ventricular changes after closed headjnnp.bmj.com/content/jnnp/6/1-2/52.full.pdfpsychoneurosis 1 8...

VENTRICULAR CHANGES AFTER CLOSED HEAD INJURY

BY

HUGH DAVIES, Major R.A.M.C., T.A. and MURRAY A. FALCONER, T/Major, R.A.M.C-

(From a Military Hospitalfor Head Injuries)

(RECEIVED 7TH MAY, 1943)

IntroductionALTHOUGH the majority of patients who sustain aclosed head injury appear to make a complete andsatisfactory recovery, some are left with residualdisabilities, which interfere with their well-beingand their adjustment to society. It is known thatin such cases permanent structural changes oftenoccur in the brain, but clinically it is difficult to ascer-tain their severity and extent. There is no singlemethod of investigation which affords this informa-tion. Such methods as neurological examination,radiological investigation of the skull, psychologicaltests, and electro-encephalography, each contributesomething to the analysis, but each has its limita-tions. The following study was undertaken in orderto evaluate air encephalography, not so much as amethod of demonstrating the presence of post-traumatic space-occupying lesions, but of assessingthe degree ofdamage which has occurred in the brain.

That changes in the outline of the ventricles oftenfollow closed head injury was clearly established inpapers from Foerster's clinic at Breslau by Schwab(1926a and b) and by Bielschowsky (1928). Bothauthors employed encephalography with air intro-duced by the lumbar route and both described threegroups of cases with abnormal encephalographicfindings, viz. (a) cases in which the ventricles didnot fill; (b) cases with enlargement and deformityof the ventricles; and (c) cases with abnormalitiesof distribution of the sub-arachnoid air over thecerebral convexities. In addition both studied thecirculation of the cerebro-spinal fluid after headinjury by injecting sodium iodide solution into theventricles or lumbar theca, and subsequently ascer-taining the time of its appearance in other parts ofthe cerebro-spinal fluid system or in the urine. Oncomparing their findings with standards obtainedfrom control cases, both of them concluded that inthe majority of cases with abnormal encephalo-grams there were disturbances of the cerebro-spinalfluid circulation, either in the form of obstructionto the cerebro-spinal fluid pathways or of delayedabsorption of the fluid into the bood stream. Biel-schowsky, whose paper was based on 106 cases ofhead injury, of both closed and open types, wentfurther than Schwab and tried to correlate theclinical features of his cases with the encephalo-graphic appearances. He showed that, while inmany cases there was an obvious relationship

between the two, in other cases this relationship wasnot apparent; and indeed the same encephalo-graphic appearances as were seen in some cases withpersistent symptoms and signs would also be seenin others without persistent symptoms or with onlya history of post-traumatic epilepsy.

Since then several other authors have confirmedthat encephalographic changes often follow headinjury, but without exception they have based theirfindings on smaller groups of cases and have notextended the scope of Bielschowsky's observations.Fischer (1927), after investigating a series of 14psychopathic patients, many of whom had sustainedhead injury several years previously, concluded thatsimilar encephalographic abnormalities could some-times be found in psychopathic patients who had nohistory of head injury, and that the correlationbetween clinical features and encephalographicfindings was not always apparent. Swift (1931),Hauptmann (1932), Friedman (1932) and othershave regarded encephalography as a means ofdifferentiating between cases with genuine dis-abilities and cases with functional disturbances,implying that those cases which have normalencephalographic appearances usually belong to thelatter group. Several others (Flugel 1932, Bennettand Hunt 1933, Lippens and Desjardin 1934,Travers 1937, Money and Susman 1932), havereported on the encephalographic changes followinghead injury without offering much comment on theirvetiological and clinical significance.

There has thus been little advance in our apprecia-tion of the encephalographic changes following headinjury since Bielschowsky's paper appeared in 1928.During the intervening years knowledge of theclinical aspects of head injury has much improved.In this paper an attempt is therefore made to re-assess, in terms of present-day clinical standards,the value of air encephalography in the investigationof cases of head injury after the acute stage.

Case MaterialOur study is based upon 100 cases of closed head

injury, which were admitted to a military hospitalfor head injuries, either as acute cases or for theinvestigation of symptoms deemed to be the resultof injury. In all of these cases it was consideredclinically that the symptoms did, in fact, result fromthe head injury. Cases with symptoms judged to be

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psychoneurotic in origin, or with symptoms con-sidered to be referable to a previous mental orphysical defect, were excluded. The series includescases with depressed fractures, but not those withpenetrating injuries. Together they form an un-selected consecutive series of cases in which the fullhospital notes and X-ray films were available and inwhich the encephalograms were satisfactory.

TechniqueThe cisternal route of injection was employed in all

except 7 cases. The cerebro-spinal fluid was replacedfractionally with air, and the technique was directed toobtaining an adequate ventricular filling, but not a com-plete dtainage of cerebro-spinal fluid, and thus a fulloutline of the sub-arachnoid spaces. The amount of airinjected was usually between 30 and 60 c.c. This methodwas generally found adequate to demonstrate the ven-tricular changes without causing much discomfort to thepatient, and without the necessity for employing a generalanesthetic. Its relative simplicity allowed of repeatedexamination in some cases.

Radiological examination with the six standardLysholm (1935) projections was carried out, producing acomposite picture of the entire ventricular system. Theanode-film distance was kept constant at 36 inches; theX-ray film was placed below the skull, and a fixed Lysholmgrid was used in order to keep the head-film distance aslow as possible and so reduce the amount of distortion,which would have resulted from the use of a Potter-Bucky diaphragm. Thus the radiological technique wasstandardized to permit of comparative measurements ofthe ventricles. It did not, however, permit of detailedstudies of the distribution of air in the cortical sub-arachnoid spaces, such as would have been possible withlumbar encephalography and full drainage.

Methods of MeasurementMethods of measuring the ventricular system after

encephalography have been described by Abramovitchand Winkler (1930), Davidoff and Dyke (1937), andEvans (1942). Abramovitch and Winkler recorded theventricular measurements with a measuring stereoscopeand related the ventricular to the cranial dimensions.Davidoff and Dyke took as their standards the maximumbreadth and the length of the ventricular system in 150cases considered to be normal. Evans compared inchildren the total breadth of the ventricular system with the

FIG. I.-Outline of the lateral ventricles as projected inthe brow-up antero-posterior view. The dotted lineindicates the measurement taken for the assessment ofventricular size.

maximum breadth of the skull. All these authors directedtheir measurements of the ventricles to the problem ofestablishing whether or not hydrocephalus was present.Our problem was to assess not only general changes in

one or both lateral ventricles but also focal changes. Thelatter occur most frequently in the frontal and temporalhorns or in the trigone. From a study of our material itbecame apparent that the diagonal width of the body ofthe lateral ventricle formed an arbitrary but reliablecriterion of the size of the lateral ventricle as a whole(Fig. 1). This measurement, which is most easily madein the standard brow-up projection, enables the size ofthe two lateral ventricles to be compared on the same film.Any variations due to inequality in filling of the twoventricles can be excluded by examination of the lateralprojection with the brow up, in which view the amountof air in each lateral ventricle can be verified. Focaldilatation can be assessed by comparing component partsof the lateral ventricles with each other. This methodof measurement was found to be reliable. In severalcases repeated examination showed no change in themeasurements obtained, thereby checking their accuracy,and also proving that repeated encephalography does notof itself lead to permanent ventricular changes.As it had been suggested that variations in intracranial

pressure, consequent upon the fractional replacement ofcerebrospinal fluid, might cause temporary ventriculardistension and so affect the measurements, some experi-ments were undertaken both on the cadaver and theliving subject.

In recently dead cadavers injection of air directly intothe ventricles under pressure was found to produce nochange in the measurements of more than I mm. Infour cases, where encephalography was well tolerated, thequantity of air injected was deliberately increased relativeto the quantity of fluid withdrawn. In a typical case filmswere obtained after the injection of 30 c.c. of air withequivalent withdrawal of fluid. A further 25 c.c. of air wasthen injected, at which point the patient complained ofincreasing severity of headache. A film was immediatelyobtained and cerebro-spinal fluid withdrawn to balancethe replacement. No increase in the ventricular measure-rrents was observed (Fig. 2), either immediately orduring the subsequent radiological procedure, extendingover a period of nearly one hour. No alteration inmeasurements was noted in the other three cases similarlyinvestigated (Table 1). It is, therefore, suggested thatthe possibility of unreliable ventricular measurements,due to pressure changes arising during the injection of air,may be ignored.

TABLE I.-VENTRICULAR MEASUREMENTS IN CON-TROL CASES AFTER INTRODUCTION OF ADDI-TIONAL AIR

Air Airinjected injectedwith without

equivalent R.L.V. L.L.V. further R.L.V. L.L.V.C.S.F. (cml.) (cn.) C.S.F. (cn;.) (cm.)with- with-drawal dr-awal(c.c.) (c.c.)

Case I 20 1-8 1 8 10 1 8 1_8Case 2 30 1 7 1 8 25 1 7 18Case 3 40 1.9 1 8 25 1 9 1.9Case 4 35 1-8 1 7 20 1-8 1-7

ControlsIn order to establish standards for the normal ven-

tricular measurements, we took a series of 50 cases(Table 11), in which encephalography was considereddesirable to exclude the presence of a space-occupyinglesion, or which were not thought clinically to be examplesof diseases usually associated with ventricular enlarge-ment. In all of them the ventricular measurements weremade tinder the same radiographic conditions as thosein the head injury series, and in all of them the outlines

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HUGH DAVIES AND MURRA Y A. FALCONER

A BFIG. 2.-Table 1. Case 3. A. Outline of ventricles after injection of 40 c.c. of air with equivalent withdrawal of c.s.f.

B. Outline after the further injection of 25 c.c. of air without any withdrawal of c.s.f.

TABLE 11.-CONTROL SERIESVentricular

measurementsR.L.V. L.L.V.

Clinical diagnosis (cm.) (cm.)Idiopathic epilepsy 1 5 1-5Idiopathic epilepsy 1 6 1 6Idiopathic epilepsy 1 6 1-6Idiopathic epilepsy 1 6 1 6

Idiopathic encephalopathy 1 6 1 6Migraine 1-6 1 6

Psychoneurosis 1-6 1-6Familial optic atrophy 1-6 1 7

Idiopathic epilepsy 1-6 1 8Idiopathic epilepsy 1-7 1-6Idiopathic epilepsy 1 7 1 7

Migraine 1 7 1 7Idiopathic epilepsy 1-7 1 8Idiopathic epilepsy 1-7 1 8

Disseminated sclerosis 1 8 1 7Migraine 1 8 1 7

Concomitant squint 1 8 1 7Idiopathic epilepsy 1 8 1 8Idiopathic epilepsy 1 8 1 8

Migraine 1 8 1l8Migraine 1 8 1 8

Psychoneurosis 1 8 1 8Psychoneurosis 1 8 1 8

Retrobulbar neuritis 1 8 1 8Idiopathic epilepsy 1 8 1.9Idiopathic epilepsy 1 8 1.9Idiopathic epilepsy 1 8 1.9Psychoneurosis 1 8 1.9

Psychopathic personality 1 8 1.9Disseminated sclerosis 1 8 1.9Idiopathic epilepsy 1 9 1 8Psychoneurosis 1.9 1-9Psychoneurosis 1 9 1.9

Vaso-vagal attacks 1.9 1 9Idiopathic epilepsy 1 9 1 9Idiopathic epilepsy 1.9 2 0Idiopathic epilepsy 1-8 2 0Psychoneurosis 1 8 20Psychoneurosis 1 8 20

Idiopathic epilepsy 20 1 8Idiopathic epilepsy 2-0 1 9Psychoneurosis 2 0 1.9

Hospitalcase no.1506940

2612*9082994314420282885

Clinical diagnosisIdiopathic epilepsyIdiopathic epilepsyIdiopathic epilepsyPsychoneurosisPsychoneurosisPsychoneurosis

Idiopathic epilepsyIdiopathic epilepsy

VentricularmeasurementsR.L.V. L.L.V.(cm.) (cm.)20 202-0 2-02-0 2-02-0 2-02-0 2-02-0 202-1 2-12-2 2-2

* Denotes the incidence of a trivial head injury.

of the two lateral ventricles were similar, except for thenormal anatomical variations in the development of theoccipital horns.

It will be observed that in no case was there a differenceof more than 2 mm. between the measurements of the twoventricular bodies and that in as many as 28 cases theventricular measurements were equal on the two sides.It was therefore considered justifiable to assume that,in the absence of gross cranial asymmetry, a variation inmeasurement between the two ventricular bodies of morethan 2 mm. was significant. The upper limit of normalitycan only be fixed arbitrarily, but, as in only 2 out of the50 cases was the oblique diameter of the body of theventricle greater than 2 cm., figures greater than this weretaken to indicate dilatation.

Measurement of the Third VentricleThe maximum breadth of the third ventricle, as seen

in the antero-posterior brow-up projection, was measuredin every case. Considerable variation was found to occurin both the head injury and in the control series. Theredid not appear to us to be any trend towards increasedmeasurement in cases with ventricular dilation. It wastherefore decided to regard the breadth of the thirdventricle as having too wide a normal range of variationto afford any significant information. This accords witha similar conclusion reached by Fischer (1927).

Analysis of Case MaterialGeneralOn the basis of the above standards of normality

we found evidence of enlargement of the lateral

Hospitalcase no.

72288114981775

*420913324019381396531

330512519053459116748531086146130892851280214062362979

* 19462365269697333842717

*1950*1176*2731

7063615H 782431t1288'291627192287

*1501

54


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VENTRICULAR CHANGES AFTER CLOSED HEAD INJURY 55ventricles in 69 out of the 100 cases, as opposed to 2 (2) Those with focal dilatation of part of theout of 50 cases in the control series. In some cases ventricular system. Table IV. (Focalthe enlargement involved only a part of the lateral dilatatio,i) 15 casesventricle (Jocal lilatadtions), whereas in others the (3) Those with generalized dilatations of thewhole of the lateral ventricle was affected (generaliZed lateral ventricles o(lilaitatiolis).AstisugseththevnrCIa (a) Of one ventricle only. Table V.blilatatiosls).As this suggested that the ventricular (ULiilatelal generalized dila-dilatations might have been produced by more than tatioln). 21one mechanism, we arranged our 100 cases into the (b) Of both ventricles. Table VI.following four radiological groups according to the (Bilatelal genieralized dila-type and extent of the ventricular changes: tatioli).. .. .. .. 26

(4) Those with focal dilatations superimposed(I) Those without dilatation of the ventricles. ongeneralizeddilatations. TableVII.

Table Ill. (Nol-Irmal eliceph/aloglranits) 3 1 cases (Focal with genieralizedl lilatationi) 7

TABLE 111.-NORMAL ENCEPHALOGRAMS

No. Diagnosis

I Head injury. Not unconscious. Post-traumatic syndrome.

2 Head injury. Not unconscious. Post-traumatic epilepsy.

3 Head injury. Not unconscious. Post-traumatic syndrome.

4 Head injury. Not unconscious. Post-traumatic syndrome.

5 Post-traumatic epilepsy6 Head injury with residual pyramidal

signs.7 Post-traumatic epilepsy8 Head injury without residual se-

quelx.9 Head injury with residual pyramidal

signs.10 Post-traumatic syndrome11 Post-traumatic syndrome

12 Post-traumatic syndrome13 Head injury with cranial nerve palsy

14 Post-traumatic epilepsy15 Post-traumatic syndrome

16 Post-traumatic syndrome17 Post-traumatic syndrome18 Head injury with cranial nerve palsy.

Post-traumatic syndrome.19 Head injury with cranial nerve palsy20 Head injury with cranial nerve palsy

21 Post-traumatic epilepsy

22 Head injiury with hypothalamic and

2324

25

2627

2829

30

31

brain stem signs. Post-traumaticintellectual deterioration.

Post-traumatic syndrome .. ..Head injury with cranial nerve palsy

Post - traumatic syndrome. Opticradiation distrubance.

Post-traumatic syndromePost-traumatic intellectual deteriora-

tion.Head injury with brain stem signsPost-traumatic intellectual deteriora-

tion.Head injury with brain stem signs . .

IHead injury with cranial nerve palsy.Post-traumatic syndrome.

P.T.A. (cR.L.V. L.L.V.P... (cm.) (cm.)

Nil

Nil

Nil

Nil

MinutesMinutes

Minutes2 hours

2! hours

3 hours12 hours

12 hours18 hours

I day2,- days

2 days2 days2 days

3 days3 days

4 days

5 days

5 days5 days

2IIweeks

l2- weeks2-- weeks

3 weeks3 weeks

4 weeks3 weeks

I2 months

1-8

1-9

1-6

1-7

1-81-8

1-91 7

1-7

*

1l8

1-9.1-9

1-71.9

1-61-61-9

1-71-6

1-7

1-61-71-61-61-6

2-0

1l81-6

191-8

1-8

1-6

1-7

1-9

1-7

1-8

1.91-92-01-91-7

*

1-8

1-81-9

1-91-9

1-71-61-9

1-71-6

1-6

1-61-71-61-61-6

2-0

1.91-6

1-91-8

1-8

1-7

Site

Frontal

Left temporal

Frontal

OccipitalLeft side

Right parietalNot knownRight frontal

Vertex

Right frontalRight frontal

Not knownFrontal

Not knownRight parietal

Right frontalOccipital

Left frontal andRight occipitalRight temporalMid-frontal

Left occipital

Not known

Left frontalRight frontal

Left occipital

Not knownLeft temporal

Not known? Occipital

? Occipital

Left side

Fractures

Nil

Nil

Compound frontal

Nil

NilNil

NilNil

Slightly depressedvertexNil

Compounddepressed

NilSlightly depressed

frontalNil

Depressed rightparietal

NilNilNilNil

Comminutedfrontal

Left posteriorparietal

Nil

Left frontalComminuted

frontalDepressed left

occipitalNil

Left temporal

NilNil

Nil

Multiple leftparietal

* Air was present in the cavum septi pellucidi, separating and angulating the ventricular bodies, which were, however, of normal sizeand outline. It was felt that the standard measurements were not applicable in such a case.


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HUGH DA VIES AND MURRA Y A. FALCONER

FIG. 3.-Focal dilatation. Case No. 35. Focal dilatation of the anterior horn of the right lateral ventricle.

FIG. 4.-Focal dilatation. Case No. 43. Focal dilatation of the trigone of the left lateral ventricle.

These figures establish that ventricular dilatationsupervenes in a high proportion of cases after headinjury. Our series, however, constitutes a highlyselected group of cases in that, with one exception,they all showed either some residual complicationdue to the head injury or else some unusual featureduring the acute stage, such as prolonged post-traumatic confusion or epileptic attacks, whichnecessitated detailed investigation (see later). Thisexception, Case 8, was our only example of thecommon straightforward type of head injury withshort duration of unconsciousness and subsequent

rapid and complete recovery, and had a normalencephalogram. Consequently our observationsare based almost entirely on the more complicatedcases which are more likely to show abnormalities.We have evidence, however, to suggest that ven-tricular dilatation seldom supervenes after trivialinjuries, whereas it occurs much more frequentlyafter severe head injuries.

In order to elucidate the factors responsible forthe enlargement of the ventricles, we attempted tocorrelate the type and extent of the ventriculardilatation with the severity of the head injury as

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VENTRICULAR CHANGES AFTER CLOSED HEAD INJURYjudged by clinical standards, with the site of injury,and with the time after injury when the dilatationbecame apparent.

It is often difficult to measure clinically theseverity of brain damage resulting from injury, assometimes even severe destruction of brain tissuemay OCCUr without much upset to the patient.Two criteria, which are often used clinically forassessing the severity of head injuries, are the dura-tion of the post-traumatic amnesia and the amountof blood in the cerebro-spinal fluid in the acute phaseof the injury. Neither of these criteria is entirelyreliable, because sometimes the brain may beseriously damaged without loss of consciousnessresulting, or without the appearance of blood in thecerebro-spinal fluid. Of these two criteria theduration of the post-traumatic amnesia is the more

easily obtained and was estimated in each of ourcases. In Table VIII the frequency and the degreeof the ventricular dilatation in our cases is analysedwith regard to the length of the post-traumaticamnesia. The table shows that the frequency ofventricLilar dilatation rises steadily with increasingduration of the post-traumatic amnesia, from 33 percent. in cases where there was no post-traumaticamnesia to 92 per cent. in cases where the post-traumatic amnesia extended longer than a month.Moreover the extent to which the ventricles dilatedalso seemed to increase with the duration of the post-traumatic amnesia. Thus out of 18 cases in whichthe post-traumatic amnesia was under I day, 2 (11per cent.) had focal dilatation and 3 cases (17 percent.) had generalized bilateral dilatation: out of13 cases in which the post-traumatic amnesia ex-

TABLE IV. FOCAL DILATATIONS

No. Diagnosis P.T.A. (cm.L) (cLm.) Local changes Site Fractures_- --I(m.(cm.Head injury with cranial nervepalsies.

Head injury without residualsequeke.

Head injury with residualpyramidal signs. Post-trau-matic intellectual deteriora-tion.

Post-traLumatic epilepsy

Post - traumatic syndrome.Post-traumatic epilepsy.

Post-traumatic syndrome

Post - traumatic syndrome.Head injury with cranialnerve palsies

Post-traumatic intellectual de-terioration.

Head injury with residualpyramidal signs. Post-traLl-matic epilepsy.

Head injury withbrain stem signs.

Head injury withpyramidal signs.

residual 2-3 weeks

residual 13-4 weeks

Head injury with residualpyramidal signs. Post-trau-matic intellectual deteriora-tion.

Head injury with residualpyramidal signs.

Head injury with residualpyramidal signs. Dysphasia.Post - traumatic intellectualdleterioration.

r'ost-traumatic intellectual de-terioration.

1.9

16

1 8

2.4*

1-8

18

17

1 8

2020

2424

1 8

1 8

2-0

2 1

1 7

Dilatation leftanterior horn

Dilatation leftanterior horn

Dilatation righttemporal hornand vestibule

Gross dilatationright anteriorhorn and bothanterior bodies

Both anteriorhorns dilated;right morethan left

Dilated rightvestibule

Dilated rightanterior horn

Dilated rightanterior horn

Dilated left an-terior hornand rightvestibule

Dilatation leftanterior bodyand anteriorhorn

Slight dilata-tion left vesti-bule

Slight dilata-tion left vesti-bule and tem-poral horn



Dilatation bothanterior horns

Frontal

Left frontal

Right side

Right frontal

Frontal

Not known

Right frontal

Right frontal

Multiple

Left vertex

Right temporal

Right parietal

Left frontal

Left side

Left parietal

* The dilatation in this case was essentially focal despite the bilateral enlargemenit.

Left frontal

Left frontal

Depressed righttemporal

Right frontalcompoundcomminuted

Depressedfrontal

Diastasis rightlambdoid

Right frontal

Right frontal

Right occipital

Nil

Nil

Right sided

Nil

Left parietal

Nil

12 hours

I day

4 days

4 days

I week

I week

1!2 weeks

weeks

2 weeks

32

33

34

35

36

37

38

39

40

41

42

43

44

45

46

18

16

18

24

18

18

20

18

1I818

192 0

1.9

18

1 6

18

17

I month

I month

2-1- months

2 months

-1- -I

-

I

T

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HUGH DA VIES AND MURRA Y A. FALCONERTABLE V.-GENERALIZED DILATATIONS-UNILATERAL

Diagnosis

Post-traumatic epilepsyPost-traumatic syndromeHead injury with optic-radiation dis-

turbances.Post-traumatic intellectual deteriora-

tion.Head injury with residual pyramidal

signs. Post-traumatic syndrome.Head injury with cranial nerve palsyPost-traumatic intellectual deteriora-

tion.Post-traumatic syndromeHead injury with residual pyramidal

signs.Head injury with residual pyramidal

signs and cranial nerve palsies.Head injury with residual pyramidal

signs. Post-traumatic epilepsy.Post-traumatic intellectual deteriora-


signs.Head injury with residual pyramidal

signs. Post-traumatic epilepsy.Head injury without residual sequelhHead injury with residual pyramidal

signs.Post-traumatic intellectual deteriora-

tion.Post-traumatic syndrome. Post-

traumatic epilepsy.Head injury without residual sequelkHead injury without residual sequelsPost-traumatic syndrome .. ..

P.T.A.

NilMinutesMinutes

4 days24 days3 days

3 days1 week

1 week1 weeks

2 weeks

2 weeks

2 weeks

2 weeks

2 weeks

3 weeks3 weeks

3 weeks

3 weeks

3-4 weeksmonths

3 weeks

R.L.V.(cm.)1-91-91-9

1-6

2-32-31 82-1

1-822

20

2-0

2-0

2-0

2-02-01.91-7

1-5

1-7

2-01-61-9

L.L.V.(cm.)252-32-2

23

1-82-0241-7

2-51 8

18

30

23

2-3

1-71-72-52-1

2-0

20

232-02-1

Site

OccipitalRight parietalRight occipital

Left parietal

Not known

OccipitalRight frontal

Left frontalRight parietal

Right parietal

? Left side

Not known

Frontal

Right side

Right temporalLeft temporal

Left parietal

Right parietal

FrontalNot knownNot known

Fractures

NilNil

Compound rightoccipital

Nil

Nil

NilNil

NilRight parietal

Right parietal

? Left parietal

Nil

Basal

Right temporal

Right frontalNil

Left parietal

Nil

NilNilNil

FIG. 5.-Unilateral general dilatation. Case No. 57. General dilatation of the left lateral ventricle without focalchanges or enlargement of the right lateral ventricle.

58

No.

474849

50

51

5253

5455

56

57

58

59

60

6162

63

64

656667


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I,

FIG. 6.-Bilateral general dilatation. Case No. 81. Dilatation of both lateral ventricles, the left being somewhatmore affected.

TABLE VI .-GENERALIZED DILATATIONS-BI LATERAL

Diagnosis

Head injury without unconsciousness.Head injury with pyramidal resi-dual signs.

Head injury with residual pyramidalsigns.

Post-traumatic syndromePost-traumatic intellectual deteriora-

tion.Post-traumatic intellectual deteriora-

tion.Head injury with cranial nerve palsy.

Post-traumatic epilepsy.Post-traumatic epilepsyHead injury with optic radiation dis-

turbance. Post-traumatic epilepsy.Head injury without residual sequels

Post-traumatic intellectual deteriora-tion. Post-traumatic epilepsy.

Head injury with cranial nerve pal-sies. Post-traumatic syndrome.

Head injury with residual pyramidalsigns. Post-traumatic intellectualdeterioration.

Post-traumatic intellectual deteriora-tion.

Post-traumatic syndromeHead injury with residual pyramidal

signs. Dysphasia and cranial nervepalsies. Post-traumatic epilepsy.

Head injury with cranial nerve pal-sies. Post-traumatic syndrome.

Head injury with residual pyramidalsigns.



Head injury without residual sequekeHead injury without residual sequekeHead injury without residual sequelxPost-traumatic intellectual deteriora-




signs. Post-traumatic intellectualdeterioration.

P.T.A.

Nil

3 minutes

1 day1 day4 days

4-5 days

I weekI week

1I- weeks

2 weeks

2 weeks

2-3 weeks

3 weeks

3 weeks3 weeks

4 weeks

+1 month

+I month

- month

I monthImonths

22 months

2{ months

2!

months2-3

months

R.L.V.(cm.)2-5

2 5

242 3

2 7

24

242 3

2 12 324

2 3

2 1

2.5

2 62 8

2-1

20

2 2

2 2

2 12 82 82-5

2-1

2 5

2 8

L.L.V.(cm.)2-1

20

2-13 2

2 8

2 5

242 3

242-524

2 3

2 3

3 0

3 12 8

2-6

24

2 7

2 7

2 32 33 02 8

2 2

2 7

2 5

Site

M id-vertex

Left side

Right sideRight frontal

Left frontal

Right side

Right temporalNot known

Right parietal

Not known

Not known

Not known

Frontal

Not knownNot known

Occipital '?

Right side ?

Not known

Frontal

Right frontalFrontalVertex

Right frontal

Right side

Not known

Not known

Fractures

Depressed vertical

Diastasis leftcoronal

NilNil

Nil

Right parietal

Right temporalLeft parietal

Nil

Nil

Right parietal

Nil

Left parietal

OccipitalRight parietal

Left sidedmultiple

Nil

Not known

Nil

Right frontalNilNilNil

Maxilla

Nil

Right parietal

No.

68

69

7071

72

73

7475

76

77

78

79

80

8182

83

84

85

86

87888990

91

92

93

59


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HUGH DAVIES AND MURRAY A. FALCONER

FIG. 7.-Bilateral general dilatation. Case No. 88. Bilateral general dilatation of the lateral ventricles, the rightside being more affected than the left but both being enlarged.

TABLE VII.-FOCAL DILATATIONS ASSOCIATED WITH GENERALIZED

Diagnosis

94 Post-traumatic syndrome .

Head injury withnyramidal signs.

residual

IHead injury with bilateral 6thnerve palsy.

Post-traumatic epilepsy



Post-traumatic intellectual de-terioration.

P.T.A.

I day

4 days

4 days

5 days

4 weeks

4 weeks

Not as-sessable

R.L.V. L.L.V.(cm.) (cm.)

2 3

20

2-1

171 72-0

18

20

2 6

2-7

2-3

2 22 21.9

2.1

20

Local changes

Left more thanright through-out but es-pecially leftvestibule andp o s t e r i o rhorns

Relative dilata-tion of leftfrontal andt e m p o r a Ihorns

Left vestibuledilated

Left a little+anteriorly

Right vestibuledilated

Left vestibulcdilated

Both anteriorhorns+

TABLE VilI. DURATION OF THE POST-TRAUMATIC AMNESIA IN THE VARIOUS TYPES OF POST-TRAUMATICVENTRICULAR DILATATION

Ventricular dilatation

No. ofDuration of cases in No ventricular Generalized Focal

P.T.A. each dilatation _ _____ andtime Focal General- All types

period Uni- Bi- iz-dl.teral lateral

31 cases 1 5 cases 21 cases 26 cases 7 cases 69 casesNo P.T.A. .. 6 4 (67 per cent. of group) 0 1 1 0 2 (33 per cent. of group)Under I day 18 10 (56 ,. ,, ) 2 2 3 1 8 (441-7 days .. 26 10 (38 ,, ,, ) 4 5 4 3 16 (62 ,1-4 weeks .. 37 6 (16 ,, ,, ) 7 11 11 2 31 (84Over I month 13 1 ( 8 ,, , ) 2 2 7 1 12 (92

No.

95

96

97

98

99

100

Site

Frontal

Left frontal

Frontal

Frontal

Not known

Occipital

Left frontal

Fractures

Basal

Left frontal

Frontal

Nil

Nil

Nil

Depressedfrontal

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FIGi. 8.-Focal dilatation associated with generalized. Case No. 99. An example of general dilatation of the leftlateral ventricle with a superimposed focal dilatation of the trigone. The right lateral \entricle is una!iected.

tended longer than a month 2 cases (15 per cent.)had focal dilatation and 7 (54 per cent.) hadgeneralized bilateral dilatation.

Records of the findings on lumbar puncture per-formed during the first week after injury were avail-able in only 17 cases. In 2 of these the cerebro-spinal fluid was normal, whereas in the remaining15 cases it contained blood. Of the 17 cases, 4,including the two with normal cerebro-spinal fluids,were later shown to have normal ventricular outlines,whereas 13 of those which had had subarachnoidhxemorrhage were later demonstrated to have dilatedventricles. Assuming that blood in the cerebro-spinal fluid is an indication of severe head injury,these observations confirm the impression derivedfrom the analysis of the post-traumatic amnesiastandards that the more severe degrees of cerebraltrauma are apt to be followed by ventriculardilatation.An analysis of the ventricular changes in relation

to the sites at which the violence had been applieddid not indicate any causal connexion between thetwo (Table IX). If, for the moment, fi-actures of

the skull are not taken into account, it would appearfrom Table IX that both focal dilatations and uni-lateral or bilateral dilatations of the ventricles arecaused just as frequently by injuries delivered in theantero-posterior axis of the skull as they are byinjuries delivered from the side. One reason whichmay account for this apparent lack of correlationbetween the site of injury and the site and extent ofthe subsequent ventricular dilatation is that in roadaccidents, which formed a large proportion of ourcases, the skull is often subjected to multiple blows,as Cairns (1941) has shown fi-om a study of thecrash helmets of injured motor-cyclists. In 9 casesthe dilatation appeared to have been caused bycontre-coup; three of these had received occipitalinjuries, which had resulted in a generalized dilata-tion of the contralateral ventricle in five cases andfocal dilatation in one.

Although the actual site of violence appears to havelittle connexion with the development of any par-ticular type of ventricular dilatation, the productionof a localized fi-acture of the skull seems to influencethe development of a focal dilatation of the ventricle

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HUGH DAVIES AND MURRAY A. FALCONER

TABLE IX.-RELATION OF VENTRICULAR CHANGES TO SITES OF INJURY

No. of Site of injury to skullEncephalographic cases in

appearances eachgroup Frontal and Lateral Vertical Not known

occipital

Cases Cases Cases CasesNormal ventricles .. 31 17 (55 per cent. 7 (23 per cent. 1 (3 per cent. 6 (19 per cent.

of group) of group) of group) of group)Focal dilatation of ven- 15 7 (47 per cent. 6 (40 per cent. 1 (7 per cent. 1 (7 per cent.

tricles.. .... of group) of group) of group) of group)Generalized dilatation 47 15 (32 per cent. 17 (36 per cent. 2 (4 per cent. 13 (28 per cent.

of ventricles of group) of group) of group) of group)(a) Unilateral .. 21 7 (33 percent. 10 (48 per cent. 4 (19 per cent.

of group) of group) of group)(b) Bilateral .. 26 8 (31 per cent. 7 (27 per cent. 2 (8 per cent. 9 (35 per cent.

of group) of group) of group) of group)Focal and generalized 7 6 (86 per cent. 1 (14 per cent.

dilatations of ven- of group) of group)tricles

TABLE X.-RELATION OF VENTRICULAR CHANGES TO FRACTURE OF SKULL.

Fracture of skullEncephalographic appearances cases in

each group Present Not present

Cases CasesNormal venttricles .. .. .. 31 13 (42 per cent. of group) 18 (58 per cent. of group)Focal dilatation of ventricles .. 15 11 (73 , ,, ) 4 (27 ,, )Generalized dilatation of ventricles 47 21 (45 ,, ,, ) 26 (55

(a) Unilateral .. .. .. 21 8 (38 ,, ,, ) 13 (62(b) Bilateral .. .. .. 26 13 (50 ,, ,, ) 13 (50

Focal and generalized dilatation ofventricles .. .. .. .. 7 4 (57 ,, ,, ) 3 (43 ,, ,, )

(Table X). Thus a fracture of the skull was observedin 15 out of 22 cases (68 per cent.) with focal or focaland generalized dilatations of the skulls as opposedto 34 out of 78 cases (44 per cent.) in which theventricles were normal or only showed a uniformenlargement. In the majority of the cases of focaldilatation of the ventricles associated with fracture,the ventricular enlargement occurred immediatelybeneath the site of fracture (9 out of 11 cases). In2 cases, however, the ventricle on the opposite sidehad dilated, apparently by contre-coup.As regards the time of onset of post-traumatic

ventricular dilatation, we have evidence which sug-gests that it is usual for dilatation to commence inless than 3 weeks and that it may reach its maximumwithin 4 weeks. This evidence is, however, scanty,as encephalography was seldom undertaken duringthe acute phase of head injury, and, moreover, wasusually performed only once in each case. Out ofthe 69 cases which showed ventricular enlargement,only 7 were examined within a month of injury.Of these, 5, which were examined between 3 and 4weeks after injury (Cases 32, 43, 53, 59, and 63),showed ventricular dilatation. In one of these(Case 43), which was first examined 1 month afterinjury, and later re-examined 2 months and 32-months after injury, the dilatation did not appear

to have progressed after the first examination. In2 cases (Cases 40 and 76), which were first examinedearlier than 3 weeks after injury, some progressionin the ventricular changes was subsequently demon-strated at a later examination. In Case 40 the firstencephalogram (2 weeks after injury), was normalbut encephalography repeated at 6 weeks and againat 8 weeks showed that a dilatation of the left anteriorhorn and right ventricle had appeared between thefirst and second examinations, but had not increasedin size after the 6th week. In the second case(Case 76), slight ventricular enlargement, whichwas present at 21 weeks, appeared to have increasedwhen examined at 5 weeks. We have no cases inour series in which we found evidence of progressionof the ventricular enlargement later than 4-6 weeksafter injury.

Correlation with symptoms and physical signsAn analysis of the clinical features of our cases,

made in conjunction with the encephalographicfindings, shows that the connexion between thedegree and type of the ventricular enlargement andthe clinical symptoms is not always obvious. Inonecase, for example, generalized bilateral ventriculardilatation of considerable degree might (Case 93),be associated with marked residual neurological

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signs, and in another case (Case 88) with none atall. Again, when one ventricle is dilated more

than its fellow, the neurological signs present, con-trary to the usual observation, may be referable tothe side with the smaller or more normal ventricle,whereas the side of the brain with the greater ven-

tricular dilatation gives rise to no symptoms or

signs.Frequently, however, the enlargement of the

ventricles could be correlated with neurologicalfeatures, such as hemiparesis, aphasia, or visual fielddisturbances, indicating permanent focal damage tothe brain. In Table Xl the frequency of ventriculardilatation in cases with persistent neurological signsis compared with that in cases without signs of focalcerebral damage. It shows that about 89 per cent.of the cases with persistent focal signs showedventricular enlargement, as compared with 62 percent. of the cases in the second group and with4 per cent. of cases in the control series.

In order to appraise the clinical significance ofpost-traumatic ventricular dilatation more fully, we

arranged our cases into the following clinical groupsand attempted to correlate the clinical features withthe encephalographic appearances.

(I) Head injury without unconsciousness .. 6 cases(2) Head injury without residual sequels .. 9(3) Head injury with residual neurological

signs .. .. .. .. .. 44(a) With pyramidal signs 24 cases(b) With hypothalamic and/

or brain stem signs 4(c) With optic radiation dis-

turbances .. 3(d) With cranial nerve pal-

sies .. .. 16(4) Post-traumatic syndrome .. .. 29(5) Post-traumatic intellectual deterioration 24(6) Post-traumatic epilepsy .. .. .. 19

A total of 131 diagnoses thus was made in the100 cases, multiple diagnoses being made in 30cases. In each instance the diagnosis was based on

the clinical features prevailing after recovery fromthe head injury and not on the signs present in theacute stage. The allocation of cases to the firstthree groups and to the last group was straight-forward. The assignment of cases to the groupsof post-traumatic syndrome and post-traumaticintellectual deterioration was necessarily more

arbitrary; those cases in which chronic headaches,often associated with giddiness and fatigue, were

prominent were allocated to the first group, and thosein which an objective personality change pre-

dominated were assigned to the second group. Nocase was placed in both groups. No separate group

was made for cases showing residual sensory signsor, in cases where the dominant hemisphere was

damaged, for residual speech disturbances, becausein no instance were such signs observed withoutmotor signs, and consequently these cases are alreadyrepresented in the group showing residual pyramidalsigns.The frequency with which these clinical states

were encountered in relation to the various gradesof post-traumatic ventricular dilatation is outlinedin Table XII. A more detailed study of each group

will be given below, but certain important generali-zations may here be stressed. Residual pyramidalsigns indicative of hemisphere damage are very

frequently associated with dilatation of the ventricleon the opposite side of the brain. Primary hypo-thalamic and brain stem signs, on the other hand,are usually not associated with ventricular dilatation.Cases of post-traumatic syndrome usually havenormal or only slightly dilated ventricles, whereascases of post-traumatic intellectual deteriorationoften show most marked ventricular dilatation. Inall these groups, therefore, an apparent connexionbetween clinical features and ventricular changescan be made out. On the other hand, no such re-

lationship is evident in cases presenting cranialnerve palsies or post-traumatic epilepsy. Our find-ings in the groups of head injury without un-

consciousness and head injury without residualsequele are not applicable to head injuries ingeneral, as our material in these two groups is toohighly selected.A more detailed analysis of each clinical group

will now be considered.

Head Injury without UnconsciousnessThere were 6 cases in this group. All had a clear

recollection of the accident, and were subsequentlyinvestigated between 3 and 15 months later on

account of persistent features considered to be dueto the injury (post-traumatic syndrome, 3 cases;post-traumatic epilepsy, 2 cases; residual pyramidalsigns, 1 case). Four cases showed normal ven-

tricular outlines, and two (Cases 47 and 68) showedsome dilatation of the ventricles presumably relatedto the head injury.

TABLE XI.-FREQUENCY OF VENTRICULAR DILATATION IN THE HEAD INJURY AND CONTROL SERIES

No. of Cases with normal Cases with ventricularcases in ventricles dilatation

each group

Total head injuries .. .. .. 100 31 (31 per cent. of group) 69 (69 per cent. of group)(a) Head injury with persistent

signs of focal cerebraldamage .. .. .. 27 3 (11 ,, ,, ) 24 (89

(b) Head injury without persistentsigns of focal cerebraldamage .. .. .. 73 28 (38 ,, ,, ) 45 (62

Control series .. .. .. 50 48 (96 ,, ,, ) 2 (4

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TABLE XII.-FREQUENCY OF THE DIFFERENT CLINICAL STATES IN THE VARIOUS TYPES OF POST-TRAUMATICVENTRICULAR DILATATION

Ventricular dilatation

No. ofDiagnostic cases in No ventricular Generalized Focalgroup each dilatation and

group Focal General- All typesUni- Bi- ized

lateral lateral

31 cases 15 cases 21 cases 26 cases 7 cases 69 cases1. Head injury without

unconsciousness 6 4 (67 per cent.) 0 1 1 0 2 (33 per cen;t2. Head injury without

residual sequels .. 9 1 (11 ,, ) 1 3 4 0 8 (89,,3. Head injury with resi-

dual neurologicalsigns.. .... 44 12 (27 ,, ) 9 9 10 4 32 (73,,

(a) Pyramidal 24 2 (8 ,, ) 6 7 6 3 22 (92(b) Hypothalamic

and brainstem 4 3 (75 ) 1 0 0 0 1 (25

(c) Optic radia-tion. .. 3 1 (35 , ) 0 1 1 0 2 (65

(d) Cranial nervepalsies 16 6 (27 , ) 3 2 4 1 10 (73,,

4. Post-traumatic syn-drome .. .. 29 14 (48 ,, ) 3 6 4 2 15 (52

5. Post - traumatic intel-lectual deterioration 24 3 (12 ,, ) 5 4 11 1 21 (88

5. Post - traumatic epi-lepsy.. . _19 6 (32 ,, ) 3 4 5 1 13 (68,.

Controls .. .. 50 48 (96 ,,) 0 0 2 0 2 (4 .,

CaKse 47. The first of these two cases with ventriculardilatation was a 22-year-old signaller, who fell 12-15 feetbackwards from a telegraph pole, striking his head onsoft earth without losing consciousness. Four hourslater he had a generalized epileptic convulsion andsubsequently he had recurrent attacks at intervals of 2 or3 months. There were no abnormal neurological signsand no previous personal or family history of epilepsy.The electroencephalogram revealed slow high-voltagewaves over both hemispheres, suggestive of idiopathicepilepsy, but because symptoms had first occurred soearly after the injury the case was considered clinically tobe one of post-traumatic epilepsy. Air encephalographydemonstrated moderate dilatation of the left lateralventricle.

Case 68.-The second case was a 39-year-old air-craftsman who received a blow over the vertex when abuilding collapsed after an explosion. He sustaineda small compound depressed fracture over the centreof the superior longitudinal sinus but did not loseconsciousness. Immediately after injury he developedslight weakness and numbness of both lower limbs, moremarked on the left side than on the right, without dis-turbance of micturition or defaecation. At operationthe depressed fragments were elevated and the dura shlownto be intact. Subsequently this patient was left withslight residual spasticity in both lower limbs, again morein the left than the right. Encephalography showedbilateral general ventricular dilatation which wasmoderate on the right side and slight on the left.

These two cases indicate that ventrictilar dilata-tion can develop after head injuries in whichconsciousness was not lost. The responsiblemechanism is not known. Possibly a thrombosis ofthe superior longitudinal sinus, directly resulting

from the injury, may have played a part in the secondcase, but sLich a mechanism was unlikely in the firstcase.

Head Injury without Residual SequelseNine cases in the series eventually made comnplete

clinical recoveries. In only one was the ventricularsystem normal. This case (Case 8) was the onlyexample of a comparatively mild and straight-forward head injury in our series. There was apost-traumatic amnesia of 2 hours. Encephalo-graphy was undertaken because, 1 hour after injury,a convulsive attack, the significance of which wasnot evident, had been observed down the right sideof the body. The other 8 cases all showed ven-tricular enlargement. In one (Case 33) a symptom-less focal dilatation of the left frontal horn developedbeneath the site of a healed compotind depressedfracture. The remaining 7 cases were all examplesof prolonged post-traumatic confusion with con-fabulatory disttirbances (Korsakow's psychosis).All seven made complete recoveries, and subse-quently showed generalized dilatations of one orboth lateral ventricles. It is interesting that two ofthem (Cases 61 and 88), both with well markedventricular dilatation, were pilots who later returnedto full flying duties.

It will be seen that, though this grotip inclidesonly cases which made complete recoveries, it isreally highly selected in that in most of the cases

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VENTRICULAR CHANGES AFTER CLOSED HEAD INJURYwere examples of post-traumatic Korsakow's syn-drome. It shows clearly that post-traumatic ven-tricular dilatation, even of moderate degree, is notnecessarily associated with permanent psychologicalor neurological disturbances.

Head Injury with Residual Neurological SignsA. With Resilual Pyr-amidal Signs

Ventricular dilatation was observed in all except2 of the 24 cases in this group. One of these twoexceptions (Case 6) sustained a head injury of com-paratively mild severity due to a blow on the rightside of the head from a falling hammer. The skullwas not fractured. The left arm was immediatelyparalysed, and slight permanent weakness of thearm was still evident 6 months later. The secondexception (Case 9), was a case with a small, slightlydepressed fracture in the mid-vertex over thesuperior longitudinal sinus, presenting slight residualsensory and motor signs in both lower limbs, moreon the left side than on the right. A possible factorin the production of the clinical features shown bythis case may have been a partial thrombosis of thesuperior longitudinal sinus beneath the depressedfracture.

In the remaining 22 cases (92 per cent.) the residualpyramidal disturbances were associated with ven-tricular dilatation. Six were examples of focalventricular dilatation, 7 of unilateral ventriculardilatation, 6 of bilateral ventricular dilatation, and3 of focal with unilateral general ventricular dilata-tion. It is interesting that with one exception thebigger ventricle was, appropriately, on the sideopposite to that of the pyramidal disturbance. Thisrelationship between the site of injury and the sideon which symptoms appeared was further em-phasized in Case 68, which showed bilateralpyramidal signs and bilateral ventricular dilatation;the side of greater ventricular dilatation was opposedto that of the greater motor signs. The exceptionto this rule was Case 44, in which a pronouncedresidual left hemiparesis was observed in associationwith a marked focal dilatation of the anterior part ofthe left lateral ventricle; there may have been somedilatation of the vestibule of the right lateralventricle in this case but the degree of enlargementwas very slight and opinions varied as to whether itwas of pathological degree.

Particularly striking were the 7 cases (Cases 51,55, 56, 57, 59, 60, 62) in which an apparently strictlyunilateral ventricular dilatation was associated withcorresponding pyramidal signs down the oppositeside of the body. In one of these (Case 55) thedegree of hemiparesis was very pronounced; inanother (Case 57) the discrepancy in size betweenthe two ventricles was particularly marked. Anillustrative case history from this group is asfollows:

Case 57.-A 24-year-old soldier received a closed headinjury in April, 1940, as a result of a motor-cycle acci-dent, which resulted in a post-traumatic amnesia of 2weeks duration. Subsequently he complained of aphasiaand of weakness of the right arm and leg which cleared

F

up completely within a further 2 weeks. About 3 monthsafter his injury he developed frequent epileptic attacks,which began with clonic movements of the fingers of theright hand, followed shortly by loss of consciousness fora few minutes. After many of the attacks he had aphasiaand a transient right hemiplegia lasting for an hour.Between attacks weakness of the right lower face wasevident, but no weakness or sensory disturbances in thelimbs. X-ray examination showed a linear fracture inthe left parietal region, and cisternal encephalographydemonstrated a moderate dilatation of the whole of theleft lateral ventricle. In view of the focal aura of hismajor attacks a left lateral craniotomy was performedand a small meningo-cerebral scar was found in the leftpre-central gyrus.

This association of residual pyramidal signs withdilatation of the opposite ventricle occurs so fre-quently that it raises the question whether cases inwhich the pyramidal signs were only transient mightnot also show ventricular dilatation when examinedat a later date. Our information as to the detailedsigns shown by our cases in the acute stage is un-fortunately incomplete, and we have records of only7 such cases with transient pyramidal disturbances(Cases 58, 65, 86, 87, 89, 90, 100). It is interestingthat either unilateral or bilateral ventricular dilata-tion was later demonstrated in all of them, and thatthe larger ventricle was always on the side oppositeto that of motor dysfunction.

B. With Hypothalamic and/or- Brain Stem SignisOf the 4 cases included in this subgroup, only one

(Case 41) showed ventricular dilatation. None hada fracture of the skull visible in the X-ray films.Three cases (Cases 28, 30, and 41), each with aprolonged post-traumatic amnesia of between 2 and4 weeks duration, exhibited residual " cerebellar "ataxia down one side of the body without motorweakness. In one instance this was associated withnystagmus and dysarthria as well. The traumaticlesion responsible for these features was presumedto lie within either the brain stem of the cerebellum.Two of these three cases had normal encephalogramsand the third some focal dilatation of the ipsolateralfrontal horn. The remaining case (Case 22) in thissubgroup was thought clinically to have had neuro-logical lesions in the hypothalamus and upper partof the brain stem, which radiological examinationshowed were associated with a normal encephalo-gram. During the acute phase immediately follow-ing injury, the characteristic postures of decerebraterigidity, associated with righting reflexes of theMagnus and de Kleyn type, were demonstrated. Inthe later stages the patient was left with a profounddementia, slight residual weakness of the right arm,and increased spasticity of both lower limbs. Thesefour cases together suggest that cases of primarybrain stem and hypothalamic injury are not usuallyfollowed by ventricular dilatation.

C. With Residual Optic Radiation DefectsAn incomplete homonymous hemianopia of con-

grous type was observed in three cases (Cases 25, 49,75). In each case there was a fracture in the parieto-occipital region, presumably associated with a

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HUGH DAVIES AND MURRA Y A. FALCONERlocalized injury of the posterior part of the cerebralhemisphere. In no case did a dilatation of therelated part of the lateral ventricle occur. In thefirst case (Case 25) the ventricular outlines werenormal, in the second case (Case 49) there was ageneralized dilatation of the opposite lateral ven-tricle from contrecoup, while in the third case (Case75) there was a generalized symmetrical dilatationof both lateral ventricles. These three cases wouldseem to indicate that a localized cerebral injury isnot necessarily followed by ventricular dilatation,but it must be remembered that ventricular changesin the occipital horns are often difficult to assess,owing to the wide range of normal anatomicalvariations.

D. With Cr-anial Nerve PalsiesIn this group are included only cases in which

cranial nerves were damaged, presumably withinthe cranial cavity, by injuries such as those involvingthe olfactory and oculomotor nerves or the opticchiasm. Cases in which the nerve was obviouslydamaged in its course through the skull, as in lesionsof the optic nerve, the facial and auditory nerves,and the divisions of the trigeminal nerve wereexcluded.

Sixteen cases were found in the series, some withmultiple lesions; 12 showed anosmia, 4 chismaticdisturbances, and 3 oculomotor nerve palsies. Themajority were associated with other residual neuro-logical lesions which rendered it very difficult todetermine the relationship between the state of theventricles and the cranial nerve palsies. In 5 cases,however, cranial nerve palsies were noted as occur-ring without other residual sequelk. Two of thesecases showed bilateral anosmia and bitemporalhemianopia, one bilateral anosmia, one bilateralsixth nerve paresis, and one unilateral sixth nervepalsy. The ventricles were normal in three, showedfocal dilatation in a fourth, and focal with general-ized dilatation in the fifth. There is probably nodirect relationship between the state of the ventriclesand these cranial nerve palsies.

Post-Traumatic Syndrome and Post-Traumatic In-tellectual Deterioration

Residual symptoms of intellectual disturbances,either subjective or objective, were observed in 53cases. According as to whether subjective orobjective features predominated, we divided thesecases, as mentioned earlier, into two groups, a groupof cases of post-traumatic syndrome in which head-aches, giddiness, and lassitude were the character-istic features, and a group of cases of post-traumaticintellectual deterioration in which objective person-ality changes were conspicuous.

Twenty-nine cases were listed as examples of thepost-traumatic syndrome. Collectively they werethe result of injuries which clinically seemed lesssevere than those in the second group. In 3 outof the 29 cases (10 per cent.) there had not been anyloss of consciousness, in 16 cases (55 per cent.) thepost-traumatic amnesia was of 1 week or less,

while in only 10 cases (35 per cent.) was it greaterthan 1 week. Radiologicalexaminationshowedthatof the cases of post-traumatic syndrome nearly half(14 cases, i.e. 48 per cent. of the group) showednormal ventricular outlines. In addition 3 cases(10 per cent.) showed focal enlargement of theventricles, 6 (21 per cent.) unilateral ventriculardilatation, and 4 (14 per cent.) bilateral ventriculardilatation, while 2 cases (7 per cent.) showed com-binations of focal and generalized ventriculardilatation.

Twenty-four cases were included in the secondgroup of post-traumatic intellectual deterioration.By comparison with the first group, the injuries inthis group were clinically more severe and werefollowed more frequently by ventricular dilatation.Thus a post-traumatic amnesia of one week or less wasobserved in only 6 cases (25 per cent.), whereas in18 cases (75 per cent. as opposed to 35 per cent. incases of post-traumatic syndrome) the duration ofthe post-traumatic amnesia exceeded a week. Nocases of head injury without loss of consciousnesswere included in this group. Twenty-one out of the24 cases (88 per cent.) showed ventricular dilatation.In 50 per cent. of these cases (12 cases), both lateralventricles were affected; unilateral ventricular dilata-tion was observed in 4 cases (17 per cent.); focalventricular enlargement in 5 cases (21 per cent.), andnormal ventricular outlines in 3 cases (12 per cent.).

Post-Traumatic EpilepsyRecurrent epileptic phenomena considered to be

the direct result of the head injury were noted in19 cases. Cases of epilepsy with antecedent attacksor with a known family history of epilepsy wereexcluded, as were all cases in which convulsive dis-turbances occurred only during the acute phasesfollowing injury. Grand mal seizures were observedin 12 out of the 19 cases, petit mal attacks in 2,grand mal associated with petit mal in 3, and focalmotor seizures in 2 cases. Usually these attacksappeared some months after the injury, but in onecase (Case 47), they apparently first appeared withina few hours of the accident, while in another case(Case 5), an interval of 3 years elapsed before theattacks appeared.The incidence of post-traumatic epilepsy in our

series appeared to bear no relation to the severity ofthe responsible injury, as measured by either theduration of the post-traumatic amnesia or the degreeof ventricular dilatation. Thus 3 cases sustainedinjuries without loss of consciousness, 3 had post-traumatic amnesia of less than 1 day, 6 post-trau-matic amnesia of 1 week, and 7 post-traumaticamnesia of more than 1 week. Again, of the 10cases in which post-traumatic epilepsy occurredwithout other residual features, half showed normalventricles and half dilated ventricles.

DiscussionIt is evident from this analysis of our case material

that ventricular dilatation of either a focal or ageneralized character often follows closed head

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injuries. Although dilatation may occur afterapparently mild injuries, the frequency with whichit is found increases with the severity of the trauma.These ventricular enlargements first appear within2-3 weeks of injury and may reach their maximumwithin a month. They do not appear to be in-fluenced so much by the site of the direction of theviolence as by the presence of a fracture of the skull.Focal dilatations in particular tend to developbeneath the site of a localized fracture of the skull.Although in some cases the correlation between

the clinical signs and the encephalographic appear-ances is not at first apparent, in most there is anobvious relationship between the two. In particular,cases with residual pyramidal signs down one sideof the body are frequently found to have dilatationof the lateral ventricle on the opposite side of thebrain. Moreover, some of the remaining cases ofventricular enlargement were known to have pre-sented signs of pyramidal disturbance in the acutephase of injury. Again, in cases with marked intel-lectual and mental deterioration both ventricles areoften enlarged, whereas in cases without objectivedeterioration, but with only disorders of a subjectivecharacter such as headaches and dizziness, theventricular system is more often normal. On theother hand the appearance of post-traumatic epilepsydoes not seem to be connected with changes in theventricular outline.We strongly deprecate the view expressed by Swift

(1932), Hauptmann (1931), Friedman (1932), andothers that air encephalography can be used asa certain means of differentiating between caseswith genuine disabilities and those with functionaldisturbances. These authorities, who have advo-cated the use of air encephalography in this con-nexion, have implied that, when the encephalogramsare normal, the case should be regarded as offunctional character. In our series of 31 cases withnormal ventricular outlines following head injury,at least 6 cases had definite objective neurologicalsigns indicating cerebral damage and 6 suffered frompost-traumatic epilepsy. We therefore feel thatthe findings of a normal encephalogram in a givencase does not prove that the symptoms are func-tional, because permanent organic damage can occurin the brain without resulting in later ventricularenlargement.

In this paper we have confined ourselves to a con-sideration of the ventricular changes, and have notpaid attention to the other encephalographicfeatures described in Bielschowsky's classical paper(1928). We do not consider non-filling of theventricles with air to be evidence of pathologicalchange, for we have observed on several occasions,after encephalography had failed to fill the ventricles,that ventriculography has revealed a normal ven-tricular system. Recently we met with a case inwhich, after lumbar encephalography had failed tooutline the ventricles, encephalography repeated afew days later with air introduced by the cisternalroute produced very satisfactory filling of theventricles, which appeared normal. As during the

period when our 100 cases were investigated therewere only 4 cases of chronic head injury in whichventricular filling was not obtained, we have notfelt justified in considering such cases as pathologicaland have consequently excluded them from ourseries.

Authors using lumbar encephalography haverightly laid great emphasis on abnormalities of dis-tribution of the subarachnoid air. In our materialthese abnormalities have not been obvious, exceptin cases which also showed ventricular changes, andso we have not considered them. Cisternal en-cephalography, as performed in this hospital withthe installation of only small quantities of air, doesnot lend itself to so clear a demonstration of the sub-arachnoid pathways as does lumbar encephalo-graphy. We feel this disadvantage of cisternal en-cephalography is outweighed by the advantage ofbeing able to outline the ventricles clearly withsmaller quantities of air, thereby causing much lessdistress to the patient.The presence of ventricular dilatation after

recovery from a head injury indicates that anatrophic process has taken place in the brain. Suchan atrophic process may be the result of obstructionto the cerebro-spinal fluid pathways, or of resolutionof the pathological changes produced in the brainitself by the trauma. Broadly speaking, post-traumatic ventricular dilatations are of two types,focal and generalized, and are probably produced bydifferent mechanisms. It is unlikely that purelyfocal dilatations, for example, are due to the backpressure effects of obstruction to the cerebro-spinalfluid pathways, although such factors may operatein producing generalized dilatations. It is morelikely that focal dilatation is the result of resolutionof local pathological changes such as focal hxmor-rhage, contusion, and laceration of brain tissuedirectly occasioned by the injury. The frequencywith which focal dilatations develop beneath alocalized fracture of the skull supports this view.In the production of generalized dilatation, otherfactors, which affect the brain more widely, mustalso operate. It is known that after head injurywidespread pathological changes may occur in thebrain, often remote from the actual site of injury,and may even overshadow the local injury (Hassin,1940). Factors, such as cedema of the cerebralhemispheres and dilatation of the cerebral capillariesand veins, often with endarteritis (Winkelman andEckel, 1934), may play a part in the widespreadpathological processes. Traumatic subarachnoidhemorrhage may also contribute to a generalizedbilateral ventricular dilatation, as indicated by theexperimental observations of Bagley (1928). How-ever, it is difficult to explain why ventricular dilata-tion is apparently so frequently confined to onelateral ventricle, and may even reach a considerabledegree in that ventricle without the other lateralventricle being affected. It is unlikely that traumaticsubarachnoid haemorrhage or obstruction to thecerebro-spinal pathways, which would affect bothventricles equally, here play a part. It seems more

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likely that the dilatation of the ventricle is the resultof a vasctular disturbance.Whatever the explanation of the ventricular

changes, the fact remains that, in addition to its usein demonstrating the presence of space-occupyinglesions such as intra-cranial hematomata, air en-cephalography is a useful adjunct in the investi-gation of chronic head injuries. It affords a mea-surable indication of the extent of the grossatrophying processes consequent upon cerebralcontusion, laceration, and traumatic vascular dis-turbance. It has its limitations in that finer degreesof cerebral injury can occur without subsequentalteration of the ventricular outlines.

Summary1. The previous literature upon the subject of air

encephalography after head injury shows that since1928 there has been no review of any large series ofcases from the aspect of correlation of the radio-graphic appearances with the clinical findings. Inview of the improved clinical standards of assess-ment it was felt that the significance of the encephalo-graphic changes should be evaluated in the light ofthese.

2. A series of 100 cases of closed head injury ispresented, all of which were examined by a stan-dardized technique, and a method of measurementof the ventricular bodies for the assessment ofdilatation is described.

3. As control a series of 50 cases, in which theventricular system was considered to be normal, wassimilarly examined.

4. The types of change in the ventricular outlineencountered are described, and their time of onsetand relation to the site of injury, to fracture and tothe symptoms and physical signs presenting arediscussed.

5. It would appear from the material that there iscorrelation between the ventricular changes and theclinical signs in the majority of cases, but that thismay not always be so.

6. The mechanism of ventricular dilatation ap-pears more likely to be due to intra-cerebral atrophic

processes than to obstruction of the cerebro-spinalfluid pathways, as has previously been held by somewriters.

7. Air encephalography cannot be regarded as acertain means of differentiating organic from func-tional post-traumatic states, as has been claimed.It does, however, afford a measurable criterion of theextent of atrophic processes occurring after cerebraldamage.

We are much indebted to the medical officers of themilitary hospital for head injuries, under whose carethese cases were, for their unfailing co-operation, andwe wish to record our thanks to our Commanding Officer,Lieut.-Col. G. 0. Chambers, M.C., for his permission topublish this paper. We also wish to express our thanksto T./Brigadier Hugh Cairns for his help and interest inthis survey.

REFERENCESAbramovitch, D., and Winkler H. (1930). Z. ges.

Neurol. Psychiat., 127, 454.Bagley, A. (1928). Arch. Surg., 17, 18.Bennett, A. E., and Hunt, H. B. (1933). Arch. Surg.,

26, 397.Bielschowsky, P. (1928). Z. ges. Neurol. Psychiat., 117,

55.Cairns, H. (1941). Brit. med. J., (ii), 465.Davidoff, L. M., and Dyke, C. G. (1937). The Normal

Encephalogram, Lea, Philadelphia.Evans, W. A. (1942). Arch. Neurol. Psychiat.

(Chicago), 47, 931.Fischer, M. (1927). Arch. Psychiat. Nervenkr., 82, 403.Flugel, F. E. (1932). Ergebn. inn. Med. Kinderheilk., 44,

327.Friedman, E. D. (1932). Arch. Neurol. Psychiat.

(Chicago), 27, 791.Hassin, G. B. (1940). Injuries of the Skull, Brain and

Spinal Cord (Edited Brock), London.Hauptmann, A. (1932). Arch. Psychiat. Nervenkr., 96,

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455.Lysholm, E. (1935). Acta radiol. Stockh., Supp. xxiv.Money, R. A., and Susman, E. (1932). Aust. N. Z. J.

Surg., 2, 47.Schwab, 0. (1926a). Z. ges. Neurol. Psychiat., 102, 294.

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