Neurol Med Chir (Tokyo) 40, 361 ~ 365, 2000

Sigmoid Sinus Thrombosis After Mild Closed Head Injury
in an Infant: Diagnosis by Magnetic Resonance Imaging
in the Acute Phase

—Case Report—

Hideki SATOH, Kiyoshi KUMANO, Ryo OGAMI, Tohru NISHI, Jun ONDA,
Shigeru NISHIMURA, and Kaoru KURISU*

Department of Neurosurgery, Kitakyushu General Hospital, Kitakyushu, Fukuoka;
*Department of Neurosurgery, Hiroshima University School of Medicine, Hiroshima

Abstract

Intracranial sinus thrombosis following a mild closed head injury without a skull fracture or in-
tracranial hematoma is extremely rare. A 23-month-old girl presented with vomiting and gait ataxia 1
day after occipital trauma. Computed tomography revealed a slightly increased density area in the
region of the left sigmoid sinus. T,-weighted magnetic resonance (MR) imaging demonstrated an
isointense area in the left sigmoid sinus and T,-weighted imaging showed a hyperintense area reflecting
the characteristics of oxyhemoglobin. MR angiography and cerebral angiography indicated occlusion
of the left sigmoid sinus. After 4 days of conservative treatment, her symptoms subsided completely.
Follow-up MR angiography and cerebral angiography showed recanalization of the sigmoid sinus. The
MR images and MR angiograms were useful for both early diagnosis and follow-up. Treatment should

reflect the severity of individual cases, and early diagnosis will help achieve a good outcome.

Key words: sinus thrombosis, sigmoid sinus, closed head injury, magnetic resonance imaging

Introduction

Intracranial sinus thrombosis is a relatively rare
event associated with a poor prognosis, largely be-
cause the diagnosis was difficult. Mild closed head
injury without skull fractures or intracranial hema-
tomas is an extremely rare cause, with only 11
reported cases.*°"?1522526 We treated an infant with
sigmoid sinus thrombosis complicated by mild
closed head injury. The thrombosis was identified in
the acute phase by magnetic resonance (MR) imag-
ing.

Case Report
A 23-month-old girl fell from a height of approxi-

mately 1 m and struck her occiput on November 8,
1998. She suffered no loss of consciousness or

vomiting and was able to walk. However, vomiting
and gait disturbance appeared by the next morning.
The patient was first taken to the pediatric depart-
ment of a local hospital and then referred to our in-
stitution for further evaluation. Her history included
medical treatment for asthma for 3 months. Her
family history was unremarkable.

Neurological signs and symptoms on admission
included moderate headache complaints, decreased
muscle tone, and gait ataxia. There were no abnor-
malities of the cranial nerves or motor or sensory
disturbances in the extremities. Fundoscopy showed
no evidence of a choked disc. No signs of dehydra-
tion were present. Biochemical and hematologic
screening tests disclosed no abnormal findings
(hematocrit 34.6%, platelet count 25.8 x 10*/ul,
white blood cell count 8.9 x 10°/ul, and C-reactive
protein 0.1 mg/dl). All bleeding and coagulation test

Received June 30,1999; Accepted March 14, 2000

Author’s present address: H. Satoh, M.D., Department of Neurosurgery, Hiroshima Prefectural Hospital, Hiroshima,

Japan.
362 H. Satoh et al.

Fig. 1 T,-weighted magnetic resonance (MR) image on admission demonstrating an isointense area
in the left sigmoid sinus (left), and T,-weighted image demonstrating a hyperintense area
(center). Phase-contrast MR angiogram (velocity encoding gradient = 15 cm/sec) showing
occlusion of the left sigmoid sinus (right). There is no midline shift of the fourth ventricle.
arrow: lateral wall of the sigmoid sinus, arrowhead: small extradural hematoma.

Fig. 2 Cerebral angiogram performed on the sec-
ond hospital day also demonstrating occlu-
sion of the left sigmoid sinus.

results were within the normal ranges (bleeding time
2 min, prothrombin activity 82% of control, activat-
ed partial thromboplastin time 32.5 sec, fibrin
degradation products 3.1 ug/ml). The control protein
S activity was 102% and the control protein C ac-
tivity was 123%, and the lupus anticoagulant was
not detectable. The lumbar puncture opening pres-

Fig. 3 T,-weighted magnetic resonance image 15
days after admission (left) and cerebral an-
giogram on the following day (right) demon-
strating that the left sigmoid sinus has
recanalized. arrow: flow void phenomenon
of the left sigmoid sinus.

sure was 240 mmH.0O, and cell numbers and protein
concentration in the cerebrospinal fluid were within
the normal ranges. Computed tomography (CT) re-
vealed a region of slightly increased density in the
sigmoid sinus, which was enhanced by administra-
tion of contrast medium. T;-weighted MR imaging
obtained on the same day showed an isointense
area, and T,-weighted imaging demonstrated a
hyperintense area in the left sigmoid sinus (Fig. 1
left, center). MR angiography (phase-contrast

Neurol Med Chir (Tokyo) 40, July, 2000
Sigmoid Sinus Thrombosis After Mild Closed Head Injury 363

method) demonstrated occlusion of the left sigmoid
sinus (Fig. 1 right). Cerebral angiography confirmed
occlusion of the left sigmoid sinus on November 10
(Fig. 2).

Intravenous drip infusion of glycerol and steroid
was administered to treat the increased intracranial
pressure. Headache and vomiting resolved 3 days
after admission, and the patient was able to walk 4
days after admission. MR imaging and MR an-
giography 15 days after admission disclosed that the
left sigmoid sinus had recanalized (Fig. 3 left). Con-
ventional cerebral angiography on the following day
showed the same finding (Fig. 3 right). The patient
was discharged from the hospital 17 days after ad-
mission with no neurological deficits. MR imaging
and MR angiography 3 months after hospital dis-
charge confirmed patency of the sigmoid sinus.

Discussion

Causes of sinus thrombosis include infection of the
head and neck, pregnancy and delivery, oral con-
traceptives, and dehydration. More recently, sinus
thrombosis has resulted from hypercoagulable states
caused by protein S deficiency, protein C deficien-
cy, or antiphospholipid antibodies.” Sinus throm-
bosis had been considered a very ominous event
until recently, when mild cases have been resolved
without residual neurological deficits because of
technical advances.” Some cases of skull fracture or
intracranial hematoma following head injury have
caused thrombosis by direct compression of the
sinus,” but thrombosis after mild closed head inju-
ty without such complications is exceptionally rare.

Symptoms of sinus thrombosis can be classified
into two groups: manifestations of increased in-
tracranial pressure such as headache, choked disc,
and impaired consciousness”; and focal signs in-
cluding convulsive seizures and hemiplegia caused
by venous infarction, which is often hemorrhagic.”
Cerebellar ataxia is not common, but gait ataxia oc-
curred in all five cases with sigmoid sinus throm-
bosis (including three with skull fractures), sug-
gesting that gait ataxia is characteristic of sigmoid
sinus involvement. The time interval between injury
and symptom onset varies from moments after inju-
ry to 8 months,” which is an obstacle to accurate
diagnosis of traumatic sinus thrombosis.

The severity of the manifestations of sinus throm-
bosis depends on the extent of the thrombus, the
anatomy of collateral veins, and the rate of progres-
sion of thrombosis.” Sinus thrombosis following
mild closed head injury in the 12 reported cases,
including the present patient, originated in the su-
perior sagittal sinus in five cases, the transverse si-

Neurol Med Chir (Tokyo) 40, July, 2000

nus in five, the sigmoid sinus in four, and the
straight sinus in one (multiple sinuses were involved
in 2 cases). Condition on discharge was described in
11 patients. No deaths occurred, and neurological
sequelae were noted in four patients, three of whom
had superior sagittal sinus thrombosis. All three
patients with sigmoid sinus thrombosis showed
favorable outcomes on discharge.

Proposed mechanisms of sinus thrombosis after
mild closed head injury have involved endothelial
damage within the venous sinus that causes throm-
bosis by activating the coagulation system. The
brain also contains an abundance of thromboplastin
that is released after injury. Thromboplastin induces
an abnormal hypercoagulable state like the destruc-
tion of platelets and erythrocytes."'*?) However,
fibrinolytic activity is higher in normal venous walls
than in artery or capillary walls, and thrombi in the
sinuses frequently recanalize with time due to
fibrinolysis.”? This mechanism may account for the
mild cases of sinus thrombosis.

The characteristic CT findings of sinus thrombo-
sis include the cord sign, dense vein sign, and
empty-delta sign following the administration of
contrast agents.*’°” Indirect evidence such as
hemorrhagic infarcts, venous infarcts, extensive
cerebral edema, and narrowing of the cerebral ven-
tricles suggest sinus thrombosis in many cases.”
Cerebral angiography, particularly digital subtrac-
tion angiography, is the method of choice for diag-
nosing sinus thrombosis. However, complete ab-
sence of the transverse and sigmoid sinus may be a
normal anatomic variation, so diagnosis of throm-
bosis in these areas should proceed cautiously.” MR
imaging findings in sinus thrombosis have also been
reported.’”’? Four phases were identified based on
sequential changes.’? In the first few hours, the
thrombi appear as isointense to slightly hypointense
on the T,-weighted images, and hyperintense on the
T.-weighted images, reflecting the presence of oxy-
hemoglobin.”” Several hours after thrombus forma-
tion, the thrombus appears as hypointense on the
T.-weighted images as deoxyhemoglobin becomes
dominant. In the present case, the MR imaging
findings were extremely valuable to establish the
diagnosis during the acute phase, within several
hours of thrombus formation, as confirmed by the
signal intensities characteristic of oxyhemoglobin.
Moreover, the phase-contrast MR angiography was
used to depict veins selectively by appropriate
flow-velocity settings.”"?? MR imaging was superior
to CT or cerebral angiography in four ways: throm-
bus in the sinus was visualized with no contrast
medium; time elapsed since thrombosis could be
estimated; the procedure was noninvasive and safe
364

for performance in a child; and sequential follow-
up imaging was facilitated.

No consensus has been reached for the treatment
of sinus thrombosis, because the severity varies
greatly from case to case. Hypertonic diuretics and
steroids are useful to treat increased intracranial
pressure, but severe cases may require barbiturate
therapy and hypothermia. Anticoagulant therapy
with heparin or warfarin is frequently administered
to limit extension of the thrombus. Secondary ex-
tension of the thrombus to cortical and deep veins
has been found in autopsy cases, stressing the need
to prevent extension.) Anticoagulant therapy for
sinus thrombosis improves outcome, even in
patients with hemorrhagic infarct, and does not in-
crease the risk of exacerbation hemorrhagic com-
ponents of infarcts.” However, since traumatic si-
nus thrombosis can be accompanied by direct
hemorrhagic injury, anticoagulant therapy should
proceed carefully with adequate monitoring for
complications such as new bleeding. Local throm-
bolytic injections of urokinase or tissue plasminogen
activator to facilitate recanalization may be given
directly into the occluded sinus by intravascular
techniques,’"*”® but evaluation of the therapeutic
effects and complications including pulmonary em-
bolism is required.

The present case of sigmoid sinus thrombosis fol-
lowing mild closed head injury in an infant was
treated successfully as MR imaging allowed early
diagnosis and observation of sequential changes.
Treatment must be both prompt and appropriate for
the individual patient to achieve a good outcome.

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Address reprint requests to: H. Satoh, M.D., Department of

Neurosurgery, Hiroshima Prefectural Hospital, 1-5-
54 Ujina-Kanda, Minami-ku, Hiroshima 734-8530,
Japan.