StrokeA Journal of Cerebral Circulation

SEPTEMBER-OCTOBER 1975

VOL. 6 NO. 5

The Contribution of Computerized AxialTomography to the Diagnosis of Cerebellarand Pontine Hematomas•Y H. R. MOLL!*, M.D.,* R. WOTHRICH, M.D.,f U. WIGOU, M.D.,|

R. H O N I O , M.D.4 AND M. O K I , M.D.J

Ab* tractiThe Contributionof ComputerizedAxial Tomographyto theDiagnosis ofCerebellarand PontineHematomas

• Case histories are reported of seven patients in whom the diagnosis of cerebellar (four) orpontine hemorrhage (three) was made by computerized axial tomography (CT). In all of thepatients except two the diagnosis, established on the basis of a space-occupying high absorptionlesion, was proved by either operation or autopsy. In the two remaining cases, the evolution onCT was typical for an intracerebral hematoma, i.e., the high absorption zone was transformedinto an area of reduced density. It is concluded that CT is a highly reliable method for thediagnosis and location of posterior fossa hematomas. A CT syndrome, observed in four of theseven cases, is described consisting of a hydrocephalus with the tips of the posterior horns beingfilled with blood. This seems to be specific for a posterior fossa hematoma having penetratedinto the fourth ventricle.

Additional K«y Wordsintraventricular hematoma

posterior fossa hematoma intracerebral hematomaobstructive hydrocephalus

• During the last two years computerized axial x-raytomography (CT)1 has been widely established as aroutine neuroradiological procedure. From the ex-perience collected since that time there is now generalagreement on the extremely high diagnostic value ofthis method.

Among the conditions whose detection profitedmost by the use of CT undoubtedly is the intracerebralhematoma. This is regularly shown on CT as a zone ofgreatly increased x-ray absorption compared with thesurrounding brain tissue, and thus can be clearlydifferentiated from a brain infarct, showing reducedabsorption.25

In an earlier paper8 we reported our experiencewith this type of CT diagnosis. It was found that thedetection of 24 intracerebral hematomas was provedto be correct by operation or autopsy in 18 cases,while the clinical course left hardly any doubt of thelesion's hemorrhagic nature in the remaining six. Noknown false-negative hematoma diagnosis was madeup to that time among the nearly 900 scans done, andnone has been made since, even though our case ex-

•Department of Neurosurgery, tDepartnient of Neurology,t Department of Radiology, University of Basel, Basel, Switzerland.

perience has almost doubled. Similarly, Scott et al.,4

who reported CT findings on 22 intracerebral or in-traventricular hematomas, did not have any false-positive or false-negative "hematoma" findingsamong the 600 investigations carried out. An equallyhigh relevance of the method was reported by Paxtonand Ambrose,' who detected 66 intracerebralhemorrhages among their first 650 patients examinedwith CT.

It would appear that maximum profit is availablefrom CT for hematomas located in the posterior fossa,when one takes into consideration the difficulty ofclinically differentiating intrapontine from cerebellarhematomas and infarcts as well as the particularproblems of these lesions arising with traditionalneuroradiological methods. Further, CT is anatraumatic technique which can be repeatedly appliedto study the radiological evolution. We thus can ex-pect to learn much on the natural history of posteriorfossa hematomas and of the secondary effects of these.

The present paper reports the data available onseven patients in whom the CT diagnosis of either acerebellar or a pontine hematoma was made, andwhose case histories and CT findings shall be dis-cussed.

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MOLLER, WOTHRICH, WIGGLI, HONIG, ELKE

MethodsAmong the first 1,500 CT investigations done at the Kan-tonsspital, Basel, 44 were intracerebral hematomas. Ofthese, four were cerebellar and three intrapontine, represent-ing the case series reported in this paper.

In all of the patients CT was carried out with the EMI-scanner, using the original program, which includes a dis-play on an 80 X 80 matrix. Most of the tomograms madewere 13 mm standard sections, whose anatomy and labelingwidely correspond to the key drawing represented in figure1.' Some of the investigations were done with thetomograms oriented about 25° steeper than demonstratedon this figure, and had a height of only 8 mm. These arelabeled with 31 A, 3IB, etc., on the figures of this paper.

Case ReportsCEREBELLAR HEMATOMAS

Cate 1 (CT 63)

A 75-year-old man, without known history of hypertension,had complained of dizziness for three months and ap-parently showed some gait ataxia during this period. On themorning of the day of admission he became somnolent, andlater complained of headache and vertigo. The patient

vomited repeatedly and the somnolence progressed to stuporand coma.

On admission at midnight he was in deep coma andshowed bilateral miosis without light reaction, and a con-jugate deviation of the eyes to the right. Tendon reflexeswere not elicitable, and there was a bilateral Babinski sign.Some minor flexion of the limbs was provoked by painfulstimuli, less definite on the left side where the muscle tonusappeared to be reduced. Blood pressure was 185/105 mmHg. There was a sinus tachycardia of 124 per minute and atachypnea of 44 per minute.

The differential diagnosis of a posterior fossa hema-toma was obvious, but because of the grave condition andthe advanced age no further diagnostic procedures were un-dertaken on admission.

A CT investigation was carried out the next morningwhen the patient's condition had been stabilized under astandard prednisone and mannitol antiedematous treatment.The pictures (figs. 2a and b) showed a large hematomawithin the left cerebellar hemisphere which had penetratedinto the fourth ventricle. There was a very large hydro-cephalus. While the greatly dilated third ventricle did notdefinitely show any blood content, there were contrastsshowing blood absorption values in both occipital horns.

468

FIGURI I

Key drawings representing anatomical landmarks for a standard set of 13-mm EMI scans (from Muller et al.').

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few hours later, dysarthria and somnolence were noticed,and shortly afterward, the patient was found to bestuporous. During transport to the hospital respiratoryarrest occurred.

On admission, while on artificial respiration, the patientwas in deep coma showing fixed dilated pupils and totalareflexia.

On CT (figs. 3a and b) the posterior fossa sections weregrossly disturbed by artifacts due to artificial respiration;however, a huge hydrocephalus with the third ventricle andthe tips of both occipital horns containing blood could beseen. The diagnosis of a posterior fossa hematoma, havingperforated into the fourth ventricle, was made from thisevidence.

After the registration of two isoelectric EEGs spaced by24 hours, artificial respiration was stopped. On autopsy ahematoma the size of a chestnut was found within the rightcerebellar hemisphere, which penetrated into the fourth ven-tricle. Massive brain edema was further demonstrated.

Cos* 4 (CT 1031)A 63-year-old man, maintained on anticoagulative treat-ment for a recent coronary thrombosis, had experiencedduring the preceding fortnight several attacks of vertigo.These were interpreted as basilar TIAs. A slight left

hemiparesis was noticed since that time by his daughter. Oneday before admission the patient had a sudden frontalheadache, vertigo and nausea. About 12 hours laterprogressive somnolence and left sixth nerve palsy werenoticed. A lumbar puncture carried out at the local hospitalshowed blood-stained CSF.

On admission a few hours later, the patient was in deepcoma. There was a bilateral miosis but light reaction waspreserved. The bulbi were in divergent positions. Except fora central left seventh nerve palsy there were no furtherpathological findings at the level of the cranial nerves. Therewas some flexion response from all four limbs on painfulstimuli, and a bilateral Babinski sign. Blood pressure, heartrate and respiration were normal; the Quick prothrombinvalue was 20%.

CT, performed immediately after admission (figs. 3cand d), showed a large midline posterior fossa hematomalocated within the vermis including the fourth ventricle andpossibly parts of the tegmentum pontis. Hydrocephalus to aconsiderable degree and some blood in both occipital hornswere evident. Vertebral angiography showed separation andflattening of the loops of the posterior inferior cerebellararteries indicating a space-occupying lesion in the inferiorparts of the vermis.

The patient was operated on by formal craniotomy and

novtis(a and b) Occlusive hydrocephalus containing blood within occipital horns in a cerebellar right hemispherehematoma, Case 3; (c and dj hematoma in the vermis. Case 4; (e and f) pontine hematoma. Case 5. Foranatomy see figure 1.

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a large intracerebellar hematoma located in the vertnis wasevacuated. This extended to the fourth ventricle, penetratinginto its floor.

After a period of hyperthermia with persistent coma,the clinical condition improved astonishingly well. Dailylumbar punctures were practiced. Referred to his localhospital, the patient gained consciousness and respon-siveness and could be fed orally. Three weeks after opera-tion, however, he relapsed into coma, showed extremehyperthermia and died. No autopsy was done.

PONTINE HEMATOMASCaie5(CT1286)A 59-year-old woman, without known history of hyper-tension, fell to the ground for unknown reasons, withouthurting her head. Four hours later she complained of nauseaand vertigo, and therefore was brought to a local hospital.On lumbar puncture the CSF was found to be bloody.

On admission two hours later, the patient was insuperficial coma. Blood pressure was 250/160 mm Hg.There were bilateral pinpoint pupils without reaction tolight, and a peripheral left seventh nerve palsy. The left cor-neal reflex was absent. On painful stimuli the patient showedsemi-intentional movements with her left arm and left leg,while on the right side only minor flexion reactions wereelicitable. The midline echo was not displaced. Thepresumptive clinical diagnosis of a pontine hemorrhage wasmade.

CT (figs. 3e and 0 confirmed this diagnosis by showinga pontine intracerebral hematoma more concentrated to theleft side but including the basis and tegmentum pontisbilaterally. While the upper part of the fourth ventricle,which was slightly displaced to the right side, appeared to befree of blood, there was a blood cast within the third ventri-cle. Some blood also was seen in both occipital horns. Thelateral ventricles were only moderately dilated.

The patient, who was treated conservatively, rapidlydeteriorated and died two days later. Autopsy confirmed thediagnosis of a pontine hematoma measuring 3 X 2 cm indiameter, extending to the substantia nigra on the left sideand having penetrated to the fourth ventricle.

Case6(CT 1301/1335/1451)A 58-year-old hypertensive man, anticoagulated since atransitory hemiparesis left two years ago, complained of asudden severe right temporal headache with accompanyingprofuse perspiration some ten hours before admission. Dur-ing the following two hours a progressive left hemiparesiswas noticed. On neurological examination at a localhospital, a left hemiplegia with extensor plantar responsewas noticed. The patient was found to be awake andcollaborative. There was anisocoria (the left pupil beingsomewhat wider than the right) and both pupils reactedpromptly to light. There was no definite neck stiffness, butlumbar puncture showed the CSF to be bloody. An in-tracerebral hematoma was suspected and the patient, whobecame comatose during the following eight hours, wasreferred for further studies.

A right carotid angiogram showed a slight hydro-cephalus. On the vertebral angiogram the cranial loop of theright posterior inferior cerebellar artery was flattened point-ing to a space-occupying lesion located in the paramedianregion of the posterior fossa.

On neurological examination, 20 hours after the first

symptoms, the patient appeared to be in deep coma. Therewas a bilateral miosis with preserved light reaction, but bothcorneal reflexes were absent. All tendon reflexes were greatlydiminished, and there was a bilateral extensor plantarresponse. On painful stimuli, the patient showed extensorspasms bilaterally, more marked on the left. The clinicaldifferential diagnosis of a pontine hemorrhage or ahemorrhagic pontine infarct was made and conservativetreatment was given.

On neurological examination 24 hours later, the leftcorneal reflex was elicitable again, and there was evidence ofa peripheral right seventh nerve palsy. Even though thepatient continued to show signs of decerebration on the leftside, he now flexed his right arm and leg on painful stimuli.The lesion thus could be clinically located at the right side ofthe pons, including the basis as well as the tegmentum pon-tis.

A CT, carried out at this stage of the clinical evolution(figs. 4a and b), confirmed this diagnosis and showed noevidence of penetration of the hematoma into the fourth ven-tricle. An EEG recorded two days later was dominated un-expectedly by a 9 cycles per second alpha rhythm blockingon passive eye opening. From this it was concluded that, inspite of the clinical impression of a coma, consciousness waspreserved. In fact, when observing the patient on visits by hisrelatives, an emotional reaction seemed to be present, asconcluded from an increase of respiration rate.

While the clinical condition as well as the EEG did notshow any substantial changes during the first two weeks, aCT examination 11 days after the event (figs. 4c and d)revealed a definite increase in ventricular size. However, ona further control made 37 days after the bleeding (figs. 4eand f)> the size of the lateral ventricles had again returned tothat measured on the first examination. The lesion in thepons, whose high density had already decreased on the sec-ond scan, was now replaced by a zone of reduced absorptionshowing partly "CSF" values.

The patient who returned to his local hospital forfurther care was seen by us again on the occasion of the thirdCT, 37 days after the event. He had been clinically awakefor two weeks, but there was a marked hypokinesia. Thepatient sporadically answered questions and was able tocooperate to some extent. There was a right trigeminal andfacial palsy, a right internuclear nystagmus and a limitationof upward and medial gaze of the left eye. Pupils wereisocoric and of normal size, and light reaction was present.The left side, excluding the face, was plegic and hypotonic,and sensitivity appeared to be grossly disturbed.*

Cat«7(CT 1429/1474/1309)A 39-year-old man, known as being hypertensive for tenyears, experienced a sudden frontal headache, and a fewminutes later lost consciousness.

On admission two hours later, he was in coma, showinga pinpoint left pupil and a right mydriasis, no light reactionbeing present on either side. Corneal reflexes were notelicitable. On painful stimuli the patient showed extensorspasms of all four limbs. There was a marked hyperreflexiaof all tendon reflexes and a bilateral extensor plantarresponse. Blood pressure was 160/100 mm Hg and the heartrate was 72 per minute. On echoencephalography the third

'These findings were unchanged on a further control two monthslater.

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The hematoma was evacuated by formal craniotomy,after a ventricular drainage had been established. Thepatient's condition improved dramatically immediately aftersurgery. He opened his eyes on acoustical stimuli and movedall four limbs. The pupils were less miotic and showed somereaction on light. There were no further changes of theclinical picture, but three days later the patient diedsuddenly.

Autopsy showed a fresh intracerebellar hematoma atthe site of the operation, and a marked generalized brainedema.

Cot* 2 (CT 269, 636)An 87-year-old woman suddenly experienced vertigo,nausea and weakness in both legs. During the followinghours she repeatedly vomited.

On admission she was disoriented in space and time.There were no pathological findings on the level of thecranial nerves but the patient showed a coarse tremor inboth arms and a marked paraparesis. The right patellarreflex and both achilles reflexes were diminished and theplantar reflexes were indifferent. Blood pressure was 190/90mm Hg, and the heart rate was 92 per minute.

The presumptive diagnosis of a brain stem infarct wasmade and the patient was treated conservatively.

During the following ten days the paraparesis definitelyimproved, the vertigo disappeared, and the patient, after aperiod of marked somnolence, became fully alert andoriented again.

On CT, ten days after admission (figi. 2c and d), aspace-occupying lesion of increased absorption, measuringabout 2 cm in diameter, was found within the rightccrebellar hemisphere rather posteriorly and near themidline, the fourth ventricle being displaced to the left. Thehigh density zone was surrounded by an area of reduced ab-sorption. Both the third and the lateral ventricles weremoderately dilated, but there was no evidence of blood con-tent. The findings were interpreted as a right intracerebellarhematoma, and this diagnosis was confirmed by a CT con-trol (figs. 2e and f) three months later, after full clinicalrecovery. At the site of the former high density lesion, therewas now an area of reduced absorption, containing CSFvalues. There was no change of ventricular size, and as onthe previous scan, there was evidence of some corticalatrophy.

Cos* 3 ( a 228)A 70-year-old normotensive man, under anticoagulativetreatment since a coronary thrombosis one year ago,suddenly had vertigo, nausea and abnormal perspiration. A

riouui(a and b) Cerebellar left hemisphere hematoma. Case 1; (c and d) cerebellar right hemisphere hematoma,Case 2; (e andf) Case 2, control scan three months later showing abnormally low absorption in the region ofthe hematoma. For anatomy see figure I.

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FKH0U4

Right pontine hematoma, Case 6. (a and b) On admission, (c and d) control 11 days later (notice increase ofhydrocephalus), (e and f) 37 days later (notice regression of hydrocephalus and low absorption area in theregion of the hematoma). For anatomy see figure I.

ventricle was found to be widely dilated. A right carotidangiogram confirmed the presence of a markedhydrocephalus. On vertebral angiography the basilar arterywas found to be pressed against the clivus. There was abackward displacement of the precentral vein and a lateraldisplacement of the right posterior mesencephalic vein. Theright inferior vermis and vein were not filled nor were thevessels within the right side of the pons and the medulla dur-ing the parenchymatous phase. The diagnosis made at thattime was a right pontine hematoma.

With regard to the advanced occlusive hydrocephalus,ventricular drainage was established from the right frontalhorn. This did not change the clinical state. On CT, however(figs. 5a and b), which was carried out ten hours afteroperation, the formerly dilated lateral ventricles were nowextremely slim. The lesion itself was confirmed by this in-vestigation to be a large intrapontine hematoma, more con-centrated to the right side. There it appeared to include thepeduncle and to have ruptured into the cerebellopontineangle and possibly to the cerebellar hemisphere. The fourthventricle could not be identified on the pictures. However,the fact that there was no blood content in the third andlateral ventricles did not suggest the presence of ventricularpenetration.

No clinical improvement was noticed on further obser-vation. Respiration was assisted during the following ten

days and the patient received antihypertensive treatment(catapresan, dihydralazine) as well as an antiedematousregimen (prednisone, mannitol).

CT controls, seven and 12 days after the bleeding (figs.5c, d, e and 0. showed a progressive reduction in size of thehigh absorption lesion, but even on the second of these con-trols there were absorption values up to 30.

A few hours after the second control scan, the patient,having been hyperthermic for two days, died fromrespiratory arrest. On autopsy a large pontine hematoma(partly coagulated, partly liquefied) was demonstrated. Thishad destroyed the tegmentum on both sides, and only smallstrips of the brain tissue within the basis pontis werepreserved. The hematoma had penetrated into the rightcerebellar hemisphere and into the fourth ventricle, while onthe left side it extended up to the thalamus.

DiscussionIt is a general experience that the clinical differentialdiagnosis of infratentorial brain hemorrhage is par-ticularly difficult.7"11 Localizing signs, expected to givethe diagnostic clue, are all too often overshadowed bycoma or decerebration as a result of occlusivehydrocephalus and tentorial herniation. Even in thosecases in which the onset is gradual rather than sudden,

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Pontine hematoma, Case 7. (a and b) On admission, after ventricular drainage, fc and d) seven days later, feand fj 12 days later (notice diminished size of high absorption area). For anatomy see figure I.

only occasionally can an accurate localization of theprocess be made.

When it comes to differentiating between brainstem infarct and posterior fossa hematoma, thisproblem too cannot be reliably solved on purelyclinical grounds. The rule, e.g., that pinpoint pupilsspeak in favor of a pontine hematoma rather than aninfarct, is frequently misleading, and so is the absenceor presence of cerebellar signs. Lumbar puncture,apart from being dangerous in both conditions, is notan appropriate test to exclude a hematoma, since theCSF need not be bloody in this condition.10'w

An important contribution to the diagnosis ofcerebellar and pontine hematomas is made byechoencephalography.18 The detection of a dilatedthird ventricle in a patient not suspected of havingbrain atrophy definitely speaks in favor of a space-occupying lesion within the posterior fossa. Thismethod, however, is not able to differentiate betweencerebellar and pontine hematomas, nor to rule out anyother infratentorial mass. As such, even a brain steminfarct can act through its local edema.

It was, therefore, the traditional neuroradi-ological methods with which the final diagnosis had to

be established. Vertebral angiography not only allowsthe location of many of the larger infratentorialhematomas, by demonstrating them as space-occupying avascular lesions, it also makes evidentvascular malformations and aneurysms as possiblesources of bleeding. Furthermore, this method allowsdetection of both downward and upward cerebellarherniation. An accurate evaluation of the size of thelateral ventricles can be made with carotidangiography. None of the angiographical methods,however, allows us to detect intraventricular blood. Aventricular dilatation, as demonstrated angiograph-ically, thus can be due to compression as well as toclotting out of the fourth ventricle and aqueduct.

From the case series reported, it would appearthat most of the problems with which we were leftusing classical neuroradiological techniques are solvedby CT. Not only was this method able to demonstrate,and locate with a fair accuracy, clinically relevantcerebellar and intrapontine hematomas, it also fur-nished important information on the secondary effectof the space-occupying lesion on CSF circulation byimaging the ventricular system and its contents.

The CT observation of three (6.8%) pontine and

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four (9.1%) cerebellar hematomas among a total of 44cerebral hemorrhages investigated may reflect thefrequency of occurrence of these hematoma locations.This was found in autopsy material to range between6%9> u and 16%u of the intracerebral hemorrhages forthe pontine and between ~ 10%'- ••ia and 14%17 for thecerebellar hematomas.

The lesions demonstrated in our series all haddiameters of more than 1 cm. This raises the questionof the minimum size of a hematoma recognizable onCT. It is obvious that this is limited not only by thesize of the tissue unit measured (3 X 3 X 13 mm in astandard EMI scan), but also by the differencebetween the absorption values of the lesion, and thoseof the surrounding structures which will be averagedwith the border zones of the process. The high absorp-tion of fresh hematomas, however, will hardly beaveraged to normal tissue values, even if a very smallhemorrhage partly occupies a cluster of four scanningunits. It is thus theoretically possible to demonstrate,in an ideal scan, hematomas having a diameter of lessthan half a centimeter. However, the artifacts fre-quently observed in the posterior fossa with its thickbone structures present further limitations.

As to the precise location of an intracerebralhemorrhage, this is limited too by the resolution of thesystem. Hematomas generally are demonstrated a fewmillimeters too large, due to averaging in the borderzones. Furthermore, with posterior fossa hematomasit may be difficult to make definite statements as to theextension of a pontine hemorrhage to the basis andtegmentum pontis, respectively, for reasons of thethickness of tissue slice scanned and its oblique orien-tation to the brain stem (demonstrated in figure 1).

Taking into consideration these limitations, thelocalizing information offered by the method in ourcases was quite astonishing. This becomes obvious notonly when considering the poor clinicoradiologicalcorrelation in our patients having cerebellar hema-tomas, but also by concentrating upon some of thefeatures presented by Case 6, a patient with a unilat-eral pontine hematoma. While the clinical syndromeobserved on admission did not show any lateralizingsign, the limitation of the hemorrhage to the right sideof the pons was clearly demonstrated by the scan, andalso proved by the clinical evolution. From this obser-vation it becomes evident that much of the initialclinical picture may be due to edema and mass dis-placement and not to the lesion itself.

A hydrocephalus was demonstrated in all of thecases reported, except in Case 7, in which ventriculardrainage had been established before scanning. Fourof the patients, whose CT demonstrated an advancedhydrocephalus, also showed some blood in both oc-cipital horns. The blood was thought to have reachedthis site by pressures opposing the intraventricularpressure through the aqueduct and third ventricle. Itssmall amount can be easily explained. The increasingcounterpressure of the CSF on progressive blocking of

the aqueduct and fourth ventricle prevents furtherblood to reach the foramina of Monro. Moreover,some unclotted blood may even be pushed back fromthis third ventricle, which appeared to contain clearCSF in two of our cases showing blood in the occipitalhorns.

The hydrodynamic situation described is clearlydifferent from that observed in supratentorial in-tracerebral hematomas perforating into the ven-tricular system. In these conditions the canal throughwhich the blood reaches the ventricles is considerablywider than the aqueduct, and also CSF (and unclottedblood) can freely escape through the aqueduct. Thisresults in a much larger amount of intraventricularblood than can be seen in the patients havinghematomas which penetrate into the fourth ventricle.In fact, none of the 24 patients we observed to havesupratentorial hematomas (which penetrated into theventricular system) showed the syndrome of asymmetrical hydrocephalus and minor quantities ofblood in both occipital horns. This syndrome then canbe expected, from our experience, to be specific for aventricular hematoma perforation being located in-fratentorially.

Further improvement in the diagnostic informa-tion furnished by CT can be expected from the highdefinition system now being introduced by the makerof the device. From our early experience with thismodification, a better demonstration of both cerebel-lar hemispheres and brain stem is possible. Also, thenew EMI system is less prone to artifacts. Thus, it isto be anticipated that by using CT in the clinicalroutine, much important diagnostic information willbe added to our present knowledge on posterior fossahematomas. This will certainly not only widen ourscope of neurology and pathophysiology of these con-ditions, but, in addition, by allowing a clinicopath-ological correlation in vivo, it will make possible theseparation of neurological phenomena caused by thelesion itself and by its secondary effects. By doing so,the method may substantially improve the clinicalmanagement of pontine and cerebellar hematomas.

AcknowledgmentThe authors wish to thank Professor A. Levy, Drs. B. Zdrojewskiand D. Stula for providing the operative findings and Professor J.Ulrich for the autopsy findings included in this paper.

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H. R. MÜLLER, R. WÜTHRICH, U. WIGGLI, R. HÜNIG and M. ELKEPontine Hematomas

The Contribution of Computerized Axial Tomography to the Diagnosis of Cerebellar and

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