the anterior inferior cerebellar artery

J. Neurol. Neurosurg. Psychiat., 1949, 12, 137.

THE ANTERIOR INFERIOR CEREBELLAR ARTERYITS VARIATIONS, PONTINE DISTRIBUTION, AND SIGNIFICANCEIN THE SURGERY OF CEREBELLO-PONTlINE ANGLE TUMOURS*

BY

W. J. ATKINSONFrom the Department of Pathology, National Hospital.

Queen Square, London

The anterior inferior cerebellar artery arisesconstantly from the basilar artery on each side atthe junction of its lowest and middle thirds andpasses laterally and downwards to cross the cere-bello-pontine angle and the eighth cranial nerve.At this point the internal auditory artery is usuallygiven off, passing almost immediately into theinternal auditory meatus. Either immediately be-fore or iimediately after crossing the eighth nerve,the main artery divides into two. (1) One branchpasses laterally and downwards on the medial andanterior border of the cerebellar hemisphere. Afterabout a centimetre or so of tortuous course it sendsa constant branch of very variable siize posteriorlyalong the medial surface of the hemisphere toanastomose with a cerebellar branch of the posteriorinferior cerebellar artery. Reference will be madeto this anastomosis later. (2) The other branch ofthe anterior inferior cerebellar artery passes directlylaterally and curls round the upper edge of theflocculus, where it lies on the surface of the middlecerebellar peduncle, and it then passes on to thecerebellar hemisphere proper and anastomoses withall three main cerebellar arteries. This latterbranch of the main artery which passes immediatelylaterally gives off small arteries which' supply themiddle cerebellar peduncle and adjoining part ofthe pons. The main artery itself also sends smallvessels into the pons, supplying chiefly its lateralpart as far superiorly as the junction of the upperand middle thirds and extending down to supplythe lateral third of the upper part of the medullaoblongata.

Plate Ha is taken from a specimen of the basilararterial system which has been injected post-mortemwith red latex. The anterior inferior cerebellarartery on each side will be seen as described,'andmost significant is that part of the artery whichcrosses the cerebello-pontine angle, for here it lies*Read to the British Society of Neurological Surgeons in Dublin in

July, 1948.This work was carried out with the aid of a grant froln the NationalHospital, Queen Square.

immediately anterior to the eighth nerve and inthis portion does not give off any branches. Thereare therefore two parts of the artery which areresponsible for pontine blood supply-themain'part of the vessel proximally and the lateral branchwhich winds round the flocculus distally. In thepast few years, Dr. J. G. Greenfield has pointed outthat those cases of acoustic neurofibromata whichcome to necropsy after operation frequently havehad occlusion of the anterior inferior cerebellarartery on the tumour side by a clip or a thrombus.He also noted that this was associated with infarctionof the pons on that side. In the past it has beenthought that such a lesion was the result oflacerationof the pons by the surgeon-in spite of his usualdenial; or it has been called malaciapontis.

It was therefore with this problem in mind thata series of normal hind-brains was injected withdyed gelatin solutions in various ways designed toillustrate (1) exactly which area was supplied by theanterior vessel in the pons: (2) which areas couldbe apportioned to the proximal and distal parts ofthat vessel as far as the pons itself was concerned,and (3) which anastomoses from the superior andthe posterior inferior cerebellar arteries could takeover the anterior inferior cerebellar arterial supply.The second question was considered the mostimportant, because only by answering it would itbe possible to ascertain the effect on life of placinga clip on the artery as it crossed the eighth nerve,that is, at the point where in effect the acousticnerve tumour would tend to displace the vesselmost away from the angle.

Variations in the Anterior Inferior Cerebellar ArteryIt has repeatedly been observed that there is a

considerable variation in the size and therefore inthe importance of the anterior inferior cerebellarartery. Fig. 1 shows the variations and findingsin a series of consecutive necropsies, and it willbe seen that not only may each case be differentbut there is usually a difference between either

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FIG. 1.-Variations of the branches of the basilar artery.(1) The "classical" and a fairly common arrange- (2) The anterior varying inversely with the posterior

ment. inferior artery (common).(3) Both posterior vessels small, their areas of supply (4) Both anterior vessels small, their areas of supply

being chiefly fed by the anterior vessels (un- being chiefly from the posterior vessels (un-common). common).

(5) Anomalous importance of vessel from the junction (6) Rare-posterior vessel being continuation ofof vertebral arteries. vertebral artery.

(7) Pathological-long-standing thrombosis of lower third of basilar, vertebral, and posterior arteries. Both areaof supply of posterior vessels supplied by right anterior inferior artery. (Patient died from other causes.)

Pc.-posterior cerebral artery; Sc.-superior cerebellar artery A. I.C.-anterior inferior cerebellar artery;P.I.C.-posterior inferior cerebellar artery; B.-basilar artery; V.-vertebral artery; Sp.-spinal artery;A.-internal auditory artery; VIII.-acoustic nerve; An.-anastomotic vessel; Anom.-anomalous vessel.




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side in the individual case. It was also foundthat usually this variation in size was in inverseproportion to the size of the posterior inferiorartery and sometimes to that of the vertebralartery. An anastomotic vessel between the anteriorinferior and the posterior inferior vessels was foundconstantly on the medial aspect of the cerebellumand was large where there was any marked degreeof difference between these arteries on each side;its possible importance in surgery will be mentionedlater. Here too was a factor that had to beeliminated in the injection of the anterior inferiorartery when we attempted to outline its pontinedistribution. Hmemostatic clips were placed on thecerebellar cortical anastomosing vessels, and themain proximal stem of the artery and the lateralbranch were injected, after perfusing the wholebasilar system with normal saline to which 1 percent. sodium nitrate had been added. Various dyeswere used to portray the areas of supply of (1) theproximal part of the artery; (2) the lateral part orbranch passing round the flocculus, and (3) theremainder of the basilar system. In later investiga-tions the areas of the posterior inferior -and thesuperior cerebellar arteries were also injected.Plate I illustrates the area of supply of the anteriorinferior cerebellar artery.

Areas of SupplyIt will be seen (Plate I a, b, c) that the anterior

inferior artery has two separate areas of supply-the proximal stem supplies the lateral area of thepons; and the lateral branch, after crossing theeighth nerve, supplies the middle cerebellar peduncleand an area of variable size in the lateral tegmentalregion of the lower two-thirds ofthe pons. Plate VIId, e, f represents a constant fiinTing when the twoparts of this artery are injected. We consider thatthe tegmentum transmits autonomic impulses whichare important for cardiovascular control. Thisconclusion is reached from physiological evidenceto be given later and from a study of other pontinepathways which can be allocated to other functionsalready established. A clip on the artery as itcrosses the eighth cranial nerve will immediatelydeprive the lateral part of the tegmentum of bloodsupply if no anastomosis exists via the posteriorinferior or the superior cerebellar arteries or theusually very small but occasionally larger (Fig. 1,No. 5) branch which may come off the basilar nearits origin from the junction of the vertebrals.Further, such a clip may well initiate thrombosisin the main proximal stem of the artery and soimpair the whole ofthe artery's pontine distribution.Moreover, we have. found that, while there arenumerous surface anastomoses between the cere-

bellar arteries over the cerebellar cortex, injectionof the anterior inferior cerebellar artery from thebasilar artery always stains the artery's distributionselectively. This is comparable with Bolton's (1939)work on the anterior spinal artery. She found thatdye injected into a segmental spinal artery passedchiefly in a caudal direction along the anteriorspinal artery, and, although a little passed rostrallyby anastomosis, it did not penetrate into thecapillary distribution of arteries entering at a morerostral level.

Again, it is widely held that when a main arteryis injured all its tributaries and the coUateralanastomoses go into spasm for a variable time.Finally, at most operations on acoustic tumourswhere removal is attempted, retraction of thecerebellum is invariably sufficient to produce asoftening of at least part of the cortex. A certainnumber of anastomoses will be occluded in thismanner.

HistoricalWallenburg (1901) appears to have been the

first to record a lesion of the anterior inferiorcerebellar artery, A clinical diagnosis of haemor-rhage from the ramus centralis arteriw radicularisnervifaciae dextri, a branch of the anterior inferiorcerebellar artery, was made. The patient livedseven years and at necropsy the right side of thepons appeared smaller than the left. Sectionrevealed a hemorrhagic cyst in the tegmentum ofthe pons extending to the floor ofthe fourth ventricle.Caudally, it reached the anterior end of the olive(inferior), and rostrally the lingula of the cerebellum.It destroyed the motor nucleus, as well as part ofthe sensory nucleus and some of the sensory rootsof the right fifth nerve. The nuclei of the sixth andseventh nerves on the right side were destroyed, aswere the nuclei of Bechterew and Deiters, parts ofthe restiform body and posterior longitudinalbundle, the dorsal fibres of the cochlear nucleus asthey passed to the trapezoid body, and part of thespino-thalamic and spinal-tectal tracts on the sameside.

Since that time there have been few observations,on the place the artery may hold in physiology ormedicine.

Case RecordsHere it is important to consider the clinical

condition of those patients who have come tonecropsy and in whom there has been clear evidenceof this vessel's occlusion following operation forthe removal of an acoustic neurofibroma. Eachcase will be described in terms of operation pro-cedure, postoperative course, and post-mortemifindings.

145




W. J. ATKINSON

Case 1.-The first case of which we have any recordrelating to the infarction of the pons was in!1938. Awoman (H.W.), aged 45 years, was admitted under thecare of Dr. Denny-Brown with a: six weeks history ofdizzy attacks and ataxia followed- by vomiting attacks.On Nov. 8 she underwent the operation ofpartial removalofan acoustic neurofibroma; after this she was reportedas being in poor condition from loss of blood. On thenext day she was conscious but had an abnormallyrapid pulse rate. Two days after operation progresswas reported as good although she had retention ofurine. On the fourth day, however, she was comatosewith ,a temperature of 1040 F., pulse rate of 150 perminute, and normal respirations. She died on the fifthpostoperative day. The post-mortem report stated thatthere was no excessive hemorrhage but there was somelaceration of the side of the pons in the region of themiddle cerebellar peduncle on the side from which anacoustic neurofibroma had been partly removed(Plate Ib).

COMMENT.-The specimen shows what has beenvariously described as a laceration of the pons, pre-sumably by the surgeon or as malacia pontis. It exactlyresembles the appearance of infarction resulting fromocclusion of the anterior inferior cerebellar artery, andlies in the area of supply of that artery.

Case 2.-The second case (D.C.) was in 1945 underthe care of Mr. Northfield who has kindly permitted meto include this case. She had had a sub-occipitaldecompression in April, 1944, following a three-yearhistory starting with weakness of the right hand. InJuly, 1945, a partial removal, and in October, 1945, acomplete removal of the acoustic tumour was accom-plished. At this operation a careful although tediousmobilization was achieved; at the lower pole of thetumour where scar tissue attached it to the lateralcerebellar lobe a relatively small vessel suddenly bled.andwas clipped. The final removal was straightforwardand the surface ofthe pons was at the end of the operationcompletely free from bruising. That evening the wardsister reported that breathing was deep, the head inclinedback to the left, the mouth twitching and drawn to theright, the' eyes turned to-the left, the jaw clenched, andthat there were generalized shaking movements, with thearms spastic, loss of consciousness, deep stertorousbreathing, excessive saliva, pulse bounding and strong,and cyanosis. The blood pressure was 150/95 mm. Hg,the pulse 140, and respirations 28 per minute. Thetemperature was 102-40 F. One hour later the pulsewas 120 and respirations 28 per minute 'and of-bubbly character, the temperature being 102-40 F. Shewas speaking, however, and two hours after that couldanswer questions although she 'was complaining ofheadache. The next day lumbar puncture pressure was250 mm. of brownish c.s.f., there being no block. Twodays after operation the temperature was 1040 F., pulse168, and respiration rate 40 per minute ; she answeredquestions and both plantars were flexor. That eveningthe pulse rate rose rapidly to 176, her respiration became

* very bubbly, and she was cyanosed. Half an hour laterthe pulse rate was 200 and the' respirations 32 Per 'minute.

Two hours later the pulse rate was uncountable,respirations 32 per minute, and temperature 1030 F.She still continued to respond to questions. At 9 p.m.that evening, about fifty-two hours after operation, aright ventricular tap revealed a pressure of 300 mm. of.crystal-clear cerebrospinal fluid., The following morningat 2.55 a.m., the pulse rate having been uncountable forthe previous nine hours, the respirations becameirregular and finally failed at 4.25 a.m., two and a halfdays after operation.NECROPSY REPORT (Dr. J. G. Greenfield).-A silver

clip was present in the anterior inferior cerebellar arteryabout an inch from the basilar. The right lobe of thecerebellum was destroyed except for a thin layer of theinner part of the upper hemisphere and for a bit of thelower posterior part of the hemisphere including theuvula and tonsils. The fourth ventricle was openedand ballooned towards the lateral angle. There wasan extensive area of infarction involving the middlepeduncle and the lateral half of the pons; it extendedinwards to a point 3 mm. to the right of themedian raphe and 10 mm. to the right of the medianraphe ventrally in the mid-pons plane. At the lowerend of the pons this area extended into the uppermostmedulla as low as a plane 3 mm. above the olive. At thelower limit of the pons the infarction reached the middleline dorsally and extended forwards 3 mm. along themid-line and extended forwards laterally at an angle300 from the mid-line. It did not appear to extend morethan 2 or 3 mm. into the medulla. At the juncture ofthe pons and mid-brain there was hiemorrhage into themid-lateral zone in the right side but not extending ashigh as the lower limit of the red nucleus in the territoryof the right anterior inferior cerebellar artery. Therewas slight dilatation ofPthe third ventricle and moderatedilatation of the lateral ventricle.

Dr. J. G. Greenfield reported that post mortem theinfarcted area on the side of the pons showed on sectionas a partly haemorrhagic and a partly necrotic area. Inthe mid-brain it inuolved the outer part of the cruschiefly in a hemorrhagic manner with a zone of earlynecrosis between the heemorrhage and the fillet tract.There was also a small oval area of necrosis midwaybetween the fillet and the posterior longitudinal bundlewith a small himorrhage near its dorsal surface, andsmall hemorrhages were seen round the iter of Sylviuson the right side. At the junction of the pons andmid-brain the dorsal and external part of the crus wasinvolved in himorrhagic necrosis. The fillet here wasfree from degeneration except for some vacuolardegeneration at its outer part but there was a zone ofearly necrosis dorsal to its outer end, under the wallof which small hemorrhages were present. In themid-pons just above the exit of the fifth cranial nervethere was much more degeneration than hemorrhage.The degeneration involved most of the bundles of thecrus except those situated most antero-medially andthose lying under the emerging fifth nerve. Betweenthis and the fillet there was a fairly large area ofdegeneration near the surface with h2morrhages in afairly wide area under the floor of the upper end of thefourth ventricle on the right side. Just below the exit

146




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FIG. 2.-Case 3. Chart during operation of bloodpressure and pulse changes.

of the fifth nerve there was a zone of degenerationextending about a third of the distance in from thesurface of the median raphe with hlmorrhages into themiddle cerebellar peduncle and under the floor of thefourth ventricle. No hemorrhage or degeneration wasseen in the medulla on this side (Plate III).

COMMENT.-In this case the surgeon stated definitelythat following the final removal of the tumour the sideof the pons was perfectly clean with no bruising or

CEREBELLAR ARTERY 147

and passed from the lateral surface of the pons to the.infero-lateral surface of the cerebellum on the right side(anterior inferior cerebellar artery)." The right side ofthe pons was considerably bruised, and the middlecerebellar peduncle was very flattened by the tumour.On histological examination it was found that consider-able haemorrhagic infarction of the pons on the rightside merged with an area of pallor of myelin stainingwhich reached nearly to the mid-line at the mid-level ofthe pons, but nowhere involved the most ventral halfof this part (Plate IV).

Case 4.-The fourth case (A.E., aged 57 years) wasadmitted under the care of Dr. F. M. R. Walshe 'inOctober, 1946, with pain behind his left ear and 'slightdeafness on the left side which began four years pre-viously. A small acoustic neurofibroma of the size ofa pigeon's egg was removed. The operation notereports that an artery running over the surface of thetumour was clipped and divided. The operation tooktwo hours, and fifty minutes after the start of operationthe blood pressure rose to 150/80 mm. Hg and the pulserate fell to 72 per minute with' normal respirations forten minutes (Fig. 3). That evening the patient failed torecover full consciousness though he reacted to stimuli.No improvement occurred with ventricular and lumbarpunctures, which revealed slightly blood-stained fluid.The blood pressure remained normal but the pulse wasreported as full and bounding; respirations werenormal. Early the following morning, however, the

damage whatever. At necropsy, the infarct, which 160must have developed subsequent to operation, was inthe territory supplied by the anterior inferior cerebellar 150artery, and the occluded artery appeared to be thatwhich caused bleeding in the final stages of operation. SYSTOLIC 140

Case 3.-The third case (G.B., aged 47 years) was1 0

admitted under the care of Dr. E. A. Carmichael in 920February, 1946, because of deafness in her right earfor the previous three years. A piecemeal removal of 110a right acoustic 'neurofibroma was accomplished. loConsiderable arterial hlmorrhage was encountered inthe later stages and was eventually controlled with 90 ,'silver clips and fibrin foam. The whole operation took PULSE -4three hours. One hour and ten minutes after the start DIASTOLIC 80the blood pressure rose from the normal 120/90 to160/110 mm. Hg, with a fall of pulse rate from 120 to110 per minute (Fig. 2). This slowly returned to normal 60over the next half hour,' to remain so for a furthertwenty minutes. In the remaining hour it fell gradually S0to 110/85 mm. Hg with a pulse rate of 140. That 40 Aevening the patient was very shocked, but regained a Ostate in which she was able to respond by blinking to 3spoken words. Her state of consciousness did not alter RESPN. -._..-, .- -:from then to near the end. Blood pressure fell to 20 ' O z'80/60 and then was unrecordable. That night a blood Y X , ztransfusion restored the circulatory state temporarily. 10She died the following morning seventeen hours after _____if_*___*_*_*___*__operation. At necropsy, there was a small blood clotover the bed of the tumour on the right side of the pons. TIME PM. 2 10 20'30 4050 3 l0 20 3040 s0" A silver clip was found on a vessel 1" from the mid- FiG. 3.-Case 4. Blood pressure, pulse, and respirationline which was thrombosed back to the basilar artery chart during operation.G**




W. J. ATKINSON'

condition deteriorated, the temperature rose to 1020 F.the pulse was feeble-150 per minute; and therespirations stertorous, 30 per minute. He died twenty-three hours after operation.

NoCRopsy REPoRT.-The cavity from which thetumour had been removed was filled with half an ounceof blood clot. The anterior inferior cerebellar arterywas double on this side though single on the other. Theupper left artery had a free end in the region of theinternal auditory meatus. Section of the pons showedalmost complete destruction of the tegmentum, passinginwards as far as the mid-line against the ependymallining and extending backwards along a line runningfrom the central fovea of the ventricle to the outermostpart of the ventral surface (Plate Va, b).

Case 5.-The fifth case (A.B., aged 58 years) wasadmitted under the care of Sir Charles Symonds becauseshe had had parnsthesie over the left side of her facefor four years.

In October, 1947, an attempt was made to remove aleft acoustic neurofibroma the size of a walnut. Alarge artery crossing its posterior surface was double-clipped and divided, after which the capsule wascoagjilated and the contents evacuated with spoon andsuction. The lateral portion was removed by morcelle-ment until the uppermost nodule of growth passingthrough the tentorium was exposed. This was graspedwith rongeurs and was delivered downwards into thewound when a sudden spurt of air followed by cerebro-spinal fluid-at first clear and later blood-stained-wasnoticed through the indwelling lateral ventricularcannula. This spurt of fluid ceased two or three seconds

' after becoming blood-stained, the whole of this processlasting no more than ten seconds after the first changein the patient's condition was noticed. "Almostimmediately after this first change in condition wasnoticed the tension of the contents of the posteriorfosta became raised and the cerebellum started toherniate., The retractor had to' be removed, andimmediately further cerebellar herniation took placeand'in the space of a minute it was quite obvious thata severe haemorrhage had taken place in the supra-tentorial chamber ..." The patient's general conditionhad immediately deteriorated, and by the time the rapidclosure ofthe wound had been completed the respirationswere very slow and shallow, the pulse very thin and rapid,and the blood pressure unrecordable. Soon, however,her irregular respirations rose to 22 per minute withoccasional deep sighs. The pulse was 120 per minuteand the blood pressure rose to 100/60 mm. Hg. Sheremained deeply unconscious and did not respond tostimuli. The left pupil had a fair r6action to light butthe right had none. The right was slightly larger thanthe left. She remained' in this condition for a further'nine hours, during which time the blood pressure slowlyfell. The right lateral ventricle was tapped and clearcerebrospinal fluid under increased pressure was found.Following this, the blood pressure was said to haveimproved. However, her temperature rose and respira-tions became stertorous. She remained deeply un-

conscious with increasing, pulmonary signs, and diedtwenty. hours after operation.At post-mortem examination there was no excessive

bleeding anywhere and the anterior inferior cerebellarartery was found clipped and divided but not throm-bosed. A small nodule of tumour one,inch long andi inch wide lay in the cerebello-pontine angle adherentto the brain and internal auditory meatus. There washemorrhagic softening of the lower pons and uppermedulla on the left side. No blood clot was found inthe lateral ventricles, only blood-stained fluid.

Microscopically, sections of the' lower two-thirds ofthe pons showed swelling and punctate haemorrhagesin the lateral area' including'the tegmentum; this areashowed as a region of pallor of myelin staining and arelative increase of interstitial spaces (Plate Vc, d, e).

Case 6.-The sixth case (B.M., aged 56 years) wasadmitted under the care of Dr. D. Brinton in March,1948, because she had had attacks of vertigo for the pastyear. At operation an acoustic neurofibroma wascompletely removed from the left cerebello-pontineangle; during this procedure two arteries were exposed,clipped, and divided. At this stage, forty minutes afterthe first incision, the blood pressure rose sharply to120/78 mm. Hg, having been falling slowly from 110/72to 94/60-1, the pulse rate falling to 78. Twenty minuteslater the blood pressure was 98/70 mm. Hg and at theend of the operation thirty minutes later it was 95/65.Four hours later -she was conscious and rational butrestless and picking at the bedclothes: five hours afteroperation the blood pressure rose to 150/100 mm. Hgand remained at about this level for five hours. Hertemperature was 1020 F. Later that day she becameconfused and drowsy. Three days later she was still

130

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448




ANTERIOR INFERIOR CEREBELLAR ARTERY -

stuporose; operation wound was re-opened but nohaemorrhage was found. She died on the following day(Fig. 4).At post-mortem examination the left side of the pons

in the region of the middle cerebellar peduncle was foundto be swollen with a rather local protrusion, which wassoft on section. A silver clip lay on the left anteriorinferior cerebellar artery and a clot was attached to thevessel just short of the clip. On section of the lowertwo-thirds of the pons a hemorrhagic infarct in thedistribution of the anterior inferior cerebellar arterywas seen (Plate VI).

Case 7.-The seventh case (J.W., aged 62 years) wasadmitted under the care of Sir Charles Symonds inFebruary, 1948, because she had had attacks of vertigoand ataxia for seven months previously. A left acousticneurofibroma was completely removed. Blood pressure

130

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remained normal throughout opqeation and for sevenhours later. It then rose to 160/100 mm. Hg andremained at this level for at least twelve hours. On thefollowing day her condition was fairly good althoughshe was incontinent of urine and feces (Fig. 5). Onthe second postoperative day the left cornea wasobserved to be ulcerated. On the third day she wasdrowsy and slightly-confused, having increased tone inall four limbs. She also had a hoarse, irritating cough.On the sixth day she was drowsy but rousable. Byevening, however, she was reported to be unconscious.The next day, seven days after operation, she died.NECROPSY REPORT.-The right side of the pons was

bruised and the right anterior inferior cerebellar arterywas thrombosed where it ran outward to the internalauditory meatus. There was slight hydrocephalus.There was an area of pallor of myelin staining in theregioft.of the junction between the lateral part of the

pons and the middle cerebellar peduncle, and the lateraltegmental area was affected. Throughout this areathere were microscopically punctate or ring himorrhagesand an apparent increase *of interstitial spaces (PlateVlla, b, c).CoMwNT.-This is the only case without operative

occlusion of the vessel ; thrombosis obviously tookplace later. This time the operation chart did notreveaI any autonomic change although in the subsequenttwenty-four hours the pulse pressure did alter in amanner similar to that seen in the other cases.

Discussion of CasesThe above series of seven cases consists of one

from Chase Farm Hospital and six from therecords of the National Hospital, London. Thesesix occurred between 1938 and 1948 and all diedfollowing the complete or nearly complete removalof acoustic nerve tumours. During the same periodthere were eight other deaths from acoustic nervetumours at the National Hospital. In one caseno operation was performed, two underwent suboc-cipital decompression only, and five had both partialremovals and suboccipital decompression. Noneof these cases had pontine infarction as describedabove.The operation and postoperative records are

given in the cases described because it appears thatclipping or injuring the artery may be associatedwith autonomic disturbances. The blood pressurerose at or near the time when the artery was oc-cluded,- but soon subsided and in most cases theimmediate postoperative state seemed fairly satis-factory. However, the pressures in the lumbartheca and lateral ventricles, when taken, remainedhigh; consciousness was disturbed and there weremany signs of generalized increase of intracranialpressure. The final deterioration resembled veryclosely that seen in patients dying of supratentorialtumours.

Correlation of DataIt will be seen that the area of infarction of the

pons id' these seven cases coincides almost exactlywith that area which accepts the dye when it isinjected into the anterior inferior cerebellar artery.The area we consider to be of primary importance,as far as the patient's life is concerned, is thetegmental area. This point will be elaboratedlater.The lateral branch of the artery which winds

around the flocculus sends back branches to thisarea which would therefore be involved if the clipwere placed on the artery as it crossed the eighthnerve. Further, the possibility ofretrograde throm-bosis provides an explanation for an ischiemia ofthe tegmental area, even if the latter were supplied

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10W. J. ATKINSON'

by the main stem of the anterior cerebellar artery.There appears to be little or no intrapontine anasto-Moses between arteries penetrating the pons or themiddle cerebellar peduncle. The anastomotic sup-ply via the posterior inferior cerebellar artery maybe lost if this artery is relatively small-on one side.The previously stated findings that anastomoses donot permit ready overflow from one arterial-distribu-tion to another and that spasm tends to occurin the branches of the injured artery, are alsofactors which may impair the recovery of circulationafter occlusion of the vessel.The study of autonomic disturbances from

brain-stem injury has interested many physiologistsand clinicians, and it is the effects of such injurywhich still prevents success in the treatment ofconditions raising intracranial pressure.

It is interesting here to note that Le Beau and'Bonvallet (1938) obtained a state of cerebral,welling in the supratentorial cerebral tissues,associated with a rise in blood pressure, followingsections of the brain stem from the medullaoblongata up to the thalamus. They submit thatthe rate at which " cerebral cedema " took placewas related to the rise in blood pressure. A recentpublication by Le Beau (1948) deals with this subjectfurther. Kabat and others (1935) have shown thatlesions in the region of the central tegmental tract,whether in upper pons or mid-brain, give rise toalterations in blood pressure in animals. A lateraltegmental lesion in the middle third of the pons inthe cat also produces a similar rise of blood pressure(personal observation); this area coincides withthat of the blood supply from the anterior inferiorcerebellar artery. A further contribution on thissubject is being prepared.There are many implications arising from this

Work, and it is suggested that the r-ise in bloodpressure which takes place during the course of theoperation on an acoustic tumour at about the timewhen the anterior inferior cerebellar artery isoccluded is caused by an ischemia of the lateraltegmental area in the region of the pons suppliedby that artery. What precisely happens to thecerebral and pulmonary circulations when thelateral tegmental areas are injured is at present amatter for further detailed investigation. The auto-nomic pathways in mid-brain and pons conveyimpulses for vasomotor and respiratory regulation,disturbance of which somehow sets up an irre-versible process whereby the brain swells and thelungs become cedematous.Some findings which surgeons have reported are

relevant here. First, as the surgeon approaches thepons, usually during the latter part of the removalof the tumour, the blood pressure is often noted as

rising temporarily to 160/100 mm. Hg with a fallin pulse rate. This is sometimes ascribed to theremoval of that last part of the tumour in thetentorial hiatus. I submit that it may be due to aspasm of the anterior inferior or superior cerebellararteries impairing the blood supply to the lateraltegmental areas. This vasomotor change does notusually persist, and Beattie and others (1938) showedexperimentally that after permanent unilaterallesions in the pons, mid-brain, or lateral hypotha-lamic area, the blood pressure tends to come downagain to normal after an interval.

Secondly, the cerebellum is seen to bulge suddenlydown into, the wound and the intraventricularpressure to rise acutely as shown by the indwellingcannula in the lateral ventricle. Such an event isoften attributed to the anesthetic; but anotherexplanation may well be that the blood pressure,and the supra-tentorial pressure, rises as thelateral tegmental area is deprived of blood supplyby the occlusion of the anterior cerebellar artery.Thus acute cerebral compression results, and thevicious circle of supra-tentorial compression occurs.

Thirdly, in two other cases following this type ofoperation complete anesthesia of the ipsilateral sideof the face and dissociated sensory loss of theopposite side of the body have been observed.This is probably due to infarction affecting thelateral pontine area in the region of the enteringfifth nerve and its principal sensory nuclei and thespino-thalamic tract.

In conclusion, the chief implication of this workis that there is a grave danger to the patient if theanterior inferior cerebellar artery is occluded duringthe operation on an acoustic tumour. This dangeris in damage to the autonomic pathways frominfarction of the tegmentum of the pons. Itmust be conceded that there are many cases ofrecovery in which the anterior inferior cerebellarartery has been intentionally occluded atoperation. Howevr, if at operation the pos-terior inferior cerebellar artery were found to beunusually small it would be reasonable to infer thatthe anterior inferior cerebellar artery is large andthat there is likely to be only a poor collateralcirculation via the posterior vessel: in which caseits operative occlusion might be dangerous.

Summary1. The course, distribution, and anastomotic

relations of the anterior inferior cerebellar arteryare described.

2. Seven cases of acoustic neuroma are describedin which an infarction of the lateral tegmentalregion of the pons, in the area correspondihg to

I.





the distribution of this artery, was found atnecropsy, sobn after operation. In all these casesthere was occlusion of the vessel in the neighbour-hood of the internal auditory meatus, either due toa clip placed on the vessel at operation or to post-operative thrombosis of the artery.

3. These cases suggest that occliusion of theanterior inferior cerebellar artery is an importantcause of death after operation. especially when thisartery is larger than usual. The recognition 'of anunusually small posterior inferior cerebellar arterymay warn the surgeon that the anterior inferiorartery is dangerously large.

4. An attempt is made to correlate certainclinical observations made on these cases, especiallythe rise of blood pressure following interferencewith the anterior inferior cerebellar artery, with the

results of experimental lesions in the lateral teg-mental region of the pons.

My grateful thanks are due to Dr. J. G: Greenfieldfor his encouragement, advice, and stimulation in thepreparation of this article. I also wish to convey mythanks to the members of the staff of the NationalHospital, and to Mr. D. W. C. Northfield of theLondon Hospital for their kind permiission to use theircases.

REFERENCESBeattie, J., Brow, G. R., and Long, C. N. H. (1938). In

Clark, W. E. LeG: "The Hypothalamus." Oliverand Boyd, Edinburgh. p. 81.

Bolton, B. (1939). J. Neurol. Psychiat., n.s., 2, 137.Kabat, H., Magoun, H. W., and Ranson, S. W. (1935).

Arch. Neurol. Psychiat. Chicago, 34, 931.Le Beau, J. (1948). Rev. canad. Biol., 7, 254.--, and Bonvallet, M. (1938). C. R. Soc. Biol. Paris,

127, 126.-- -.-(1938). Ibid., 129, 833.Wallenburg, A. (1901). Dtsch. Z. Nervenheilk., 19, 227.

151




ANGLE TUMOURSCEREBELLO-PONTINESURGERY OF SIGNIFICANCE IN THEDISTRIBUTION, AND VARIATIONS, PONTINECEREBELLAR ARTERY: ITS THE ANTERIOR INFERIOR

W. J. Atkinson

doi: 10.1136/jnnp.12.2.137137-151

1949 12:J Neurol Neurosurg Psychiatry

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