84 STROKE VOL 11, No 1, JANUARY-FEBRUARY 1980

11. Kennedy C, Sakurada O, Shinohara M et al: Local cerebralglucose utilization in the normal conscious Macaque monkey.Ann Neurol 4: 293-301, 1978

12. Welsh FA, Ginsberg MD, Rieder W et al: Diffuse cerebralischemia in the cat: II. Regional metabolites during severeischemia and recirculation. Ann Neurol 3: 493-501, 1978

13. Blair RDG, Waltz AG: Regional cerebral blood flow duringacute ischemia. Neurology (Minneap) 20: 802-808, 1970

14. Yamaguchi T, Waltz AG, Okazaki H: Hyperemia and ischemia

in experimental cerebral infarction: Correlation of his-topathology and regional blood flow. Neurology (Minneap) 21:565-578, 1971

15. Ginsberg MD, Reivich M, Frinak S et al: Pyridine nucleotideredox state and blood flow of the cerebral cortex following mid-dle cerebral artery occlusion in the cat. Stroke 7:125-131, 1976

16. Lowry OH, Passonneau JV, Hasselberger FX, Schulz DW:Effects of ischemia on known substrates and cofactors of theglycolytic pathway in brain. J Biol Chem 239: 18-30, 1964

Primary Pontine Hemorrhage:Clinicopathological Correlations

NOBORU GOTO, M.D., MITSUO KANEKO, M.D.,

YASUAKI HOSAKA, M.D., AND HIROAKI KOGA, M.D.

S U M M A R Y In 18 autopsies from patients with primary pontine hemorrhage we studied the sites ofbleeding, the volumes and development of hematomas and clinicopathological correlations. A modular opticalelectronic planimeter was introduced to measure the size of hematomas. The series of patients can be dividedinto 2 groups from the viewpoint of bleeding sites, their development and clinical symptomatology. These are1) the tegmentobasiiar type and 2) the tegmentai type. The precise location of the orgin of hemorrhage, and theapproximate volume of hematomas can now be determined with the help of computerized tomography. This in-formation will be of help in understanding clinical symptoms. Two different typical patient reports, selectedfrom the collection, are presented.

Stroke, Vol 11, No 1, 1980

PRIMARY pontine hemorrhage is a relatively rarecondition compared with supratentorial cerebralhemorrhage. It is generally accepted that about 10%of all cerebral hemorrhages occur in the pons,1"* andthe symptoms of this kind of hemorrhage have been ofinterest to clinicians for over a century.10

Clinicopathological investigations, however, wererather scarce at the time KSrnyey (1939)1 reported hisclinical and anatomic study of this condition. Epstein(1951)2 reported clinical and pathological findings of 7patients with primary pontine hemorrhage studiedover a 33-year period. Silverstein (1972)' reviewedpast research on primary pontine hemorrhage andpresented a clinicopathological series of 50 patients.

Calculations of the volume of a pontine hemorrhageand its correlations to clinical symptoms were not in-cluded in previous publications.1"8 The authors haveinvestigated this correlation and present the results oftheir findings.

Methods

For the study of primary pontine hemorrhage, 38clinical observations were available with 19 autopsies.One of these, in which the origin of hemorrhage was

From the Department of Neuroanatomy, Nihon UniversitySchool of Medicine, 30 Oyaguchi, Itabashi, Tokyo 173, Japan (Dr.Goto) and the Department of Neurosurgery, Hamamatsu MedicalCenter Hospital, 328 Tomizuka, Hamamatsu, Shizuoka 432, Japan(Drs. Kaneko, Hosaka and Koga).

Reprints: Dr. Goto.

easily detected, due to arteriovenous malformation inthe midbrain, was excluded. In the remaining 18patients no evidence of traumatic injury, neoplasm,supratentorial mass effect, or blood dyscrasia,described in previous publications,4'7 was found. Thecondition most likely to lead to primary pontinehemorrhage was hypertension, which affected abouttwo-thirds of the patients.

The brain stems and cerebelli, including thediencephali of 18 patients, were cut transversely intosections about 1 cm thick after fixation in a 10% solu-tion of formalin. After macroscopic observations,photographs were taken of the sections containinghematomas together with a scale for measurements.Each color transparency was enlarged to exactly theoriginal brain size using a photographic enlarging ap-paratus, and traced on paper. Then the area of thehematoma on each trace was measured with amodular optical planimeter (Digiplan, Kontron Co.).The volume of the hematomas was calculated fromthe average measured sectional areas and the length oftheir axial extensions.

For histological investigations, the sections werefixed in a solution of 5% potassium dichromate and5% potassium chromate with several changes of solu-tion for 3 weeks after the macroscopic observations.The sections were then washed in running water,dehydrated with alcohol, embedded in celloidin, cut in30jt-thick slices, and stained in the following ways:Kultschitzky's method for myelin, method of Klflverand Barrera, Goldner's modification for Masson's tri-

by guest on April 18, 2018

http://stroke.ahajournals.org/D

ownloaded from

PRIMARY PONTINE HEMORRHAGE/Go/o et at. 85

chrome stain, phosphotungstic acid hematoxylin stain,hematoxylin and eosin.

Results

1) Age: The age of patients at the onset of pontinehemorrhage was between 40 and 70 years. Theaverage age was 53.7 years. 2) Sex: This series com-prised 12 males and 6 females. 3) Duration of Sur-vival: Survival after onset ranged from 2 to 9Vi mo.4) Clinical Manifestations: The main clinical signs andsymptoms, blood pressures on admission and pasthistories of hypertension are given in tables 1 and 2.5) Initial Sites of Bleeding: From macroscopic andmicroscopic investigations of the 18 autopsiedpatients, 2 different areas of the brain stem were foundto be the site of initiation of bleeding in primary pon-tine hemorrhage. The initial sites of bleeding weredetermined as follows: in a massive hemorrhage, thearea of hemorrhage mainly consisted of blood clotwithout mixture of nervous tissue. In this instance theinitial site of hemorrhage, in most cases, is located inits center, but the peripheral parts of the hemorrhagemay contain mixtures of small blood clots and nervetissue. Using this definition, we found that hemor-rhage started from the median border area betweenbasilar and tegmental parts at the middle level of thepons in 15 patients. This group, designated as the"tegmentobasilar type," can be divided into 2 furthersub-groups: upper and lower. Nine patients belongedto the upper sub-group, and 6 to the lower sub-group.Three patients showed the beginning of hemorrhageon one side of the tegmentum at the middle level of thepons (tegmental type). The sites of hemorrhage andthe number of patients are shown in figure 1. 6) De-velopment of the Hematomas (fig. 2): In the tegmen-tobasilar type, the spread of pontine hematomas canoccur in 3 different directions as follows: 1) extensionto the opposite side which results in bilateralhematoma, 2) ventrodorsal extension, 3) upward ex-tension. Bilateral and ventrodorsal extension wereobserved in 15 patients and upward extension oc-curred in 13. In 12 patients hemorrhages spon-taneously broke into the fourth ventricle as the resultof ventrodorsal extension. With upward extension, thehematomas reached the midbrain in 11 patients, andthe thalamus in 2. In 5, hematomas were localizedwithin the pons. No direct extension of a hemorrhagewas observed into the medulla oblongata. In thetegmental type, the hematomas were localized in thetegmentum on one side with slight upward extensionlimited to the pons. 7) Volumes of the Hematomas:Hematoma volumes in all patients collected in thestudy, are shown in table 1. The volumes include theintraventricular mass of hemorrhage as it is often notclearly distinguishable from the intracerebral hemor-rhage because of the destruction of pontine structures.The intraventricular fluid blood from the intracerebralhemorrhage which did not form a mass, even after fix-ation, was not included in the measurements.

In 3 patients operated upon, the volumes listed in

the table refer to the hematomas which were notremoved during the operation.

In the 15 non-operated patients, the volumes rangedfrom 2.39 ml to 96.99 ml (under 40 ml in 13).

Patient I (A-348)

A 66-year-old woman suddenly complained of ver-tigo, and immediately lost consciousness. On admis-sion, the patient was in deep coma, showing no reac-tion to painful stimuli, with weak, regular respiration,fixed dilated pupils, fixed eyes in midposition withoutany ocular movement, no corneal reflexes, anddecerebrate rigidity with a posture of hyperextendedand pronated extremities. Her blood pressure was198/104 mm Hg and her CSF was bloody. The patientwas diagnosed as having primary pontine hemor-rhage of the fulminant type, and she was treated con-servatively. She died 4 days after the onset. Pasthistory showed a preexistent hypertension which hadbeen controlled with medication for 3 years.

An autopsy examination disclosed that the brainweighed 1,380 g; moderate scattered atheromatousplaques were found in the basal arteries of the brain;cerebral gyri were flattened on both sides; uncal her-niation was observed on the right, and markedbilateral prominent tonsillar herniations were present.

Upon sectioning of the brain, a bilateral pontinehematoma was found which extended from the deepbasilar part of the pons to the tegmentum with markeddestruction of pontine structures. The hemorrhageseemed to have started from the median border areabetween the basis and the tegmentum slightly abovethe level of the midpons, with rupture into the fourthventricle (fig. 3). The hematoma extended upward andbilaterally, into the midbrain tegmentum (fig. 4), andcontinued into the ventral parts of the dorsomedialthalamic nuclei on both sides. No macroscopicchanges were observed in the telencephalon and themedulla oblongata.

The volume of the hematoma, measured andcalculated as mentioned before, was 41.47 ml.

Histological examination snowed only lamellarfibrin networks mingled in the blood clot, but no ab-normal vessels nor ruptured microaneurysms.

Pathological diagnosis: Primary pontine hemor-rhage (tegmentobasilar type) with extension to themidbrain and the thalamus, and rupture into thefourth ventricle.

Patient II (A-275)

A 69-year-old man who was hypertensive for 5years and had not been treated properly, suddenly lostconsciousness after complaining of nausea andheadache.

On admission, his level of consciousness variedfrom stupor to coma. His blood pressure was 250/110mm Hg; his respiration was irregular, and his pupilswere myotic, 1.5 mm in diameter for both eyes. A lefthemifacial palsy and right hemiparesis were found.Sensory loss of the right half of the body, including the

by guest on April 18, 2018

http://stroke.ahajournals.org/D

ownloaded from

86 STROKE VOL 11, No 1, JANUARY-FEBRUARY 1980

TABLE 1 18 Autopsy-Proved Patients with Primary Pontine Hemorrhage

Patient Age/8exDuration of BP

surrival on iPreexistent

hypertension Clinical manifestationa

A-196

A-209

A-234

A-275

A-276

A-317

A-325

A-333

A-348

A-365

A-382

A-397

A-418

A-447

A-473

A-483

A-511

A-559

46/M

58/M

47/M

69/M

61/M

55/M

65/M

52/F

66/F

51/F

41/M

69/M

50/F

63/M

46/F

44/M

41/F

42/M

35hs

23hs

28hs

9^ms

3ds

2ds

5ds

2ds

4ds

21ds

4hs

2ds

7ds

29ds

24hs

5ds

3hs

2hs

200/110

180/90

120/0

250/110

140/80

226/90

210/120

140/80

198/104

158/104

250/120

178/90

140/70

190/120

218/94

180/110

246/138

240/120

No

3 or 4 ys

Yes

5ys

No

Controlled,10ys

Controlled,lOys

No

Controlled,3ys

Yes

Controlled,iyNo

?

Controlled

Yes

Controlled,iyYes

Coma, irregular respiration, myosis, tetraplegia, cyanosis,hyperpyrexia, etc.

Coma, irregular respiration, myosis, tetraplegia, hyper-pyrexia, etc.

Coma, left myosis, decerebrate rigidity, etc.

Coma, myosis, insufficient respiration, left facial pasly,right hemiplegia, one-and-a-half syndrome, pseudobulbarpalsy, etc.

Coma, irregular respiration, decerebrate rigidity, etc.

Coma, decerebrate rigidity, conjugate deviation of the eyestoward the nose, etc.

Stupor, irregular respiration, myosis, skew deviation, lefthemifacial palsy, right hemiplegia, etc.

Stupor, irregular respiration, myosis, left hemiplegia, ver-tical involuntary eye movement, decerebrate rigidity, etc.

Coma, mydriasis, fixed eyes in the midposition, deoerebraterigidity, etc.

Stupor, anisocoria (L>R), disturbed horizontal eye move-ment, right hemifacial palsy, left hemiplegia, etc

Coma, irregular respiration, cyanosis, fixed eyes in the mid-position, tetraplegia, etc.

Coma, irregular respiration, myosis, conjugate eye devi-ation toward the nose, etc.

Coma, insufficient respiration, myosis, fixed eyes in the mid-position, stiff neck, tetraplegia, decerebrate rigidity, etc.

Stupor, anisocoria (L<R), conjugate deviation to L, righthemiparesis, vertical involuntary eye movement, decere-brate rigidity, etc.

Coma, insufficient respiration, decerebrate rigidity, etc.

SAH, coma after an operation (L-MCA aneurysm), righthemiparesis, decerebrate rigidity, etc.

Coma, disturbed horizontal eye movement, left decerebraterigidity, etc.

Coma, apnea, myosis, vertical involuntary eye movement,decerebrate rigidity, etc.

Abbreviation*: a. b, e, d, e and f are identical with figs. 1 and 6; B — bilateral _ . . . . . _ .intestinal; L — left: ha — hours; MCA — middle cerebral artery; ma — months; R — right; SAH — snbaraohnoid hemorrhage; T — tesmentaltegmentobasilar; VH — fourth ventricular hemorrhage; y(a) — year(s).

;_BA - basilar ju-tery; BP — blood pressure; d s j - days; GI — @ s t r ° -; TB ™

face, was suspected by his reaction to noxious stimuli.His tendon reflexes biceps, triceps, supinator,quadriceps, and ankle jerks were all reduced on bothsides. He had bilateral extensor plantar responses andthe clinical picture indicated that the patient had avascular lesion in the left pontine tegmentum.

Air ventriculography was performed and showed amass lesion in the suspected area.

Two hours after onset, he was operated upon toremove the hematoma, which was seen through thefloor of the fourth ventricle at the level of the facialcolliculus on the left. The volume of the hematomaremoved was 3 to 4 ml. After the operation, hisirregular respiration improved immediately.

On the seventh day, he showed good response toverbal commands and regained movements of the leftarm and leg, subsequently of the right arm and leg.Horizontal ocular movements were strikingly dis-turbed, showing no movements of the left eye which

was fixed in mid-position and slow movements of theabducted right eye up to the mid-line (one-and-a-halfsyndrome").

The patient had a gastrocutaneous fistula because ofsevere difficulty in swallowing due to pseudobulbarpalsy. He continued to have a left peripheral facialpalsy, right hemiparesis and dysarthria, until his deathdue to pneumonia 9'A months after onset.

At autopsy his brain weighed 1,300 g.Atheromatous plaques were observed all over thebasal arteries. The basilar artery was thrombosed inits first third, with the lumen occluded 60 to 90% overabout 10 mm. The thrombus was histologically wellorganized.

The brain stem and the cerebellum were sliced tomake complete serial sections for a precise localiza-tion of the lesion and secondary changes. At thetransverse sections through the facial colliculus, afocus of softening was observed, located in the left

by guest on April 18, 2018

http://stroke.ahajournals.org/D

ownloaded from

PRIMARY PONTINE HEMORRHAGE/Gofo el al. 87

TABLE 1 (Continued)

Type

TB

TB

TB

T

TB

TB

T

TB

TB

T

TB

TB

TB

TB

TB

TB

TB

TB

Site ofbleeding

be

d

d

lefttegment.

be

be

lefttegment.

be

be

righttegment.

be

d

be

d

be

be

d

be

Intrapontinedevelopment

abed

abedf

abedef

lefttegment.

abed

abed

lefttegment.

abed

abedf

righttegment

abedf

abed

abc

abed

abed

abed

abedf

abed

Upwarddevelopment

Midbrain,thalamus

Midbrain

Midbrain

No

Midbrain

Midbrain

No

Midbrain

Midbrain,thalamus

No

Midbrain

Midbrain

No

Midbrain

Midbrain

Midbrain

Midbrain

No

Latendi ty

B

B

B

L

B

B

L

B

B

R

B

B

B

B

B

B

B

B

VH

Yes

Yes

Yes

No

No

Yes

Yes

Yes

Yes

No

Yes

Yes

No

No

Yes

Yes

Yes

Yes

Volume ofhematoma

(in ml)

96.99

37.63

37.67

(0.5)

21.72

27.18

(8.35)

26.77

41.47

(7.67)

20.77

10.31

2.39

18.98

12.85

20.24

34.93

12.59

Miscellaneous

GI bleeding

Operated,BA thrombosis

Operated,GI bleeding

Operated,GI bleeding, ileus

Aneurysm(L-MCA)

pontine tegmentum with a small 0.5 ml hematomaremaining in its center (fig. 5). The softening lesion ex-tended orocaudally within one side of the pontinetegmentum. At higher levels the sections revealed asmall cavity between the small hematoma and the sur-rounding softened area. An accumulation of foamcells could be seen around the hematoma and thecavity, but there was no proliferation of capillaries.The ipsilateral facial root was not stained due to com-plete degeneration. The left reticular formation wasalmost completely destroyed longitudinally except apart of it near the medial lemniscus. No centraltegmental tract could be observed on that side. Therewas moderate degeneration in the right mediallongitudinal fasciculus. In the medulla oblongata, apseudohypertrophy of the olivary nucleus wasobserved on the left. The medial lemnisci weredestroyed bilaterally in the pontine lesion, and showedorocaudal degeneration. The nerve cells of the nucleusambiguus showed secondary sclerotic changes, es-pecially on the left.

Pathological diagnosis: Primary pontine hemor-rhage (left tegmental type) accompanied by basilarartery thrombosis.

Discussion

Clinicopathological Correlations

In the series of primary pontine hemorrhagescollected here, it was often difficult to use symptomson admission, especially in the tegmentobasilar type,to accurately diagnose the site of hemorrhage becauseof rapid progression, and often deep coma.

In 8 patients tetraplegia and hemiplegia alternanswere highly suggestive of a pontine lesion. In 5 of thesepatients hemorrhages developed in the basilar part ofthe pons to destroy the bilateral pyramidal tracts. In 3patients who had hemiplegia alternans facialis on ad-mission, the ipsilateral pyramidal tract was found tobe compressed.

Disturbances of horizontal eye movements were

by guest on April 18, 2018

http://stroke.ahajournals.org/D

ownloaded from

88

TABLE 2 Clinical Manifestations (in 18 Patients)

STROKE

Disturbances of consciousness (on admission)ComaStupor

Hypertension (over 150 mm Hg on admission)

Decerebrate rigidity

Respiratory disturbances

Motor palsyTetraplegiaHemiplegia alternans fad aliaHemiplegia including hemiparesis

Myosis

Disturbance of horizontal eye movements

Vertical involuntary eye movements

Conjugate deviation of the eyes toward the nose

Anisocoria

Hyperpyrexia

One-and-a-half syndrome

Skew deviation of the eyes

Pseudobulbar palsy

Gastrointestinal hemorrhage

No. ofpitienta

18144

14

12

11

11533

9

6

3

2

2

2

1

1

1

3

VOL 11, No 1, JANUARY-FEBRUARY 1980

TD(2)

observed in 6 patients, and vertical involuntary eyemovements in 3. These symptoms were helpful indiagnosis and indicated more precisely the location ofa lesion involving the ipsilateral or bilateral pontinetegmentum, generally slightly below the middle level.9

Twelve patients had decerebrate posture which in-

FIGURE 1. Sites of initiation of hemorrhage. Figures in-dicate number of patients.

FIGURE 2. Development of pontine hemorrhages. Ab-breviations: IPL: intrapontine localization; MD: mid-braindevelopment, R4 V: rupture into the fourth ventricle; TBD:tegmentobasilar development; TD: thalamic development;TL: tegmental localization. Numbers in parentheses indicatethe frequency in 18 patients.

dicated additional destruction or dysfunction of themidbrain.

In the tegmental hemorrhages, the characteristicsymptoms correlated with the site of the lesion. Thesymptoms included hemiplegia alternans facialis,Foville's syndrome, and, in addition, the "one-and-a-half syndrome."'

Respiratory disturbances comprising irregular, ster-torous, frequent, shallow, slow labored, and failure ofrespiration were observed in 11 patients. In thesepatients lesions were found in the bilateral tegmento-basilar or the ipsilateral tegmental parts of the pons.

Myosis (pinpoint or constricted pupils) has beenconsidered one of the typical diagnostic signs sinceMagoun et al (1938)11 noted it was due to a disorder ofthe sympathetic pupillary pathways in the pontinetegmentum. This sign was seen only in 9 patients inspite of extensive destruction of the pontine tegmen-tum in all patients, Steegmann (1951)10 observed it in14 cases (65%) and Silverstein (1973)' in 25 cases(64%).

Hypertension

On admission, systolic blood pressures over 150mm Hg were observed in 14 patients (over 200 mm Hgin 8). Four patients were normotensive (under 150 mmHg).

by guest on April 18, 2018

http://stroke.ahajournals.org/D

ownloaded from

PRIMARY PONTINE HEMORRHAGE/Go/o et al.

•\

FIGURE 3. Patient I: transverse sectionthrough the midpons, Kultschitzky's stain.

Twelve patients had a history of hypertension, 6 un-der medical control, and no information about treat-ment of 6 others was available. Four patients had nohistory of hypertension and no information was avail-able about pre-existing hypertension for the other 2.

Sites of Bleeding

In the tegmentobasilar type of hematoma, rupturedvessels are arterial in view of the mode of onset andthe speed of the formation and the quantity of thehematoma. No histological proof has been obtained tosupport this as yet. The sites and frequencies ofbleeding show in figure 6 that the common sites ofhemorrhage are between c and b, and in d.

In the tegmental type of hematoma the initiation ofbleeding is thought to occur on one side of the tegmen-tum at the level of midpons, but no ruptured vesselscould be histologically identified. The origin of rup-tures could be capillary or venous in view of the modeof the onset of these hematomas.

Development of Hemorrhage

The distinctive features in the development oftegmentobasilar hematomas are: 1) hemorrhage and

destruction can be extensive in comparison with theother type; 2) hemorrhages easily extend to the op-posite side; 3) they can extend tegmentobasilarly; 4)they may break into the fourth ventricle; 5) they caneasily extend upward to destroy the midbrain; and 6)no direct extension of a hemorrhage into the medullaoblongata was observed.

In the tegmental type the characteristic features are:1) hemorrhages have a tendency to extend upward; 2)they are always localized on one side of the tegmen-tum; 3) no extension outside the pons were seen; 4) thedestruction in the pons is limited in comparison withthe other type; and 5) these hemorrhages may breakspontaneously into the fourth ventricle.

Volumes of the Hematomas

In the study of primary pontine hemorrhage calcu-lations of the volume of hemorrhage have not been in-cluded in previous publications.17 The volumes of thehematomas found in this study are listed in table 1.The characteristic features of the volume of primarypontine hemorrhage are summarized as follows: 1)hematomas localized in the tegmentum are generallyunder 10 ml in volume; 2) hematomas localized in the

FIGURE 4. Patient I: horizontal sectionthrough the junction between the diencephalonand the midbrain, Kultschitzky's stain.

by guest on April 18, 2018

http://stroke.ahajournals.org/D

ownloaded from

90 STROKE VOL 11, No 1, JANUARY-FEBRUARY 1980

FIGURE 5. Patient II: transverse sectionthrough the facial colliculus of the pons,Kultschitzky's stain.

v g ;

pons (tegmentum and basis) can be up to about 20 mlin volume; 3) hematomas of the tegmentobasilar typecan be up to 40 ml in volume when they extend into themidbrain; and 4) hemorrhages reaching the thalamusare usually over 40 ml in volume.

These findings can be useful to supplement findingsobtained by computerized tomography. Using thistechnique a rough idea of the volume of a hematomacan thus be obtained, and then they can be classified asto size and inferences can be made about their site andextension.

FIGURE 6. Arterial supply from the basilar artery to themedian pontine areas (Goto).

No histological proof of the causes of the primarypontine hemorrhage could be detected. It is possiblethat the tegmentobasilar hematoma might be due torupture of an abnormal vessel such as cryptic arterio-venous malformation, microaneurysm, or angio-necrosis. In the tegmental hematoma occlusivearterial disease with hemorrhagic infarction is thoughtto be the most probable pathogenesis.

References

1. Kornyey S: Rapidly fatal pontile hemorrhage, clinical andanatomic report. Arch Neurol Psychiat (Chicago) 41:793-799,1939

2. Epstein AW: Primary massive pontine hemorrhage. JNeuropathol Exp Neurol 16: 426^*48, 1951

3. Silverstein A: Primary pontine hemorrhage. In Vinken PJ,Bruyn GW (eds) Handbook of Clinical Neurology, Vol 12,Amsterdam, North Holland Publishing Co, p 37-53, 1972

4. Mutlu N, Berry RG, Alpers BJ: Massive cerebral hemorrhage.Arch Neurol (Chicago) 8: 644-661, 1963

5. Brewer DB, Fawcett FJ, Horsfield GI: A necropsy series ofnon-traumatic cerebral haemorrhages and softenings, with par-ticular reference to heart weight. J Pathol Bact 96: 311-320,1968

6. Freytag E: Fatal hypertensive intracerebral haematomas: a sur-vey of the pathological anatomy of 393 cases. J NeurolNeurosurg Psychiatry 31: 616-620, 1968

7. McCormick WF, Rosenfield DB: Massive brain hemorrhage: areview of 144 cases and an examination of their causes. Stroke4: 946-954, 1973

8. Fisher CM: Some neuro-ophthalmological observations. JNeurol Neurosurg Psychiatry 30: 383-392, 1967

9. Cohen B, Komatsuzaki A, Bender MB: Electrooculographicsyndrome in monkeys after pontine reticular formation lesions.Arch Neurol (Chicago) 18: 78-92, 1968

10. Steegman AT: Primary pontile hemorrhage, with particularreference to respiratory failure. J Nerv Ment Dis 114: 35-65,1951

11. Magoun HW, Ranson SW, Hetherington A: Descending con-nections from the hypothalamus. Arch Neurol Psychiat(Chicago) 39: 1127-1149, 1938

12. Foix C, Hillemand P: Les arteres de l'axe encephalique jus-qu'au diencephale inclusivement. Rev Neurol II: 705-739, 1925

13. Gopa N: Anatomy of the Blood Vessels of the Central NervousSystem. Tokyo, Ishiyaku Publishers Inc, p 96-107, 1971

by guest on April 18, 2018

http://stroke.ahajournals.org/D

ownloaded from

N Goto, M Kaneko, Y Hosaka and H KogaPrimary pontine hemorrhage: clinicopathological correlations.

Print ISSN: 0039-2499. Online ISSN: 1524-4628 Copyright © 1980 American Heart Association, Inc. All rights reserved.

is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231Stroke doi: 10.1161/01.STR.11.1.84

1980;11:84-90Stroke. 

http://stroke.ahajournals.org/content/11/1/84World Wide Web at:

The online version of this article, along with updated information and services, is located on the

  http://stroke.ahajournals.org//subscriptions/

is online at: Stroke Information about subscribing to Subscriptions: 

http://www.lww.com/reprints Information about reprints can be found online at: Reprints:

  document. Permissions and Rights Question and Answer available in the

Permissions in the middle column of the Web page under Services. Further information about this process isOnce the online version of the published article for which permission is being requested is located, click Request

can be obtained via RightsLink, a service of the Copyright Clearance Center, not the Editorial Office.Stroke Requests for permissions to reproduce figures, tables, or portions of articles originally published inPermissions:

by guest on April 18, 2018

http://stroke.ahajournals.org/D

ownloaded from