Appearance and Disappearance of Empty Delta

1282
Appearance and Disappearance of Empty Delta Sign in
Superior Sagittal Sinus Thrombosis
YUKITO SHINOHARA, M . D . ,
MIEKO YOSHITOSHI, M . D . ,
FUMIHITO YOSHII,
AND
M.D.
SUMMARY The diagnostic value of the empty delta sign on post-infusion CT films was investigated in five
patients with superior sagittal sinus thrombosis subsequently verified angiographically and/or pathologically. The empty delta sign, which has been considered to be unique and reliable in the diagnosis of cerebral
venous sinus occlusion, was observed only on CT films taken one to four weeks after onset, and was not seen
in the extremes of the acute or the chronic stage of the illness. These observations may explain why this sign
has not been apparent in some reports concerning the CT findings of superior sagittal sinus thrombosis.
Recanalization within the thrombus may be the reason why this sign was no longer apparent in the chronic
stage of the patients with superior sagittal sinus thrombosis.
Stroke Vol 17, No 6, 1986
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ALTHOUGH COMPUTED TOMOGRAPHY (CT)
has gained wide acceptance as an accurate and noninvasive technique for the evaluation of intracranial lesions, the value of CT in the diagnosis of superior
sagittal sinus (SSS) thrombosis remains unsettled.
Several reports1"14 have described CT findings in SSS
thrombosis and emphasized the importance of the socalled empty delta sign, clot in the sinus, dilated cerebral veins, multiple focal bilateral parasagittal hemorrhages, and gyral and tentorial enhancement. Among
these findings, the empty delta sign was considered to
be unique and reliable in the diagnosis of SSS occlusion. However, this sign was sometimes not apparent
even in patients in whom cerebral sinus and venous
occlusion was subsequently verified pathologically.
The purpose of this paper is to describe this CT
finding, especially in connection with the diagnosis of
SSS thrombosis.
Report of Patients
Patient One
A 37-year-old male had suddenly developed high
fever up to 38.4°C, diarrhea and headache. He was
admitted to a hospital, but headache and diarrhea lasted for almost five days. Four days before transfer to
our hospital, he showed right-sided hemisensory disturbance followed by hemiparesis on the right side and
total aphasia. After that, repeated generalized convulsions developed and the level of consciousness declined gradually. On admission, the level of consciousness corresponded to stupor, and there was right
hemiparesis including the face; there was total aphasia.
CT scans on admission (four days after onset of hemiparesis) showed a large low density area and multiple
hemorrhages over the left parieto-occipital region, but
the so-called empty delta sign was not apparent on the
enhanced CT films at regular window settings. A cerebral angiogram showed displacement of the anterior
From the Department of Neurology, Tokai University School of
Medicine.
Address correspondence to: Yukito Schinohara, M.D., Department
of Neurology, Isehara, Kanagawa, 259-11, JAPAN.
Received February 6, 1986, revision # 1 accepted June 17, 1986.
cerebral artery from left to right on the AP view of the
arterial phase. The SSS together with the torcular herophili was not visualized and, instead, abnormal corkscrew-like veins which did not reach the sagittal sinuses were observed in the venous phase. Follow-up CT
scans at regular window settings taken 10 days (fig 1,
left) and two weeks after onset both showed a filling
defect at the level of the torcular herophili corresponding to the so-called empty delta sign. The patient was
submitted to a craniectomy to reduce the intracranial
pressure, and at this time the obstructed SSS and engorged superficial cerebral veins were observed. The
empty delta sign was still present on the enhanced CT
films one month later, but it has disappeared three
months later (fig 1, right). Since then, this sign has
never been observed in spite of repeated CT examinations over a period of more than five years.
Patient Two
A 28-year-old female, eight weeks pregnant, suddenly developed severe nausea and headache together
with lassitude, followed by the development of a slight
right hemiparesis. On admission she had neck stiffness
and a mild right hemiparesis. She had a known history
of epilepsy and had had an episode of mild head trauma
two months previously. CT scans taken two years before and two months before admission for evaluation
of epilepsy and head trauma, respectively, showed no
abnormal findings even on enhanced CT films. CT
scans taken two and three weeks after the onset of
nausea and headache both showed a low density area
on the left parietal region, and the empty delta sign was
visualized on the enhanced CT film, both at regular
and at higher window settings (fig 2, left). A cerebral
angiogram confirmed that this patient had an occlusion
of the SSS, but the filling defect within the torcular
herophili was no longer clearly apparent on the CT
films taken 1 month later and had completely disappeared on those taken 3 months later even with increased window width (fig 2, right). CT examinations
repeated at approximately three months and four years
did not show the delta sign.
In addition, CT films of three other patients with
SSS thrombosis verified angiographically were care-
EMPTY DELTA SIGN IN SSS THROMBOSIS/5/i/no/iaro et al
1283
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FIGURE 1. Left — CT scan taken 10 days after onset. The
white arrow indicates empty delta sign. Right — CT scan taken
3 months later. Empty delta sign was not apparent at any scan
level.
FIGURE 2. Left — CT scan taken 2 weeks after onset (Window; 103 HU, Center; 73 HU). The white arrow indicates
empty delta sign. Right — CT scan taken 3 months later. No
empty delta sign was observed.
fully examined retrospectively. The characteristic delta sign was not seen in the acute stage, within 5 days
after the onset of symptoms, nor in the chronic stage,
more than 2 months after the onset, despite repeated
examinations. All five patients described here have
survived to date.
CT scan was no longer apparent in a follow-up CT scan
two months later, but did not discuss the reason for
this.
Fresh blood clot is isodense to the brain8 or may
have slightly increased attenuation on CT films.14 This
might be one of the reasons why we could not observe
the empty delta sign on post-contrast images in patients
in the extremely acute stage although we could not
demonstrate an increased density in the SSS on unenhanced CT films. The obstructed sinus in the chronic
stage usually shows numerous channels of recanalization within the thrombus. 8 '" This perhaps explains
why the empty delta sign was no longer apparent in the
chronic stage of SSS thrombosis.
The empty delta sign is very important for the CT
diagnosis of SSS obstruction, but it may not be apparent in the extremes of the acute or chronic stages of
SSS thrombosis.
Discussion
Barnes and Winestock1 were the first to describe the
CT findings of SSS thrombosis, but they emphasized
the diagnostic value of dynamic radionuclide scanning
for sinus thrombosis rather than CT scanning. Thereafter, several authors2"14 described CT findings in SSS
thrombosis, but the reported findings ranged from normal3' 10- l2 ' l3 to various specific2'4- 6~9-14 and nonspecific3 findings. Among the specific findings on CT, the
empty delta sign of Buonanno et al2 is considered to be
unique and reliable. 6 - 8 - 9 - l4 However, even Buonanno
et al2 found this empty delta sign in only 2 out of 11
patients. Many other workers'- 3~y '•10-'3 failed to detect
this sign despite careful examinations. This discrepancy could be explained by our results. Some of the
above reports did not indicate precisely when the CT
scans were taken in relation to the onset of the illness.
When the CT examinations were repeated not only in
the extremes of the acute or chronic stages, but also in
the sub-acute stage, the frequency of appearance of the
empty delta sign on CT in SSS thrombosis seems to be
higher. When CT scans were taken between one and
four weeks after the onset of symptoms this specific
finding was seen more frequently. Furthermore, the
empty delta sign was more apparent at high display
levels and narrow display windows 6 ' 9 - 14 of CT.
The appearance or disappearance of the empty delta
sign has been described previously by some authors
without comment. Crimmings et al14 described a patient with SSS thrombosis in which CT films did not
show the empty delta sign at five days but shows it
clearly after eight weeks at high display levels and/or
narrow display windows. Brant-Zawadzki et al9 reported that the empty delta sign seen on a post-infusion
References
1. Barnes BD, Winestock DP: Dynamic radionuclide scanning in the
diagnosis of thrombosis of the superior sagittal sinus. Neurology
(Minneap) 27: 656-661, 1977
2. Buonanno FS, Moody DM, Ball MR, Laster DW: Computed cranial tomographic findings in cerebral sinovenous occlusion. J Comput Assist Tomogr 2: 281-290, 1978
3. Kinsley DPE, Kendall BE, Mosely IF: Superior sagittal sinus
thrombosis: an evaluation of the changes demonstrated on computed tomography. J Neurol Neurosurg Psychiat 41: 1065-1068, 1978
4 Manna M, Groves JT: Deep vascular congestion in dura] venous
thrombosis on computed tomography. J Comput Assist Tomogr 3:
539-541, 1979
5. Brisma J: Computer tomography in superior sagittal sinus thrombosis. Acta Radiol Diagn 21: 321-326, 1980
6. Ziljha A, Daiz AS: Computed tomography in the diagnosis of
superior sagittal sinus thrombosis. J Comput Assist Tomogr 4:
124-126, 1980
7. Steinherz PG, Miller LP, Ghavimi F, Allen JC, Miller DR: Dural
sinus thrombosis in children with acute lymphoblastic leukemia.
JAMA 246: 2837-2839, 1981
8 Patronas NJ, Duda EE, Mirfakhraee M, Wollmann RL. Superior
sagittal sinus thrombosis diagnosed by computed tomography.
Surg Neurol 15: 11-14, 1981
Brant-Zawadzki M, Chang GY, McCarty GE: Computed tomography in dural sinus thrombosis. Arch Neurol 39: 446—447, 1982
1284
STROKE
10. Di Rocco C, Iannelli A, Leone G, Moschini M, Valori VM: Heparin-urokinase treatment in aseptic dural sinus thrombosis. Arch
Neurol 38: 431-435, 1981
11. Beal MF, Wechsler LR, Davis KR: Cerebral vein thrombosis and
multiple intracranial hemorrhages by computed tomography. Arch
Neurol 39: 437-438, 1982
12. Shinohara Y, Takagi S, Kobatake K, Gotoh F: Influence of cerebral venous obstruction on cerebral circulation in humans. Arch
Neurol 39: 479-481, 1982
VOL
17, N o
6, NOVEMBER-DECEMBER
1986
13. Barnes BD, Brant-Zawadzki M, Mentzer W: Digital subtraction
angiography in the diagnosis of superior sagittal sinus thrombosis.
Neurology 33: 508-510, 1983
14. Crimmings TJ, Rockswold GL, Yock DH Jr: Progressive postraumatic superior sagittal sinus thrombosis complicated by pulmonary
embolism. J Neurosurg 60: 179-182, 1984
15. Kuramochi S, Hosoda Y, Matsuyama H, Shinohara Y: Thromboendophlebitis obliterans of the dural sinuses associated with hypertrophic pachymeningitis. Vase Surg 13: 104-110, 1979
Effect of Allopurinol on Ischemia and
Reperfusion-Induced Cerebral Injury in
Spontaneously Hypertensive Rats
TORU ITOH, M . D . , MASATO KAWAKAMI, M . D . , * YOICHI YAMAUCHI, B . S . ,
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SADAHIRO SHIMIZU, B . S . , AND MASAKI NAKAMURA, PH.D.t
SUMMARY In spontaneously hypertensive rats, we studied the participation of xanthine oxidase-linked
free radical in ischemia and reperfusion-induced cerebral injury, using allopurinol, a xanthine oxidase
inhibitor. The loss of righting reflex was noted in some animals after a 4 hour occlusion of bilateral common
carotid arteries and 19 of 25 animals died within 72 hours after reperfusion. One hour after reperfusion, the
cerebral water content increased significantly, with an increase in sodium content and a decrease in
potassium content. In 7 animals treated with oral administrations of allopurinol (200 mg/kg) 24 hours and 1
hour before occlusion, no death was found either during occlusion or after reperfusion, and the loss of
righting reflex was noted in only one animal 24—72 hours following reperfusion. The increase in cerebral
water content and accompanied changes in electrolyte contents were clearly prevented by allopurinol. These
results suggest the possibility that the production of xanthine oxidase-linked free radical participates in
cerebral injury due to ischemia and reperfusion in spontaneously hypertensive rats.
Stroke Vol 17, No 6, 1986
XANTHINE OXIDASE ACTIVITY is a major factor
in the generation of superoxide radical, and the production of free radical from xanthine oxidase has been
considered to play an important role in the genesis of
tissue injury due to ischemia and reperfusion. li2 This
has been proved by the evidence that allopurinol, a
tight-binding competitive inhibitor of xanthine oxidase,3 prevents the ischemia and reperfusion-induced
tissue injuries in the stomach, intestine, kidney, and
heart.2' *~* Such a free radical also seems to be implicated in the genesis of ischemia-induced enzyme damage
in the gerbil cerebral cortex.7
In the present study, we studied the effect of allopurinol, a xanthine oxidase inhibitor, on ischemia and
reperfusion-induced cerebral injury after bilateral
common carotid artery occlusion in spontaneously hypertensive rats in order to investigate the importance of
xanthine oxidase-linked free radical in cerebral injury.
Materials and Methods
Fifty-nine male spontaneously hypertensive rats
(Okamoto and Aoki;8 23-37 weeks old, weighing
From the Department of Neurology, St. Marianna University School
of Medicine, Kawasaki, Japan,* and Tokyo Research Laboratories,
Kowa Company, Ltd., Higashimurayama, Tokyo, Japan.t
Address correspondence to: Toru Itoh, M.D., Division of Neurology,
Tokyo Hospital, St. Marianna University School of Medicine, 3-435
Kosugi, Nakahara-ku, Kawasaki, 211, Japan.
Received November 8, 1985; revision # 2 accepted May 30, 1986.
350—450 g), which had systolic blood pressure of
160-200 mm Hg as measured with electrosphygmomanometer (PE-300, Narco Biochem Inc., Houston),
were used.
The animals were anesthetized with ether and fixed
in supine posture, the skin was incised in the ventrolateral neck region and the common carotid arteries were
separated from the surrounding tissue in the bilateral
manner. A cotton thread was put on both arteries and it
was passed through a polyethylene tube (20 mm
length, PE 160, Clay Adams) and then pulled to obstruct completely the blood flow. Then, the tube was
exposed out of the ventrolateral neck region and the
skin was sutured. After the operation under ether anesthesia, the animals were transferred to individual
cages. Four hours following the occlusion, the thread
passing through the tube was cut to reperfuse the blood
flow, and 1, 2, 3, 24 and 72 hours after reperfusion,
neurological symptoms and mortality were observed.
For the study of water and electrolyte contents, animals were anesthetized with intraperitoneal administration of pentobarbital-Na (Somnopentyl, PitmanMore Inc.) 40 mg/kg at 1 hour after reperfusion. In this
study, spontaneously hypertensive rats having the surgical preparation but without carotid artery occlusion
were used as sham-operated animals. Brains were removed immediately after decapitation under anesthesia. The posterior two-thirds of the cerebral hemi-
Appearance and disappearance of empty delta sign in superior sagittal sinus thrombosis.
Y Shinohara, M Yoshitoshi and F Yoshii
Stroke. 1986;17:1282-1284
doi: 10.1161/01.STR.17.6.1282
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