Traumatic intracranial hemorrhage

TRAUMATIC

INTRACRANIAL

E. S. GURDJIAN,

HEMORRHAGE*

M.D. AND J. E. WEBSTER,

M.D.

Detroit, .\licbigan

I

hemorrhagic collecNTRACRANIAL tions resulting from injury have been classified upon the basis of an anatomic location within the crania1 cavity. The main groups include: (I ) Epidural hemorrhage, produced by tearing of the middle meningeal vessels or dural sinuses, (2) subdural collections resulting mainly from disruption of cortical pial vessels, (3) subarachnoid hemorrhage produced by cerebral contusion and laceration and (4) intraparenchymatous hemorrhage due to intracerebra1 bleeding. The type of hemorrhage may be correlated to some degree with the nature of the injuring force. ilrhen a direct blow or force strikes the non-moving or slower moving head, localized vascular injury is produced, the middle meningeal vessels mav b,e torn, a venous sinus disrupted or a pial Lxessel ruptured as cerebral tissue is bruised and lacerated. The forces of indirect injury, when the head is decelerated as it rapidI) moves against a slower moving or nonmoving object, produce more complex, diffuse and combinations of vascular damage. The greater the velocity of the energ) involhred, the more extensive the pattern of vascular disruption. The frequency of combinations of both vascuIar and parenchymatous damage must be emphasized since both the diagnosis and management are influenced by this circumstance. Thus, an extradural hemorrhage ma? co-exist hvith cerebral contusions, intracerebral petechial hemorrhages, subarach noid and subdural bleeding. (Fig. I.) However, one lesion is usualI!, predominant and its clinical-surgical chnracteristics are sufficiently typical to warrant separate classification and discussion.

The following classification of vascular lesions is used in this analysis with a review of the pertinent findings in surgicalI>treated and nutopsied cases. I. Epidural hemorrhage 2. Subdural hemorrhage (a) Acute type (b) Subacute chronic type (c) Acute and chronic types in infants 3. Subarachnoid hemorrhage 4. Intraparenchymntous hemorrhage (a) Petechial (b) Massive 5. Subdural accumulation of spinal fluids EPIDURAL

HEMOKHHAGE

The most common type of extrndural hemorrhage is of middle meningeal vessel Epidural hemorrhage origin. (Table I.) from the sagittsl sinus is occasionally seen. The latter may occur from depressed, comminuted fractures near the midline of the vault. In one of the cases studied an ice pick perforated the sinus, causing extensive extradural and intradural hemorrhage. A large clot collected between the two hemispheres in this instance and o\rerlay the corpus collosum. Extradural hemorrhage of occipital emissary vein origin was noted in several cases of depressed fracture posterior and superior to the mastoid region. Occasionally the lateral sinus was involved, an occurrence associated with penetrating wounds. Since extradural hemorrhage is usually of middle meningeal origin, the terms middle meningeal, epidural and extradural hemorrhage are used interchangeably. This type of collection is usually unilateral. Two cases of bilateral extradura1 clots have been

U~O’I :I concussix-e state mnl- be so r:~pid ;LS to preclude a conscious period. mortem table. A frequent clinical finding is dil:ltation Etiology. F:\lls, biq.clc wcidents 3nd of the pupil on the side of the lesion. Estradirect head blo\vs :\re frequentl~~ the cause ocul:lr pnlsies occur. The enI:Irging clot 1n;1\ c)t‘extrndur:~l hemorrhirge. I II a series of I 58 COJ~l~~~~~SS the ocul:lr nerve or nt‘r\~es ;15 the\ tr;i\.erse thr superior orbit:11 fissure or the pressure ITI:IJ occur b!. the bulging innet aspect ot the tempornl lobe medinll!, in\x)l\-ing ::nd interrupting the nerx’c (11 ner\.es in their intracrnninl course from lxxin stem to the cavernous sinus. ,4 dil:tted pupil uithout other signs of oculomotol 1x1ml ysis ina~ also be attributed .to the above described etiology or to p:lrnl\,sis ot I ;\,-gc’rOII S:lll,c SidC 25 I argtT 011I~ppoSitt?Si& I the corticnl pupilI:lry constricting mech;lL~.C(Ud. 0 nism. In f:tvor of a peripheral mech:lnisnl I-.stmwiil:ir. p:ds,! is the fact th:lt \vhen ;L clot is loc:lted ;lt thr ‘l‘l,irtl 4 l*‘l,ul-l II I bnse, pupillary manifest:ltions ;trc the rule. SiYtt1. I ( Fi(rc. 2. I LVhen the clot co\.ers the pariet:lI t.oc;~I sigm and tempor:ll :lreas, the pupils :lre likely to t’l.Ok ICI2 ‘l‘clnpci-“tur< seen onl! once in this series. Par:11 vsis of Spimil-tluitl lindings the third nc‘r\-e 1~;~s observed in four c;Lses. I’rcssurc. Incrensing nexkness :lnd Ixltxlysi~ result In I- CXSC’S In I c:lsc’ (:lc,:lIfrom compression of the clot o\‘er the motet .Aswci:ctctl msssivc Itsions centers. Th e p:lr”lysis is usu:~Il~- on the Sul,duml iI~mcIrrll:lgc. opposite side from the clot. OCC:ISIOI-sally it 7‘~n~t~~~rc~-st~l~~~l~~id;~l-l~~b~ clot -l 2 C;ulxtur:~l accumuhtion of spinal lluitt nxty be seen on the snme side :ls the clot. In 20 tz- obser\-ed. Depressed tempornl fractures rn:l>’ kle :ISSOA “ Iucij interv:\l ” may be nbsent due to ci:Lted with hemorrhnge; five C;ISC’Soccurred co-existing p:lthoIogic damage within the in this series. Recluse of this :lssoc*i;ltion, hemorrhqe crani:~l c;xvity. 0 ccasionall~ Ijatients ~1ith simp!c del>ression5, I.‘\ en it from the meninge:ll \-essels superimposed

‘wen in this series. One patient \vns operated upor~ and the other was seen :lt the post-

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minor, deserve close observation, particularly if continued unconsciousness and focal signs exist. In two cases, demonstrated I>? postmortem examination, the fractures were of such degree that roentgen studies could not have revealed them. In one case of bilateral middle meningeal hemorrhage both temporal areas were explored because of the extensive fracture from one temple to the other. The patient presented bilateral neurologic signs. In patients with a pineal calcification, the presence of a shift may be diagnostic and may Iocate the lesion accurateI>;. (Fig. 7. ) Pathologic Obserzvztions. The initial hemorrhage from the middle rneningenl lressels may be instantaneous and rapid or delayed and slowly progressi\-e. In progressi\:e lesions, various venous channels of the durn and bone contribute as the separation of the dura from the bone proceeds. Accompanying subdural bleeding was noted in eleven out of thirty cases. In tmw patients there was an associated subdural nccumulation of spinal fl uicl. In three instances, a

Hemorrhage

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massive temporosphenoidal clot was founcl to accompany the extradural collection. Treatment. In our experience the operation of choice is that of a subtemporal decompression on the side of the lesion. If the cIot is be>-ond the area of the temporal bone, a small bone fIap may be required. Bleeding points are controlled. The middle meningeal artery is ligated or occluded b\. silver cIips or cauterx. Deep hemorrhage at the base may require retraction of the temporal lobe for exposure of the foramen spinosum into which a plug of cotton or wood may be introduced. The dura is opened, if necessar?, to remove a subdural or intraparenchymatous clot. UsuaIl~. a gauze drain is used for hemostasis. Local or general anesthesia may be used. In our experience pentothal sodium has been dangerous. ACUTE

SUBDURAL

HEMORRHAGE

Acute subdural hemorrhage usuallv resuits from a tear of pial lressels associated with contusion and laceration of cerebral

tissue. (Table 11.) At times it is extensive, covering the surface of a hemisphere. Bilateral collections may be present. As a rule, the hematoma is located in the frontoparieto-temporal region of one or both sides. Occasionall\; an unusual localization .\(.I II> s, ,11,1Khl. III;\IOKI
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of the clot is seen. (Fig. 5.) In two patients there was an extensive subdural hematoma between the thvo hemispheres. The common fronto-parieto-temporal clot site can be explained on the basis of anatomic relations between brain and bone. The frontal and temporal lobes are snugly titted into a bony encasement having projecting and irreguIar surfaces. In indirect blows when the rapidly moving head strikes a non-moving or slowly moving object, the intracranial contents by a mass movement abut against the irregular surfaces with resulting vascular disruption in this region. Clinical Q6.serm~ion.s. The conscious state ma?’ manifest changes which correspond with those observed in patients with extradural hemorrhage. The “lucid interval ” is common and is seen as frequently as in middle meningeal hemorrhage. The interva1 may varb- from a few hours to several days or weeks. Since expansion of the subdural lesion occurs more SIOWIJ- than the epidural, resulting physiologic events are usually less prompt in appearance. The longer the period of lucidity and freedom from major symptoms, the better the prognosis. Patients may remain semiconscious or comatose from the time of injury. Focal neurologic signs may be meager, those present being the result of increased intracranial pressure. Frequent examinations mapre\-enl :L gradually deepening stupor

with a dulling of responses to stimuli. A sIowing of the pulse may occur. Occasionally the blood pressure rises with increasing stupor but as a rule it shows little or no change. Convulsions are common. PupilIary inequality and extraocular palsies occur. A dilated pupil, if present, is usualI?on the same side as the lesion. Unilateral extraocular muscle paralyses are also usualIy ipsilateral. There is most commonly an absence of papilledema. Increasing paresis of one-half of the body may be seen. This paresis or paralysis may be on the same side as the subdural collection, resulting in false localization. The spinal fluid pressure is usually elevated but surprisingly lo\n pressures have been noted. The cerebrospinal fluid is often bloody but may be xanthochromatic or clear. Severe bloodl? spina fIuid most frequently indicates diffuse intracerebral injur?; but exceptions to this conclusion are commonly encountered. Failure of a patient who has sustained a crania1 injury to improve normall! suggests the possibility; of an existing complication which may well be a subdural collection. By means of pneumoencephalography or multiple burr holes the diagnosis may be made. Roentgen 0bservaLon.s. A fracture of the skull may be present on the same or on the side opposite the hematoma with equal frequency. (Fig. 6.) A fracture is commonI>absent. The presence of a fracture line does not locate the collection in cases of acute subdural hemorrhage. The presence of a shifted pineal shadow may be diagnostIc. (Fig. 7.) Pathologic Observations. As a rule, the disruption of pial vessels is the source of a subdural hemorrhage. Occasionally a massive intraparenchq-matous clot may extrude through the cortex and seep into the subdural space. The latter is more common in non-traumatic cases. Contusion and Incerntion of the cerebral substance may accompany pial tears; deeper multiple small hemorrhages may be seen. These associated lesions complicate the syndrome of the subdural collection and serve as a cause for

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FIG. 7. Pineal h cmatoma.

FIG. 6. fracture patient patient

Subdural hcmorrhagr (Aj in a GLSC with :I on the s:~mr side as the hemorrhage; (n) in :I with :I fracture on the opposite sidr; ic’l in :L with no fracture.

prolonged disability or death. A subdural hemorrhage may be of non-surgical proportions producing minor or no symptoms and signs. Upon the initiaI size and source of the hemorrhage depends the expanding nature of the mass with slow or rapid progression of symptoms and signs. A disruption of a large pial vein may produce practically instantaneous signs and symp-

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toms. In the slowly expanding forms, the absorption of tissue Auids and cerebrospinal fluid by the coIIection m_ay onIy gradually add volume and only insidiously result in a dynamic intracrania1 condition. This process becomes characterized by its chronicity and is so described by the term chronic subdural hematoma. In instances in which the Iocalizing signs are on the wrong side there probabIy occurs compression of the brain stem on the opposite side from the hemorrhage against the tentorial border, compressing the pyramida tract on the opposite side. Treatment. The acute subdura1 hemorrhage presenting dynamic signs usually necessitates operative intervention. Both hemispheric surfaces should always be explored. A trephine opening at the frontoparietal junction 2 inches on either side of the midIine uncovers the greatest majority of collections. If the two initia1 openings fail to reveal a hematoma, an air study may be employed in place of further random openings. If a subdura1 hemorrhage has been Iocated, a subtempora1 decompression

i, then performed on the side of the lesion. The liquid rind,‘‘‘’ semi-solid clots are irrip;:lted from the subdural space b?, means of wlinv and a brain spatula. The subdural spat” i$ drained from twelve to eighteen hours;. SI

BACUTE

AND

CHRONIC

SUBDURAL

HEMATOMAS

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hemorrhage into the subdural small in amount or of quantit), not suflicient to jeopardize the relationships and requirements

Lvithin the cranial csvit!., symptoms maq be absent for bveelis or months. 13~ osmosis and the difFusion of cerebrospinal fluid and other tissue Huids into the collection (harythe subdural ing a higher specific gra\.it\.), hematomn g-aduall~ expands. Additional \.olume is contributed by occxsional hemorrhages into the colt from \~cssels in the granulation tissue on the proliferating dural side of the cvllection. (Fig. 8.) UltimatelF the expansion results in cerebral symptoms. The prolonged, lucid, ~!.mptom-free inter\.al can be explained upon these circumstances. (Table III. I

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Gurdjinn,

Webster---Intracranial

(~linicul Oh.ser~u/io~~s. Chronic, subdural hematoma may follow minor types of In some instances the cranial injury. trauma may be entirely forgotten by the patient and relatives. On the other hand, se\.ere cerebral damage may be accom-

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personalit) defects appear and Mit.hin ;t week the patient progresses into a stupor, and finally coma if recognition of this complication has not been made. Pupillay inequality may occur with the enlarged pupil on the ipsilateral side. The fundi may exhibit papilledema although this is the exception rather than the rule. VisuaI field studies in those patients who are cooperative have proved of little help. Headache is a constant complaint and may be localized to the side of the lesion. An overlying hyperpathic zone of the scalp Dihtctl on sitlv of Icsion may be present. In some patients increasing : 1:::: :. k: I~:C~u;lI 3 drowsiness Dilatctl ~,nsi~lt’oI)I)ositr Irsion. may be the only finding. As I-\t r:1ocul;rr p:II’~ a general rule, focal neurologic signs obtain 4 Third. in the acl\vancecl cases. Bilateral focal signs 0I None. l’r:K2urc 01’ skull and findings implicating the “wrong side” 21 Prcscnr are common. This is the result of pedunNow 11 cular compression against the tentorium Sitlc involvctl IxCt 32 on the side opposite the lesion. The cerebro2Right. spinal fluid pressure is usually ele\-ated. : I : I 6 Hilat~~r:II The fluid itself may be clear but is freSpinal fluid lintlings Pressure ;IIIOVC 3~10 I” quently xanthochromatic. The grossly clear 200 j,,t, 12 fluid may contain an ele\-nted total protein 101,-200 j with minimal pleocytosis. 13lootl or \:Intllochl-(,tn:lti~ Opcrxtion of choice.: Changes in pulse, respiration, bloocl presBil:llcr:II, c~plorator~, t rcphinc subdural k~mpord sure and temperature are of little dingnos&conq~rc.ssion on tlw side of Irsion or ostw~plnstic tic significance until advanced cerebral Ilap if clot is solid $0 licco\~crCtl, compression has occurred. At times a 0 Dirtl bradycardia may be obser\.ed usually acpanied and complicated by this condition. companied by headache. The electroenceIn such cases there may be fracture of the phalogram may be of important diagnostic skull with disabilitv from the onset of the assistance. (,Figs. 9 and I I.) injury. Roentgen Ohermtions. A fracture of the If chronic subdural hematoma compliskul1 may or may not be present and its cates a severe injury, the patient ma) represence does not indicate the side of the main unconscious or semi-conscious for hematoma. As a rule, the complication varying periods from days to weeks, profollows minor trauma to the head and thus gressing from the unconsciousness caused a majority of patients show no fracture. by- the initial severe cerebral damage into a Pneumoencephalograms are very helpful semi-consciousness caused by the cerebral and patients with subdural hematomas compression of the subdural hematoma. A tolerate this procedure surprisingly well. If number of patients in this series had assothe ventricles are visualized, there‘is a midciated se\-ere, diffuse cerebral injury. line shift and cortical air markings on the In the more typica case the patient ma) affected side are characteristically absent. be normal following a cranial injury for (Figs. 9 and IO.) A collection of air nla~’ Lrarying periods. Then in a brief period of show medial to the hematoma and this but several days headache, previousI>, of column may appear as a “pointer” bvithin mild order, becomes intense. Conduct and the cranial cavity. This finding is pathog-

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nornonic of’ ;I subdura1 hernntorna. Pineal shado\v shif’t may be diagnostic of the locat ion of the lesion. (Fig. 7. ) Electroencephnlographic studies mav be diagnostic (Fig. I 11, although in our experience correct localization of the lesion has been accomplished by this technic in about _~o per cent of the cases. I’alholo~ic Observations. In the genesis subdural hernntornn there is :\ 01’ chronic

prompt cellular reaction with connt.cti\.t tissue proliferation on the dural side of tht collection. (Fig. 8.) On the :~rachnoitl side :\ membrane forms. ‘The subdural limiting mass increases in size by the :Ibsorption of’ tissue fluids and spinal fluid through the process of osmosis and ditfusion. The innet I:1ycr- of the s:xc ser\w as :I sc,mi-l”rrl~e;‘blI /“‘ocess membrane. Thus an esp~ncling occurs (usunll~ co\.ering :I \\,itlc arc;\ of the

this tissue to retain its characteristics semi-permeabIe membrane is lost.

IN

cerebral surface, since the subdural space is not limited) rather than an absorption of the collection. Within the sac of the hematoma the blood may partialI). or completeI> hemolyze. It is not unusual, however, for the cIot to remain semi-solid. Treatment. Bilateral trepanation at the 2 inches on frontoparietal junction about either side of the midline followed by a subtemporal decompression on the side of the collection is the method of choice if the lesion is mostly Auid. A small osteoplastic flap is used if the clot is mostly solid. A single or two trephine openings may be adequate for the evacuation of unclotted hematomas when combined with irrigation. Changin g the position of the head may also be of assistance. It is no\v generall>- admitted that the membrane of the hematoma sac need not be remo\ved. After c\acuation of the sac contents the ability of

of a

INFANTS

NeLvborn infants occasionally are afflicted with subdural hemorrhage. Birth injuries, injur\; by forceps, falls and other etiologic factors may be responsible. In acute subdural hemorrhage, the infant does not react normally to its environment, presenting often a lethargy and dulled response to stimuli. A weak, inconstant cry replaces the lusty ability of the normal infant. Cyanosis appears with w:eak, irregular respirations. High concentrations of oxygen ma>- have Iittle effect. Neurologic findings ma! be of a minor order. Occasionally spasticity is present on the contralateral side. Pupillary irregularities occur. Convulsions are common, being either localized or generalized. An important finding is a tenseness, fullness or bogginess of the anterior fontanel. Lumbar puncture usunhy shows a grossly bloody fluid uncler increased pressure. The infant with a chronic type of subdural hemorrhage or hvdrorna has progressed satisfactorily in‘ its early months until a parent or pediatrician notices enlargement of the head. In other patients, a convulsion first draws attention to a n interruption of normal progress. In all other respects, the growth, sleep, feeding, Head measvision, etc., maJ- be normal. urements indicate an enlargement abo\-e normaI. A cracked pot sound may be noted on percussion of the head. The fontanel is wide and the sutures may be separated. Roentgen studies may shoiv this same suture separation. Focal neurologic signs and fundus changes are usually absent. The lesion may be accurately diagnosed 6). tap with a No. 18 gauge needle through the lateral aspect of the fontanel on both sides. When present, the cohection may be evacuated through appropriate trephine openings on the a tfected side. Occasionally. aspiration alone has been sufIicient to drain the collection.

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Gurdjian,

Webster-Intracranial

The chronic subdural collection is suitably managed 23). means of t\vo frontopartetnl openings of an exploratory type. If a clot is encountered with a thick membrane, it may be necessary by means of a small bone flap to remove this layer in order to allow expansion of the depressed hemisphere. (Fig. I 2.) Clots may be irrigated from the surface through two openings. A hydromn may be evacuatecl through :I single opening. SUBDURAL

ACCUMULATION

OF SPINAL

FLUID

Consideration must be gi\,en to the currence of a subdural accumulation

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Hemorrhage

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injur),. It is almost ne\‘er diagnosed prior to operation. That there is a cause and effect relationship between this condition and clinical findings is prox.ed by the rather remarkable results following treatment in some cases. Pathologically, the collection has been stated to be caused b,v a rent in the arachnoid kvith a resulting val\.e-like action kvhich permits cerebrospinal fluid to enter the subdural space and not return. a patient fails to iniprol,e after \I’hen may be drainage of a collection, air studies necessary to rule out :I co-existent disturbance. W’e have seen middle meningeal hemorrhage occur kvith this lesion. In some cases this abnormalitv may be seen without a history of cranial iijury. The treatment is that of simple drainage of the subdural collection through trephine openings. Not infrequently the collections are bilateral. SIASSIVE

TYPE

I~TlIAP.~I~E~C~1Y~l.~TOUS

HE&lOKKH;\GE

spinal fluid. (Table IV.) This curious condition is seen in less sex.ere grades of head

&lassi\.e intraparench~nlntous hemorrhage or intrncerebrnl hemorrhage in acute head injury is uncommon in autopsy n1:1-

var. I-XXV,N<).,

Gurdjian,

Webster---IntracraniaI

terial. The most vuInerabIe area seems to be in the region of the temporosphenoidal Iobe. CIinicaIIy the same rarity of such cases is evident. In our series of over 200 operations for head injury with massive hemorrhage, there have been live instances of massive intracerebra1 clot; three occurred in the left temporosphenoidal lobe. The clinical findings observed were similar in each instance to left temporosphenoidal cIot. A progressive faiIure characterized by a right Iower facia1 weakness, right upper limb paresis, eventual aphasia and stupor was noted. Because of the localizing signs, trephine with a left subtemporaI decompression was performed and in each instance a massive clot from the temporosphenoidal lobe with an overlying subdural hemorrhage was evacuated. Much necrotic brain tissue was encountered which was aIso removed. (Fig. 13.) In the diagnosis of such cases, Iocalizing neuroIogic signs aided by air studies shouId accurately locate the Iesion. SUBARACHNOID

HEMORRHAGE

Subarachnoid hemorrhage is the most common variety of traumatic intracrania1 hemorrhage. It may co-exist with epidura1, subdura1 and intraparenchymatous hemorrhage. The associated subarachnoid hemorrhage is usuaIIy brought about by Iaceration and contusions of brain surfaces. TABLE

v’

Diiated pupil.. II Hemiparesis or hemipIegia. 15 Lucidinterval................................. Continued unconsciousness or disorientation. z0 DiIated pupi with contraIateraI paraIysis. IO Convulsions (Jacksonian). 1 Convulsions (generaIized) 3 Total cases. Deaths........ ._.._,___._._._._. ?z * In thirty-four cases the above signs and symptoms led to exploration, but the Iatter reveaIed no massive clots. Usually edema of the brain, contusions and subarachnoid hemorrhage were seen.

At times it is extensive enough to cover ant or both hemispheres. The diagnosis is confirmed by a Iumbar puncture. The cere-

Hemorrhage

American JournaI ofSurgct,y

97

FIG. 13. Extensive contusion of brain in right parietal region. Such a lesion may eventuaIIy result in softening and hemorrhages causing an intraparenchymatous intraparenchymatous hemormass Icsion. Traumatic rhage is almost always associated with softening and necrosis of brain tissue resulting in severe cerebral deficit.

brospinal fluid obtained from the spine may contain much Iess blood than that obtained from the cisterna magna or the ventricIes. LocaIized subarachnoid hemorrhage with edema may cause focal signs of a progressive nature so as to resembIe cIoseIy the picture of subdural hematoma or massive intracrania1 hemorrhage. The presence of bIood in the spina Auid shouId not deter operative intervention, for in cases of epidural and subdural hemorrhage there is frequently associated subarachnoid hemorrhage. The patient with subarachnoid hemorrhage usuaIIy gradually improves, the conscious or semi-conscious state lightens and focai signs resolve. Conservative supportive treatment is thus wiseIy continued in the presence of gradual improvement. PETECHIAL

HEMORRHAGE

Brief mention of petechial hemorrhages is made to complete the subject. How often they occur in those with severe crania1 injury is diffrcuIt to estabhsh, but 34 per cent of cases seen at the autopsy tabIe show these small hemorrhages throughout the cerebra1 tissue. The association of petechinl hemorrhages with other forms of operative

cwnctitions makes for longercon~:~lescence and Iess complete recol’ery due to sequeIae of n permanent nature.

A similarity of sqmptonis and signs is evident III the discussion of the \rnrious types of acute traumatic intracranial hemorrhagic collections. The state of consciousness and its alterations are signif;cantlJ. important. An increasing stupor, abolition of the conscious state after a lucid inter\-al are indications for possible operative inter\.ention. The neurologic status of the patient should be studied frequently. The progress of neurologic findings ma,v be suggesti1.e of an enlarging mass lesion. On repeated esaminations, if the patient sho\\;s increasing lvealiness of one-half of the body, e\-entuating in paraI~.sis, he may be afflicted \I-ith an enlarging blood clot. On the other hand, if :I paresis or paralysis has been found to exist soon after injur!., its causation by contusions and bruises of cerebral tissue is much more likely and, therefore, operati\.e interx.ention may not be considered in such a case. The presence of inequality of pupils may be significant. The dilated pupil is usually- on the side of the lesion. Pnpilliclema mav be present although this is rare. The \yital functions IllLiJ shon alterations from normal. A slowing pulse rate and ;i loitering respira-

tor). rate may accompan~~ mass lesions. An increase in blood pressure, although rare, may signify increasing intracranial tension. In acute hemorrhagic collection the one single important symptom justifying is increasing drowsiness or exploration stupor. Pupillar?inequalities, changes in vital functions and focal neurologic signs may corroborate the presence of an enlarging clot. Ho\ve\-er, a dilated pupil, :I low pulse rate or hemiplegia in :L perfectl! conscious patient does not justif) operative intervention. In subacute and chronic subdural hematomns the presence of unilateral headache and hyperpnthia of the scalp over the pathologic lesion are important. The association of severe brain injur? M.ith subdural hemntoma produces long disabilit>and the recognition of a complicating subdural hematoma in long continued unconsciousness is important. Post-traumatic epilepsy is rare in epidural and chronic subdural hematomas. In acute subdural hematomas it is seen in almost a third of the patients. This fa\,or-s the assumption that in these patients the subdural hematoma is associated with contusions and bruises of the cerebral surface eventuating in cerebrodural cicatrization. Headaches, dizzy spells and personalit?changes are surprisingly uncommon as seyuelae in postoperative mass lesions.