Neurol Med Chir (Tokyo) 42, 383¿386, 2002

Complete Superior and Inferior Sagittal Sinus Thromboses
With Multiple Cranial Nerve Pareses and Transient
Ischemic Attack
—Case Report—
Cahide TOPSAKAL, Mutlu CIHANGIROGLU*, Metin KAPLAN,
Ismail AKDEMIR, and Murat TIFTIKCI
Departments of Neurosurgery and *Radiology, Firat University School of Medicine, Elazig, Turkey

Abstract
A 27-year-old woman with headache and right peripheral facial nerve paresis persisting for over 25
days, and left hemiparesis for 2 days, which had all been gradually improving, was admitted to our
hospital as she suddenly developed horizontal and vertical diplopia. She had right fourth and sixth
cranial nerve pareses, papilledema, and right orbital venous congestion, and also experienced a seizure
on the day of admission. Magnetic resonance (MR) imaging and MR venography revealed complete superior and inferior sagittal sinus thromboses and significant collateral venous channels, but no parenchymal lesion. Fourth and seventh cranial nerve pareses and the left hemiparesis resolved completely
within 2 days, but she concurrently developed an episode of right hemiparesis, which lasted for 30
minutes. The patient recovered with medical therapy. MR venography showed recanalization of both
sinuses. She was neurologically intact except for minimal right abducens nerve paresis at discharge, 40
days after admission. Multiple cranial nerve pareses with transient ischemic attack is an extremely rare
manifestation of superior sagittal sinus thrombosis. Transient functional disturbance due to temporary
reduction of tissue perfusion caused by overload of the collateral channels is more likely to be responsible for the transient ischemic attack and reversible ischemic neurological deficit.
Key words: cranial nerve paresis, reversible ischemic neurological deficit,
sinus thrombosis, transient ischemic attack

Introduction

and inferior sagittal sinus thromboses.

Case Report

Dural sinus thrombosis is a rare but life-threatening
pathology which requires special care for correct
diagnosis and treatment. The clinical manifestations
of superior sagittal sinus (SSS) thrombosis are nonspecific but characterized by the symptoms of either
isolated intracerebral hemorrhage (ICH), i.e.,
headache, papilledema, blurred vision,2,9,12,16) or ICH
symptoms together with seizures, focal deficits,
progressive coma, and death.6,10,12,14) Sporadic cases
of cranial nerve pareses associated with SSS thrombosis are rare,1,4,6,15) and only three cases with transient ischemic attack (TIA) have been reported since
1966.3,5)
We describe a case of multiple cranial nerve
pareses associated with TIA due to complete SSS
Received

January 18, 2002;

Accepted

sagittal sinus,

A 27-year-old woman with complaints of headache
and right facial nerve paresis persisting for over 25
days, and left hemiparesis for 2 days, which had all
been gradually improving, was admitted to our
hospital on May 30, 2000 as she suddenly developed
horizontal and vertical diplopia. On the same day,
she suffered vomiting and generalized convulsion.
Neurological examination found she was somnolent
and disoriented (Glasgow Coma Scale score 9) with
neck stiffness, right fourth, sixth, and mild seventh
cranial nerve pareses, papilledema, right orbital
venous congestion, and mild left hemiparesis
(Fig. 1). Lumbar puncture revealed increased intracranial pressure (ICP) (31 cmH2O) and xanthochromia. Computed tomography (CT) had previ-

June 8, 2002

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C. Topsakal et al.

Fig. 1

Photographs showing peripheral facial (A)
and abducens nerve pareses (B) on the right.

Fig. 2

Coronal T1-weighted (A) and axial T2weighted (B) magnetic resonance images
showing the signal changes consisted with
indolent flow in the sagittal sinus.

ously been evaluated as normal, but magnetic
resonance (MR) imaging on the day of admission
revealed sagittal sinus thrombosis (Fig. 2). Carotid
angiography and MR venography demonstrated
complete SSS and inferior sagittal sinus thromboses
and prominent collateral venous circulation (Fig. 3).
Fourth and seventh cranial nerve pareses and the
left hemiparesis resolved completely within 2 days.
However, she suffered an episode of right hemiparesis, which lasted for 30 minutes, and depression of
consciousness, so she was monitored in the intensive care unit until she recovered within 3 days.
Detailed hematological and biochemical profiles,
including serum protein C, protein S, and antithrombin III levels, were investigated. Coagulation
profiles and collagen assays were measured. Focal
or systemic sepsis was excluded. Medical therapy
included heparin and warfarin administration with
repeated prothrombin time controls, anticonvulsant

Fig. 3

Right carotid angiogram, venous phase (A)
and magnetic resonance venogram (B)
showing no filling of the superior and inferior sagittal sinuses, and dilation of the
vein of Labb áe and other anastomotic veins
together with a large number of collateral
veins.

Fig. 4

Magnetic resonance venogram after treatment clearly showing both sagittal sinuses
due to recanalization.

and isotonic hydration therapies, and cerebrospinal
fluid (CSF) drainage by lumbar puncture.
MR venography 18 days later displayed good
recanalization of both sinuses (Fig. 4). Lumbar puncture findings and CSF pressure were within the
physiological ranges. She was neurologically intact
except for minimal right abducens nerve paresis at
discharge 40 days later.

Discussion
SSS thromboses are identified at autopsy in 50% of
cases, and the mortality is 56%. Thromboses of large
dural sinuses may be spontaneous or follow direct
infection, either systemic or of the adjacent epidural
or subdural spaces. Aseptic (primary) intracranial
venous occlusive disease tends to favor unpaired
sinuses and is associated with pregnancy and puer-

Neurol Med Chir (Tokyo) 42, September, 2002

Sinus Thromboses With Multiple Cranial Nerve Pareses and TIA
perium, malignancy, hypercoagulable state (thrombophilia), lupus erythematosus, Behçet's disease,
familial Mediterranean fever, oral contraceptives,
intracranial surgery, trauma, dehydration, cachexia,
cardiac diseases, diabetes mellitus, and homocysteinuria.2,6,9,12) In our case, no etiological factor
could be found. The ratio of women to men is 2:1.
The mean age at the time of diagnosis was 27
years.14) Our female patient was also 27 years old.
Sinus thrombosis can only be identified by MR imaging, angiography, or MR venography. CT shows
multiple irregular high dense foci mainly in the
parietal lobes and the ventricular shift to one side,
and the so-called ``empty triangle'' sign and gyral enhancement may be observed after administration of
contrast medium.10) However, CT was not helpful in
our case. MR imaging demonstrated the sinus
thrombosis. Carotid angiography reveals delayed
circulation, poor filling of the cortical veins, and absent or narrow SSS with a zigzag-shaped margin.10)
In our case, the absence of both sagittal sinuses and
presence of disseminated collateral venous circulation on angiography were confirmed by MR
venography, which is the most reliable and noninvasive method for evaluating the venous sinuses.
Thromboses of the transverse and sigmoid sinuses
are usually asymptomatic if the thrombosed sinus is
nondominant or associated with rich collateral circulation.9) Furthermore, the clinical manifestation
remains silent in chronic cases as good collateral
venous circulation can develop. However, acute
venous outflow obstruction leads to venous hypertension and resultant acute ICP increase. SSS
thrombosis either occurs as isolated ICH, i.e.,
pseudotumor cerebri,2,9,12,16) which manifests as
headache, papilledema, and/or blurred vision. The
only presenting symptom in 53–66.7% of cases is
persistent headache of variable duration, location,
and severity.12,14) Papilledema occurs in 33% of
cases,10–12,14) whereas visual loss in 25% of cases may
progress to optic atrophy.12,14) CSF pressure usually
increased to over 20 cmH2O.2) SSS thrombosis does
not usually occur as isolated ICH, but manifests as
seizures, focal deficits, progressive coma, and death
(38%). Seizure is the second commonest sign (49%)
after headache, which may progress to status epilepticus.12,14) In our patient, the headache suggestive of
ICH preceded the focal neurological disturbance by
1–3 days.12) Hemiparesis, quadriparesis, or paraparesis is the third most common symptom (19–
48%).6,10,12,14)
SSS occlusion alone will not cause cranial nerve
findings except for visual obscuration and abducens
nerve paresis due to increased ICP. Thus, the clinical findings may be due to increased ICP. Pseu-

Neurol Med Chir (Tokyo) 42, September, 2002

385

dotumor cerebri is known to be associated with ocular motility deficits, most commonly sixth cranial
nerve paresis as a false-localizing sign.1,10) Very seldom fourth cranial nerve paresis15) and facial nerve
involvement1,4,6) have been reported as false-localizing signs. In our case, fourth, sixth, and seventh
cranial nerve pareses occurred together and were
reversible. Fourth cranial nerve paresis was a reversible ischemic neurological deficit (RIND) which
lasted for 2 days. The right hemiparesis lasted 30
minutes occurred as a TIA.
Fourth, sixth, and seventh cranial nerve pareses
are individually reported to be false-localizing signs
of intracranial hypertension. However, multiple
cranial nerve pareses are hard to attribute only to intracranial hypertension. Venous thrombosis reduces
the venous outflow from the brain and diminishes
the effective blood flow to the involved area. Such
venous engorgement causes white matter edema.
The increased venous pressure may also cause
hemorrhage. These processes may all contribute to
ICP increase, but focal findings can be expected due
to edema, hemorrhage, and/or venous infarction. In
our patient, no edema, infarction, or hemorrhage
could be identified, with the xanthochromic blood
providing only evidence of minimal hemorrhage.
The more likely mechanism of RIND and TIA in this
patient is thought to be a transient functional disturbance due to a temporary reduction of tissue perfusion caused by the overload of the collateral channels.5)
A better outcome can be achieved with earlier
diagnosis and treatment, particularly in patients
with identifiable disorders causing SSS thrombosis,
as well as thrombosis with relatively minimal extension.14) Systemic heparin administration remains the
best treatment. Hydration with intravenous administration of isotonic fluids should be maintained
to avoid an increase in ICH. If the presentation is
delayed, treatment with acetazolamide and nonsteroid anti-inflammatory drugs, and lumbar puncture (possibly shunt placement) can avoid the
ophthalmologic complications of pseudotumor
cerebri.9) Papilledema and visual disturbances
should improve immediately after venous drainage
is established from the retina and head of the optic
nerve. If the diagnosis is established shortly after the
thrombosis occurs, direct endovascular thrombolysis with urokinase, streptokinase, or tissue plasminogen activator may be the best therapeutic option but should only be considered in a selective
group of patients, probably those worsening under
medical therapy.7,8,13) Long-term treatment after
resolution of the acute phase consists of heparin
and/or warfarin for over 3–6 months. In our case, no

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386

surgical intervention was needed since almost complete cure was achieved with medical therapy.
10)

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Address reprint requests to: C. Topsakal, M.D., Department of Neurosurgery, Firat University School of
Medicine, 23100, Elazig, Turkey.
e-mail: cdtopsakal＠yahoo.com.

Neurol Med Chir (Tokyo) 42, September, 2002