Background

Thrombosis of the venous channels in the brain is an uncommon cause of cerebral infarction relative to arterial
disease, but it is an important consideration because of its potential morbidity. (See Prognosis.)
Knowledge of the anatomy of the venous system is essential in evaluating patients with cerebral venous
thrombosis (CVT), since symptoms associated with the condition are related to the area of thrombosis. For
example, cerebral infarction may occur with cortical vein or sagittal sinus thrombosis secondary to tissue
congestion with obstruction. (See Presentation.)
Lateral sinus thrombosis may be associated with headache and a pseudotumor cerebrilike picture. Extension
into the jugular bulb may cause jugular foramen syndrome, while cranial nerve palsies may be seen in
cavernous sinus thrombosis as a compressive phenomenon. Cerebral hemorrhage also may be a presenting
feature in patients with venous sinus thrombosis. (See Presentation.)
Imaging procedures have led to easier recognition of venous sinus thrombosis (see the images below), offering
the opportunity for early therapeutic measures. (See Workup.)

Left lateral sinus thrombosis demonstrated on magnetic resonance venography (MRV). This 42-year-old woman presented
with sudden onset of headache. Physical examination revealed no neurologic abnormalities.

Axial view of magnetic resonance (MR) venogram demonstrating lack of flow in transverse sinus.

The following guidelines for CVT have been provided by the American Heart Association and the American
Stroke Association[1] :

In patients with suspected CVT, routine blood studies consisting of a complete blood count, chemistry
panel, prothrombin time, and activated partial thromboplastin time should be performed.
Screening for potential prothrombotic conditions that may predispose a person to CVT (eg, use of
contraceptives, underlying inflammatory disease, infectious process) is recommended in the initial clinical
assessment.
Testing for prothrombotic conditions (including protein C, protein S, or antithrombin deficiency),
antiphospholipid syndrome, prothrombin G20210A mutation, and factor V Leiden can be beneficial for the
management of patients with CVT. Testing for protein C, protein S, and antithrombin deficiency is generally
indicated 2-4 weeks after completion of anticoagulation. There is a very limited value of testing in the acute
setting or in patients taking warfarin.
In patients with provoked CVT (associated with a transient risk factor), vitamin K antagonists may be
continued for 3-6 months, with a target international normalized ratio of 2.0-3.0.
In patients with unprovoked CVT, vitamin K antagonists may be continued for 6-12 months, with a
target international normalized ratio of 2.0-3.0.
For patients with recurrent CVT, venous thromboembolism (VTE) after CVT, or first CVT with severe
thrombophilia (ie, homozygous prothrombin G20210A; homozygous factor V Leiden; deficiencies of protein
C, protein S, or antithrombin; combined thrombophilia defects; or antiphospholipid syndrome), indefinite
anticoagulation may be considered, with a target international normalized ratio of 2.0-3.0.
For women with CVT during pregnancy, low-molecular-weight heparin (LMWH) in full anticoagulant
doses should be continued throughout pregnancy, and LMWH or vitamin K antagonist with a target
international normalized ratio of 2.0-3.0 should be continued for 6 weeks postpartum (for a total minimum
duration of therapy of 6 months).
It is reasonable to advise women with a history of CVT that future pregnancy is not contraindicated.
Further investigations regarding the underlying cause and a formal consultation with a hematologist or
maternal fetal medicine specialist are reasonable.
It is reasonable to treat acute CVT during pregnancy with full-dose LMWH rather than unfractionated
heparin.
For women with a history of CVT, prophylaxis with LMWH during future pregnancies and the
postpartum period is reasonable.

Etiology
Many causative conditions have been described in cerebral venous thrombosis (CVT). These may be seen
alone or in combination. For example, a prothrombin gene mutation in association with oral contraceptive use
raises the odds ratio for developing CVT.

Sinusitis
Infection may occur by extension from the paranasal sinuses. These cases also may be associated with
subdural empyema. Bacterial meningitis as a coexistent condition should be considered in these cases. Frontal
sinuses are the most common source of infection, with spread through the emissary veins between the
posterior sinus mucosa and the meninges. Rarely, sphenoid sinusitis may be associated with cavernous sinus
thrombosis. Multiple organisms are to be considered, Staphylococcus aureus being the most common. In
chronic infections, gram-negative organisms and fungi such as Aspergillus species may be found.

Trauma and surgery

Trauma may also be an etiologic event. Cerebral sinus thrombosis easily may be overlooked in cases of minor
head trauma. Neurosurgical procedures such as dural taps and infusions into the internal jugular vein have
been implicated as well.

Hypercoagulable states
Many medical conditions have been associated with CVT. For example, hypercoagulable states associated with
the antiphospholipid syndrome, protein S and C deficiencies, antithrombin III deficiency, lupus anticoagulant,
and the Leiden factor V mutation may result in CVT. Antibodies against the fibrinolytic receptor, annexin A2
(titer >3 standard deviations), are significantly associated with CVT.[2]Pregnancy also is associated with a
hypercoagulable tendency. Malignancies may be associated with hypercoagulable states as well, and therefore
may be risk factors.

Intracranial hypotension
Isolated cortical venous thrombosis has been associated with intracranial hypotension syndrome, but only
rarely. In a study, Schievink and Maya found that CVT was present in only 3 (2.1%) out of 141 patients with
spontaneous intracranial hypotension. [3]

Lumbar puncture
A few cases of CVT have been reported after lumbar puncture (LP), suggesting a causal association. In a study
by Canhao et al, LP induced a sustained decrease in mean blood flow velocity (BFV) in the straight sinus (SS),
suggesting that the decrease in venous blood flow is a possible mechanism contributing to the occurrence of
CVT. In the study, the investigators used transcranial Doppler ultrasonography to register the mean BFV of the
SS before, during, and after LP. LP induced a decrease of 47% in mean BFV in the SS, with the mean
decrease being significant immediately at the end, 30 min after, and more than 6 hours after LP.[4]

Medications
Several medications are reported to increase the risk of CVT, including the following:

Oral contraceptives - Including the third-generation formulations

Corticosteroids
Epsilon-aminocaproic acid
Thalidomide
Tamoxifen
Erythropoietin
Phytoestrogens
L-asparaginase
Heparin - Heparin therapy has been reported to produce thrombotic thrombocytopenia with associated
venous sinus thrombosis

Additional disease risk factors

Other diseases that have been described as risk factors for CVT include the following:

Inflammatory bowel diseases, such as Crohn disease and ulcerative colitis, are described as risk
factors for venous thrombosis [5] ; corticosteroids used in treatment of these conditions may play a causative
role
Pregnancy and puerperium are important considerations in women of childbearing age
Hematologic conditions, including paroxysmal nocturnal hemoglobinuria, thrombotic thrombocytopenic
purpura, sickle cell disease, and polycythemia, are to be considered
Collagen-vascular diseases, such as systemic lupus erythematosus, Wegener granulomatosis, and
Behet syndrome, have been reported to be associated with CVT
Hyperhomocysteinemia is a strong and independent risk factor for CVT, being present in 27-43% of
patients with CVT but in only 8-10% of the general population; whether treatment with folate, pyridoxine,
and/or cobalamin reduces the risk of CVT is unclear
Nephrotic syndrome
Dehydration
Spontaneous intracranial hypotension
High altitude
Hepatic cirrhosis
Sarcoidosis

Epidemiology
International occurrence
The incidence of cerebral venous thrombosis (CVT) is difficult to determine, but generally, it is believed to be an
uncommon cause of stroke, with the reported ratio of venous to arterial strokes being 1:62.5. In 1973, Towbin
reported CVT in 9% of 182 autopsies,[6] while in 1995, Daif reported a frequency in Saudi Arabia of 7 cases per
100,000 hospital patients.[7]
However, with the advent of newer imaging techniques, the reported incidence of CVT is likely to increase as
less severe cases are found.

Sex- and age-related demographics

CVT is believed to be more common in women than in men. In a series of 110 cases, Ameri and Bousser found
a female-to-male ratio of 1.29:1.[8]
In 1992, Ameri and Bousser reported a uniform age distribution in men with CVT, while 61% of women with
CVT were aged 20-35 years.[8] This difference may be related to pregnancy or the use of oral contraceptives. [9]

Prognosis
Smith demonstrated the efficacy of anticoagulant and thrombolytic therapy in patients with cerebral venous
thrombosis (CVT). In his study, he compared outcomes of patients who were treated with heparin and local
infusion of urokinase (12 patients) with those of patients who received no treatment (21 patients). [10] The results
appear in the Table, below.
Table. Patients With Cerebral Venous Thrombosis Treated With Heparin and Local Infusion of Urokinase vs
Nontreated Group (Open Table in a new window)
Treated Group, % (n = 12)

Nontreated Group, % (n = 21)

Full recovery

62.5

29

Mild disability

12.5

13

Severe disability

12.5

9.6

Fatal outcome

12.5

48

Morbidity and mortality

Herniation attributable to unilateral mass effect is the major cause of death in CVT. In CVT patients with large
parenchymal lesions causing herniation, decompressive surgery has been lifesaving and often results in good
functional outcome, even in patients with severe clinical conditions. [11]
Mortality in untreated cases of venous thrombosis has been reported to range from 13.8-48%; this high
mortality rate may be a reflection of clinical severity at entrance into the study. Between 25% and 30% of
patients have full recovery.
In a Portuguese study that prospectively analyzed 91 patients with CVT over a mean 1-year follow-up interval,
the majority of patients experienced complete recovery.[12] Of the patients analyzed, 7% died in the acute phase,
1% died during the one year follow-up, 82% recovered completely, and 1% were dependent; 59% developed
thrombotic events during the follow-up, 10% had seizures, 11% complained of severe headaches, and 1 patient
experienced severe visual loss.
In 2003, Buccino et al found a good overall outcome in their reinvestigation of a series of 34 patients with
confirmed CVT.[13] However, 10 patients (30%) had episodic headaches, 3 patients (8.8%) had seizures, 4
patients (11.7%) had pyramidal signs, and 2 (5.9%) had visual deficits. Mild nonfluent aphasia was seen in 3
patients. Working memory deficit and depression of mood were seen in 6 patients (17.6%)

History
Patients with cerebral venous thrombosis (CVT) may present with headache. [14]Although thunderclap headache
usually indicates subarachnoid hemorrhage (SAH), it may also be seen in sinus thrombosis.
SAH has been described as the presenting event with CVT. CVT should be considered in the workup of SAH,
especially when the basilar cisterns are not involved. [15]
Patients with lateral sinus thrombosis may present with a pseudotumor cerebrilike syndrome. Using a
technique called auto-triggered elliptic-centric-ordered 3-dimensional gadolinium-enhanced magnetic
resonance venography (MRV), Farb et al found that 27 of 29 patients with idiopathic intracranial hypertension
had bilateral sinovenous stenosis; this was seen in only 4 of 59 control subjects. [16]
Nausea and vomiting may also be associated with CVT. In some cases, seizures, which can be recurrent,
occur. Some patients may experience a decreased level of consciousness that progresses to coma.
Focal neurologic deficit may develop, depending on the area involved. Hemiparesis may occur, and in some
cases of sagittal sinus thrombosis, weakness may develop in the lower extremity. This also may occur as
bilateral lower extremity involvement. Aphasia, ataxia, dizziness, chorea, and hemianopia all have been
described.
Cranial nerve syndromes are seen with venous sinus thrombosis. These include the following:

Vestibular neuronopathy
Pulsatile tinnitus
Unilateral deafness
Double vision
Facial weakness
Obscuration of vision

Site of headache versus location of sinus involvement

Wasay et al found little association between headache location and the site of sinus involvement in patients
with CVT. In their study, the authors described the pattern and location of headache in 200 consecutive patients
with a proven diagnosis of CVT to identify an association between the site of the headache and location of
sinus involvement. The quality of headache was reported as throbbing (9%), bandlike (20%), thunderclap (5%),
and other (pounding, exploding, stabbing, etc) (20%).

The authors found no association between headache location and the site of sinus thrombosis except in cases
of sigmoid sinus thrombosis, in which 17 of 28 patients (61%) with involvement of the sigmoid sinus alone or in
combination with the transverse sinus had pain in the occipital and neck region. There was no association
between lateralization of pain and the site of thrombosis. [17]

Physical Examination
The effect of cerebral venous thrombosis (CVT) on mental status is quite variable, with some patients showing
no change in alertness, others developing mild confusion, and still others progressing to coma.
Cranial nerve findings may include papilledema, hemianopia, oculomotor and abducens palsies, facial
weakness, and deafness. If the thrombosis extends to the jugular vein, the patient may develop involvement of
cranial nerves IX, X, XI, and XII with the jugular foramen syndrome.
Thrombosis of the superior sagittal (longitudinal) sinus may present with unilateral paralysis that then extends
to the other side secondary to extension of the clot into the cerebral veins. Because of the location, this may
present as a unilateral lower extremity weakness or paraplegia.
Cavernous sinus thrombosis with obstruction of the ophthalmic veins may be associated with proptosis and
ipsilateral periorbital edema. Retinal hemorrhages and papilledema may be present. Paralysis of extraocular
movements, ptosis, and decreased sensation in the first division of the trigeminal nerve often are observed.
Although unusual, cortical vein thrombosis may be seen in the absence of dural sinus involvement. These
cases are associated with varied focal deficits, including aphasia, hemiparesis, hemisensory loss, and
hemianopia.

Differential Diagnoses

Abducens Nerve Palsy

Blood Dyscrasias and Stroke

Cavernous Sinus Syndromes

Cytomegalovirus Encephalitis in HIV

Head Injury

Intracranial Epidural Abscess

Neurosarcoidosis

Pediatric Status Epilepticus

Pseudotumor Cerebri

Staphylococcal Meningitis

Subdural Empyema

Systemic Lupus Erythematosus (SLE)

 Approach Considerations

The diagnosis of cerebral venous thrombosis (CVT) is made on the basis of clinical presentation and
imaging studies (see the images below), while clinical laboratory studies are useful for determining the
possible causes of CVT.

Axial view of magnetic resonance

(MR) venogram demonstrating lack of flow in transverse sinus.

Coronal view of magnetic resonance

(MR) venogram demonstrating lack of flow in the left transverse and sigmoid sinuses.

Lab studies

A complete blood count (CBC) is performed to look for polycythemia as an etiologic factor. Decreased
platelet count would support thrombotic thrombocytopenic purpura; leukocytosis might be seen in
sepsis. (If heparin is used as treatment, platelet counts should be monitored for thrombocytopenia.)
Antiphospholipid and anticardiolipin antibodies should be obtained to evaluate for antiphospholipid
syndrome. Other tests that may indicate hypercoagulable states include protein S, protein C,

antithrombin III, lupus anticoagulant, and Leiden factor V mutation. These evaluations should not be
made while the patient is on anticoagulant therapy.
Sickle cell preparation or hemoglobin electrophoresis should be obtained in individuals of African
descent.
Erythrocyte sedimentation rate and antinuclear antibody studies should be performed to screen for
systemic lupus erythematosus, Wegener granulomatosis, and temporal arteritis. If levels are elevated,
further evaluation, including of complement levels, anti-deoxyribonucleic acid (DNA) antibodies, and
neutrophil cytoplasmic antibodies (ANCA), could be considered.
Urine protein should be checked and, if elevated, nephrotic syndrome considered. Liver function
studies should be performed to rule out cirrhosis.

EEG

An electroencephalogram (EEG) may be normal, show mild generalized slowing, or show focal
abnormalities if a unilateral infarct occurs. An EEG is helpful in evaluating a seizure focus.

Procedures

Lumbar puncture (LP) is helpful in evaluating for meningitis as an associated infectious process in
cerebral venous thrombosis (CVT). However, a large, unilateral hemispheric lesion or posterior fossa
lesion demonstrated on CT or MRI scan is a contraindication for LP.
In the past, compression of the jugular vein unilaterally with pressure measurement was utilized.
Pressure may be elevated if thrombosis of the contralateral transverse sinus is present. However,
collateral circulation or incomplete compression of the jugular vein may yield a false-negative result.
Moreover, elevation of the intracranial venous pressure is a concern, as it may precipitate herniation.
As the maneuver adds little to the diagnosis, it usually is not performed.

D-Dimer Levels

D-dimer values may be beneficial in screening patients who present in the emergency department for
headache evaluation.
In a study of 18 patients with cerebral venous thrombosis (CVT), Tardy et al reported that D-dimer
levels of less than 500 ng/mL had a negative predictive value for ruling out the diagnosis in patients
with acute headache.[18]
In a prospective study of 54 consecutive patients with headache suggestive of CVT, Lalive found that
12 had CVT and, of those, 10 had D-dimer levels greater than 500 ng/mL. [19] The 2 patients with
confirmed CVT and a D-dimer level of less than 500 ng/mL had a history of chronic headache lasting
longer than 30 days.
In a study by Kosinski et al, D-dimers were positively correlated with the extent of thrombosis and
negatively correlated with the duration of symptoms in patients with cerebral sinus thrombosis. The
investigators prospectively studied 343 patients with symptoms suggesting cerebral sinus thrombosis.
[20]
The diagnosis was confirmed in 35, with 34 of these patients showing elevated D-dimer levels
greater than 500 mcg/L. Of the 308 patients not having CVT, 27 had positive values. Sensitivity was
97.1%, with a negative predictive value of 99.6%. Specificity was 91.2%, with a positive predictive
value of 55.7%.
The D-dimer test does not establish the diagnosis of CVT, and more definitive studies, such as
magnetic resonance venography (MRV), are necessary. Likewise, if a high suspicion for CVT exists,
the test cannot definitely exclude the diagnosis but can indicate that the presence of CVT is very
unlikely.

CT Scanning

Computed tomography (CT) scanning is an important imaging technique, as it is often the first imaging
study obtained. It may show evidence of infarction that does not correspond to an arterial distribution.
However, in the absence of a hemorrhagic component, demonstration of the infarct may be delayed for
as long as 48-72 hours. (See the image below.)

Computed tomography (CT) scan

demonstrates a left posterior temporal hematoma in a 38-year-old woman on oral contraceptives (the only
identified risk factor).

CT scanning is also useful for ruling out other conditions, such as neoplasm, and in evaluating
coexistent lesions, such as subdural empyema. CT scanning of the sinuses is useful in evaluating
sinusitis, while CT scanning of the mastoids may be helpful in lateral sinus thrombosis.
An empty delta sign appears on contrast scans as enhancement of the collateral veins in the superior
sagittal sinus (SSS) walls surrounding a nonenhanced thrombus in the sinus. However, the sign is
frequently absent. Early division of the SSS can give a false delta sign. The dense triangle sign formed
by fresh coagulated blood in the SSS and the cord sign representing a thrombosed cortical vein are
extremely rare.

CT angiography

CT angiography has also been used to visualize the cerebral venous system. Ozsvath et al compared
CT and MR projection in the identification of cerebral veins and thrombosis. [21] CT venography was
superior to MR in identification of cerebral veins and dural sinuses. CT was equivalent to MR in
identification of dural sinus thrombosis and therefore is a viable alternative to MRV in the examination
of patients with suspected dural sinus thrombosis. The maximum-intensity-projection technique used,
however, did not allow direct visualization of the thrombus by CT or MR technique.

MRI

MRI shows the pattern of an infarct that does not follow the distribution of an expected arterial
occlusion. It may show absence of flow void in the normal venous channels. Mas et al described MRI
findings of increased intraluminal signal on all planes and with all pulse sequences in patients with
lateral sinus thrombosis. (See the image below.) [22]

Contrast-enhanced magnetic
resonance imaging (MRI) scan showing lack of filling of left transverse sinus.

MRV

MRV is an excellent method of visualizing the dural venous sinuses and larger cerebral veins. (See the
images below.)

Left lateral sinus thrombosis

demonstrated on magnetic resonance venography (MRV). This 42-year-old woman presented with sudden onset
of headache. Physical examination revealed no neurologic abnormalities.

Same patient as in the previous image.

One week after treatment with heparin, the magnetic resonance (MR) venogram displayed increased flow in the
left lateral sinus consistent with early recanalization of the sinus; headache had resolved at this point.

Magnetic resonance venogram (MRV)

- axial view; A = lateral (transverse) sinus; B = sigmoid sinus; C = confluence of sinuses; and D = superior sagittal

sinus.
Magnetic resonance venogram (MRV) - sagittal view; A =
lateral (transverse) sinus; C = confluence of sinuses; D = superior sagittal sinus; and E = straight sinus.

Since thunderclap headaches are not limited to SAH and may be seen with cerebral venous
thrombosis (CVT), lack of evidence of SAH in a patient with such headaches should prompt
examination with MRV.

SSPCA

Single-slice phase-contrast angiography (SSPCA) takes less than 30 seconds and provides rapid and
reliable information. Many neurologists now consider it to be the procedure of choice in diagnosing
cerebral venous thrombosis. In a study of 21 patients, Adams demonstrated a specificity and sensitivity
of 100% for SSPCA when compared with alternative imaging techniques. [23]

Flow gap versus thrombosis in MRV

Ayanzen described transverse sinus flow gaps in 31% of patients with normal MRI findings who were
studied with MRV; 90% of these were in the nondominant transverse sinus, and 10% were in the
codominant sinuses. None was seen in the dominant sinus.[24] These should not be mistaken for
thrombosis.

Contrast Studies

Carotid arteriography with delayed filming technique to visualize the venous system was the procedure
of choice in the diagnosis of venous thrombosis prior to the advent of MRV. It is an invasive procedure
and is therefore associated with a small risk.
If MR studies are not diagnostic, conventional angiography should be considered. Direct venography
can be performed by passing a catheter from the jugular vein into the transverse sinus, with injection
outlining the venous sinuses.

Approach Considerations
With regard to stabilization, medical management of patients with cerebral venous thrombosis (CVT) is similar
to that of patients with arterial stroke.
Specific therapy for CVT involves anticoagulation or thrombolytic therapy.[25, 26]However, the use of
anticoagulation in CVT has been a subject of consternation among neurologists as concern has been

expressed over the possibility of increasing hemorrhage in patients treated in this manner. Existing data
support the use of systemic anticoagulation as an initial therapy in all patients, even in the presence of
intracranial hemorrhage.[25]
Studies by Einhaupl in 1991[27] and by de Bruijn and Stam in 1999[28] indicated that anticoagulation can be used
safely in CVT.

Frontal sinusitis
Frontal sinusitis should be aggressively treated before it leads to subdural empyema or CVT

Altered mental status or hemiplegia

Patients with altered mental status or hemiplegia should be given nothing by mouth to prevent aspiration.
Intravenous (IV) fluids should not be hypotonic solutions. Normal saline is recommended at a rate of
approximately 1000 mL in 24 hours. To decrease intracranial pressure, the patients head should be elevated
30-40 at all times. In the treatment of stroke patients, supplemental oxygen has not been shown to be
beneficial unless the patients level of consciousness is decreased.

Surgical care
In cases of severe neurologic deterioration, open thrombectomy and local thrombolytic therapy have been
described as beneficial.[25, 26, 29, 30]
Herniation attributable to unilateral mass effect is the major cause of death in cerebral venous thrombosis
(CVT). In CVT patients with large parenchymal lesions causing herniation, decompressive surgery has been
lifesaving and often results in good functional outcome, even in patients with severe clinical conditions. [11]

Thrombolytic Therapy
Thrombolytic therapy has been described in several case reports as beneficial in patients with cerebral venous
thrombosis (CVT). These patients were treated with infusion of a thrombolytic agent into the dural venous
sinus, utilizing microcatheter technique. This treatment at present is limited to specialized centers but should be
considered for patients with significant deficit.
A report describes the use of a rheolytic catheter device in a patient who had not responded to microcatheter
instillation of urokinase. The rheolytic catheter was designed for use in the coronary circulation and delivers 6
high-velocity saline jets through a halo device at the tip of the catheter. This leads to a Bernoulli effect that
breaks up the thrombus. In addition, the particulate debris is directed into an effluent lumen for collection in a
disposable bag. The catheter was advanced into the sagittal sinus, resulting in restoration of venous flow and
reduction of intracranial pressure.

Anticonvulsant Therapy
Seizures should be treated with appropriate anticonvulsants. Fosphenytoin is recommended for the treatment
of seizures in patients who require a parenteral formulation. Alternatively, phenobarbital or sodium valproate
injection may be utilized if the patient is allergic to phenytoin. Diazepam or lorazepam may be used to treat

status epilepticus, but the patient also should be given an anticonvulsant with a longer duration of action to
prevent recurrent seizures.

Consultations
Consultation with a neurosurgeon is indicated in patients with subdural empyema or brain abscess.
Consultation should also be considered for patients who have severe deterioration despite aggressive medical
management.
Consultation with an infectious disease specialist is to be considered for patients with cerebral venous
thrombosis (CVT) who have an associated infection, such as meningitis or sinusitis. Consultation with an
otolaryngologist may also be helpful in patients with associated sinusitis.

Medication Summary
Heparin should be considered seriously in the management of cerebral venous thrombosis (CVT), with
subsequent conversion to warfarin as maintenance therapy suggested. Subcutaneous low molecular-weight
heparin (Lovenox) also has been used in patients with venous sinus thrombosis.
Thrombolytic therapy may be effective in CVT, but all studies so far describe its use only with local instillation
by microcatheter or direct instillation at the time of surgical thrombectomy.

Anticoagulants, Cardiovascular
Class Summary
These medications are used to prevent propagation of the clot to more extensive areas of the cerebral venous
system. Studies indicate a tendency toward better outcome in patients treated with anticoagulant therapy than
in those who are not treated with anticoagulants. In Einhaupl's study, even patients with cerebral hemorrhage
appeared to benefit from anticoagulation.[27]
View full drug information

Heparin
Heparin increases the action of antithrombin III, leading to inactivation of coagulation enzymes thrombin, factor
Xa, and factor IXa. Thrombin is the enzyme that is most sensitive to inactivation by heparin.
Because heparin is not absorbed from the GI tract, it must be given parenterally. When given intravenously, its
effect is immediate. Metabolism of heparin is complex; rapid zero-order metabolism is followed by slower firstorder renal clearance. The saturable phase of heparin clearance is thought to be due to binding to endothelial
cell receptors and macrophages in which it is depolymerized. Zero-order process is saturable, leading to an
increase in half-life from 30 minutes with a low dose bolus to 150 minutes with a high dose bolus. Weightbased protocol is now often used for dosing. When choosing this therapy, the risks of its contraindications must
be weighed against the potential benefits of the drug.
View full drug information

Enoxaparin (Lovenox)
Enoxaparin is a low-molecular-weight heparin (LMWH) produced by partial chemical or enzymatic
depolymerization of unfractionated heparin (UFH). It binds to antithrombin III, enhancing its therapeutic effect.
The heparin-antithrombin III complex binds to and inactivates activated factor X (Xa) and factor II (thrombin).
LMWH differs from UFH by having a higher ratio of antifactor Xa to antifactor IIa.
Enoxaparin does not actively lyse thrombi but is able to inhibit further thrombogenesis. It prevents
reaccumulation of clot after spontaneous fibrinolysis. Its advantages include intermittent dosing and a
decreased requirement for monitoring. Heparin antifactor Xa levels may be obtained if needed to establish
adequate dosing. There is no point in checking the aPTT; the drug has a wide therapeutic window, and aPTT
does not correlate with anticoagulant effect.

View full drug information

Warfarin (Coumadin, Jantoven)

Warfarin interferes with the action of vitamin K, a cofactor essential for converting precursor proteins into
factors II, VII, IX, and X. Warfarin does not affect the activity of coagulation factors synthesized prior to
exposure to warfarin. Depletion of these mature factors by normal metabolism must occur before the
therapeutic effects of the newly synthesized factors can be seen; thus, warfarin may take several days to
become effective.
The dose of warfarin administered is influenced by differences in absorption, metabolism, and hemostatic
responses to given concentrations; the dose must be monitored closely by following the prothrombin time (PT)
and international normalized ratio (INR). Higher initial doses do not appear to improve the time required to
achieve therapeutic levels but do increase the bleeding risk.
The expert opinion is that warfarin treatment should be maintained for 3-6 months, but no randomized,
placebo-controlled trials have addressed this issue.

Thrombolytics
Class Summary
These agents cause the lysis of clots. All studies concerning the use of these agents in cerebral venous
thrombosis (CVT) involve either direct instillation into the sinus at the time of surgery or the use of
microcatheters to reach the venous sinus.
View full drug information

Alteplase (Activase)
Alteplase is a biosynthetic form of human tissue plasminogen activator. Tissue plasminogen activator exerts an
effect on the fibrinolytic system that results in the conversion of plasminogen to plasmin. Plasmin degrades
fibrin, fibrinogen, and procoagulant factors V and VIII.
Alteplase is not given as an IV infusion to treat CVT. Refer the patient to a facility with the expertise to perform
venous sinus catheterization.
View full drug information

Reteplase (Retavase)
Reteplase is a recombinant tPA that forms plasmin after facilitating cleavage of endogenous plasminogen. In
clinical trials, it has been shown to be comparable with tPA in achieving patency at 90 minutes. Heparin and
aspirin are usually given concomitantly and afterwards.
View full drug information

Tenecteplase (TNKase)
Tenecteplase is a modified version of alteplase that is made by substituting 3 amino acids. It has a longer halflife than alteplase and thus can be given as a single bolus infused over 5 seconds (as opposed to the 90
minutes required for alteplase). It appears to cause less nonintracranial bleeding than alteplase but carries a
comparable risk of intracranial bleeding and stroke.
Base the dose on the patient's weight. Initiate treatment as soon as possible after the onset of AMI symptoms.
Because tenecteplase contains no antibacterial preservatives, it must be reconstituted immediately before use.

Latar belakang
Trombosis saluran vena di otak merupakan penyebab umum dari infark serebral relatif
terhadap penyakit arteri, tetapi merupakan pertimbangan penting karena morbiditas
potensinya. (Lihat Prognosis.)
Pengetahuan tentang anatomi sistem vena sangat penting dalam mengevaluasi pasien
dengan trombosis vena serebral (CVT), karena gejala yang berhubungan dengan kondisi
yang berkaitan dengan bidang trombosis. Misalnya, infark serebral dapat terjadi dengan
vena kortikal atau trombosis sinus sagitalis sekunder kemacetan jaringan dengan obstruksi.
(Lihat Presentasi.)
Trombosis sinus lateral dapat berhubungan dengan sakit kepala dan pseudotumor cerebriseperti gambar. Ekstensi ke dalam bola jugularis dapat menyebabkan sindrom foramen
jugularis, sedangkan kelumpuhan saraf kranial dapat dilihat di trombosis sinus kavernosus
sebagai fenomena tekan. Pendarahan otak juga mungkin fitur menyajikan pada pasien
dengan trombosis sinus vena. (Lihat Presentasi.)
Prosedur pencitraan telah menyebabkan pengakuan mudah trombosis sinus vena (lihat
gambar di bawah), menawarkan kesempatan untuk langkah-langkah terapi awal. (Lihat hasil
pemeriksaan.)
Berikut panduan untuk CVT telah disediakan oleh American Heart Association dan American
Stroke Association [1]:
Pada pasien dengan dugaan CVT, studi darah rutin terdiri dari hitung darah lengkap, panel
kimia, waktu protrombin, dan waktu tromboplastin parsial teraktivasi harus dilakukan.
Skrining untuk kondisi prothrombotic potensial yang dapat mempengaruhi seseorang
untuk CVT (misalnya, penggunaan alat kontrasepsi, penyakit radang yang mendasari, proses
infeksi) dianjurkan dalam penilaian klinis awal.
Pengujian untuk kondisi prothrombotic (termasuk protein C, protein S, atau kekurangan
antitrombin), sindrom antifosfolipid, protrombin G20210A mutasi, dan faktor V Leiden dapat
bermanfaat untuk pengelolaan pasien dengan CVT. Pengujian untuk protein C, protein S, dan
defisiensi antitrombin umumnya ditunjukkan 2-4 minggu setelah selesai antikoagulan. Ada
nilai yang sangat terbatas pengujian dalam pengaturan akut atau pada pasien yang
memakai warfarin.
Pada pasien dengan diprovokasi CVT (terkait dengan faktor risiko transient), vitamin K
antagonis dapat dilanjutkan selama 3-6 bulan, dengan rasio normalisasi internasional target
2,0-3,0.
Pada pasien dengan CVT tak beralasan, vitamin K antagonis dapat dilanjutkan selama 6-12
bulan, dengan rasio normalisasi internasional target 2,0-3,0.

 Untuk pasien dengan CVT berulang, tromboemboli vena (VTE) setelah CVT, atau CVT
pertama dengan trombofilia berat (yaitu, homozigot protrombin G20210A; faktor homozigot
V Leiden, kekurangan protein C, protein S, atau antitrombin; cacat trombofilia gabungan,
atau antiphospholipid sindrom), antikoagulan terbatas dapat dipertimbangkan, dengan rasio
normalisasi internasional target 2,0-3,0.
Untuk wanita dengan CVT selama kehamilan, rendah berat molekul heparin (LMWH) dalam
dosis antikoagulan penuh harus dilanjutkan selama kehamilan, dan LMWH atau antagonis
vitamin K dengan rasio normalisasi internasional target 2,0-3,0 harus dilanjutkan selama 6
minggu postpartum (untuk total durasi minimal terapi 6 bulan).
Hal ini masuk akal untuk menyarankan wanita dengan riwayat CVT bahwa kehamilan masa
depan tidak kontraindikasi. Penyelidikan lebih lanjut mengenai penyebab dan konsultasi
formal dengan hematologi atau ibu spesialis kedokteran janin yang wajar.
Hal ini wajar untuk mengobati CVT akut selama kehamilan dengan dosis penuh LMWH
daripada heparin tak terpecah.
Untuk wanita dengan riwayat CVT, profilaksis dengan LMWH selama kehamilan masa
depan dan masa postpartum adalah wajar.

Etiologi
Banyak kondisi penyebab telah dijelaskan dalam trombosis vena serebral (CVT). Ini
dapat dilihat sendiri atau dalam kombinasi. Misalnya, mutasi gen protrombin dalam
hubungan dengan penggunaan kontrasepsi oral meningkatkan rasio odds untuk
mengembangkan CVT.
Radang dlm selaput lendir
Infeksi dapat terjadi dengan ekstensi dari sinus paranasal. Kasus-kasus ini juga
dapat dikaitkan dengan empiema subdural. Meningitis bakteri sebagai kondisi hidup
berdampingan harus dipertimbangkan dalam kasus ini. Sinus frontalis adalah
sumber yang paling umum dari infeksi, dengan penyebaran melalui pembuluh
darah utusan antara mukosa sinus posterior dan meninges. Jarang, sinusitis
sphenoid dapat berhubungan dengan trombosis sinus kavernosus. Organisme
beberapa yang harus dipertimbangkan, Staphylococcus aureus yang paling umum.
Pada infeksi kronis, organisme gram negatif dan jamur seperti Aspergillus spesies
dapat ditemukan.
Trauma dan operasi
Trauma juga dapat menjadi ajang etiologi. Trombosis sinus Cerebral mudah dapat
diabaikan dalam kasus-kasus trauma kepala ringan. Prosedur bedah saraf seperti
keran dural dan infus ke dalam vena jugularis internal telah terlibat juga.
Negara hiperkoagulasi
Banyak kondisi medis telah dikaitkan dengan CVT. Misalnya, keadaan hiperkoagulasi
terkait dengan sindrom antifosfolipid, protein S dan C kekurangan, antitrombin III
kekurangan, lupus antikoagulan, dan Leiden faktor V mutasi dapat menyebabkan
CVT. Antibodi terhadap reseptor fibrinolitik, annexin A2 (titer> 3 standar deviasi),
secara signifikan berhubungan dengan CVT. [2] Kehamilan juga dikaitkan dengan

kecenderungan hiperkoagulasi. Keganasan mungkin berhubungan dengan keadaan

hiperkoagulasi juga, dan karena itu mungkin menjadi faktor risiko.
Hipotensi intrakranial
Terisolasi trombosis vena kortikal telah dikaitkan dengan sindrom hipotensi
intrakranial, tapi jarang. Dalam sebuah penelitian, Schievink dan Maya menemukan
bahwa CVT hadir hanya 3 (2,1%) dari 141 pasien dengan hipotensi intrakranial
spontan. [3]
Pungsi lumbal
Beberapa kasus CVT telah dilaporkan setelah pungsi lumbal (LP), menunjukkan
hubungan sebab-akibat. Dalam sebuah studi oleh Canhao et al, LP disebabkan
penurunan berkelanjutan dalam kecepatan aliran darah rata-rata (BFV) di sinus
lurus (SS), menunjukkan bahwa penurunan aliran darah vena adalah mekanisme
yang mungkin berkontribusi terhadap terjadinya CVT. Dalam studi tersebut, para
peneliti menggunakan transcranial Doppler ultrasonografi untuk mendaftarkan BFV
rata-rata dari SS sebelum, selama, dan setelah LP. LP diinduksi penurunan 47%
dalam mean BFV di SS, dengan penurunan rata-rata menjadi signifikan segera di
akhir, 30 menit setelah, dan lebih dari 6 jam setelah LP. [4]
Obat
Beberapa obat yang dilaporkan meningkatkan risiko CVT, termasuk berikut:
Kontrasepsi oral - Termasuk formulasi generasi ketiga
Kortikosteroid
Asam Epsilon-aminokaproat
Thalidomide
Tamoxifen
Erythropoietin
Fitoestrogen
L-asparaginase
Heparin - terapi Heparin telah dilaporkan untuk menghasilkan trombositopenia
trombotik dengan terkait trombosis sinus vena
Faktor risiko penyakit tambahan
Penyakit lain yang telah digambarkan sebagai faktor risiko untuk CVT meliputi
berikut ini:

 Penyakit radang usus, seperti penyakit Crohn dan kolitis ulserativa, yang
digambarkan sebagai faktor risiko untuk trombosis vena [5]; kortikosteroid
digunakan dalam pengobatan kondisi ini dapat memainkan peran penyebab
Kehamilan dan masa nifas pertimbangan penting pada wanita usia subur
kondisi Hematologi, termasuk hemoglobinuria paroxysmal nocturnal, thrombotic
thrombocytopenic purpura, penyakit sel sabit, dan polisitemia, yang harus
dipertimbangkan
Penyakit kolagen-vaskular, seperti lupus eritematosus sistemik, Wegener
granulomatosis, dan sindrom Behet, telah dilaporkan berhubungan dengan CVT
hyperhomocysteinemia merupakan faktor risiko yang kuat dan independen untuk
CVT, yang hadir dalam 27-43% pasien dengan CVT tetapi hanya 8-10% dari
populasi umum; apakah pengobatan dengan folat, piridoksin, dan / atau cobalamin
mengurangi risiko CVT jelas
Sindrom nefrotik
Dehidrasi
hipotensi intrakranial spontan
ketinggian tinggi
Hati sirosis
Sarkoidosis
Epidemiologi
Terjadinya International
Insiden trombosis vena serebral (CVT) adalah sulit untuk menentukan, tetapi
umumnya, diyakini menjadi penyebab umum dari stroke, dengan rasio dilaporkan
vena ke arteri stroke menjadi 1: 62,5. Pada tahun 1973, Towbin dilaporkan CVT di
9% dari 182 otopsi, [6] sementara pada tahun 1995, Daif melaporkan frekuensi di
Arab Saudi dari 7 kasus per 100.000 pasien di rumah sakit. [7]
Namun, dengan munculnya teknik pencitraan baru, kejadian dilaporkan CVT
cenderung meningkat sebagai kasus kurang parah ditemukan.
Seks dan demografi yang berkaitan dengan usia
CVT diyakini lebih sering terjadi pada wanita dibandingkan pria. Dalam serangkaian
110 kasus, Ameri dan Bousser menemukan rasio perempuan-ke-laki-laki 1,29: [8] 1.

Pada tahun 1992, Ameri dan Bousser melaporkan distribusi usia seragam pada pria
dengan CVT, sementara 61% dari wanita dengan CVT berusia 20-35 tahun. [8]
Perbedaan ini mungkin berhubungan dengan kehamilan atau penggunaan
kontrasepsi oral. [9]
Prognosa
Smith menunjukkan kemanjuran antikoagulan dan terapi trombolitik pada pasien
dengan trombosis vena serebral (CVT). Dalam studinya, ia membandingkan hasil
dari pasien yang diobati dengan heparin dan infus lokal urokinase (12 pasien)
dengan orang-orang dari pasien yang tidak menerima pengobatan (21 pasien). [10]
Hasil muncul dalam Tabel, di bawah ini.
Meja. Pasien Dengan Cerebral vena Trombosis Diobati Dengan Heparin dan Infusion
Daerah Urokinase vs Nontreated Grup
Morbiditas dan mortalitas
Herniasi disebabkan efek massa unilateral adalah penyebab utama kematian di CVT.
Pada pasien dengan lesi parenkim CVT besar menyebabkan herniasi, operasi
dekompresi telah menyelamatkan nyawa dan sering mengakibatkan hasil fungsional
yang baik, bahkan pada pasien dengan kondisi klinis yang parah. [11]
Kematian pada kasus yang tidak diobati trombosis vena telah dilaporkan berkisar
13,8-48%; Tingkat kematian yang tinggi ini mungkin merupakan cerminan dari
keparahan klinis di pintu masuk ke ruang kerja. Antara 25% dan 30% dari pasien
mengalami pemulihan penuh.
Dalam sebuah penelitian Portugis yang prospektif dianalisis 91 pasien dengan CVT
lebih berarti 1 tahun follow-up selang, mayoritas pasien mengalami pemulihan
lengkap. [12] Dari pasien dianalisis, 7% meninggal dalam fase akut, 1% meninggal
selama satu tahun tindak lanjut, 82% sembuh sepenuhnya, dan 1% bergantung;
59% dikembangkan peristiwa trombotik selama tindak lanjut, 10% memiliki kejang,
11% mengeluh sakit kepala parah, dan 1 pasien mengalami kehilangan penglihatan
yang parah.
Pada tahun 2003, Buccino et al menemukan hasil keseluruhan baik di
reinvestigation mereka serangkaian 34 pasien dengan dikonfirmasi CVT. [13]
Namun, 10 pasien (30%) memiliki sakit kepala episodik, 3 pasien (8,8%) memiliki
kejang, 4 pasien (11,7%) memiliki tanda-tanda piramidal, dan 2 (5,9%) memiliki
defisit visual. Mild aphasia nonfluent terlihat pada 3 pasien. Bekerja defisit memori
dan depresi suasana hati terlihat pada 6 pasien (17,6%)
Sejarah

Pasien dengan trombosis vena serebral (CVT) dapat hadir dengan sakit kepala. [14]
Meskipun sakit kepala petir biasanya menunjukkan perdarahan subarachnoid (SAH),
itu juga dapat dilihat di trombosis sinus.
SAH telah digambarkan sebagai acara presentasi dengan CVT. CVT harus
dipertimbangkan dalam pemeriksaan dari SAH, terutama ketika tangki basilar tidak
terlibat. [15]
Pasien dengan trombosis sinus lateral yang mungkin hadir dengan pseudotumor
cerebri-seperti sindrom. Menggunakan teknik yang disebut auto-dipicu eliptiksentris-memerintahkan 3-dimensi gadolinium-ditingkatkan resonansi magnetik
venography (MRV), Farb et al menemukan bahwa 27 dari 29 pasien dengan
hipertensi intrakranial idiopatik memiliki stenosis sinovenous bilateral; ini terlihat
hanya 4 dari 59 subyek kontrol. [16]
Mual dan muntah juga dapat dikaitkan dengan CVT. Dalam beberapa kasus, kejang,
yang dapat berulang, terjadi. Beberapa pasien mungkin mengalami tingkat
penurunan kesadaran yang berkembang menjadi koma.
Defisit neurologis fokal dapat mengembangkan, tergantung pada daerah yang
terlibat. Hemiparesis dapat terjadi, dan dalam beberapa kasus trombosis sinus
sagittal, kelemahan dapat berkembang pada ekstremitas bawah. Ini juga dapat
terjadi sebagai keterlibatan ekstremitas bawah bilateral. Afasia, ataksia, pusing,
chorea, dan hemianopia semua telah dijelaskan.
Sindrom saraf kranial terlihat dengan trombosis sinus vena. Ini meliputi:
vestibular neuronopathy
berdenyut tinnitus
tuli unilateral
Penglihatan ganda
Kelemahan Facial
mengaburkan visi
Situs sakit kepala versus lokasi keterlibatan sinus
Wasay et al menemukan sedikit hubungan antara sakit kepala dan lokasi situs
keterlibatan sinus pada pasien dengan CVT. Dalam studi mereka, penulis
menggambarkan pola dan lokasi sakit kepala di 200 pasien berturut-turut dengan
diagnosis terbukti dari CVT untuk mengidentifikasi hubungan antara situs dari sakit
kepala dan lokasi keterlibatan sinus. Kualitas sakit kepala dilaporkan sebagai
berdenyut (9%), mirip pita (20%), petir (5%), dan lainnya (berdebar, meledak,
menusuk, dll) (20%).

Para penulis tidak menemukan hubungan antara sakit kepala dan lokasi situs
trombosis sinus kecuali dalam kasus-kasus trombosis sinus sigmoid, di mana 17 dari
28 pasien (61%) dengan keterlibatan sinus sigmoid sendiri atau dalam kombinasi
dengan sinus melintang mengalami nyeri di oksipital dan daerah leher. Tidak ada
hubungan antara lateralisasi dari rasa sakit dan situs trombosis. [17]
Pemeriksaan Fisik
Pengaruh trombosis vena serebral (CVT) pada status mental cukup bervariasi,
dengan beberapa pasien tidak menunjukkan perubahan kewaspadaan, orang lain
mengembangkan kebingungan ringan, dan yang lain maju koma.
Temuan saraf kranial mungkin termasuk edema papil, hemianopia, oculomotor dan
abducens kelumpuhan, kelemahan wajah, dan tuli. Jika trombosis meluas ke vena
jugularis, pasien dapat mengembangkan keterlibatan saraf kranial IX, X, XI, dan XII
dengan sindrom foramen jugularis.
Trombosis superior sagital (longitudinal) sinus dapat hadir dengan kelumpuhan
unilateral yang kemudian meluas ke sisi lain sekunder untuk perpanjangan bekuan
dalam pembuluh darah otak. Karena lokasi, ini dapat hadir sebagai unilateral
kelemahan ekstremitas bawah atau paraplegia.
Trombosis sinus kavernosus dengan obstruksi vena mata dapat berhubungan
dengan proptosis dan ipsilateral edema periorbital. Perdarahan retina dan edema
papil dapat hadir. Kelumpuhan gerakan ekstraokular, ptosis, dan penurunan sensasi
di divisi pertama dari saraf trigeminal sering diamati.
Meskipun tidak biasa, trombosis vena kortikal dapat dilihat dengan tidak adanya
keterlibatan sinus dural. Kasus-kasus ini berhubungan dengan defisit fokal
bervariasi, termasuk aphasia, hemiparesis, kehilangan hemisensorik, dan
hemianopia.
Pertimbangan Pendekatan
Diagnosis trombosis vena serebral (CVT) dibuat atas dasar klinis dan studi
pencitraan (lihat gambar di bawah), sedangkan penelitian laboratorium klinis
berguna untuk menentukan kemungkinan penyebab CVT.
Axial pandangan resonansi magnetik (MR) Venogram menunjukkan kurangnya
aliran di sinus melintang. Lihat koronal resonansi magnetik (MR) Venogram
menunjukkan kurangnya aliran dalam melintang kiri dan sinus sigmoid.
studi Lab
Hitung darah lengkap (CBC) dilakukan untuk mencari polisitemia sebagai faktor
etiologi. Penurunan jumlah trombosit akan mendukung thrombotic
thrombocytopenic purpura; leukositosis dapat dilihat pada sepsis. (Jika heparin

digunakan sebagai pengobatan, jumlah trombosit harus dipantau untuk

trombositopenia.)
antifosfolipid dan anticardiolipin antibodi harus diperoleh untuk mengevaluasi
sindrom antifosfolipid. Tes-tes lain yang mungkin menunjukkan keadaan
hiperkoagulasi termasuk protein S, protein C, antitrombin III, lupus antikoagulan,
dan Leiden faktor V mutasi. Evaluasi ini tidak boleh dilakukan saat pasien berada
pada terapi antikoagulan.
persiapan sel sabit atau hemoglobin elektroforesis harus diperoleh pada individu
keturunan Afrika.
studi tingkat endap darah dan antibodi antinuclear harus dilakukan untuk
menyaring eritematosus sistemik lupus, Wegener granulomatosis, dan arteritis
temporal. Jika kadar yang tinggi, evaluasi lebih lanjut, termasuk tingkat pelengkap,
asam anti-deoksiribonukleat (DNA) antibodi, dan antibodi sitoplasma neutrofil
(ANCA), bisa dipertimbangkan.
protein urin harus diperiksa dan, jika ditinggikan, sindrom nefrotik
dipertimbangkan. Studi fungsi hati harus dilakukan untuk menyingkirkan sirosis.
EEG
Sebuah electroencephalogram (EEG) mungkin normal, menunjukkan perlambatan
umum ringan, atau menunjukkan kelainan fokal jika infark unilateral terjadi. EEG
sangat membantu dalam mengevaluasi fokus kejang.
Prosedur
Pungsi lumbal (LP) sangat membantu dalam mengevaluasi untuk meningitis
sebagai proses infeksi terkait dalam trombosis vena serebral (CVT). Namun, besar,
unilateral hemisfer lesi atau posterior fossa lesi menunjukkan pada CT scan atau
MRI merupakan kontraindikasi untuk LP.
Di masa lalu, kompresi vena jugularis secara sepihak dengan pengukuran tekanan
dimanfaatkan. Tekanan mungkin meningkat jika trombosis sinus melintang
kontralateral hadir. Namun, sirkulasi kolateral atau kompresi lengkap dari vena
jugularis dapat menghasilkan hasil negatif palsu. Selain itu, ketinggian tekanan
vena intrakranial adalah kekhawatiran, karena dapat memicu herniasi. Sebagai
manuver menambahkan sedikit untuk diagnosis, biasanya tidak dilakukan.
Tingkat D-Dimer
nilai D-dimer mungkin bermanfaat dalam skrining pasien yang hadir di
departemen darurat untuk evaluasi sakit kepala.
Dalam sebuah studi dari 18 pasien dengan trombosis vena serebral (CVT), et al
Terlambat melaporkan bahwa tingkat D-dimer kurang dari 500 ng / mL memiliki nilai

prediktif negatif untuk mengesampingkan diagnosis pada pasien dengan sakit

kepala akut. [18]
Dalam sebuah studi prospektif dari 54 pasien berturut-turut dengan sugestif sakit
kepala CVT, lalive menemukan bahwa 12 memiliki CVT dan, dari mereka, 10
memiliki tingkat D-dimer lebih dari 500 ng / mL. [19] 2 pasien dengan dikonfirmasi
CVT dan tingkat D-dimer kurang dari 500 ng / mL memiliki sejarah sakit kepala
kronis berlangsung lebih dari 30 hari.
Dalam sebuah studi oleh Kosinski et al, D-dimer berkorelasi positif dengan tingkat
trombosis dan berkorelasi negatif dengan durasi gejala pada pasien dengan
trombosis sinus otak. Para peneliti mempelajari prospektif 343 pasien dengan gejala
yang menunjukkan trombosis sinus otak. [20] Diagnosis dikonfirmasi di 35, dengan
34 pasien menunjukkan tingkat D-dimer tinggi lebih dari 500 mcg / L. Dari 308
pasien yang tidak memiliki CVT, 27 memiliki nilai-nilai positif. Sensitivitas adalah
97,1%, dengan nilai prediksi negatif 99,6%. Spesifisitas adalah 91,2%, dengan nilai
prediksi positif 55,7%.
Tes D-dimer tidak menegakkan diagnosis CVT, dan studi lebih pasti, seperti
magnetic resonance venography (MRV), diperlukan. Demikian juga, jika kecurigaan
tinggi untuk CVT ada, tes tidak bisa pasti mengecualikan diagnosis tetapi dapat
menunjukkan bahwa kehadiran CVT sangat tidak mungkin.
CT Scanning
Computed tomography (CT) scanning adalah teknik pencitraan yang penting,
seperti yang sering studi pencitraan pertama diperoleh. Ini mungkin menunjukkan
bukti infark yang tidak sesuai dengan distribusi arteri. Namun, dengan tidak adanya
komponen hemoragik, demonstrasi infark mungkin tertunda selama 48-72 jam.
(Lihat gambar di bawah ini.)
Computed tomography (CT) Scan menunjukkan posterior kiri hematoma temporal
seorang wanita 38 tahun dari kontrasepsi oral (satu-satunya faktor risiko
diidentifikasi).
CT scan juga berguna untuk mengesampingkan kondisi lain, seperti neoplasma,
dan dalam mengevaluasi lesi hidup berdampingan, seperti empiema subdural. CT
scan sinus ini berguna dalam mengevaluasi sinusitis, sementara CT scan dari
mastoids dapat membantu dalam trombosis sinus lateral.
Tanda delta kosong muncul di scan kontras sebagai peningkatan pembuluh darah
agunan superior sinus sagital (SSS) dinding yang mengelilingi trombus
nonenhanced di sinus. Namun, tanda sering absen. Pembagian awal SSS dapat
memberikan tanda delta palsu. Tanda segitiga padat dibentuk oleh darah beku
segar di SSS dan tanda kabel mewakili vena kortikal thrombosed sangat langka.
CT angiografi

 CT angiography juga telah digunakan untuk memvisualisasikan sistem vena

serebral. Ozsvath et al dibandingkan CT dan proyeksi MR dalam identifikasi
pembuluh darah otak dan trombosis. [21] CT venography lebih unggul MR di
identifikasi pembuluh darah otak dan sinus dural. CT adalah setara dengan MR di
identifikasi trombosis sinus dural dan karena itu merupakan alternatif untuk MRV
dalam pemeriksaan pasien yang diduga trombosis sinus dural. Teknik maksimum
intensitas-proyeksi yang digunakan, bagaimanapun, tidak memungkinkan
visualisasi langsung dari trombus oleh CT atau MR teknik.
MRI
MRI menunjukkan pola infark yang tidak mengikuti distribusi dari oklusi arteri
yang diharapkan. Ini mungkin menunjukkan adanya aliran kekosongan dalam
saluran vena normal. Mas et al temuan MRI menggambarkan peningkatan sinyal
intraluminal pada semua pesawat dan dengan semua urutan pulsa pada pasien
dengan trombosis sinus lateral. (Lihat gambar di bawah ini.) [22]
Kontras disempurnakan magnetic resonance imaging (MRI) menunjukkan
kurangnya pengisian meninggalkan sinus melintang.
MRV
MRV merupakan metode yang baik memvisualisasikan sinus vena dural dan vena
serebral yang lebih besar. (Lihat gambar di bawah.)
Waktu trombosis sinus lateralis menunjukkan pada magnetic resonance
venography (MRV). Wanita ini 42 tahun disajikan dengan tiba-tiba sakit kepala.
Pemeriksaan fisik mengungkapkan tidak ada kelainan neurologis. Pasien yang sama
seperti pada gambar sebelumnya. Satu minggu setelah pengobatan dengan
heparin, resonansi magnetik (MR) Venogram ditampilkan peningkatan aliran dalam
sinus lateral kiri konsisten dengan rekanalisasi awal sinus; sakit kepala telah
diselesaikan pada saat ini. Magnetic resonance Venogram (MRV) - Tampilan aksial; A
= lateral (melintang) sinus; B = sigmoid sinus; C = pertemuan sinus; dan D = sinus
sagital superior. Magnetic resonance Venogram (MRV) - Tampilan sagital; A = lateral
(melintang) sinus; C = pertemuan sinus; D = sinus sagital superior; dan E = lurus
sinus.
Sejak sakit kepala petir tidak terbatas SAH dan dapat dilihat dengan trombosis
vena serebral (CVT), kurangnya bukti SAH pada pasien dengan sakit kepala tersebut
harus meminta pemeriksaan dengan MRV.
SSPCA
Single-slice fase-kontras angiography (SSPCA) Kurang dari 30 detik dan
memberikan informasi yang cepat dan dapat diandalkan. Banyak ahli saraf
sekarang mempertimbangkan untuk menjadi prosedur pilihan dalam mendiagnosis
trombosis vena serebral. Dalam sebuah studi dari 21 pasien, Adams menunjukkan

spesifisitas dan sensitivitas 100% untuk SSPCA bila dibandingkan dengan teknik
pencitraan alternatif. [23]
kesenjangan Arus dibandingkan trombosis di MRV
Ayanzen dijelaskan kesenjangan aliran sinus melintang di 31% dari pasien dengan
temuan MRI yang normal yang belajar dengan MRV; 90% dari mereka dalam sinus
melintang dominan, dan 10% berada di sinus kodominan. Tidak ada terlihat di sinus
dominan. [24] ini tidak boleh keliru untuk trombosis.
Studi Kontras
arteriografi karotis dengan teknik pembuatan film tertunda untuk
memvisualisasikan sistem vena adalah prosedur pilihan dalam diagnosis trombosis
vena sebelum munculnya MRV. Ini merupakan prosedur invasif dan karena itu
dikaitkan dengan risiko kecil.
Jika studi MR tidak diagnostik, angiografi konvensional harus dipertimbangkan.
Venography langsung dapat dilakukan dengan melewati kateter dari vena jugularis
ke sinus melintang, dengan injeksi menguraikan sinus vena.