135

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DURAL SINUS THROMBOSIS: REPORT OF TWO CASES Mitsunobu IDE, Minoru JIMBO, Masaaki YAMAMOTO, Yutaka UMEBARA and Shinji HAGIWARADepartment of Neurosurgery (Director: Prof. MinoruJIMBO), Tokyo Women's Medical College Daini Hospital

(Received July 2, 1993)

Diagnosis of dural sinus thrombosis is frequently difficult and may be delayed due to

lack of specific neurological signs. The initial diagnostic clues are usually present on

computed tomographic (CT> seans. We report two cases of dural sinus thrombosis, in

which routine precontrast CT scans visualized thrombi as increased attenuation within

the sinuses. We stress that recognition of this specific CT finding of dural sinus

thrombosis on routine precontrast study can lead to early diagnosis and prompt

appropriate therapy.

Introduction

Dural sinus thrombosis may occur more fre-

quently than is suspected. Towbin found dural

sinus thrombosis in 9% of 182 consecutive au-

topsies of adult casesi}. Dural sinus thrombosis

can be asymptomatic or present with only mild

neurological deficits, but it may also have an

acute, rapidly fatal course. Diagnosis of dural

sinus thrombosis is frequently difficult and may

be delayed due to lack of specific neurological

signs. Early diagnosis and prompt appropriate

treatment can lead to decreased risk of mortality

and morbidity. The initial diagnostic clues are

usually present on computed tomographic (CT)

scans. We report two cases of acute dural sinus

thrombosis and discuss the CT findings of this

condition; hyperdense intraluminal thrombi de-

tected on precontrast CT scans.

Case Report

Patient 1.

A six-year-old boy began to vomit frequently

and complained of continuous headache, and was

admitted to a local hospital. Four days later, he

was transferred to our facility immediately after a

generalized seizure. On arrival, he was stuporous

and exhibited left hemiparesis and nuchal stif-

-1429

fness. Platelet count, bleeding time and coagula-

tion time were within normal limits. Coagulation

studies demonstrated normal prothrombin and

partial thromboplastin times. Low fibrinogen (120

mg/100 ml) and high fibrin degradation product

concentrations (O.45 mg/1) were considered to

have resulted from aggravated intravascular

coagulation and fibrinolysis, respectively. Precon-

trast CT scans on admission revealed a hyper-

dense hematoma in the right temporal lobe, as-

sociated with hypodense edema in the right hem-

isphere. The precontrast CT scans also demon-

strated areas of increased attenuation in the

regions of the superior sagittal, straight and right

transverse sinuses and the Galenic and internal

cerebral veins (Fig. 1). The attenuation value in

these intraluminal regions was 75-90 Hounsfield

units (HU). Based on these CT findings, a diagno-

sis of dural sinus thrombosis was made and ther-

apy with fructose added glycerol (GLYCEOL@)

and low molecular weight dextran was initiated.

Cerebral angiography could not be performed.

Despite aggressive medical treatment, his neuro-

logical condition deteriorated rapidly and he be-

came comatose on the second hospital day. Repeat

CT scans demonstrated a new hematoMa in the

right thalamus and widespread hypodense areas

in the midbrain and the bilateral basal ganglia. He

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Fig. 1 Patient 1. Precontrast computed tomographic scans demonstrating areas of increased attenuation

in the region of the superior sagittal, straight, and right transverse sinuses and the Galenic and internal

cerebral veins. The attenuation value in these regions is 75-90 Hounsfield units. Hemorrhagic venous

infarcts are also present in the right temporal lobe.

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The right transverse and sigmoid sinuses, which have

been peeled from the skull with forceps, are occluded by

fresh thrombus.

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Fig. 3 Patient 1. Transectional view of the superior

sagittal sinus, demonstrating an anternortem thrombus.

(hematoxylin and eosin ×40)

died on the third hospital day.

At autopsy, the brain was edematous andweighed 1,350 g. The cerebral surface was enti-

rely covered with severe subarachnoid hemor-

rhage. The superior sagittal, straight, bilateral

transverse and sigmoid sinuses were occluded by

fresh antemortem thrombi (Figs. 2 and 3). The left

transverse and sigmoid sinuses were hypoplastic.

The internal cerebral and Galenic veins were also

thrombosed. On brain section there were exten- '

sive hemorrhagic infarcts of the midbrain, both

thalami and the basal ganglia.

Patient 2.

A 38-year-old woman was admitted to our faci-

lity with a 24-hour history of worsening headache

and frequent vomiting. On admission, her con-

sciousness was clear. There was neither neuro-

logical deficit nor papilledema. She had no definite

past history of otic disease. She had been taking

oral contraceptives for 10 months. Routine coagu-

- 1430 -

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Fig. 4 Patient 2. Precontrast computed tomographic scans demonstrating areas of increased attenuation

in the region of the left transverse and superior sagittal sinuses. The attenuation value of these regions is

80-90 Hounsfield units.

Fig. 5 Patient 2. Anteroposterior (A) and lateral (B) views of digital subtraction angiQgram demonstrating

occlusion of the superior sagittal and left transverse sinuses.

lation studies showed normal findings. Precon-

trast CT scans revealed areas of increased at-

tenuation within the superior sagittal and left

transverse sinuses, but neither parenchymal

lesions nor subarachnoid hemorrhage (Fig. 4).

Digital subtraction angiography (DSA) demon-

strated obstruction of the superior sagittal and

left transverse sinuses (Fig. 5). Magnetic reson-

ance (MR) imaging demonstrated hyperintense

areas in the superior sagittal and left transverse

sinuses on both Tl- and T2-weighted images with

concurrent mastoiditis on the left side (Fig. 6). A

diagnosis of dural sinus thrombosis was made and

therapy with low molecular weight dextran and

systemic fibrinolytic agent was initiated. Uro-

kinase was administered through continuous

venous infusion (2 X 105 units/day) fpr five days.

In addition, an otologist was consulted for man-

agement of the mastoiditis. Headache and vomit-

ing subsided within a week. She was discharged a

month later and had no neurological deficits.

Follow-up MR imaging demonstrated recanaliza-

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138

Fig. 6 Patient 2. Axial Tl- (A) and T2-weighted (B) and coronal Tl-weighted (C) magnetic resonance

images demonstrating hyperintense areas in the superior sagittal and left transverse sinuses (arrows)

with concurrent mastoidotis on the left side.

Fig. 7 Patient 2. Coronal Tl-weighted magnetic reson-

ance image two months after the onset demonstrating

recovery of flow void sign in the superior sagittal and left

transverse sinuses <arrows).

tion of

(Fig. 7).

the left transverse and sagittal slnuses

Discussion

Dural sinus thrombosis has various etiologies.

Septic dural sinus thrombosis may be a serious

complication of meningitis or encephalitis2}. It can

also occur as a result of middle ear or paranasal

sinus infections. Aseptic dural sinus thrombosis is

seen during pregnancy and the puerperium3). It

has been reported in several young women given

oral contraceptives4)5). Dehydration and cachexia,

as well as a number of hematological and vascular

diseases, have been reported to be associated with

aseptic dural sinus thrombosis6)nyiO). In patient 1,

neither antemortem nor postmortem examination

revealed the etiology of the disease. The clinical

course of patient 1 was fulminant because in-

volvement of the deep venous system caused

hemorrhagic infarcts in the midbrain and thal-

amus. Factors contributing to increased mortality

include rapid thrombus evolution and involve-

ment of the deep venous system. The internal

cerebral vein is often affected in childrenii). We

speculate that oral contraceptives and mastoiditis

were the major causes of dural sinus thrombosis

in patient 2.

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139

DSA, MR imaging and MR angiography areexcellent tools for the diagnosis of dural sinus

thrombosisi2}i3). However, the initial diagnostic

clues are usually present on CT scans, and their

recognition can lead to early diagnosis and prompt

appropriate therapy. The use' of CT scanning for

diagnosing dural sinus thrombosis has been re-

ported by a number of authors2)ii)i4}i5}. Buonanno

et al. have advocated the "empty triangle" sign as

a CT finding specific to superior sagittal sinus

thrombosisi4). Infusion of contrast medium and a

narrow CT display window, and a high window

level, may be necessary to demonstrate this sign.

However, these special window settings are not

likely to be implemented unless dural sinus

thrombosis is suspected. Less specific signs in-

clude cerebral edema, small ventricles, hemor-

rhage within the cerebral parenchyma, and gyral

enhancementi4)i6}i7).

We wish to cali attention to other CT signs of

dural sinus thrombosis. In our two patients,

routine precontrast CT scans visualized thrombi

as increased attenuation within the sinuses be-

cause of the high hemoglobin concentration of

fresh thrombi. Direct visualization of a thrombus

as increased attenuation within the sinuses and

veins on precontrast CT scans has been reported

previously2}ii)i5)i8}. In fact, the attenuation value of

the superior sagittal sinus ranges from 50 to 68

HU. This could be misleading if the diagnosis

were made without measuring the actual attenua-

tion value of the lesioni5). In our two patients, the

attenuation value of the affected sinuses and

veins was 75--90 HU, which is in good agreement

with that of fresh thrombus'9>. These areas of'

increased attenuation corresponded closely with

the extent of thrombosis revealed by the autopsy

or DSA.

We could not treat patient 1 with fibrinolytic or

anticoagulant therapy because the hemorrhagic

infarction was far advanced on admission. In

contrast, we successfully treated patient 2 with

systemic fibrinolytic therapy following early

diagnosis. According to Kalbag and Woolf, seizure

onset signals the development of hemorrhagic

infarction and systemic use of anticoagulants is

contraindicated thereafter20). From this view-.

point, early diagnosis and prompt appropriate

therapy are crucial. Di Rocco et al. reported

successful systemic use of anticoagulant and

fibrinolytic agents2i}. Successful treatment by

local infusion of fibrinolytic agents has recently

been reported22>N24). These reports encourage clini-

cians to attempt these innovative therapies in

otherwise hopeless cases of dural sinus throm-

bosis.

Referecnes

1) Towbin A: The syndrome of latent cerebral venous

thrombosis: Its frequency and relation to age and

congestive heart failure. Stroke 4: 419-430, 1973.

2) Wendling LR: Intracranial venous sinus thrombosis:

Diagnosis suggested by computed tomography. AJR 130: 978-980, 1978.

3) Cross JN, Castro PO, Jennett WB: Cerebral strokes

associated with pregnancy and the puerperium. Br Med

J 3: 214, 19684) Atkinson EA, Fa' irburn B, Heathfield KWG: In- tracranial venous thrombosis as a complication of oral

contraceptives. Lancet 1: 914-918, r970

5) Shende MC, Lourie H: Sagittal sinus thrombosis related to oral contraceptives. Case report.J Neurosurg

33: 714-717, 1970

6) Bousser MG: Cerebral vein thrombosis in Behcet's syndrome: Arch Neurol 39: 322, 1982

7) David RB, Hadfield MG, Vines FS et al: Dural sinus occlusion in leukemia. Pediatrics 56: 793-796,

19758) Donhowe SP, Lazaro RP: Dural sinus thrombosis in paroxysmal nocturnal hemoglobinuria. Clin Neurol

Neurosurg 86: 149-152, 1984

9) Dunsker SB, Torres-Reyes E, Peden JC Jr: Pseu- dotumor cerebri associated with idiopathic cryofi-

brinogeneMia: Report of a case. Arch Neurol 23: 120-127, 1970

10) Iijima S, Nakamura S, Shio H et al: A case of superior sagittal sinus thrombosis with primary thrombocythemia. Rjnsho Shinkeigaku 20: 333-338,

198011) Justich E, Lammer J, Fritsch G et al: CT diagnosis

of thrombosis of dural sinuses in childhood. EurJ Radiol

4: 294-295, 1984

l2) McMurdo SK Jr, Brant-Zawadzki M, Bradley WG et al: Dural sinus thrombosis: Study using intermediate field strength MR imaging. Radiology

161: 83-86, 1986

13) Padayachee,TS, Bingham JB, Graves wo et al: Dural sinus thrombosis: Diagnosis and follow-up by

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140

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16）Virapongse　C，　Cazenave　C，　Quis董ing　R　et　a1：The

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　　．cases　of　dural　s査nus　thrombosis．　Radiol．ogy　162：

　　779－785，1987

17）Zil㎞a　A，　Daiz　AS：Computed　tomography　in　the

　　diagnosis　of　superior　sagittal　sinus　thrombosis．JCom－

　　put．　Assist　Tomogr　4：124－126，1980

18＞Crimmins　TJ，　Rockswold　GL，　Wock　DH：Progres－

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静脈洞血栓症の2例

東京女子医科大学　附属第二病院脳神経外科．

イデ　ミツノブジン．ボ井出　光信・神保ウメバラ　　　ユタカ　　ハギワラ

梅原　　裕・萩原

　ミノル　　ヤマモト　　マサァキ

　実・山本　昌昭シン　ジ

信司

　頭痛，嘔吐などを主訴に来院し，初期には特異的な症候を呈さない静脈洞血栓症の診断は，しばし

ぽ困難で，診断が遅れることが多い．

　静脈洞血栓症は早期に診断し，速やかに適切な治療を開始せねぽ，症例1のように致命的となるこ

と．が少なくない．　　　　　　　　　　　　　　　　　　　・

　本症の確定診断は脳血管撮影によってなされることが多いが，本．症を疑わなけれぽ実施されること．

は少ない．本症を疑うきっかけは，やはりCT　scanであると考えられる．これまで，静脈洞血栓症に

特異的なCT所見としては㌔mpty　triangle　sign”が知られているが，これは，慢性期の所見であり，

造影剤の投与および特殊なwindow　settingを要する．．やはり，本症を疑ってかからなければ見落とさ

れる可能性が高い．

　我々の2症例ではplain　CT　scanで静脈洞内の新鮮血栓がhigh　density　areaとして描出されてお

り，その範．囲は，剖検所見あるいは脳血管撮影所見と一致していた．この所見は静脈洞血栓症の早期

の診断，治療の上で重要なものと考え報告する．

一． P434一