIIy and experimentaIIy that the barbiturates, morphine

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and avertin produced a sharp decrease in oxygen saturation of the bIood and oxygen utiIization by brain tissues. UnfortunateIy in trying to interpret pathoIogic findings no one can be certain which of the postmortem ceIIuIar changes were present before and were a part of the cause of death, and which changes deveIoped during the agonaI stages which just precede death. The mechanism of post-traumatic brain sweIIing and edema is a probIem about which there is stiI1 no unanimity of opinion in spite of much experimenta work. Because of the inherent difficulties, no one has yet been abIe definiteIy to prove the exact reIationships of the various factors. PiIcher,” from a study of sixty experimentaIIy traumatized dogs’ brains, was unabIe to find conclusive evidence of edema and expIained the increased pressure by disturbances of the bIood and cerebrospina1 circuIations. Shapiro and Jackson16 studied brains of fata traumatic cases and by various methods of dehydration found that the subarachnoid Auid was not increased, but decreased, the brain swoIIen but not edematous. Part of the sweIIing was thought to be by ventricuIar distention and part by scattered hemorrhages. Both of these articles17.18 contain excehent bibIiographies. As a result of the divergent views on this subject, therapy now varies between two extremes, on the one hand marked dehydration as advocated by Faylg and Iumbar punctures advised by Munro20and on the other, the extreme conservatism of Sachs21 and Dandy.22 Other factors which cause an increase in cerebrospina1 fluid pressure are bIood, as shown by BagIey23 and Parker and Lehman.z* Schnedorf,26 in experiments on dogs, found an increase in cerebrospina1 &id pressure and proteins, from simpIe cisternal withdrawa and immediate repIacement of the fluid. Oxygen given intranasaIIy Iessened these rises. The factor of hemorrhage also is not compIeteIy understood. In the severeIy injured or fata cases it is not known how

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much of the bleeding is the direct resuIt of the trauma and how much is due to disturbed physioIogic functions incidenta to

CHART

I.

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reported cases of rapid death, apparently beIonging to the concussion group, which seemed to be due to paraIysis of the

The vital signs of a rapidly fata case, in which death occurred due to a basal hemorrhage.

the treatment and termina1 states. Nor is it definiteIy known whether or not spinal drainages are entireIy benefrcia1 in the presence of subarachnoid bIeeding. A number of informative articIes on this subject have appeared during Iate years, to which the reader is referred. Hemorrhage is of course by far the most serious compIication of cerebra1 trauma and offers the greatest chaIIenge to us a11 to find ways to lessen or control in the earIy stages. PromptIy IocaIized epidura1 and subdura1 hematomata often can be successfuIIy treated surgicaIIy if there is not too much brain damage in addition. Another important probIem about which there is as yet no genera1 agreement, is the accurate definition of the diagnostic terms concussion and contusion. MiIIer,26 in an exceIIent summary of the theories of concussion, defined this as a transient state with immediate unconsciousness and with spontaneous recovery without sequeIae. He

respiratory center. Forbes and Wolff’7 concIuded from experiments on dogs that the cerebra1 circuIation is in part at least controIIed by cerebra1 vasomotor nerves. SchaIIer, Tamaki and Newman28 reported eIeven fata cases and experimental data on albino rats a11 of which had died of petechia1 hemorrhages which were judged to have been caused by refIex vasomotor phenomena, and not by the direct action of the trauma. These and other experiments on the vasomotor contro1 of circuIation may uItimateIy give us a more scientific expIanation of the cases which show post-mortem diffuse punctate hemorrhages, apparentIy out of proportion to the severity of trauma. And this may force us to add another group in our cIinica1 cIassifIcation of cases. From the above review, it is apparent that the resuIts of brain trauma stiI1 present many unsoIved probIems,2g which

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chaIIenge the best efforts of cIinicians and scientists. Regarding diagnosis, unti1 some more

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signs. Chart I iIIustrates a rapidIy fata case due to basa1 hemorrhage. Chart II is a rough diagram we use to show the average

CHART II.A diagrammatic chart of averages of many fatal cases. The vital signs are shown during the period of shock and then traced through the four stages of meduIIary compression. ChronoIogicaIly, the third and fourth stages may be much Ionger than shown here.

satisfactory cIassification is avaiIabIe, we shaI1 continue to group our cases as concussion, contusion and Iaceration. Hemorrhage may accompany any of these three. With the Iatter two the brain may become swoIIen and engorged, depending upon the many variabIe factors mentioned above. Before one can safely evaIuate a recentIy injured patient, one must insist upon obtaining fuI1 details of the mechanism and severity of trauma, the duration of primary unconsciousness. AIso it must be determined earIy if there is probabIy a rapidIy developing hemorrhage or if there is any condition requiring surgica1 interference so that effective appropriate treatment may be made avaiIable without deIay, even though this may mean a carefuI transfer by ambuIance to the nearest suitabIe hospita1. There are two sets of signs and symptoms to interpret, the meduIIary and the cerebraI. In our teaching we spend considerable time emphasizing the meduIIary

course in fata cases. It wiI1 be seen that the temperature and respirations usuaIIy change a IittIe more promptIy than the puIse and bIood pressure. As has been pointed out by Browder and Meyers,30 death occurs in some cases without showing these characteristic signs, but this represents the usua1 case. The important point to remember is, that if measures to reIieve developing meduIIary compression are to be instituted, they must be done before the third stage deveIops with its stertorous, irreguIar or Cheyne-Stokes respiration, rapid, progressiveIy weakening pulse and sharpIy rising temperature. These are evidences of beginning meduIIary failure and the resuItant cerebra1 anoxia which in a few minutes wiII bring about hopeIess or fata destruction of ceIIs. One must be on the aIert, if anticipating possible middle meningea1 bIeeding, not to be IuIled into a sense of security by the apparentIy favorabIe, fuI1, bounding, sIow puIse and the

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slowed, deeper respirations of the fateful second stage. Here usuaIIy the temperature gives a helpfu1 cIue, and one is further J.R. *213@91 MALZ$Q,

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because it thus masks importa .nt diagnostic signs. During the first few hours in a potentiaIIy ADX. 3-2 4 -35. 7: 30 EN. - in cozw;; ~nu$sion. es I 30 I

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III.An iIlustrative case of delayed death. In such cases the pathoIogic changes are mainly microscopic. Evidences of sweIIing, edema and gross hemorrhage may be absent.

CHART

informed by the cerebra1 signs of progressiveIy deepening stupor (after the Iucid interva1 of two to six hours), and the IocaIizing sign of first constricting and soon diIating pupi on the side of hemorrhage. The muscIe tone of the face and upper extremity and deep tendon reflexes on the opposite side compIete the diagnosis. It is by frequent comparison of these various findings that one can best judge the course. Chart III iIIustrates a common type of fata case. Death occurs after several days, and often the pathologic findings after death do not seem severe enough to be incompatible with Iife. It is with this group of cases that we must strive for better resuIts. Such conditions as toxic dehydration and hypogIycemia must be guarded Repeated arteria1 bIood oxygen against. determinations shouId be done. Depression by drugs must be avoided. Morphine, especiaIIy, is undesirabIe because of its depressant action on the meduIIary centers and

serious case, frequent checks of vita1 and neuroIogic signs shouId be recorded by competent observers. Nurses can be taught to render vaIuabIe data if properly trained. During the examination one must remember the possible compIicating presence of an accompanying injury to the chest or an intra-abdomina1 viscus, with its resuItant profound shock. Gentleness of handling and avoidance of unnecessary exposure of the patient’s body are important precautions. SpurIing and Bradfords’ have given an exceIIent outIine of neuroIogic diagnosis. Management of the different types of cases was outIined in our previous communications.3**33 A compIete report on over I 200 cases is pIanned in the near future. We wouId stress again the importance of adequate treatment of shock, carefu1, thorough and prompt debridement of wounds, and the taking of x-rays when and if shock is past. AI1 unconscious patients shouId be hospitaIized at Ieast one or two

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days to be assured against sIowIy deveIoping hemorrhage. We institute oxygen therapy earIy in

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point to remember if hypogIycemia exists. We combine sucrose and gIucose according to conditions, and keep carefu1 track of

w. A case of deIayed edema. Markedly reIieved by strenuous r&gime of glucose, sucrose and Iumbar punctures.

cases with persisting unconsciousness, particuIarIy if the arteria1 bIood oxygen is at a11 Iow. The norma bIood oxygen saturation is g5 per cent. With IeveIs beIow 85 per cent, the deveIopment of anoxia is speeded by such factors as hyperthermia, hypogIycemia, acute aIcohoIism, sedation by drugs and the progressive sweIIing, edema and hemorrhage of trauma. A preliminary communication regarding oxygen therapy in some of our cases has been made.34 A more compIete report awaits more experience. Measures advocated are to keep the bIood oxygen and sugar IeveIs as near to norma as possible to support the blood pressure at time of shock, and to avoid use of sedative and hypnotic drugs if at a11 possibIe. With the Hartman oxygen apparatus it is possibIe to keep the patient in as high oxygen atmosphere as desired (80 per cent to IOO per cent). It shouId be remembered that sucrose, whiIe it is an effective dehydrating agent, may be toxic to some kidneys and is not utiIized as nourishment by the tissues, an important

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bIood sugar during dehydration and of the urine when using sucrose. Lumbar punctures give vaIuabIe data regarding intraspina1 pressure and indicate the presence and amount of bIeeding. They usuaIIy are not necessary or desirabIe unti1 the stage of acute hemorrhage is past, but may then be heIpfu1 in removing bIood from the subarachnoid spaces. They shouId not be done routinely in every case, but shouId rather be Iimited to cases which present generaIIy accepted indications.20*33’3g We advocate and appIy the principIes of dehydration, in cases where edema deveIops as a compIicating factor, but in our experience these cases occur reIativeIy infrequentIy. Chart IV is of an iIIustrative case of effective resuIts of repeated periodic use of gIucose, sucrose and Iumbar punctures. We have failed to see benefit from this procedure in cases where Iacerations and hemorrhage were the main Iesions. Our experience Ieads us to agree with Browder and Meyers4’ who state that intracrania1 tension is not the basic probIem in the

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so often leads to the deveIopment of management of craniocerebra1 trauma. We psychoneuroses. wouId aIso warn against the indiscriminate use of hypertonics. SUMMARY In comatose or moribund patients, where the respirations are stertorous and puII. The management of craniocerebral monary and IaryngeaI edema are beginning, injuries in this country is becoming a pneumonia may be avoided if the foot of probIem of increasing importance. the bed is eIevated and the face turned 2. Success depends upon a thorough sideways and beIow the IeveI of the trachea working knowledge of the anatomy, physias advocated by CoIeman.35 In cases of oIogy and pathoIogy of the brain and the persistent cerebrospina1 drainage from ear ceIIuIar changes caused by trauma. or nose, in addition to operative cIosure of 3. AIthough there are stiI1 many unsolved the defect in the dura, we administer probIems, new data are accumuIating suIfaniIamide earIy as a preventative which in time should pIace management against meningitis. We have had some on a more scientific basis with better cases where this treatment apparentIy did resuIts. prevent such a compIication. For further 4. A pathoIogic process of great impordetaiIs on therapy, the reader is referred to tance is the destructive celIuIar change such articIes as those of Munro,20~36’37~38 which resuIts from such conditions as Swift,40’41 Craig,42 Ney,43 BattIe, Jackanemia, hyperthermia, hypogIycemia, tisson, Dickerson and Gunther45 and Mock.46 sue sweIIing, shock, metaboIic depression The surgica1 aspects of the problem are by hypnotic or sedative drugs and acute too extensive and speciaIized to be included aIcohoIic intoxication. here. Surgery is indicated in: (I) a11 com5. Oxygen therapy, from our experience pound fractures; (2) extradura1 hemorrhage; thus far, promptIy increases diminished (3) depressed fractures, which shouId be oxygen saturation in the bIood. If used operated on immediateIy if compound or if earIy enough and in sufficient concentrasigns of compression are present, otherwise tion, 80 to IOO per cent, it may heIp to at a Iater date; (4) fractures resuIting in prevent the deveIopment of dangerous cerebrospina1 rhinorrhea; and (5) as a anoxia, particuIarIy if the bIood pressure is decompressive measure in a few cases where supported in shock. medica means have faiIed to prevent danREFERENCES gerous compression. (6) SubduraI hemorI. RAND, C. W. Histologic studies of brain in cases of rhages and hydroma can often be diagnosed fata iniurv to head; preiiminarv report. Arch. only after exploratory trephines are Surg., 22: $38-753 (May) 1931. ” 2. RAND. C. W.. and COURVILLE. C. B. HistoIoeic made. changes in brain in cases of fata injury to heid; The end rest&s, compIications, sequelae reaction of microglia and oligodendrogha. Arch. and prognosis are probIems which wiI1 be Neurol. EdPsycbiat., 27: 605-644 (March) 1932. discussed fuIIy in a subsequent communicaa. RAND. C. W.. and COURVILLE. C. B. HistoIoeic studies of brain in cases of fata injury to he:d; tion. Sufhce it to say, that aIthough the changes in choroid plexus and ependyma. Arch. immediate and end results have seemed to .%Tg, 23: 3f7-425 (Sept.) 1931. improve sIightIy from year to year, we 4. RAND. C. W.. and COURVILLE, C. B. HistoIoaic studies of brain in cases of fata injury to he:d; shouId strive to save more patients from reIation of cIassic neurogIia. Arch. Neural. Ed preventabIe deaths, to overcome where Psycbiat., 27: 1342-1379 (June) 1932. possible, in the early stages, the unfavor5. RAND, C. W., and COURVILLE, C. B. Change in nerve fibres. Arch. Neural. @YPsycbiat., 3 I : 527abIe processes which may resuIt in sIow 555 (March) 1934. death or in persistent unfavorable sequeIae 6. RAND, C. W., and COURVILLE, C. B. Cytoarchitecor even in permanent menta1 impairment. tonic aIterations. Arch. Neural. ETPsycbiat., 36: 1277-1293 (Dec.) 1936. AIso by attention to the psychic factors, we 7. COURVILLE, C. B. Asphyxia as consequence of shouId try to avoid, where possibIe, the nitrous oxide anesthesia. Medicine, I 5 : I zg-245 train of events which, in the predisposed, (May) 1936.

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C. B. Pathogenesis of necrosis of cerebra1 gray matter following nitrous oxide anesthesia. Ann. Surg., 107: 37x-379 (March)

1938. g. SCHREIBER F., and GATES, N. Cerebra1 injury in the newborn due to anoxia at birth. J. Michigan M. Sot., 37: 145-150 (Feb.) 1938. IO. SCHREIBER. F. Apnea of the newborn and associated cerebra1 in&; cIinicaI and statistica study. J. A. M. A., I;I:-1263-1269 (Oct. I) 1938. I I. HARTMAN. F. W. Some etioIonicaI factors and Iesions in cerebral anoxia. Am.-J. Clin. Patb., 8: 629-650 (Nov.) 1938. 12. HARTMAN, F. W. Lesions of brain foIIowing fever therapy; etioIogy and pathogenesis. J. A. M. A., log: 2116-2121 (Dec.) 1937. 13. HARTMAN, F. W., and MAJOR, R. C. PathoIogicaI changes resulting from accurateIy controlled artificia1 fever. Am. J. Clin. Patb., 5: 392-410 (Sept.) 1935. 14. GILDEA, E. F., and COBB, S. Effects of anemia on cerebra1 cortex of cat. Arch. Neural. EdPsycbiat., 23: 876-903 (May) 1930. 15. GERARD, R. W. Anoxia and neural metabolism. Arch. Neural. @Y Psycbiat., 40: 985-996 (Nov.) 1938.

I 6. GELLHORN, E., INGRAHAM, R. C., and MOLDAVSKY,

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L. InfIuence of hypoglycemia on sensitivity of central nervous system to oxygen want. J. Neuropbysiol., I : 301-312 (July) 1938. PILCHER, C. Experimental cerebra1 trauma; Auid content of brains after trauma of head. Arch. Surg., 35: 512-527 (Sept.) 1937. SHAPIRO, P., and JACKSON, H. SweIIing of brain in cases of injury _ _ to head. Arch. Surg., 38: 443-456 (March) 1939. FAY., T. Treatment of acute and chronic cases of cerebraI trauma by methods of dehydration. Ann. Surg., IO!: 76-132 (Jan.) 1935. MUNRO, D. Therapeutic vaIue of Iumbar puncture in the treatment of crania1 and intracraniaI injury. Boston M. w S. J., rg3: I 187-1189 (Dec. 24) 1935. Diagnosis treatment and immediate prognosis of cerebra1 trauma: introductory study of 1494 cases. New England J. Med., 2 IO: 287-294 (Feb. 8) 1934. SACHS, ERNEST. Diagnosis and treatment of head injuries. J. A. M. A., 81: 215g-2161 (Dec. 29) 1923. Head injuries. Znternat. J. Med. +Y Surg., 46: 567 (Dec.) 1933. DANDY, W. E. Diagnosis and treatment of injuries of head. J. A. M. A., IOI: 772-775 (Sept. 2)

1933. 23. BAGLEY, C., JR. BIood in cerebrospina1 fluid; resuItant functional and organic aberations in centraI nervous system; experimental data. Arch. Surg., 17: 18-38 (July) 1928. 24. PARKER, W. H.. and LEHMAN, E. D. Studies in brain injury; increased cerebrospinal pressure from blood in the spina &id; experimental study. Ann. Surg.. 104: 1192-506 (Oct.) 1936. 25. MCCLURE, R. D., HARTMAN, F. W., !%HNEDORF, J. G., AND SCHELLING,V. “Anoxia.” Ann. Surg., Nov. rg3g. 26. MILLER, G. G. Cerebra1 concussion. Arch. Surg., 14: 891-916 (ApriI) 1927.

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