Unusual association of diseases/symptoms

CASE REPORT

Transient ischaemic attack: an exceptional
presenting syndrome of a superior sagittal sinus
thrombosis
Assunta Scuotto, Raffaele D’Avanzo, Massimo Natale, Michele Rotondo
Department of Neuroscience,
Second University of Naples,
Naples, Italy
Correspondence to
Professor Assunta Scuotto,
assunta.scuotto@unina2.it

SUMMARY
We report a case of a transient ischaemic attack (TIA) as
an exceptionally rare form of cerebral vein thrombosis.
A 41-year-old man presented with a headache and five
episodes of a transient left hemiparesis lasting
approximately 10–15 min over the course of 2 weeks.
Arterial origins of the disease were ruled out by detailed
investigations. However, MR venography revealed a
superior sagittal sinus thrombosis with numerous
prominent collateral venous channels. No parenchymal
lesion was seen. After medical therapy, no further
transient neurological deficit occurred. Follow-up MR
venography showed sinus recanalisation.

BACKGROUND
Interest in this case lies in the fact that venous sinus
thrombosis (VST), a rare life-threatening pathology,
unusually presents transitory focal deficits in its
course. Although exceptional, venous sinus thrombosis (TIA)-like events due to VST should be taken
into account, requiring special care to ensure
correct diagnosis and treatment.

CASE PRESENTATION
A 41-year-old man was admitted because of a headache and recurrent transient left hemiparesis. During
the last 2 weeks, he experienced a total of five episodes of mild left-sided weakness, lasting 10–15 min
without any lapses of consciousness. His headache
was unresponsive to analgesics and was increasing in
intensity during the attacks; it was diffuse and dull,
sometimes accompanied by nausea. No triggers for
the neurological events were identified. On admission, the neurological examination was normal.
Physical examination showed no abnormalities.
His medical history was unremarkable. In terms
of vascular risk factors, he had been smoking <5
cigarettes/day for the past 12 years. Family history
was non-contributory.
Initial working diagnoses included TIAs, seizures
and hemiplegic migraines. Focal seizure episodes,
generally lasting a few minutes or less, were previously excluded: routine EEG performed during an
episode of hemiparesis was normal.

To cite: Scuotto A,
D’Avanzo R, Natale M, et al.
BMJ Case Rep Published
online: [ please include Day
Month Year] doi:10.1136/
bcr-2013-200894

INVESTIGATIONS
Brain CT was normal. Electrocardiography, echocardiography, carotid ultrasonography, MRI of the
brain and MR angiography (MRA) of the cerebral
arterial vessels were unremarkable, while MR venography (MRV) detected superior sagittal sinus

Scuotto A, et al. BMJ Case Rep 2013. doi:10.1136/bcr-2013-200894

thrombosis (figure 1A). The haematological and
biochemical profiles were normal. Thrombophilia,
vasculitis and infective screening were negative.

DIFFERENTIAL DIAGNOSIS
The differential diagnosis chiefly included cerebral
arterial thromboembolism and/or cardiogenic embolism, which are the most common causes of TIAs.
Although less frequent and/or exceptional, other conditions such as vasculitis, cerebral vasospasm due to
sympathomimetic drugs, hypercoagulable state,
syncope, migraine, partial seizures, hypoglycaemia,
labyrinthine disorders and exceptional subepidural
haematomas, subarachnoid haemorrhage and neurobrucellosis were likewise considered and excluded.
Detailed laboratory investigations (ie, hypercoagulability tests as protein C, protein S, antiphospholipid
antibodies, homocysteinemia, antithrombin, rheumatoid factor, erythrocyte sedimentation rate, C reactive
protein) along with neuroradiological procedures
allowed for the proper diagnosis.

TREATMENT
Medical treatment included subcutaneous lowmolecular-weight heparin administration for 3 weeks.
He was discharged on anticoagulant therapy (warfarin)
for 3 months.

OUTCOME AND FOLLOW-UP
The headache subsided 1 week after anticoagulation therapy. No further attacks presented during
hospitalisation or at the 14-month follow-up. MRV,
performed 1 and 12 months after treatment (figure
1B), detected full recanalisation of the affected
sinus. Actually, it would be better to plan and recommend a neuroimaging follow-up 3–6 months
after diagnosis to assess the recanalisation of the
occluded cortical vein/sinuses in stable patients.

DISCUSSION
Cerebral venous thrombosis is a rare life- threatening pathology with an estimated annual incidence
of 3–4 cases per million in adults and 7 cases per
million in neonates.1
Among the most common risk factors are the use
of oral contraceptives, pregnancy and puerperium,
which contribute to making the disease more frequent in women than in men. Other causes such as
cerebral neoplasms, infections and traumas are less
frequently encountered. In 15–20% of patients,
cerebral venous thrombosis remains unprovoked.
Also, in the present case, no aetiological factor
1

Unusual association of diseases/symptoms
Figure 1 (A) MR venography show
extensive thrombosis in the superior
sagittal sinus, with extensive cortical
venous collateral formation. (B) MR
venography 12 months later depicts
complete recanalisation of the superior
sagittal sinus.

could be found. The most frequently encountered sinuses are
the superior sagittal (62% of patients) and the transverse (40%),
but in two-thirds of cases more than one sinus is involved.
Clinical manifestations are variable and not specific, depending on the oedema and/or increased intracranial pressure, cerebral haemorrhages and cerebral infarcts. Signs and symptoms
include headache (the most common one with no specific features), seizures, focal neurological deficits, papilloedema and
consciousness alteration. Recurrent transient focal deficit is an
exceedingly rare manifestation of cerebral venous thrombosis.
To the best of our knowledge, less than half a dozen cases have
been previously reported in the literature.2–7
At present, the pathogenesis of TIA caused by VST still
remains debatable. In the absence of parenchymal lesions as in
the described case, a functional/metabolic disturbance, probably
related to perfusion failure, might be considered the origin of
the neurological deficit.
VST should be regarded as a continuing process of disequilibrium between prothrombotic and thrombolytic mechanisms
rather than as an abrupt monophasic process. Consequently,
local areas of the brain could be only functionally/metabolically
disturbed but not irreversibly damaged.8
Although collateral pathways in venous sinus disease are generally believed to be well established because of the slow growth
of the venous thrombus, a discrepant moment of venous drainage can occur before the adequate opening of the collateral
channels. Flow dynamic forces can collide at the level of capacitance vessels after which the tissue perfusion pressure may be
reduced, which results in a neurological deficit.3
Early diagnosis is essential to minimie morbidity and improve survival of patients with VST. However, diagnosis may be overlooked or
delayed mainly because of the wide spectrum of clinical presentations
along with the possible lack of indirect imaging signs such as parenchymal abnormalities, that is, venous infarcts, brain oedema, etc.
Usually MRV allows a proper diagnosis, seldom requiring
additional digital angiography.
Anticoagulant treatment, initially with heparin and subsequently with oral vitamin K antagonists, is crucial. Usually oral
anticoagulant is administered only for 3 months if the risk
factor of VST is transient and/or removed; otherwise, it can be
prolonged as in the case of severe thrombophilia or of other
permanent risk factors such as myeloproliferative neoplasms.1 9
Other treatments, such as local or systemic thrombolysis, are
currently still under evaluation. These options could be associated
with a high risk of intracranial bleeding and should therefore be
considered only for patients who deteriorate despite adequate
anticoagulation.9 Conversely, according to a recent report,10
2

endovascular thrombolytic treatment might cure the chronic
thrombosis and recanalise the cerebral venous sinus.

Learning points
▸ We suggest that patients with transient ischaemic attack
(TIA)-like episodes and headache should be carefully investigated
in terms of cerebral venous thrombosis, especially if detailed
investigations for arterial–cardiac thromboembolic aetiologies are
completed and common causes of TIA are excluded.
▸ MR venography should be additionally performed when
neuroradiological studies exclude arterial origins of the
disease. Digital subtraction angiography could be required in
selected cases.
▸ Early diagnosis and anticoagulant treatment reduce
morbidity and improve survival.
▸ The optimal duration of anticoagulant treatment is not
currently well established.

Competing interest None.
Patient consent Obtained.
Provenance and peer review Not commissioned; externally peer reviewed.

REFERENCES
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Published Online First: 27 May 2013. doi: 10.1016/j.jstrokecerebrovasdis.2013.04.005

Scuotto A, et al. BMJ Case Rep 2013. doi:10.1136/bcr-2013-200894

Unusual association of diseases/symptoms

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