1

Revista Chilena de Radiología. Vol. 16 N 4, Año 2010; 175-187.

INTRACRANIAL VENOUS THROMBOSIS: IMAGING SIGNS AND COMMON

PITFALLS

Drs. Michael Hirsch S1, Alejandra Torres G2.

1Radiology Resident, Hospital Clínico Universidad de Chile.

2Neuroradiologist, Hospital Clínico Universidad de Chile.

Corresponding Author:

Michael Hirsch S.

Postal Address: Av. Santos Dumont #999. Independencia, Santiago.

Phone: 9789191

E-mail: mphirsch@gmail.com

Abstract

Although intracranial venous thrombosis is a relatively rare disease, it

constitutes an entity that must be timely and accurately diagnosed in

emergency services, given the need for prompt treatment to avoid serious

complications, including neurological deficits or even death. There are several

imaging signs that can be visualized on both computed tomography (CT) and

magnetic resonance (MR) imaging scans that allow for this early diagnosis. On

the other hand, some differential diagnoses need to be performed to prevent

mistaking intracranial venous thrombosis for any other entity.

2

Key words: Cranial Sinuses; Sinus Thrombosis, Intracranial; Tomography,

Spiral Computed Tomography; Magnetic Resonance Imaging; Radiology.

Introduction

Intracranial venous thrombosis (IVT) is a cerebrovascular condition that may

affect all ages, occurring predominantly in infants and in adults around the third

decade of life (1,2). It may include cerebral veins (CV) as well as dural venous

sinuses (DVS). There are over a hundred causes described as etiopathogenic

factor of IVT (Table I) (1), summarized in the classic “Virchow's triad” which

encompasses states of hypercoagulability, vessel wall damage and disturbance

of venous flow (3). However, the causal factor of IVT may be found only in 75 to

85% of patients, even though when all available examinations and laboratory

tests are performed (1, 4).

By reviewing the clinical presentation of IVT, a wide range of symptoms and

signs, ranging from headache and intracranial hypertension to coma and even

death, may be observed (Table II). Headache is the most commonly

encountered symptom─seen in 75 to 95% of patients with IVT─, usually

preceding by days, weeks or exceptionally months (2,5) the manifestation of

other neurological disorders (70-75%). Headache has been associated with

manifestations of intracranial hypertension in 20 to 40% of cases (2); it can be

mild, moderate, or severe in intensity, and predominantly diffuse (2). Given the

variability and nonspecificity of presenting symptoms of the IVT, an imaging

diagnostic technique is essential to understand the etiology of symptoms,

mainly because an early diagnosis allows the implementation of a timely

anticoagulant therapy, thus reducing the rate of complications and neurological

sequelae.

3

Table I. Causes and risk factors associated with

intracranial venous thrombosis.

Prothrombotic genetic conditions

Antithrombin deficiency

Protein C and S deficiency

Factor V-Leiden mutation

Prothrombin mutations

Homocysteinemia caused by mutations in the

methyltetrahydrofolate reductase gene.

Acquired prothrombotic conditions

Nephrotic sindrome

Antiphospholipid antibodies

Homocysteinemia

Pregnancy

Puerperium

Infections

Otitis, mastoiditis, sinusitis

Meningitis

Systemic infectious disease

Inflammatory diseases

Systemic lupus erythematosus

Wegener’s granulomatosis

Sarcoidosis

Inflammatory bowel disease

Behçet’s syndrome

Hematologic conditions

Polycythemia, primary and secondary

Thrombocythemia

Leukemia

Anemia, including paroxysmal nocturnal hemoglobinuria

Drugs

Oral contraceptives

Asparaginase

Mechanical/ traumatic causes

Head trauma

Injury to sinuses or jugular vein, jugular catheterization

Neurosurgical procedures

Lumbar puncture

Miscellaneous

Dehydration, especially in children

Cancer

4

Table II. Clinical features of intracranial venous thrombosis

Symptoms

Headache

Visual disturbances

Impairment of consciousness

Nausea, vomiting

Signs

Papilledema

Focal neurological deficit

Cranial nerve palsies

Convulsions, coma

Imaging aspects

There are several imaging findings that allow us to suspect or make the

diagnosis of IVT, both on computed tomography and magnetic resonance

imaging scannings:

A) Signs of vein occlusion

B) Parenchymal alterations and other changes secondary to venous stasis

C) Signs of recanalization.

Each of them will be discussed.

A) Signs of venous occlusion

1) The Empty Delta Sign

This finding was originally described on CT cuts with intravenous contrast

agent; it corresponds to a triangular and hypodense filling defect associated

with a hyperdense peripheral area, which is produced by contrast material

enhancement in the thrombosed superior sagittal sinus (SSS) (Figure 1) (3.6).

Currently, it is possible to observe the empty delta sign not only in the SSS, but

also in the transverse (TS) and sigmoid sinuses (SS) on multiplanar

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reconstructions from multidetector CT, as well as on contrast-enhanced MR

imaging studies.

Figure 1. Contrast enhanced CT sequence (a, b) where empty delta sign in superior sagittal

sinus at various levels is identified in the same patient

DVS exhibit an elongated and triangular shape in cross section; they are

valveless structures with a plexus of adjacent venous channels that act as a

collateral pathway for drainage in the event of thrombosis (Figure 2) (7).

Numerous hypotheses intended to explain the appearance of this sign have

been formulated, including:

Recanalization of the thrombus within the venous sinus

Organization of the blood clot

Blood-brain barrier breakdown

6

Dilatation of collateral peridural and dural venous channels.

Seemingly, the latter would be the most likely explanation since contrast-

enhancement of dural venous collateral circulation─primarily consisting of

lateral lacunae, vascular mesh (dural cavernous spaces), and meningeal

venous tributaries─would produce the empty delta sign in the thrombosed sinus (3, 6, 7).

In up to 90% of cases the location of thrombosis involves more than one sinus,

particularly the ST and SS, collectively termed as lateral sinus. (Table III) (4, 8, 9).

Figure 2. Coronal sections of an anatomical preparation. a) Identifies the superior sagittal sinus

(S) formed by the divergence of the periosteal and meningeal layers of the dura mater. The

latter converge at the falx cerebri (H). Around the sinus there is a collateral venous plexus

(asterisks). b) In the transverse sinus (TS) the meningeal layers of the dura mater converge at

the tentorium (T), also giving it a triangular appearance. Calotte (C), cerebellum (Ce).

7

Table III.

Thrombus location

%

Superior sagittal sinus 62.0

Left lateral sinus 44.7

Right lateral sinus 41.2

Straight sinus 18.0

Cortical veins 17.1

Deep venous system 10.9

Cerebellar veins 0.3

Late-phase contrast-enhanced CT scans have proved to be a reliable method to

investigate the cerebral venous structures (especially by multiplanar

reformatting), with a sensitivity of 95% when compared with angiography, as

reported in several publications (10). This capability allows a high performance,

thus avoiding the inherent risks of the interventional procedure.

The empty delta sign is observed in 25 to 75% of cases of DVS thrombosis,

depending on the different techniques applied. Ideally, it has to be detected by

means of multiplanar reformation at different spatial planes, especially in the

SSS and TS horizontal portions (Figure 3) by using wider window settings than

those normally used for brain parenchyma, with a window width of 260 HU and

a level of 130 HU (Figure 4) (5). It should be noted that the empty delta sign may

disappear in the chronic stages due to enhancement of organized clot (5).

8

Figure 3. Coronal plane reformation Contrast-enhanced CT. The empty delta sign in the right

transverse sinus is identified; to compare with contralateral sinus.

9

Figure 4. Contrast-enhanced CT. A small thrombus in the superior sagittal sinus can be

observed only by changing window width and window level.

2) The hyperdense sinus sign and the cord sign

In 20% of cases the clot can be seen in its early stages at the level of the DVS

(6) as a hyperdense image on non-contrast-enhanced CT scans (Figure 5, 6a,

7a), since the thrombus retracts and its water content decreases while the

concentration of hemoglobin increases, thus achieving an attenuation value of

50-80 HU, which normalizes within 1-2 weeks’ time (11). The tentorium and

beam hardening artifacts caused by bones may obscure this finding or it may be

confused with a subarachnoid hemorrhage, an underlying subdural hematoma,

or it can be caused by a high hematocrit (11).

The cord sign corresponds to the same principle as that of the hyperdense

sinus, but applied to cortical veins (Figure 7a), which are rarely involved in

isolation in IVT (4).

3) Absence of flow void and hyperintense vein sign

On non-contrast MR images, vessels are usually hypointense on all sequences

due to its flow; this is called flow void sign, also known as "flow void." When this

flow-void is absent, vessels become hyperintense, which may be indicative of

thrombosis (Figures 6c, 8a); nevertheless, a slow or turbulent flow can cause

changes in DVS signal intensity, thus leading to misdiagnosis (4). Moreover, the

various states of hemoglobin degradation may alter the appearance of the

thrombus and make it less obvious, mimicking the typically observed absence

of flow void signal (12,13). For example, deoxyhemoglobin will cause the acute

thrombus to appear as a very hypointense area on T2-weighted sequences

(Figure 9), mimicking the normal flow void, and isointense on T1-weighted

sequences, resembling the adjacent brain parenchyma, so that it may go

unnoticed unless a contrast medium is used. The presence of the empty delta

sign will facilitate the right diagnosis (Figure 8b) (4). Something similar occurs on

non-contrast enhanced TOF angiographic sequences in which the subacute

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thrombus composed of methemoglobin is hyperintense, resembling the signal

intensity that flow normally exhibits on this view. Performance of T1-weighted

SE sequences allows discrimination between the hyperintense thrombus and

the normal absence of flow void sign (4); on the other hand, 3D-contrast-

enhanced MR angiographic sequences with improved spatial resolution and

visualization of filling defects of the venous system have increased sensitivity

and specificity levels in comparison with unenhanced TOF sequences. Among

these are, for example, the FLASH sequence (fast low-angle shot) and ATECO

(auto-triggered elliptic centric-ordered) view (Figures 7f, 10) (14 - 17).

11

Figure 5. CT scan without contrast. a) The superior sagittal sinus is hyperdense. b) In a cut at a

superior level than the preceeding one, this finding disappears, which supports the diagnosis of

thrombosis. Note that the great cerebral vein (vein of Galen) does appear hyperdense in this

cut.

12

13

Figure 6. a) Unenhanced CT scan showing hyperdense right transverse sinus, associated with

temporal lobe hematoma, surrounded by scarce vasogenic edema. b) After contrast

administration and at a more superior cut, absence of filling of the transverse sinus is shown

and the hematoma is best viewed. c) T1 MRI sequence shows the absence of normal flow void

at the level of the lateral sinus and signal intensity changes caused by degradation of

hemoglobin in the hematoma, as visualized on T2 d) and GRE T2 * sequences, e) appearing on

the latter the magnification of the magnetic susceptibility artifact.

The hyperintense vein sign is similar to the cord sign observed on CT scanning

(Figure 11) and corresponds to the absence of flow void in the cortical veins,

visualized on T1 and T2 MRI sequences, with the exception of visible signal

hypointensity caused by the hemoglobin degradation process (Figure 7c) (4).

The above data demonstrate the importance of being aware of MRI appearance

at the various stages of hemoglobin degradation process, a common issue in

general radiologists training but outside the scope of this review.

4) Magnetic susceptibility artifact

Lately, there has been much emphasis on T2*-weighted gradient-echo (GRE)

sequences (18) due to its capability to highlight the magnetic susceptibility artifact

produced by the paramagnetic states of hemoglobin degradation, such as

deoxyhemoglobin, methemoglobin, and hemosiderin. These elements are seen

as hypointense images generating the "blooming" phenomenon, effect that

corresponds to an amplification of their actual area of deposition produced by

the magnification of the artifact on this sequence (Figure 6 and 7). This allows

to detect thrombosis in small-caliber veins, such as the cortex veins (Figure 12),

or to make thrombosis evident, when there are only subtle changes in signal

intensity on classic T1- and T2-weighted sequences (4). There is a 3D- GRE

sequence technique with post-processing phase and high spatial resolution

referred to as “susceptibility-weighted imaging” (SWI), which amplifies the

above described phenomenon and several studies have shown it to be superior

to conventional techniques (19, 20).

14

15

16

17

Figure 7. SSS thrombosis and left frontal cortical vein thrombosis; unenhanced CT image

shows the hyperdense sinus sign and the cord sign a). MRI view shows magnetic susceptibility

artifact with "blooming" effect on T2* GRE sequence b), which is not evident on the T2

sequence c). Involvement of brain parenchyma causing slight cortical hyperintensity on T2

sequence d) and restriction of proton mobility represented on DWI sequence e) and ADC map

f). Cortical vein thrombosis is associated with thrombosis of SVD; in the case of SSS thrombosis

it is represented in the ATECO sequence g). In a control at 5 months, no changes on T2 h),

DWI i), or ADC map j) are observed and on an ATECO sequence, recanalization of the SSS is

shown k).

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B) Parenchymal alterations and other changes secondary to venous

stasis

Changes in the brain parenchyma may be observed in 50 to 57% of IVT

patients (4, 21), especially on MRI sequences. Varying in degree, type of

alteration and time reversibility, they can be divided into manifestations

secondary to vasogenic edema, secondary to the restriction of proton mobility

on diffusion-weighted sequences (DWI) with cytotoxic edema-like pattern, and

hemorrhagic manifestations (4).

The primary underlying mechanism for these parenchymal abnormalities is an

increased venous pressure secondary to obstruction of venous drainage that

can lead to an increase in caliber or number of visible veins, particularly on MRI

and / or meningeal enhancement due to venous congestion (5). If collateral

pathways of venous drainage are insufficient, which is especially evident in

cortical venous thrombosis, a vasogenic edema in the adjacent parenchyma

begins to be formed. If venous pressure continues to increase, a corresponding

reduction of arterial perfusion pressure may be expected and a cytotoxic edema

and cell death may occur. If adequate collateral pathways develop or

recanalization occurs before cell death or intracranial hemorrhage, parenchymal

abnormalities can be partially or completely resolved. Clearly, this is not a linear

process and vasogenic edema and cytotoxic edema pattern can often coexist,

(4); some authors have found evidence of cytotoxic edema early after the

development of an IVT, so its exact pathophysiology remains controversial (21).

Brain edema, which on CT scans is seen as hypodense areas or loss of

differentiation between gray and white matter, can be better characterized by

MRI sequences, using DWI and T2 FLAIR images. In this way we can

differentiate an alteration of parenchymal signal intensity with hyperintensity on

DWI sequence and restriction of proton mobility in the apparent attenuation

coefficient (ADC) map, similar to the cytotoxic edema seen in the arterial

ischemia, but that in venous thrombosis is highly likely to reverse in time, which

lead us to assert that it does not correspond exactly to the same phenomenon,

19

or that it may constitute a reversible stage of this effect (Figure 7) (21-23). This

difference in behaviour when compared to blood cytotoxic edema makes it

advisable not to use the term "venous infarction" to refer to this type of

parenchymal lesion, since it does not reflect the potential reversibility of the

damage (4); in this context, it seems to be more appropriate to speak of venous

ischemia. Some authors have correlated the degree of restriction of protons

mobility with a potential irreversibility when the mobility coefficient in the ADC

mapping is less than 0.20 x10-5 cm2 /s (23), but this finding has not been

documented in other studies (25).

On the other hand, vasogenic edema shows hyperintensity on T2-weighted MRI

sequences and hypointensity on T1- weighted MRI images, with a tendency to

respect the cortex; it shows no restriction on ADC map and usually is not

hyperintense on diffusion-weighted imaging, unless it represents an artefactual

image due to T2 effects (Figure 11), commonly associated with an increase of

mass effect due to increased water content in the area involved. The vasogenic

edema is one of the most commonly encountered parenchymal abnormalities in

IVT patients, closely related to pathophysiological events triggered after

intracranial venous thrombosis. When capillary fluid pressure increases, it may

cross the blood brain barrier resulting in early and wide-spread vasogenic

edema, which may constitute the predominant disturbance, reaching up to one

third of the cases, as reported by some studies (22, 25).

Increase in parenchymal volume without attenuation or signal intensity

alterations can be found in up to 42% of IVT cases, possibly as a reflection of

the capillary venous congestion, with effacement of sulci, decrease in the width

of the cisterns as well as in the size of the ventricular system (4, 24).

Up to one third of the IVT may show signs of intracranial hemorrhage and T2 *-

weighted sequences are especially useful for detecting them (4); depending on

the state of the hemoglobin, diverse areas of signal intensity alteration may be

found in the hematoma (Figure 6). Venous thrombosis should always be viewed

as a cause of benign-appearing hematoma, in absence of any other apparent

cause (arterial hypertension, vascular malformation, etc.); the search for the

signs already described is essential to suggest or confirm its etiology.

20

In TVI, subarachnoid hemorrhage is occasionally found, a finding scarcely

reported in the literature despite its common occurrence in lumbar puncture

studies. Ruling out cases that include intraparenchymal hematomas with some

degree of leakage into the subarachnoid space, there are some publications

that have correlated subarachnoid hemorrhage with cortical venous thrombosis

more often than with dural venous sinus thrombosis (25, 26); it has also been

described as a rare initial presentation of cortical venous thrombosis, so it is

necessary to consider this diagnosis within the spectrum of causes of

nonaneurysmal subarachnoid hemorrhage (26).

C) Signs of recanalization

When IVT begins to recanalize, multiple intrasinus channels and dural collateral

vessels may be observed, mainly on MR venographic projections (Figure 7k,

13). Several studies have demonstrated the usefulness of anticoagulant and

thrombolytic therapies for achieving patient recovery and reducing mortality

rates as well as serious sequelae in IVT patients (2); nevertheless, a complete

recanalization is not required for clinical recovery (27) and it is not directly

correlated with the extent of recanalization, apparently due to the presence of

collateral veins that would help to improve drainage of the areas involved (4). As

for time of recanalization, it has been shown that the majority of recanalizations

occurs before 6 months and that there is no difference in recanalization rates

between controls at 3 months and after 6 months (28, 29).

21

Figure 8. a) T1-weighted MRI without contrast shows absence of flow void in the superior

sagittal sinus. Compare with cerebral vein (vein of Galen) b). Thrombosis was confirmed in the

sequence with contrast.

22

Figure 9. T2-weighted MRI a) and T1 with contrast sequences b). Note the superior sagittal

sinus hypointense on T2, which may suggest a normal flow void; however, after contrast

administration the empty delta sign is observed.

23

Figure 10. ATECO MR sequence in coronal plane shows left transverse sinus thrombosis.

Figure 11. Coronal T2 FLAIR sequence shows hyperintense vein sign in a left parietal cortical

vein and partial absence of flow void of ipsilateral transverse sinus, with involvement of the

temporal lobe, predominantly at the level of subcortical white matter, with the appearance of

vasogenic edema.

24

Figure 12. GRE T2 * sequence a) showing magnetic susceptibility artifact in the right superior

anastomotic vein (vein of Trolard), without visualization on 3D venographic sequence b).

25

Figure 13. ATECO MR sequence shows lateral sinus thrombosis with partial recanalization.

Common pitfalls

Anatomical variations at the confluence of the sinuses are common (Figure 14)

(30) and may result in false positives. A 49% of asymmetric TS has been

described, with partial or complete absence in up to 20% (4), which can produce

artifacts due to slow, fast or turbulent flow on MRI sequences, even on ATECO

MR angiographic sequences, giving the false impression of thrombosis.

26

The asymmetrical bifurcation of the confluence of the sinuses, or at a superior

level, may cause a triangular image called "the pseudo empty delta” sign

(Figure 15) (4, 31), which has been visualized in 18% of contrast-enhanced CT

scans (32). This error can be avoided by exploring the entire route of the sinuses

and documenting the density of this pseudodefect, which has the same

attenuation (on CT) or signal intensity (on MRI) as that of the subarachnoid

CSF.

The presence of hypodense collections (such as abscesses) in the epidural

space adjacent to the sinuses has been described as a possible cause of a

"pseudo empty delta" sign (31). Fenestrations or septa within dural sinus are also

mentioned as causes of a false positive diagnosis (33).

Arachnoid granulations (Figure 16) are identified in 24% of contrast-enhanced

CT scans (34), usually in the SSS and the TS, specifically in the lateral aspect

(Figures 17,18) near the entrance of superficial veins such as the inferior

anastomotic vein (vein of Labbé) (4), although they are also found in the

cavernous, superior petrosal, and straight sinuses, in descending order of

frequency (5). Arachnoid granulations can protrude directly into the sinus lumen,

thus resulting in a potential false positive for the empty delta sign (5). One way to

identify them is by their rounded shape that produces a focal filling defect, with

the same attenuation as that of the subarachnoid CSF (on CT) or the same

signal intensity (on MRI) (4).

27

Figure 14. Diagram of coronal view of the anatomical variations found at the confluence of the

sinuses (Retrieved from Reference 30). a) Confluent: 35%, b) Bifurcation: 14%, c) left

Dominance: 10%, d) right Dominance: 40%. In the last two types we have observed that the

nondominant side flow mainly comes from a division of the straight sinus.

28

Figure 15. Sign of the "pseudo empty delta." a) contrast-enhanced CT view with triangular

image posterior to the confluence of the sinuses, which can be misinterpreted as thrombosis. b)

In the phase without contrast no hyperdense image can be seen. c) Reconstruction in the

coronal plane shows the bifurcated configuration that the confluence of the sinuses exhibits.

29

Figure 16. Coronal section of an anatomical preparation in which an arachnoid granulation

(asterisk) in the transverse sinus (TS) is identified.

30

31

Figure 17. CT sequence at the level of transverse sinuses. a) filling defects consistent with

arachnoid granulations are identified b) Compare the defect density with the sinus on non-

contrast phase. c) The reconstruction in the coronal plane also helps to evaluate the defect.

Figure 18. MR ATECO sequence. a) In the coronal plane, arachnoid granulations in the SSS

are observed. b) In the same patient, arachnoid granulations in the transverse sinus are seen.

32

Final Comment

While the venous-phase angiography with digital subtraction imaging technique

remains to be the "gold standard" for diagnosis of IVT─an invasive and risky

method─, the possibility of making an accurate diagnosis by noninvasive

methods, such as CT or MRI studies, has been considered. As already

discused, these techniques reveal several signs that allow a proper diagnosis of

IVT. For instance, the empty delta sign described on contrast-enhanced CT

scans as well as on MRI sequences is a sign widely known for imaging

specialists; nevertheless, the "false positives" that this sign may originate

(anatomic variants, arachnoidal granulations or slow flow on MRI) or some

conditions that may mimic a "false negative" result (such as the chronic

development of a thrombus on CT and MRI sequences) not always are properly

recognized.

Another relevant issue that radiologists must be acquainted with is the

sensitivity and specificity of imaging methods, the use of contrast materials,

along with the noninvasive angiographic techniques that yield the highest

diagnostic performance in identifying IVT. It is our task to be fully familiar with all

these imaging techniques in order to make accurate and timely diagnoses to

provide the most appropriate treatment to patients presenting IVT (5) as well as

to protect misdiagnosed patients against unnecessary exposure to

anticoagulant therapy with it inherent risks. Likewise, if we are able to recognize

the existence of venous thrombosis on CT and MRI studies, we can spare

patients with hematoma from undergoing conventional angiography.

In summary, adequate knowledge of signs favouring an accurate imaging

diagnosis of IVT as well as of pitfalls arising from artifacts, physiological and

anatomical variants, constitute issues to be mastered by radiologists.

33

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