8
Fong Y. Tsai 1 . 2 James S. Teal 1 . 3 Grant B. Heishima 4 Ch i-Shing Zee 1 Verity S. Grinnell 4 C. Mark Mehringer 4 Hervey D. Sega l1 1 Received August 1 3. 1 980; accepted after re- vision October 22, 198 1. 'Department of Radiology. Los Angeles County- University of Southern California Medi ca l Center, Los Angeles, CA 90033. ' Present address: Department of Radiology, University of California Irvin e Medical Center, 101 City Dr. S., Orange, CA 92668. Address reprint requests to F. Y. Tsai. 3Present address: Department of Radiology, Howard University Hospital, Washington, DC 20060. ' Department of Radiology, Harbor General- University of California at Los Angeles Medical Center, To rr ance, CA 90509. AJNR 3:149 - 156, March / April 1982 0195-6 108 / 82 / 0302-0 149 $00.00 © American Roentgen Ray Soc iety Computed Tomography in Acute Posterior Fossa Infarcts 149 Thirty-one cases of acute posterior fossa infarcts are reported . CT evidence of obliterated posterior fossa cisterns and hydrocephalus indicates a grave prognosis due to brainstem compression . Progressive obliteration of posterior fossa cisterns may be used as an i ndicator for surgical decompression. Patients with intac t posterior fossa cisterns had good recoveries without surgical treatment. CT can be used to diagnose the very early phase of an acute posterior fossa infarct and has prognostic value in predicting the outcome. Acute infar cts involving the pons, medulla oblongata , and cerebellum are assoc iated with high morta li ty. Early diagnosis is essential [1- 4], but has been difficu lt until the introdu ction of co mputed tomography (CT). We r eviewed litera- ture on' this entity [1-25] and carefully analyzed 31 cases seen over the past 3 years. CT plays an import a nt role in the diagnostic and pr og nos ti c impli ca tions of acute posterior fossa infarcts. Materials and Methods Over a 3 yea r period, we have atl ended at least 31 patients with ac ute i nfarc ts in th e poster ior fossa. The 18 men and 13 women were aged 23-73 years (average, 49.9 years). Almost a ll patients had dizziness , lethargy, and weakness on admission. Four had sudden onse t of co ma without pr eceding sy mptom s. Nine had headac he, and 14 had vomiting (table 1) . The interval from onse t of sy mptoms to initial CT sca n was a few (4-6) ho ur s to 2 weeks. Th e 31 patient s were divided into thr ee gro ups acco rding to age: (1) nine patients under 40 years o ld-three died , two b ecame permanen tly vegetativ e, and the o th er fo ur had good recovery; (2) 13 patients aged 40 - 59 years- fi ve died and eight had good recovery; and (3) nine patients aged 60 or older-four died and fi ve had good r ecove ry. Results Fi ve cases demonstrated isodense posterior fossas by CT (Cases 1, 2, 8, 14 , and 16) a few hour s to 2- 3 days (case 2) after onset of sy mptom s. Twenty-five had hypo density a few hours to 5 days ( case 12) after th e onset of sympto ms. One of these 25 had mi xe d hyp er- and hypod ensities. One pat ient with mi xed hyp er- and hyp odensities was initia ll y scanned abo ut 2 weeks after the onset of symptoms. Ther e were 12 fatal cases (table 1) . Among th ese, 10 showed co mplete obliteration of th e posterior fossa ciste rns, with a sma ll or an absent fourth ventricl e. Nine of the 12 fatal cases had hydrocephalus related to swe lling of the posterior f ossa str uc tur es. Two had no h ydrocepha lu s; in one of (case 5) those two , pontine and cerebellopontine angle cisterns were maintained and the perimesencep halic c isterns were obliterated.

Computed Tomography in Acute Posterior Fossa Infarcts · CPA, and PM cisterns, Hydrocephalus, CCT: Nonopacification of bas il ar artery, Angio: P artia l occlusion o f basilar, superior

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Fong Y. Tsai 1. 2

James S. Teal 1. 3

Grant B. Heishima4

Ch i-Shing Zee 1

Verity S. Grinnell 4

C. Mark Mehringer4

Hervey D. Sega l1 1

Received August 13. 1980; accepted after re­vision October 22, 1981.

' Department of Radiology. Los Ange les County-Universi ty of Southern Californi a Medica l Center , Los Ange les, CA 90033.

' Present address: Department of Radiology, University of Ca li forn ia Irvine Medica l Center , 10 1 City Dr. S., Orange, CA 92668. Add ress reprin t requests to F. Y. Tsai.

3Present address: Department of Rad iology, Howard University Hospital, Washington, DC 20060.

' Department of Rad iology, Harbor General­University o f California at Los Angeles Medical Cen ter , Torrance, CA 90509.

AJNR 3:149- 156, March / April 1982 0 195-6108 / 82 / 0302-0149 $00.00 © American Roentgen Ray Society

Computed Tomography in Acute Posterior Fossa Infarcts

149

Thirty-one cases of acute posterior fossa infarcts are reported . CT evidence of obliterated posterior fossa cisterns and hydrocephalus indicates a grave prognosis due to brainstem compression . Progressive obliteration of posterior fossa cisterns may be used as an indicator for surgical decompression. Patients with intact posterior fossa cisterns had good recoveries without surgical treatment. CT can be used to diagnose the very early phase of an acute posterior fossa infarct and has prognostic value in predicting the outcome.

Acute infarcts involving the pons, medulla oblongata , and cerebellum are assoc iated with high mortali ty . Early diagnosis is essential [1-4], but has been difficult unti l the introduc tion of computed tomography (CT) . We reviewed litera­ture on 'this entity [1-25] and carefully analyzed 3 1 cases seen over the past 3 years . CT plays an important role in the diagnostic and prognosti c implicati ons of acute posterior fossa infarcts.

Materials and Methods

Over a 3 year period, we have atlended at least 3 1 pat ients with acute infarcts in th e posterior fossa. Th e 1 8 men and 13 wo men were aged 23-73 years (average, 49.9 years). Almost all patients had dizziness , lethargy, and weakness on admission. Four had sudden onset of co ma without preceding symptoms. Nine had headache, and 1 4 had vom iting (table 1). The interval from onset of symptoms to initial CT scan was a few (4-6) hours to 2 weeks.

The 3 1 patients were divided into three groups according to age: (1 ) nine patients under 40 years old-three died , two became permanen tl y vege tative, and the other four had good recovery; (2) 1 3 patients aged 40- 59 years- fi ve died and eigh t had good recovery; and (3) nine patients aged 60 or older-four d ied and five had good recovery.

Results

Fi ve cases demonstrated isodense posterior fos sas by CT (Cases 1 , 2, 8, 14, and 16 ) a few hours to 2 - 3 days (case 2) after onset of symptoms. Twenty-five had hypodensity a few hours to 5 days (case 12) after the onset of symptoms. One of these 25 had mixed hyper- and hypodensities. One patient with mi xed hyper- and hypodensities was initiall y scanned about 2 weeks after the onset of symptoms.

There were 12 fata l cases (table 1). Among these, 10 showed complete obl iteration of the posterior fossa ciste rns, with a small or an absent fourth ventricl e. Nine of the 12 fatal cases had hydrocephalus related to swelling of the posterior fossa structures. Two had no hydrocephalus; in one of (case 5) those two , pontine and cerebellopontine ang le c istern s were maintained and the perimesencephalic c isterns were obliterated.

TA

BL

E 1

: S

um

mar

y o

f C

ase

s

Cas

e N

o.

(ag

e, g

en

de

r)

Die

d w

ith

ou

t su

rge

ry:

1 (3

9,F

)

2 (2

3,F

)

3 (4

9,F

)

4 (6

2,M

)

5 (6

4,M

)

6 (6

5,F

)

7 (4

6,F

)

8 (4

9,M

)

9 (5

3,M

)

10

(3

8,M

)

Clin

ical

Fin

din

gs

Le

tha

rgy

and

vom

itin

g,

1 d

ay

be

fore

ad

mis

sio

n,

Co

ma

tose

and

ap

ne

ic s

eve

ral

ho

urs

aft

er

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on

, D

ow

nw

ard

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mu

s, f

ixe

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nd d

i­la

ted

pu

pils

, A

bse

nt

do

ll's

eye

mo

vem

en

t an

d co

rne

al

refl

exe

s,

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ad

ac

he,

leth

arg

y,

and

vom

itin

g 2

-3

da

ys b

fore

ad

mis

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n,

Ob

tun

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n a

dm

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en

co

ma

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vera

l h

ou

rs l

ate

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on

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bse

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corn

ea

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fle

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pu

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hth

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ad

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the

n b

eca

me

co

ma

­to

se o

ver

24

hr,

Pu

pil

s fix

ed

and

dila

ted

, F

lac­

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d a

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on

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hyp

ert

en

sive

dia

be

tic,

Su

dd

en

on

set

of

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ea

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ht

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l re

fle

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o s

po

nta

neo

us

resp

irat

ion

, in

­cr

ea

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rig

ht

de

ep

te

nd

on

re

flex,

Ext

en

sor

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gid

ity,

Pro

gre

ssiv

ely

in

cre

asi

ng

we

akn

ess

2 d

ays

be

­fo

re a

dm

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, S

ud

de

n o

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t o

f co

ma

a f

ew

h

ou

rs b

efo

re a

dm

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on

, N

on

resp

on

sive

, fl

ac­

cid

, a

nd

are

fle

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, N

o s

po

nta

ne

ou

s re

spir

ati

on

(i

ntu

ba

ted

),

Le

tha

rgy

an

d w

ea

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ss o

n d

ay

of

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issi

on

(f

ou

nd

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resp

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sive

at

ho

me

), R

esp

on

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to

pa

in b

y m

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ng

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ft s

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(rig

ht

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ery

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mm

, w

ea

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, E

yes

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via

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to r

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t.

Hyp

ert

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sion

fo

r 6

yea

rs,

Su

dd

en

on

set

of

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with

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le

tha

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we

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pils

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),

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dd

en

on

set

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ith

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bra

te p

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, P

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mm

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ht

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esp

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with

d

ece

reb

rate

po

stu

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g,

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dd

en

on

set

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com

a,

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nre

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nsi

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im­

uli.

Are

fle

xic

, fla

ccid

, N

o sp

on

tan

eo

us

resp

ira­

tion

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l e

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e d

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ca

rdia

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the

teri

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tion

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tun

da

tio

n w

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ub

seq

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nt

com

a s

eve

ral

ho

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la

ter,

Re

spo

nsi

ve t

o d

ee

p

pa

in w

ith d

ece

reb

rate

po

stu

rin

g,

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corn

ea

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r g

ag

re

fle

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or

do

ll's

eye

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vem

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t. P

up

ils

fixe

d a

nd

dil

ate

d,

CT

an

d A

ng

iog

rap

hic

Fin

din

gs

NC

T:

Iso

de

ns

ity

in p

ost

eri

or

foss

a,

Ab

sen

ce o

f P

, C

PA

, a

nd P

M c

iste

rns,

Sm

all

fou

rth

ve

ntr

i­c

le,

Hyd

roce

ph

alu

s,

CC

T:

No

no

pa

cifi

cati

on

of

ba

sila

r a

rte

ry,

An

gio

: O

cclu

sio

n o

f b

asi

lar

art

ery

pro

xim

al t

o A

ICA

, N

CT

: Is

od

en

sity

in p

ost

eri

or

foss

a,

Sm

all

fou

rth

ve

ntr

icle

, d

isp

lace

d t

o le

ft.

Ab

sen

ce o

f P

, C

PA

, an

d P

M c

iste

rns

, H

ydro

cep

ha

lus

, C

CT

: N

on

op

aci

fica

tio

n o

f ba

sila

r a

rte

ry,

An

gio

: P

art

ial o

cclu

sio

n o

f b

asi

lar,

su

pe

rio

r ce

r­e

be

llar,

an

d p

ost

eri

or

cere

bra

l a

rte

rie

s,

NC

T:

De

cre

ase

d d

en

sity

in b

rain

stem

and

ce

re­

be

llum

, P

, C

PA

, a

nd P

M c

iste

rns

and

fou

rth

ve

ntr

icle

ob

lite

rate

d,

Hyd

roce

ph

alu

s,

CC

T:

No

ab

no

rma

l enh

an

cem

ent

. N

CT

: D

ec

rea

sed

de

nsi

ty in

up

pe

r p

on

s,

mid

­b

rain

, a

nd

su

pe

rio

r ve

rmis

, P

and

CP

A c

is­

tern

s a

nd

fou

rth

ven

tric

le n

orm

al.

PM

cis

tern

s p

art

ially

ob

lite

rate

d,

No

su

pra

ten

tori

al v

en

tric

­ul

ar

dila

tati

on

, C

CT

: N

o a

bn

orm

al e

nh

an

cem

en

t.

NC

T:

Lo

w d

en

sity

in m

ed

ulla

, p

on

s,

and

mid

­b

rain

, M

inim

al

he

mo

rrh

ag

ic d

en

sity

in b

rac

ium

po

ntis

, F

ou

rth

ve

ntr

icle

an

d p

ost

eri

or

foss

a c

i ste

rns

ob

lite

rate

d,

Hyd

roce

ph

alu

s,

NC

T:

De

cre

ase

d d

en

sity

in b

rain

ste

m a

nd c

ere

­b

ellu

m,

Po

ste

rio

r fo

ssa

cis

tern

s a

nd

fo

urt

h

ven

tric

le c

om

ple

tely

ob

lite

rate

d,

Hyd

roce

ph

lus

,

NC

T:

De

cre

ase

d d

en

sity

in b

rain

ste

m a

nd

le

ft

an

d m

idlin

e c

ere

be

llum

an

d le

ft o

ccip

ital

lo

be

, P

ost

eri

or

foss

a c

iste

rns

an

d f

ou

rth

ve

ntr

icle

n

ot

visu

aliz

ed

, H

ydro

cep

ha

lus

, N

CT

: D

ec

rea

sed

de

ns

ity

in p

on

s a

nd

mid

bra

in,

Po

ste

rio

r fo

ssa

cis

tern

s an

d fo

urt

h v

entr

icle

n

ot

visu

aliz

ed,

Hyd

roce

ph

alu

s,

NC

T:

Iso

de

nsi

ty i

n p

ost

eri

or

foss

a,

Hyd

roce

ph

a­lu

s, P

ost

eri

or

foss

a c

iste

rns

and

fo

urt

h v

en

tri­

cle

no

t vi

sua

lized

, N

CT

: D

ec

rea

sed

de

nsi

ty in

rig

ht

cere

be

llum

, O

lite

ratio

n o

f p

ost

eri

or

foss

a c

iste

rns

and

fou

rth

ve

ntr

icle

, H

ydro

cep

ha

lus,

C

CT

: N

on

op

aci

fica

tio

n o

f b

asi

lar

art

ery

,

Res

ult

s

Die

d 2

da

ys l

ate

r. B

asi

lar

art

ery

o

cclu

sio

n,

bila

tera

l ce

reb

ella

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rcti

on

, an

d b

rain

ste

m c

om

pre

s­si

on a

t a

uto

psy

,

Die

d 1

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ter.

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top

sy n

ot

pe

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rme

d.

Die

d 4

da

ys l

ate

r, E

xte

nsi

ve c

ere

­b

ella

r an

d p

ost

eri

or

po

nti

ne

in

­fa

rcts

at

aut

op

sy,

Die

d 2

da

ys l

ate

r, A

uto

psy

no

t p

er­

form

ed

,

Die

d 1

da

y la

ter,

Au

top

sy n

ot

pe

r­fo

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Die

d a

few

da

ys la

ter,

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d 4

da

ys l

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Die

d 2

da

ys l

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d 2

da

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to r

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igh

t fa

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ea

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ined

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ee

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then

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refl

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it fo

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w

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ith

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ry d

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ral

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cra

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l n

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e p

als

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ter.

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pn

ea

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ma

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n a

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.

Diff

icu

lty

spe

ak

ing

(su

dd

en

on

set)

. Q

ua

dri

pa

r­e

tic

, b

eca

me

qu

ad

rip

leg

ic.

De

cort

ica

te p

ost

ur­

ing

la

ter.

Hea

d d

ev

iate

d t

o le

ft.

Do

ll's

eye

m

ove

me

nt

an

d c

orn

eal

refl

exe

s w

ea

k.

Dia

be

tes

me

llitu

s fo

r ye

ars

. O

ccip

ita

l h

ea

da

che

, le

tha

rgy,

an

d w

ea

kn

ess

1 d

ay

be

fore

ad

mis

­si

on.

Rig

ht

ho

mo

nym

ou

s h

em

ian

op

sia

. D

is­

con

jug

ate

ga

ze.

De

cre

ase

d l

eft

co

rne

al

refl

ex.

Le

ft f

aci

al

we

akn

ess

.

Occ

ipit

al

he

ad

ach

e r

ad

iati

ng t

o n

eck

fo

r 3

da

ys.

Ve

rtig

o,

diz

zin

ess

, a

nd

vom

itin

g 1

da

y b

efo

re

ad

mis

sio

n.

Wid

e-b

ase

d g

ait.

Fa

llin

g t

o ri

gh

t.

Nys

tag

mu

s,

left

la

tera

l ga

ze.

Diz

zy s

pe

lls,

un

ab

le t

o w

alk

fo

r 1

da

y. A

taxi

c,

falli

ng t

o le

ft.

Nys

tag

mu

s o

n ri

gh

t la

tera

l an

d

up

wa

rd g

aze

s. D

ec

rea

sed

se

nsa

tio

n i

n le

ft l

eg

and

tru

nk

. R

igh

t o

ph

tha

lmo

ple

gia

, h

ea

da

che

, d

izzi

ne

ss a

nd

vom

itin

g.

Be

cam

e c

om

ato

se 2

da

ys l

ate

r. C

or­

neal

re

fle

xes

we

ak

. P

up

ils 4

mm

, re

act

ive

. D

oll'

s e

ve m

ove

me

nt

pre

sen

t.

NC

T:

De

cre

ase

d d

en

sity

in r

igh

t ce

reb

ellu

m w

ith

dis

pla

cem

en

t o

f sm

all

fou

rth

ven

tric

le t

o le

ft.

P,

rig

ht

CP

A,

an

d P

M c

iste

rns

no

t vi

sua

lize

d.

Le

ft C

PA

cis

tern

sm

all.

Mild

hyd

roce

ph

alu

s.

NC

T:

De

cre

ase

d d

en

sity

in v

erm

is,

mid

bra

in,

an

d u

pp

er

po

ns

. P

os

teri

or

foss

a c

iste

rns

ab­

sen

t. S

ma

ll fo

urt

h v

en

tric

le.

No

hyd

roce

pha

­lu

s.

NC

T:

De

cre

ase

d d

en

sity

in r

igh

t ce

reb

ellu

m.

Po

ste

rio

r fo

ssa

cis

tern

s vi

sua

lize

d.

Ven

tric

ula

r si

ze (

incl

ud

ing

fo

urt

h)

wit

hin

no

rma

l lim

its.

Re

pe

at

NC

T:

Sm

all

, co

mp

ress

ed

fo

urt

h v

en

tri­

cle

. S

ma

ll P

and

PM

cis

tern

s. O

blit

era

tio

n o

f C

PA

cis

tern

s.

Hyd

roce

ph

alu

s.

An

gio

: O

cclu

sio

n o

f ri

ght

po

ste

roin

feri

or

cere

­b

ella

r a

rte

ry.

NC

T:

Sm

all

are

a o

f h

ypo

de

nsi

ty in

rig

ht

cere

bel­

lum

. F

ourt

h a

nd o

the

r ve

ntr

icle

s an

d p

ost

eri

or

foss

a c

iste

rns

wit

hin

no

rma

l lim

its.

NC

T:

Lo

w d

en

sit

y in

rig

ht

cere

be

llum

. F

ou

rth

ve

ntr

icle

co

mp

ress

ed

and

dis

pla

ced

to

left.

S

ma

ll P

cis

tern

. P

M a

nd C

PA

cis

tern

s o

blit

er­

ate

d.

Hyd

roce

ph

alu

s.

NC

T:

Iso

de

nsi

ty i

n p

ost

eri

or

foss

a;

sma

ll fo

urt

h

ven

tric

le a

nd p

ost

eri

or

foss

a c

iste

rns.

No

hy­

dro

cep

ha

lus

. A

ng

io:

Pa

rtia

l o

cc

lusi

on o

f b

asi

lar

and

left

sup

rio

r ce

reb

ella

r a

rte

ries

. R

ep

ea

t N

CT

: E

nh

an

cem

ent

in

po

ns

and

low

de

sity

in

left

cere

be

llum

.

NC

T:

De

cre

ase

d d

en

sity

in

left

in

feri

or

cere

be

l­lu

m,

righ

t ce

reb

ellu

m,

and

le

ft o

ccip

ital

lobe

. S

ma

ll fo

urt

h ve

ntr

icle

dis

pla

ced

to

rig

ht.

Mild

h

ydro

cep

ha

lus

. S

ma

ll P

an

d C

PA

cis

tern

s.

NC

T 1

da

y la

ter,

aft

er

on

set

of

com

a:

Co

mp

lete

o

blit

era

tion

of

po

ste

rio

r fo

ssa

cis

tern

s.

In­

farc

ted

are

as

mo

re a

pp

are

nt.

Pro

gre

ssio

n o

f h

ydro

cep

ha

lus.

N

CT

: D

ecr

ea

sed

de

nsi

ty in

le

ft c

ere

be

llum

. F

ou

rth

ve

ntr

icle

dis

pla

ced

to

rig

ht.

No

hyd

ro­

cep

ha

lus

.

NC

T:

De

cre

ase

d d

en

sity

in l

eft

ce

reb

ellu

m.

Po

s­te

rio

r fo

ssa

cis

tern

s in

tac

t. F

ou

rth

ve

ntr

icle

co

mp

ress

ed

bu

t n

ot

dis

pla

ced

.

NC

T:

De

cre

ase

d d

en

sity

in l

eft

ce

reb

ellu

m a

nd

bra

chiu

m p

on

tis.

P,

left

CP

A,

an

d P

M c

iste

rns

visu

aliz

ed

. O

blit

era

tion

of

rig

ht

CP

A c

iste

rn.

No

hyd

roc

ep

ha

lus

.

Die

d 2

da

ys a

fte

r o

nse

t o

f co

ma

.

Die

d 2

mo

nth

s la

ter.

Bas

ila

r a

rte

ry

occ

lusi

on

and

in

farc

tio

n o

f b

rain

­st

em

and

ce

reb

ellu

m a

t a

uto

psy

.

Su

rviv

ed a

fte

r su

rge

ry;

no

de

fici

t 5

mo

nth

s la

ter.

Su

rgic

al d

eco

mp

ress

ion

with

re

­m

ova

l of

infa

rcte

d ri

gh

t ce

reb

el­

lum

.

Su

rgic

al d

eco

mp

ress

ion

with

re­

mo

val o

f h

ug

e in

farc

ted

rig

ht

cere

bellu

m.

Re

cove

red

with

out

si

gn

ifica

nt n

eu

rolo

gic

de

fici

t.

Su

rviv

ed

; sl

ow

ly i

mp

rove

d o

ver

2 m

on

ths

; q

ua

dri

pa

resi

s; o

be

yed

co

mm

an

ds

.

Su

rviv

ed

; n

od

de

d h

ead

and

mo

ved

ha

nd

s in

re

spo

nse

to

qu

est

ions

; ap

has

ia;

qu

ad

rip

are

sis

; h

om

nym

ou

s h

em

ian

op

sia

.

Re

cove

red;

no

de

fici

t 3

mo

nth

s la

ter.

Re

cove

red;

ab

le t

o w

alk

with

w

alk

er;

nys

tag

mu

s o

n ri

gh

t la

t­er

al g

aze

1 m

on

th l

ate

r.

Su

rviv

ed

with

pe

rsis

ten

t q

ua

dri

pa

­re

sis

. A

lert

and

aw

ake

1 m

on

th

late

r; d

isch

arg

ed

to

ho

me

.

» '­ z :n .w ;:: '" (l :T

"­ » ~ to

(Xl '" o -I

o "Tl » o c -I

m

-U

o UJ

-I

m

JJ

(5

JJ

"Tl o UJ

UJ » Z

"Tl » JJ

o -I

UJ

(J1

Ta

ble

1 (

con

t'd

.)

Ca

se N

o.

(ag

e. g

end

er)

21

(54

,F)

22

(54

,M)

23

(25

,M)

24

(3

4,M

)

25

(4

5,M

)

26

(5

3,M

)

27

(6

4,M

)

28

(6

5,M

)

29

(7

0,F

)

30

(3

1,M

)

31

(59

,M)

Clin

ica

l Fi

nd

ing

s

He

ad

ac

he,

leth

arg

y,

an

d v

om

itin

g f

or

24

hr.

W

ea

kne

ss a

nd

lo

ss o

f b

ala

nc

e. C

ou

ld n

ot

wa

lk,

bu

t c

ou

ld m

ove

all

ext

rem

itie

s o

n c

om

­m

an

d.

Lo

ss o

f b

ala

nce

an

d f

alli

ng

to

rig

ht

for

2 w

ee

ks.

Le

ft h

ea

rin

g l

oss

an

d d

ecr

ea

sed

le

ft c

orn

ea

l re

flex

. L

eft

5th

an

d 7

th c

ran

ial

ne

rve

pa

lsie

s.

Dip

lop

ia o

n le

ft l

ate

ral

an

d u

pw

ard

ga

zes

.

Le

tha

rgy

, vo

mit

ing

with

asp

ira

tio

n p

ne

um

on

ia.

Pu

pils

4 m

m,

rea

ctiv

e.

Dis

con

jug

ate

ga

ze w

ith

rig

ht

me

dia

l re

ctu

s p

als

y.

Su

dd

en

ly i

ncr

ea

sin

g le

tha

rgy

; su

bse

qu

en

t co

ma

an

d a

ton

ic b

rea

th­

ing

2 d

ays

la

ter.

Wit

hd

raw

al

fro

m p

ain

. C

or­

ne

al

refle

xes

pre

sen

t. P

upi

ls s

ma

ller

(2 m

m)

an

d w

ea

kly

re

act

ive

. D

izzi

ne

ss,

leth

arg

y, s

tag

ge

rin

g g

ait,

an

d v

om

it­

ing

on

mo

rnin

g o

f ad

mis

sio

n.

Un

ab

le t

o s

tan

d

or

wa

lk.

Pu

pils

3 m

m,

rea

ctiv

e.

Co

rne

al

re­

fle

xes

inta

ct.

Le

tha

rgy

, n

au

sea

, vo

mit

ing

, a

nd

in

ab

ility

to

wa

lk.

Fa

llin

g to

rig

ht.

Pu

pil

s 4

.5 m

m,

rea

ctiv

e.

Co

r­n

eal

refl

exe

s in

tact

. S

ud

de

n o

nse

t o

f d

izzi

ne

ss.

Fe

ll; f

ou

nd h

avin

g

gra

nd

mal

se

izu

re.

Dis

ori

en

tati

on

, le

tha

rgy

, d

izzi

ne

ss,

and

we

ak

nes

s. N

eu

rolo

gic

exa

mi­

na

tio

n o

the

rwis

e n

orm

al.

S

ud

den

on

set

of

vert

igo,

na

use

a,

an

d h

ea

da

ch

e,

wit

h o

cca

sio

na

l vo

mit

ing

. R

igh

t-s

ided

we

ak­

ne

ss a

nd

ata

xia

. R

om

be

rg t

est

to

rig

ht.

Diz

zin

ess

, ve

rtig

o,

an

d l

eth

arg

y 2

da

ys b

efo

re

ad

mis

sio

n.

Un

ste

ad

y g

ait

with

le

ft-s

ide

d a

tax

ia.

Le

tha

rgy,

sh

ort

ne

ss o

f b

rea

th,

an

d v

om

itin

g 1

d

ay

be

fore

ad

mis

sio

n.

Aw

ake

an

d a

lert

, b

ut

diz

zy a

nd

qu

ad

rip

are

tic.

Rig

ht

faci

al

pa

lsy

and

p

tosi

s.

Le

tha

rgy

and

we

ak

ne

ss f

or

2 d

ays

. P

up

ils 4

mm

(r

igh

t) a

nd 2

mm

(le

ft),

we

akl

y re

ac

tive

. R

igh

t 3

d c

rani

al

ne

rve

pa

lsy.

Fa

llin

g to

rig

ht.

Dis

rie

nta

tio

n o

f tim

e a

nd p

lace

. S

eve

re h

ea

da

ch

e, n

au

sea

, vo

miti

ng,

an

d v

er­

tig

o.

Le

ft-s

ide

d p

are

sth

esi

a a

nd w

ea

kne

ss;

falli

ng

to

left

. L

eft

-sid

ed

ata

xia

. D

ecr

ea

sed

re

­sp

on

se t

o p

inp

rick

and

vib

ratio

n o

n r

igh

t si

de.

CT

an

d A

ng

iog

raph

ic F

ind

ing

s

NC

T:

De

cre

ase

d d

en

sity

in

verm

is.

Fo

urt

h v

en

tri­

cle

co

mp

ress

ed

an

d d

isp

lace

d f

orw

ard

. N

o h

ydro

ce

ph

alu

s. P

ost

eri

or

foss

a c

iste

rns

pre

s­e

nt.

N

CT

: P

atc

hy

de

cre

ase

d d

en

sity

with

min

ima

l h

em

orr

ha

gic

de

nsi

ty i

n le

ft c

ere

be

llum

. F

ou

rth

ve

ntr

icle

dis

pla

ced

to

rig

ht.

CP

A c

iste

rns

sm

all.

PM

an

d P

cis

tern

s in

tact

. N

o h

ydro

­ce

ph

alu

s.

NC

T:

De

cre

ase

d d

ens

ity

in m

idb

rain

wit

h o

blit

er­

atio

n o

f P

M c

iste

rns

. F

ou

rth

ve

ntr

icle

an

d P

a

nd

CP

A c

iste

rns

inta

ct.

No

hyd

roce

ph

alu

s.

NC

T:

De

cre

ase

d d

en

sity

in

left

ce

reb

ellu

m a

nd

bra

chiu

m p

on

tis.

Fou

rth

ven

tric

le c

om

pre

sse

d

and

dis

pla

ced

to

rig

ht.

Pos

teri

or

foss

a c

iste

rns

int a

ct,

exc

ep

t ri

gh

t C

PA

cis

tern

. N

o h

ydro

­ce

ph

alu

s.

NC

T:

De

cre

ase

d d

en

sity

in

rig

ht

cere

be

llum

. P

ost

eri

or

foss

a c

iste

rns

and

fo

urt

h v

en

tric

le

inta

ct.

No

hyd

roce

ph

alu

s.

NC

T:

De

cre

ase

d d

en

sity

in r

igh

t ce

reb

ellu

m.

Po

ste

rio

r fo

ssa

cis

tern

s a

nd f

ou

rth

ve

ntr

icle

in

tact

. N

o h

ydro

cep

ha

lus.

NC

T:

De

cre

ase

d d

en

sity

in r

igh

t ce

reb

ellu

m.

Fo

urt

h v

entr

icle

dis

pla

ced

to

left

. P

os

teri

or

fos

sa c

iste

rns

inta

ct.

No

hyd

roce

ph

alu

s.

CC

T:

No

ab

no

rma

l enh

an

cem

en

t.

NC

T:

De

cre

ase

d d

en

sity

in l

eft

ce

reb

ellu

m.

Fo

urt

h v

en

tric

le c

om

pre

sse

d b

ut

no

t d

is­

pla

ced

. R

igh

t C

PA

cis

tern

ab

sent

; P

, P

M,

and

le

ft C

PA

cis

tern

s p

rese

nt.

No

hyd

roce

ph

alu

s.

NC

T:

De

cre

ase

d d

en

sity

in

left

cere

be

llum

. S

ma

ll fo

urt

h v

en

tric

le d

isp

lace

d t

o ri

gh

t. P

and

C

PA

cis

tern

s in

tac

t; P

M c

iste

rns

sm

all.

No

hy­

dro

cep

ha

lus.

N

CT

: D

ecr

ea

sed

de

nsi

ty in

rig

ht

cere

be

llum

. N

o

dis

pla

cem

en

t o

f fo

urt

h v

en

tric

le.

Pos

teri

or

foss

a c

iste

rns

inta

ct.

l'Jo

hyd

roce

ph

alu

s.

NC

T:

De

cre

ase

d d

en

sity

in l

eft

cere

be

llum

. F

ou

rth

ve

ntr

icle

and

po

ste

rio

r fo

ssa

cis

tern

s n

orm

al.

No

hyd

roce

ph

alu

s.

Res

ult

s

Re

cove

red

; m

ild w

ea

kne

ss 2

w

ee

ks l

ate

r.

Re

cove

red

with

he

ari

ng

lo

ss.

Co

uld

w

alk

wit

h a

ssis

tan

ce

1 m

on

th

late

r.

Sl o

wly

re

cove

red

ove

r o

ne

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AJNR :3, Marchi April 1982 CT OF ACUTE POSTERIOR FOSSA INFARCTS 153

Fig. 1.-Case 1. A , Conlrast CT. For­ward displacement of small fourlh ven­Iricle and complete obliterati on of pon­line, ce rebellopontine angle, and peri ­mesencephalic c islern s; dilalalion of both temporal horns secondary 10 hydro­cephalus. Posterior fossa structures were isodense. Nonopacification o f bas­ilar artery. B, Left ve rtebral angiogram. Occ lusion o f basilar artery just distal to anteroinferior ce rebellar artery. Good filling of posteroinferior cerebellar ar­tery.

A B

A

Fig. 2 .- Case 2. Contrast CT. Isodense posterior fossa structures, dis­placement of small fourth ventric le to left and anteriorly, dilatati on of both temporal horn s, obliterati on of posteri or fossa cistern s, and nonopaci ficat ion of basila r artery. Low densities within brainstem (B) were believed to be artifactual.

There were 19 survivors (table 1). One had nearly com­plete ob literation of the posterior fossa cisterns; another three had progressive ob literation of the posterior fossa cisterns plus hydrocephalus on the second CT examination . Three of these four patients had surgery resulting in better recovery than the one receiving nonsurgical treatment. The other 15 surviving cases had varying degrees of recovery with nonsurgical treatment. All of these 15 cases had visible posterior fossa cisterns and fourth ventricles .

The most common abnormality demonstrated by contrast CT was nonvisualization of the basilar artery.

In cases 1 - 3 (figs. 1 -3), the cause of the posterior fossa infarct was occlus ion of the basilar artery . In cases 1 and 2,

B

Fig . 3 .- Case 3. Noncontrast CT. Low density in center of posterior fossa with complete obliterati on of posterior fossa c istern s and fourth ventricle. Dilatal ion of both temporal horn s secondary to hydrocephalus.

CT demonstrated posteri or fossa isodensity; case 3 had hypodensity in the infarc ted pons and vermi s. In these cases there were some common features on CT, such as complete obliteration of the posterior fossa cisterns and hydroceph­alus. These three pati ents, who were treated nonsurgicall y , died .

In cases 4, 5 , and 16 (figs. 4-6), the infarct was primarily in the brainstem , with less involvement of the cerebellum. In case 16, the posterior fossa structures were isodense on the first CT; an enhancing infarc t of the pons was demon­strated 5 days later after angiography . The posterior fossa cistern s and fourth ventri c le were not obliterated . In case 4 there were infarc ts in the pons, midbrain , and cerebellum . The perimesencephalic ciste rns were obliterated . The out­come in case 4 was far worse than in case 16, possibly due to more ex tensive invo lvement of the midbrain . In case 5 there was much more extensive infarcti on in the brainstem than in case 4 . The posterior fossa c istern s and fourth ventric le were completely obliterated , and hydrocephalus

154 TSAI ET AL. AJNR :3, Marchi April 19B2

A

A

Fig. 4.-Case 15. A, Contrast CT after angiography. Enhanc ing lesion in pons and low density in left cere­bellum and brachium pontis. B, Re­formatted sagittal CT. Posterior compression of fourth ventricle (ar­row).

Fig. 5. -Case 4. Contrast CT. Low density in right side of brainstem and superior vermis, and partial ob­literation of left ambient c istern .

B

Fig. 5. -Case 5. CT before (A) and after (B) contrast. Low density in brainstem, patchy hemorrhag ic density in left brachium pontis (arrow), and obliterat ion of posterior fossa c istern s.

was present. These three cases demonstrated that the larger the area of involved brainstem, the worse the prognosis.

In cases 13, 14, and 17 (figs. 7-9), the in itial CT showed

A B

Fig . 7. -Case 17. Noncontrast CT. Displacement of small fourth ventric le to right , hypodensity of left cerebellar hemisphere, complete obliteration of peri mesencephalic cisterns, small pontine and cere bello pontine cistern s, and hydrocephalus.

c o Fig . B. - Case 13. Noncontrast CT. A and B, Slightly decreased density in

right cerebellum , slight displacement of fourth ventricle to left, intact posterior fossa c isterns , and absence of hydrocephalus. C and D, Repeat scans. Complete obliteration of posterior fossa cisterns and fourth ventric le, hydro­cephalus, and more distinc t hypodensity in right cerebellum.

varying degrees of infarction in the posterior fossa. In case 17 there was also an occ ipital lobe infarct. Initially the posterior fossa cisterns were visualized and no hydroceph-

AJNR:3, March i April 1982 CT OF ACUTE POSTERIOR FOSSA INFARCTS 155

A B

Fig. 9. - Case 14. Noncontrast CT. A , Small area of low density in right cerebellum , intact fourth ventri cle and c isterns, and absence of temporal horn dilatation. B , Repeat scan . Larger area of hypodensity in right cerebel­lum , displacement of fourth ven tric le to left. and dilatation of right temporal horn .

Fig . 1 D. - Case 18 . Noncontrast CT. Large area of low density in left cerebe llum , displacement of fourth ven tric le to right , and intact c istern s.

alus was demonstrated. However, when the posterior fossa cisterns became obliterated and hydrocephalus developed, the patient's condition deteriorated . Cases 13 and 14 had emergency surgical removal of infarcted brain in order to decompress the swelling and 'thus prevent brainstem compression . These patients recovered without neurologic deficit within 1 -6 months, Case 17 recovered with nonsur­gical treatment, but had persistent severe neurologic defi­cits, In these three cases the cerebellar infarction was quite extensive; initial CT did not show cisternal or fourth ventric­ular obliteration or hydrocephalus. But follow-up CT did show obliteration of the cisterns and hydrocephalus that correlated with the progressive brainstem compression,

Surgical decompression is a life-saving procedure. Al­though case 17 showed survival without surgery, the result was a persistent vegetative state, In case 18 (fig . 10), the infarct in the cerebellum was also very extensive, compress­ing the fourth ventricle, Although there was very mild early brainstem compression, there was still enough space avail­able for expansion of the infarcted cerebe llum , Injury to the

brainstem was not demonstrated . The outcome of this pa­tient was excellent, with no surgical treatment required ,

Five patients (cases 1 , 2 , 13 , 14, and 16) had vertebral angiography, Occlusive changes were noted in each patient.

Discussion

Acute posterior fossa infarcts may result from occ lusion of the vertebrobasilar artery and / or its branches [2,3,6-9, 14-19]. The c linica l diagnosis of posterior fossa infarct may be difficu lt. Cerebellar infarcts are often associated with and complicated by infarcts of the lateral brainstem (which is supplied by the same arteri es), The manifestation of cere­bellar disturbance has often been overshadowed by the more obvious brainstem dysfunction [3 , 7-9]. Angiographic diagnosis may also be difficult in the presence of isolated occlusion of a small arterial branch. Acute cerebe llar infarcts and accompanying cerebellar swelling may result in brain­stem compression; a large cerebe llar infarct may require surgical decompression in order to reduce injury to the brainstem [4 , 7, 8 , 10-13, 20-25]. However, there are reports of good results after acute cerebellar infarcts without surgical intervention [2 , 14, 17]. Surgery is certain ly not indicated in acute brainstem infarction. Therefore, accurate diagnosis of the type and size of the posterior fossa infarct is essential for clinical management. In our experience, CT is often useful in differentiating cerebe llar from brainstem infarcts,

The mortality rate seems to increase only slightly with increasing age: 34% , group 1; 38.5% , group 2; and 44.5%, group 3 . However , the combined rate of mortality and poor recovery (persistent vegetative states) for group 1 was 56% , indicative of grave prognosis even for the younger patients. In reviewing the CT findings, the younger patients tended to have more associated mass effect than the older patients,

Although angiography is capab le of demonstrating vas­cular occlusions (cases 1, 2, 13, 14 , and 16) [6, 18], the precise site and the size of the infarct was often not c learly identified without CT. CT can demonstrate very early infarcts in the posterior fossa [5]. The fourth ventric le is a good landmark in locating a cerebellar infarct in those cases with isodense infarcts . In cases 1 and 2 , displacement of the fourth ventricle was the major finding of cerebellar infarction (other than the nonvisualization of the posterior fossa cis­terns) . In case 17 there were infarcts on both sides, but the fourth ventri c le was sh ifted away from the larger infarct.

In cases of large or massive infarction , the posterior fossa c isterns and the fourth ventricle were obliterated , Nonvi­sualization of the posterior fossa c isterns may be correlated with clinical manifestations of brainstem compression [11, 13, 26-28]. Obliteration of the posterior fossa cisterns plus hydrocephalus were CT signs of a grave prognosis, (cases 1-3 and 5, table 1). Progressive obliteration of the posterior fossa ciste rns indicated that there was increasing brainstem compression (cases 13 , 14, and 17). This may be an indi­cation for surgical intervention to prevent death or vegetative states from brainstem injury [4 , 21 , 22 , 26- 28].

In those cases with intact posterior fossa cisterns and no hydrocephalus by CT, there was good recovery with non-

156 TSAI ET AL. AJNR:3, March i April 1982

surgical treatment. These CT findings may be used in the c linical monitoring for nonsurgical management (table 1),

We believe that CT should be promptly used for the diagnosis of acute posterior fossa infarcts. These patients should be closely monitored by CT to assist in directing the c linical management in order to prevent grave complica­tions.

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