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Clinical Case Report

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Cerebral venous sinus thrombosis presenting
with multifocal intracerebral hemorrhage and
subarachnoid hemorrhage
A case report
Jing Sun, MD, PhDa, Zhidong He, MDb, Guangxian Nan, MD, PhDa,

∗

Abstract
Rationale: Multifocal cerebral hemorrhage refers to the cerebral hemorrhage in 2 or more lesions at the same time or 48 h in the

brain caused by various causes, which has an acute onset, high mortality rate, and poor clinical treatment effect. Subarachnoid
hemorrhage (SAH) is caused by the direct flow of blood into the subarachnoid cavity due to the rupture of the diseased vessels at the
base or surface of the brain. Cerebral venous sinus thrombosis (CVST) affects approximately 5 people per million and accounts for
approximately 1% of all stroke events. CVST with both SAH and multifocal intracerebral hemorrhage (ICH) as the first presentation is
extremely rare.
Patient concerns: A 57-year-old woman presented with dizziness, nausea, and vomiting.
Diagnosis: Neuroimaging confirmed a diagnosis of CVST.
Interventions: The patient was treated with dehydration, scavenging free radicals, and nerve protection therapy.
Outcomes: After 4 weeks of systematic treatment, the patient resumed independent daily activities and was discharged with only
slight non-fluent aphasia. She did not exhibit recurrent thrombosis at an 18-month follow-up point.
Main Lessons: The usual treatment for sinus thrombosis is anticoagulation or local thrombolysis. Systemic anticoagulation is the
first-line treatment for CVST, even in patients with cerebral hemorrhage or SAH. The present patient’s hemorrhage clearly
contraindicated heparin; therefore, no anticoagulants or thrombolytic agents were administered during the 4-week hospitalization.
We discuss issues for consideration in similar cases and provide an example of determining an individualized approach to treatment.
Abbreviations: CT = computed tomography, CVST = cerebral venous sinus thrombosis, ICH = intracerebral hemorrhage, MRA

= magnetic resonance angiography, MRI = magnetic resonance imaging, MRV = magnetic resonance venography, SAH =
subarachnoid hemorrhage.

Keywords: cerebral venous sinus thrombosis, multifocal hemorrhage, subarachnoid hemorrhage

but can further complicate treatment and prognosis. Here we
describe the case of a 57-year-old woman with interior and
superior sagittal sinus thrombosis, who presented with SAH and
multifocal hemorrhage as the first manifestations. The value of
early diagnosis using computed tomography (CT) and magnetic
resonance venography (MRV) is emphasized because it is
important to identify possible causes of symptoms; it may be
possible to reverse symptoms with appropriate individualized
treatments.

1. Introduction
Cerebral venous sinus thrombosis (CVST) is a rare special
cerebrovascular disease, accounting for 1% of all strokes, but the
mortality rate is as high as 10%.[1,2] There are many causes and
risk factors of CVST, such as pregnancy, oral contraceptive,
infection, trauma, central nervous system tumor, and coagulation
dysfunction diseases. Initial presentation with subarachnoid
hemorrhage (SAH) and intracerebral hemorrhage (ICH) are rare
Editor: N/A.

2. Case report

The authors have no conflicts of interest to disclose.
a

b

The patient was admitted to our hospital with complaints of
dizziness, nausea, and vomiting. She had a clinical history of the
patent oval foramen and ischemic stroke with residual glossolalia. She denied any history of diabetes, hypertension, major
surgery, trauma, nonsteroidal anti-inflammatory drug use, or
illicit drug use. On admission, she was afebrile with blood
pressure of 121/85 mmHg and heartbeat of 63/min. Neurological
examinations revealed incomplete motor aphasia, nystagmus,
and right hemihypalgesia. A CT scan demonstrated linear
high-density images in the partial gutter of the right frontal,
parietal, and occipital lobes, as well as patchy high-density
images in the right parietal lobe and left temporal lobe (Fig. 1).

Department of Neurology, Department of Neurosurgery, China-Japan Union
Hospital of Jilin University, No. 126 Xiantai Street, Changchun, Jilin 130000,
China.

∗

Correspondence: Guangxian Nan, Department of Neurology, China-Japan
Union Hospital of Jilin University, No. 126 Xiantai Street, Changchun, Jilin
130000, China (e-mail: ngx0415@hotmail.com).

Copyright © 2018 the Author(s). Published by Wolters Kluwer Health, Inc.
This is an open access article distributed under the Creative Commons
Attribution License 4.0 (CCBY), which permits unrestricted use, distribution, and
reproduction in any medium, provided the original work is properly cited.
Medicine (2018) 97:50(e13476)
Received: 7 September 2018 / Accepted: 7 November 2018
http://dx.doi.org/10.1097/MD.0000000000013476

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Figure 1. On admission, a CT scan revealed linear high-density images in the partial gutter of the right frontal, parietal, and occipital lobes, as well as patchy highdensity images in the right parietal and left temporal lobes. CT = computed tomography.

Pertinent laboratory findings at the time of initial presentation
revealed that cardiac troponin, coagulation, homocysteine, and
ions, as well as renal and liver function, were normal.
Additionally, the patient’s white blood cell count was 10.22
thousand/cu mm. On the fourth day of hospitalization, the
patient experienced an epileptic seizure. CT re-examination
demonstrated that the right occipital and parietal lobes exhibited
multiple patchy high-density shadows (Fig. 2). Magnetic
resonance angiography (MRA) and MRV confirmed the CT
findings and revealed interior and superior sagittal sinus
thrombosis (Fig. 3). However, both tests were negative for
aneurysms or other vascular malformations. The patient was
diagnosed with CVST and was treated with dehydration,
scavenging free radicals, and nerve protection therapy. No
anticoagulants or thrombolytic agents were administered during
the 4-week hospitalization. At discharge, the patient could
complete independent daily activities and had only slight nonfluent aphasia. Follow-up brain CT at 12 weeks after onset
demonstrated encephalomalacia in the right frontal, temporal,
and parietal lobes, as well as in both the left temporal and
occipital lobes. During the 18-month follow-up, the patient did
not experience recurrent thrombosis, the symptoms of non-fluent

aphasia were improved but did not return to normal, and the
right limb muscle strength was slightly worse than normal,
without sensory disorder.
The study was approved by the Institutional Review Board and
Ethics Committee of China-Japan Union Hospital of Jilin
University. The patient provided written informed consent for
publication of this case report.

3. Discussion
CVST occurs when a blood clot forms in any of the venous
sinuses of the brain. Approximately 5 people per million are
affected by CVST and it accounts for approximately 1% of all
stroke events.[1] Although CVST is observed with increasing
frequency in daily practice and has a variety of nonspecific
clinical symptoms that overlap with other disorders, its
presentation with an associated SAH or ICH via CT and
magnetic resonance imaging (MRI) is infrequent. However, SAH
is becoming more frequently recognized as a potential complication of CVST. Panda et al[3] reported that 10 (4.3%) of 233
patients with CVST exhibited evidence of cortical SAH.
Furthermore, Oda et al[4] found that CVST resulted in 3% of

Figure 2. On the fourth day of hospitalization, CT reexamination demonstrated multiple patchy high-density shadows in the right occipital and parietal lobes. CT =
computed tomography.

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Figure 3. On the fourth day of hospitalization, MRA was normal, whereas MRV revealed interior and superior sagittal sinus thrombosis. MRA = magnetic resonance
angiography; MRV = magnetic resonance venography.

treatment for CVST, due to high efficacy, safety, and feasibility,
even in patients with cerebral hemorrhage or SAH. The 2011
American Heart Association/American Stroke Association
guidelines recommend that once imaging confirms CVST,
anticoagulation should be initiated regardless of whether ICH
is evident at presentation.[1] However, some patients with CVS
and ICH present a quintessential example of the controversy
regarding anticoagulation treatment,[8] thereby emphasizing a
careful consideration of the risks and benefits of anticoagulation
in patients with combined CVST and ICH. The patient in the
present study had SAH and multifocal hemorrhage; therefore,
the extension and severity of the bleed indicated that anticoagulation should not be initiated. Fortunately, the patient
experienced successful recovery after 4 weeks of systematic
treatment. There are no specific recommendations about the
timing of anticoagulation in CVST patients with ICH.[9]
Considering that this patient has many cerebral hemorrhage
lesions, we recommend the patient take oral anticoagulant drugs
after the absorption of intracranial hemorrhage, but the patient
and her family refused.

SAH in a retrospective review, indicating that the presence of
cortical SAH without involvement of the basal cisterns may be an
early indicator of underlying CVST.[3,4] However, the cooccurrence of SAH and multifocal hemorrhage with CVST has
not previously been described.
The distribution of SAH associated with CVST typically differs
from the characteristic pattern of SAH with arterial origins.
Specifically, when SAH is localized at the cerebral convexity and
spares the basal cisterns and skull base, CVST should be
considered. The exact mechanism of cortical CVST-induced SAH
is unknown, although rupture of venous parenchymal hemorrhagic infarcts into the subarachnoid space is a possibility.[5,6]
This mechanism is potentially applicable to the current patient
because signs of multifocal hemorrhage were observed on her CT
scans. Another possible mechanism is venous hypertension and
subsequent rupture of dilated, thin-walled, bridging subarachnoid cortical veins devoid of smooth muscle fibers.[5] In these
cases, SAH typically occurs in the region adjacent to thromboses
in veins or sinuses. This second mechanism may have also
occurred in our patient, who had bleeding in the partial gutter of
the right frontal, parietal, and occipital lobes, adjacent to the
superior sagittal sinus.
In patients with CVST, spontaneous intracranial hemorrhage
accounted for 30% to 40% of ICH.[7] CVST-induced ICH
includes simple cerebral hemorrhage and venous infarction
hemorrhage. Furthermore, the distribution of venous infarction
hemorrhages typically does not conform to the normal distribution of simple cerebral hemorrhage; the hematoma usually occurs
closer to the surface of the brain, with a large area of low density
around the focal point. Intramedullary or subcortical meniscus
hemorrhage is the earliest manifestation of CVST combined with
ICH, and the "zebra striated” hemorrhage is also a common
characteristic of this combination. In the present case, bleeding in
the right occipital and parietal lobes was considered a venous
infarction hemorrhage, which may be attributed to the blockade
of venous sinuses. Increased venous and capillary pressure results
in diapedesis of red blood cells and subsequent rupture of small
vessels. Therefore, ICH may be an extension of this sequence of
events.
Because thrombosis is typically treated with anticoagulation or
local thrombolysis. Systemic anticoagulation is the first-line

4. Conclusion
Cerebral venous thrombosis rarely presents as acute SAH, and
the clinical presentation may mimic an aneurysmal bleed. CVST
should be considered in the differential diagnosis of patients
presenting with SAH without evidence of an aneurysm. The
radiologist plays an essential role in making this oftenunsuspected critical diagnosis to enable prompt and appropriate
treatment.
While anticoagulants are recommended in theory for treatment
of cerebral sinus thrombosis, the present case report illustrates the
imperativeness of individualized therapy. Similarly, intracerebral
hematomas should theoretically be evacuated, although individualized therapy is critical. The present patient’s hemorrhage was
a clear contraindication to heparin. We recognize that successful
neurological recovery was certainly not guaranteed in the present
patient, nor would the same management work in every case;
rather, this case illustrates the issues that must be considered in
similar cases and provides an example of determining an
individualized approach to treatment.
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[4] Oda S, Shimoda M, Hoshikawa K, et al. Cortical subarachnoid
hemorrhage caused by cerebral venous thrombosis. Neurol Med Chir
(Tokyo) 2011;51:30–6.
[5] Cuvinciuc V, Viguier A, Calviere L, et al. Isolated acute nontraumatic
cortical subarachnoid hemorrhage. AJNR Am J Neuroradiol 2010;31:
1355–62.
[6] Kato Y, Takeda H, Furuya D, et al. Subarachnoid hemorrhage as the
initial presentation of cerebral venous thrombosis. Intern Med 2010;49:
467–70.
[7] Girot M, Ferro JM, Canhao P, et al. Predictors of outcome in patients
with cerebral venous thrombosis and intracerebral hemorrhage. Stroke
2007;38:337–42.
[8] Skeik N, Strak MM, Tubman DE. Complicated cerebral venous sinus
thrombosis with intracranial hemorrhage and mastoiditis. Vasc Endovasc
Surg 2012;46:585.
[9] Pizzi MA, Alejos DA, Siegel JL, et al. Cerebral venous thrombosis
associated with intracranial hemorrhage and timing of anticoagulation after hemicraniectomy. J Sroke Cerebrovasc Dis 2016;25:
2312–6.

Author contributions
Data curation: Zhidong He.
Supervision: Guangxian Nan.
Writing – original draft: Jing Sun.
Writing – review and editing: Jing Sun.

References
[1] Saposnik G, Barinagarrementeria F, Brown RDJr, et al. Diagnosis and
management of cerebral venous thrombosis: a statement for healthcare
professionals from the American Heart Association/American Stroke
Association. Stroke 2011;42:1158–92.
[2] Coutinho JM, Zuurbier SM, Stam J. Declining mortality in cerebral
venous thrombosis: a systematic review. Stroke 2014;45:1338–41.
[3] Panda S, Prashantha DK, Ravi Shankar S, et al. Localized convexity
subarachnoid haemorrhage-a sign of early cerebral venous sinus
thrombosis. Eur J Neurol 2010;17:1249–58.

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