Read the signs of sinus thrombosis in one article!

Clinical features

Cerebral venous sinus thrombosis is a special type of vascular disease, which is divided into two categories
: non-infectious and infectious.
The former is mostly caused by trauma, wasting diseases, certain blood diseases, pregnancy, severe dehydration, oral contraceptives, etc.
, and the latter is mostly secondary to head and face infections, as well as purulent meningitis, brain abscess, sepsis and other diseases
.
The main clinical manifestations are intracranial hypertension, such as headache, vomiting, decreased vision, papilledema, hemifacial limb weakness, hemiplegia, etc
.

pathogenesis

The pathogenesis and pathological changes of this disease are different from arterial thrombosis, cerebral venous return disorder and cerebrospinal fluid absorption disorder are the main changes
.
If the sinuses are completely blocked and involve a large number of collateral veins, or when the thrombus expands to the cerebral cortical veins, intracranial pressure increases and cerebral vein and cerebrospinal fluid circulation disorders occur, resulting in cerebral edema, hemorrhage, and necrosis
.
In the advanced stages of the disease, severe venous blood stasis and intracranial hypertension slow secondary arterial blood flow, leading to ischemia, hypoxia, and even infarction of brain tissue
.
Therefore, the diversity of clinical manifestations is the result of different etiology and disease stages, different ranges and locations of thrombus, and the combined effect of
secondary intracerebral lesions.

CT findings

1.
Direct signs of cerebral vein thrombosis

Direct signs of cerebral vein thrombosis are signs that directly reflect intravenous sinus thrombosis and include banding signs, high-density triangulations, and Delta or empty triangular signs
.

(1) Banding sign This sign can be seen on CT non-contrast scanning, which is a high-density thrombus image
of cortical vein creeping.
A positive sign suggests a neocortical vein thrombosis, but it is rarely seen
.

(2) High-density triangulation This sign can also be displayed on non-contrast CT images, indicating fresh thrombosis at the back of the superior sagittal sinus, with a rate of less than 2%, manifested as a triangular high density, which is difficult to distinguish from the slightly higher density of the superior sagittal sinus and sinus sink under normal circumstances, and abnormally high density can also be seen in other venous sinuses, such as transverse sinuses and straight sinuses, but this sign should be determined with caution because the venous sinuses can be spontaneously high density, especially in children or dehydrated patients
.

Both banding signs and high-density triangulation signs are non-contrast CT scan, which are essentially caused
by high-density direct development of thrombosis in the veins (sinuses).
The band sign indicates intravenous thrombosis on the surface of the cerebral cortex, while the high-density triangulation sign generally refers to the thrombus of the superior sagittal sinus, so the two signs can also be classified as manifestations of different parts of the sinus thrombosis
.
Non-contrast CT scan shows high-density foci of thrombosis in the sinuses, brain surface and deep veins, often 1~2 weeks after thrombosis, and the CT value is 50~90HU, representing fresh thrombosis
.
The morphology of thrombosis in these cerebral veins (sinuses) can be varied, depending on the orientation of the CT scan level and the relationship between the diseased blood vessels, and is most clearly displayed at the level perpendicular to the thrombus, which is dotted or triangular; At the parallel level, it is striped
.

(3) Delta sign (or empty triangle sign) This sign was first described
by Buonanno et al.
in 1978.
On contrast scanning, it appears as a triangular dural venous sinus section, and the dural sinus wall enhancement contrasts with the low-density thrombus in the cavity, similar to the Greek letter ", hence the name
.
This sign is common on cross-sectional CT scans at the posterior third of the superior sinus and on the top superior sagittal sinus
on coronal CT scans.
The mechanism of formation is due to the occlusion of the venous sinuses, the contrast agent enters the sinus space around the thrombus through the anastomosis of the collateral branches of the dural sinus, the incompletely occluded veins and the hyperplastic capillaries, and at the same time, due to the strengthening of the dura mater that constitutes the sinus wall, the basis for
marginal strengthening is formed.

Delta sign is the best and most common direct sign of CT for the diagnosis of cerebral venous sinus thrombosis, with a 35%
positive rate reported in the literature.
However, its incidence varies greatly and depends mainly on the location of the thrombus, the timing of the CT scan, and the choice of technical parameters applied at the
time of examination.
On the other hand, the degree of understanding of the clinical and radiographic manifestations of cerebral venous sinus thrombosis is also an important factor
affecting the determination of intrinsics.
If the possibility of the disease is not considered in time from the clinical manifestations, CT scanning is usually performed according to the conventional method, which is easy to cause the missed diagnosis
of this sign.
When cerebral venous sinus thrombosis is clinically suspected, there is a conscious search for signs such as coronary and thin-slice scanning, multi-window width and window position observation, and continuous multiplane correction, which can improve the display
of Delta sign.

2.
Indirect signs of cerebral vein thrombosis

(1) Abnormal enhancement of sickles and cerebellar tentacles The occurrence rate of this sign is about 20%.

Reinforcement of the cerebellar tentacle is easy to identify, and determining sickle enhancement of the brain can be difficult, especially in older people
.
Enhancement of the cerebellar screen is generally thought to indicate a straight sinus thrombus or thrombosis
involving the posterior superior sagittal sinus.

(2) Cerebral permedular vein dilation CT enhancement showed that the cerebral permedullary vein dilatation, manifested by many enhanced vascular structures
in the white matter of the brain and the gray-white matter junction.
This sign is usually associated with
extensive sinus thrombosis.

(3) Ventricular enlargement Ventricular enlargement is a common sign of the disease, caused by cerebral edema, accounting for 20%~50% of the total number of reported cases, usually coexisting
with other abnormal signs.
However, it can also be the only abnormality of the disease, accounting for 20%
of all cases.
When it occurs alone, it has no real value
because of its difficulty in evaluating its significance and lack of specificity.

(4) Low density of white matter without intensification This manifestation indicates cerebral edema, and the incidence rate of this disease can reach 75%.

It is easier to identify in adults than in children, and because nonphospholipidated white matter can produce similar changes, it is difficult to confirm the presence of
this sign in neonates.
Low-density lesions may be seen in bilateral diffuse or focal distribution
in both cerebral hemispheres.
They can sometimes be accompanied by a mass effect, manifested by ventricular displacement and shallow, disappearance
of the sulci.
Cerebral oedema may be the result of cerebral vein thrombosis parenchymal lesions alone, but may indicate concurrent venous infarction
.

(5) Venous cerebral infarction Venous cerebral infarction can produce a variety of changes on CT, including:

Hemorrhagic infarction, which is the most common sign, occurs in 10%~50% of cases of
this disease.
Lesions can be large or small, but in most cases the bleeding foci are small, surrounded by normal brain tissue or low-density lesions of varying sizes, which are usually multiple
.
Larger bleeding foci have also been reported, which are difficult to distinguish from spontaneous bleeding in the brain, manifested as multiple blood foci
with irregular margins under the cortex.
Rarely, subarachnoid hemorrhage or subdural hematoma may be present, and this change may even be the only abnormal sign
of cerebral vein thrombosis.

Non-hemorrhagic infarction Non-hemorrhagic infarction is as common as hemorrhagic infarction, accounting for 10%~40% of
patients with cerebral vein thrombosis.
They manifest themselves in a variety of forms, the most common type being accompanied by intensified subcortical low density and varying degrees of mass effect
.
Intensification is most common in the gyrus and subcortex, but is also seen in others, such as focal or quasi-circular lesions, which sometimes mimic metastases
.
In some cases, there is no spontaneous low density, only a single contrast enhancement is seen, which is very large in size and morphology, and is linearly, gyrus, or nodular intensifying
.

Hemorrhagic or non-hemorrhagic venous infarct lesions can be unilateral or bilateral, single or multiple
.
They often coexist with edema and mass effects, which can occasionally be more pronounced
.
These lesions are completely inconsistent with the distribution of the arteries and are most commonly complicated by thrombosis of the superior sagittal sinus, superficial infarction sites, and involvement of the cortex and adjacent white matter
.
Infarctions due to deep venous thrombosis are bilateral and rarely bleed, and can involve all or part of the corresponding drainage area, including the basal ganglia, surrounding white matter, and upper midbrain
.
The same is true for cerebellar venous infarction, which can be low-density (with or without contrast enhancement) or high-density, seen unilaterally or bilaterally, often with fourth ventricular compression and secondary hydrocephalus
.

MR performance

MRI has advantages in diagnosing sinus thrombosis and generally does not require enhanced scanning
.
MRV can be used as an alternative to DSA inspection
.
Cerebral venous sinus thrombosis most commonly occurs in the superior sagittal sinus, and MRI is complex and diverse depending on the length of formation, which makes diagnosis difficult
.
Acute sinus thrombosis is usually moderately or markedly high-intensity on TIWI, with T2WI showing very low intravenous sinus signal and sinus wall hyperintensity
.
With the prolongation of the disease course, TIWI or T2WI are hyperintensive; Sometimes at T1WI, the thrombus has a high signal at the edge and an equal signal in the center, which coincides with
the evolution of the hematoma in the brain.
T2WI shows that the empty signal in the venous sinus disappears, and even atrophies and occludes
with the course of the disease.

It should be noted that shortening the TR time can increase the T1WI signal of normal human cerebral sinuses, which is confused
with sinus thrombosis.
Due to the enhanced inflow effect of magnetic resonance, the normal human cerebral venous sinuses in TIWI can change from empty signals to bright signals, which behaves the same as
sinus thrombosis.
In addition, slow blood flow can increase the intensity of sinus signals; The presence of large counterflow in the temporal veins can make some of the less developed transverse sinuses highly intensive; Vortexes within the sigmoid sinus and jugular bulb are also often hyperintense
in SE images.
Therefore, suspected cases should be further differentiated
by extending the TR time, changing the scanning level, and MRV examination.

MRV can reflect the morphology and blood flow status of the cerebral sinuses, and has certain advantages
in diagnosing venous sinus thrombosis.
Direct signs of sinus thrombosis are occlusion of the affected sinuses, irregular stenosis, and filling defects
.
Due to venous return disorders, dilation of the surface and deep veins of the brain, venous blood stasis, and collateral circulation formation
are common.
However, when sinus dysplasia is present, MRI and MRV are difficult to
diagnose.
Contrast-enhanced MRV can compensate for this shortcoming
by obtaining clearer images of veins.
In addition to the superficial venous system, the brain also has a deep venous system
.
The latter consists of
the Galen vein and the basilar vein.
Enhanced MRV shows deeper veins clearer
than MRV.
If a thrombus develops in the Galen vein, local drainage areas (eg, bilateral thalamus, caudate nucleus, putamen, globus pallidus) may be oedema and lateral ventricles may be enlarged
.
Monro foramen obstruction is thought to be due to edema rather than increased venous pressure
.