Cortical vein thrombosis

Cortical vein thrombosis also called superficial cerebral vein thrombosis, cortical venous thrombosis or cerebral cortical vein thrombosis is a rare type of cerebral venous thrombosis involving the superficial cerebral veins besides the dural sinus, often coexisting with deep cerebral vein thrombosis or dural venous sinus thrombosis (Figures 1 to 4) ¹, ², ³, ⁴, ⁵, ⁶, ⁷, ⁸. Cerebral venous thrombosis is a condition where blood clot (thrombus) occurs in the cerebral veins and the dural sinuses in your brain ⁹. Blood clots are tangles of molecules and blood cells that clump together that occur when blood hardens from a liquid to a solid. Normally the venous sinuses drain blood from your brain. Cerebral venous sinus thrombosis blocks the blood from draining and can cause a hemorrhagic stroke in young and middle-aged adults, with a sex ratio heavily skewed towards women ¹⁰. Cerebral venous sinus thrombosis generally occurs in children and young adults and accounts for less than 1% of all strokes ¹¹. Cerebral venous thrombosis peak incidence rate in adults occurs in the third decade of life with the incidence rate being higher in women compared to men ¹². Isolated cortical vein thrombosis without sinus involvement is reported to be extremely rare condition and often difficult to diagnose, both clinically and radiologically ¹³. Cortical vein thrombosis clinical presentations are non-specific and the typically described ‘cord sign’ is seen rarely ¹⁴. The neuroimaging features of isolated cortical venous thrombosis include direct visualization of the blood clot (thrombus), localized hemorrhage or venous infarction. Visualization of the blood clot (thrombus) within a thrombosed cortical vein on CT scans is often described as the ‘cord sign’ (Figure 5) ⁵. The cord sign refers to cordlike hyperattenuation within a dural venous sinus on non-contrast enhanced CT of the brain due to dural venous sinus thrombosis ¹⁵. The cord sign is pathognomonic of cortical vein thrombosis ⁵. The cord sign is most commonly seen in the transverse sinus because along the origin of the tentorium it runs approximately in the axial plane such that it is visible on one image. It is important to appreciate that normal blood within the dural sinuses is usually of slightly increased density relative to brain tissue and that true hyperdensity is the key to recognizing thrombosis ¹⁵. A false positive cord sign may also be seen in the setting of generalized cerebral edema when it is actually the brain which is of reduced density rather than the sinus being hyperdense ¹⁵. MRI equivalent of the cord sign can be difficult to identify, especially during the early phase as the blood clot (thrombus) tends to be isointense with brain on T1-weighted images and hypointense on T2-weighted images, appearing as flow void ⁴. From 3 to 7 days after thrombosis, the blood clot (thrombus) becomes hyperintense on both T1- and T2-weighted images and is therefore easier to identify ⁴.

It is important to note that cortical veins are highly variable in number, size, and location ¹⁶. The cortical cerebral veins involved in cortical vein thrombosis are (Figure 1, 2 & 6):

Superficial middle cerebral vein
Inferior anastomotic vein (vein of Labbe)
Superior anastomotic vein (vein of Trolard)
Small (unnamed) cortical veins

Venous infarctions will be directly related to the presence or not of a collateral outflow.

Cortical vein thrombosis symptoms are nonspecific, ranging from no symptom (asymptomatic) to seizure, coma, and death, depending on the extension, collateral flow and association with deep cerebral vein thrombosis and dural venous sinus thrombosis. Cerebral venous thrombosis can present with variable signs and symptoms that range from a patient seen at the clinic with a 1-month history of headache, benign intracranial hypertension, subarachnoid hemorrhage (SAH), focal neurological deficit, stroke, seizures, unexplained changes in brain function such as confusion, loss of memory, loss of alertness, disorientation, poor judgment or thinking, meningoencephalitis (a rare and life-threatening condition in which you have meningitis and encephalitis at the same time) to a comatose patient admitted to the emergency room ¹⁰, ¹¹, ¹⁷, ¹⁸. Headache is the most common symptoms and presents as thunder clap headache. Patients can also present with focal or generalized seizures, focal central nervous system (CNS) deficits (hemianopsia, aphasia, motor or sensory defects), and coma. Consequently, the diagnosis of cerebral venous thrombosis is often delayed or overlooked. Results of the International Study on Cerebral Vein and Dural Sinus Thrombosis demonstrated that the median delay from onset of the symptoms to admission was 4 days and from onset of symptoms to diagnosis was 7 days ¹⁹. Therefore, having a high index of suspicion for cerebral venous thrombosis is crucial to ensure timely diagnosis and treatment ²⁰, ²¹.

Treatment of cortical vein thrombosis includes: (1) treatment of the underlying cause or removal of the identified risk factors, (2) antithrombotic treatment and (3) symptomatic treatment of intracranial hypertension, seizures and other complications. Management of isolated cortical venous thrombosis aims to recanalize the occluded vessel and prevent its extension to other parts of the venous system ²². This recanalization goal may be achieved through anticoagulation therapy with low molecular weight heparin (LMWH) subcutaneously or heparin intravenously, with low molecular weight heparin (LMWH) being the drug of choice ²³, ²⁴, ²⁵, ²⁶. Low molecular weight heparin (LMWH) and heparin are contraindicated in the setting of any recent cerebral hemorrhage, severe hypertensive episodes, hemorrhagic disorders, and peptic ulcer disease. Particular attention is necessary for patients with chronic kidney disease, as low molecular weight heparin (LMWH) can accumulate in kidney insufficiency. In such instances, heparin may be a more appropriate option ²⁷.

In patients with evidence of cerebral herniation, neurosurgery should be consulted, and decompressive craniectomy should be performed, similar to cerebral venous thrombosis ²⁸. Endovascular thrombolysis does not seem to be an option because the cortical veins cannot be reached with a microcatheter without a high-risk perforation ¹².

In patients who have evidence of worsening neurologic symptoms despite adequate treatment with low molecular weight heparin (LMWH) or heparin, mechanical thrombectomy or endovascular thrombolysis may also be an option.

In the setting of isolated cortical venous thrombosis, there is a risk of increased intracranial pressure (ICP). A neuro-intensive care admission should be considered as frequent intracranial pressure (ICP) monitoring, elevating the head of the bed, administering osmotic agents such as mannitol or hypertonic saline, and allowing permissive hyperventilation with a partial target pressure of carbon dioxide of 30 to 35 mmHg may be required ¹. Intravenous dexamethasone is not recommended in treating isolated cortical venous thrombosis ¹.

Patients that initially present with seizures, edema, infarction, or hemorrhaging on imaging should be placed on seizure prophylaxis ²⁹. Levetiracetam or valproate are the first-line drugs of choice.

Once the patient is stabilized and discharged, anticoagulation therapy with either warfarin or dabigatran should be considered for a minimum of three months to prevent recurrence of isolated cortical venous thrombosis ³⁰.

Figure 1. Cerebral venous system

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Figure 2. Dural venous sinuses

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Figure 3. Cortical vein thrombosis

Footnotes: 38 years old man with right parietal cortical vein thrombosis. Magnetic resonance imaging (MRI) of the brain: (A) Sagittal T1 sequence shows a hyperintense signal in the right parietal region, (B) axial gradient echo sequence demonstrates the hemorrhagic component as susceptibility artifact, (C) diffusion weighted imaging (DWI) shows a bright signal in the right parietal region with a corresponding hyperintense signal on (D) axial T2 weighted imaging. (E and F) Normal patency of the major cerebral venous sinuses is seen on magnetic resonance venography (MRV).

[Source ⁴ ]

Figure 4. Isolated cortical vein thrombosis

Footnotes: A case of a 25-year-old Chinese woman who had been abusing nitrous oxide for twenty months. She had a history of peripheral neuropathy and subacute combined degeneration in between. The young woman presented with headache, motor aphasia and right arm paralysis of eight hours after intermittently consuming nitrous oxide for one week. D-dimer was increased (1.1 mg/ml). Blood vitamin B12, folate, homocysteine and beta-HCG levels were normal. Head CT showed hemorrhagic infarction and subarachnoid hemorrhage. MR angiography (MRA) and venography (MRV) were normal. Head MRI identified left frontal isolated cortical vein thrombosis. Her muscle strength and verbal fluency significantly improved after initiation of Low Molecular Weight Heparin and serial head MRI showed continuous reduction in the size of thrombus.(Top image A to C, arrow) Head CT on admission showing hemorrhagic infarction mainly involving the left parietal lobe and (C, arrow heads) subarachnoid hemorrhage. (Bottom image) Head MRI 10 days after admission showed isolated cortical vein thrombosis (arrow head) over the frontal cortical surface and expanding hematoma and edema (double arrow head) that caused cingulate herniation in the sagittal, coronal and axial section (A to C) on T2 SPACE sequence. The sizes of thrombosis (arrow head), hematoma and edema (double arrow head) continuously decreased on T1 CUBE sequence after five days (D to F) and twelve days (G to I) of anticoagulation, respectively

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Figure 5. Cord sign of cortical vein thrombosis

Footnote: Noncontrast CT (computed tomography) shows the cord sign (black arrowheads). It is present at multiple continuous sections. A small low attenuated lesion (white arrowhead) is observable.

[Source ⁵ ]

How common is isolated cortical venous thrombosis?

Of all cerebral venous and sinus thrombosis, only 6.3% are from isolated cortical venous thrombosis, and isolated cortical venous thrombosis accounts for less than 1% of all cerebral infarctions ¹. One systematic review of 47 case reports/case series found that the mean age of diagnosed patients was 41and 68% of these patients are women ¹². Because isolated cortical venous thrombosis is rarely diagnosed, more research is needed to determine additional epidemiological patterns.

In general, cortical vein thrombosis, isolated cortical vein thrombosis, and cerebral venous thrombosis affect patients younger on average than patients diagnosed with arterial strokes. Women are also at a higher risk than men ³³.

Venous Drainage of the Central Nervous System

The venous drainage of the brain is complex, and the intracranial veins, unlike the systemic veins, do not follow their arterial counterparts and thus differ in their drainage territory from the arteries. There is also considerable variability in the venous drainage of the brain and skull ³⁴, ³⁵, ³⁶, ³². There are also numerous interconnections between venous drainage systems. Variations in cerebral venous anatomy is a rule rather than an exception ³¹. These variations must be kept in mind while evaluating a scan for pathologies like cerebral venous sinus thrombosis or assessment of their patency in tumors encasing the venous sinuses ³⁷, ³⁸.

The cerebrum, cerebellum and brainstem are drained by numerous veins, which empty into the dural venous sinuses. The spinal cord is supplied by anterior and posterior spinal veins, which drain into the internal and external vertebral plexuses.

Figure 6. Venous drainage of the brain

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Dural Venous Sinuses

The dural venous sinuses lie between the periosteal and meningeal layers of the dura mater. The dural venous sinuses are best thought of as collecting pools of blood, which drain all of the venous blood from the cerebral hemispheres, the face, and the scalp ⁴⁰. All the dural venous sinuses ultimately drain into the internal jugular vein. Unlike most veins of the body, the dural venous sinuses do not have valves; therefore, dural venous sinuses can promote a forward or backflow of blood to other associated structures, allowing pathogens and neoplastic cells to travel to different parts of the brain ³².

There are eleven venous sinuses in total ⁴¹. There are 7 major dural venous sinuses located within the cranial cavity, specifically between the periosteal and meningeal layer of the dura mater: superior sagittal, inferior sagittal, straight, transverse, sigmoid, cavernous, and superior petrosal sinuses ³². Most of these sinuses are found adjacent to the falx cerebri and tentorium cerebelli. The cavernous sinus is clinically the most important dural venous sinus ³².

The straight, superior, and inferior sagittal sinuses are found in the falx cerebri of the dura mater. They converge at the confluence of sinuses (overlying the internal occipital protuberance). The straight sinus is a continuation of the great cerebral vein and the inferior sagittal sinus.

From the confluence, the transverse sinus continues bilaterally and curves into the sigmoid sinus to meet the opening of the internal jugular vein.

The cavernous sinus drains the ophthalmic veins and can be found on either side of the sella turcica. From here, the blood returns to the internal jugular vein via the superior or inferior petrosal sinuses.

The dangerous triangle of the face is a triangular area bounded by the medial angle of the eyes, sides of the nose and the upper lip as its boundaries. This anatomy is important because it serves as the passageway of pathogens from the face into the brain via the cavernous sinuses. Infection coming from the superficial and deep layers of the face can easily travel into the cavernous sinuses leading to the development of a thrombus, a condition termed as cavernous sinus thrombosis. Cavernous sinus thrombosis may result in the swelling of the affected sinuses and pertinent damage to the associated cranial nerves. Patients may develop internal strabismus caused by the lesion in the cranial nerve 6, which is usually the first cranial nerve affected, which is then followed by damage to further movement and sensation of the eyes and skin of the face as well as the scalp, respectively. Ophthalmoplegia or paralysis of the eye muscles can also be manifestations of other damaged cranial nerves. Pulsatile proptosis characterized by a combination of pulsation and protrusion of the eyeball can also present in patients with affected venous sinuses ⁴², ⁴³, ⁴⁴, ⁴⁵.

Veins of the Cerebrum

The veins of cerebrum are responsible for carrying blood from the brain tissue, and depositing it in the dural venous sinuses ⁴¹.

The veins of cerebrum can be divided into superficial and deep groups, which are arranged around the gyri and sulci of the brain. Upon exiting the cerebral parenchyma, the veins run in the subarachnoid space and pierce the meninges to drain into the dural venous sinuses.

Superficial veins of cerebrum

The superficial veins of cerebrum is largely responsible for draining the cerebral cortex:

Superior cerebral veins: Drain the superior surface, carrying blood to the superior sagittal sinus.
Superficial middle cerebral vein: Drains the lateral surface of each hemisphere, carrying blood to the cavernous or sphenopalatine sinuses.
Inferior cerebral veins: Drain the inferior aspect of each cerebral hemisphere, depositing blood into cavernous and transverse sinuses.
Superior anastamotic vein (Trolard): Connects the superficial middle cerebral vein to the superior sagittal sinus.
Inferior anastamotic vein (Labbé): Connects the superficial middle cerebral vein to the transverse sinus.

Deep veins of cerebrum

Subependymal veins: There are numerous subependymal veins, which will not be described here in detail. These receive blood from the medullary veins and carry it to the dural venous sinuses. The great cerebral vein (vein of Galen) is worthy of a mention; it is formed by the union of two of the deep veins, and drains into the straight sinus.
Medullary veins: Originate 1 to 2cm below the cortical grey matter, and drain into subependymal veins. These drain the deep areas of the brain.

Veins of the Cerebellum

There are two main veins responsible for the venous drainage of the cerebellum – the superior and inferior cerebellar veins. They empty into the superior petrosal, transverse and straight dural venous sinuses.

Veins of the Brainstem

Venous drainage of the brainstem is carried out by numerous vessels – many of which are beyond the scope of this article. Examples of veins that drain the brainstem include the transverse pontine vein, anteromedian medullary vein, and the anterior and posterior spinal veins.

Veins of the Spinal Cord

The spinal cord is supplied by three anterior and three posterior spinal veins. These veins are valveless, and form an anastamotic network along the surface of the spinal cord. They also receive venous blood from the radicular veins.

The spinal veins drain into the internal and external vertebral plexuses, which in turn empty into the systemic segmental veins. The internal vertebral plexus also empties into the dural venous sinuses superiorly.

Cortical vein thrombosis causes

Cortical vein thrombosis patients usually have at least one of these risk factors ¹, ⁴⁶:

Thrombophilia, a tendency to develop blood clots due to abnormalities in coagulation, e.g. factor V Leiden, deficiency of protein C, protein S or antithrombin, or related problems
Nephrotic syndrome, a kidney problem causing protein loss in the urine (proteinuria)
Chronic inflammatory diseases, such as inflammatory bowel disease (Crohn’s disease and ulcerative colitis), systemic lupus erythematosus (autoimmune disease that occurs when your body’s immune system attacks your own tissues and organs) and Behçet’s disease (inflammation in blood vessels of unknown cause)
Pregnancy and puerperium (the period after giving birth)
Particular blood disorders, especially polycythemia vera (a rare blood disorder in which there is an increase in all blood cells, particularly red blood cells) and paroxysmal nocturnal hemoglobinuria (is a rare disease in which red blood cells break apart prematurely that presents clinically with a variety of symptoms, the most prevalent of which are hemolytic anemia, hemoglobinuria, and somatic symptoms including fatigue and shortness of breath)
Use of estrogen-containing forms of hormonal contraception
Meningitis and infections of the ear, nose and throat area such as mastoiditis and sinusitis
Direct injury to the venous sinuses
Medical procedures in the head and neck area
Sickle cell anemia
Dehydration, primarily in infants and children
Homocystinuria

In general, cortical vein thrombosis is common in any condition that leads to a hypercoagulable state (prothrombotic state or thrombophilia, which is the tendency to venous thrombosis due to an abnormality in the coagulation system), including pregnancy, the post-partum state, or those on oral contraceptives. In the International Study on Cerebral Vein and Dural Sinus Thrombosis (ICSVT), genetic and acquired thrombophilia were present in 34% of patients with cerebral venous thrombosis. Inherited thrombophilia includes protein C and protein S deficiencies, antithrombin deficiency, factor V Leiden mutation, prothrombin gene mutation 20210, as well as hyperhomocysteinemia ⁴⁷, ⁴⁸.

At least one risk factor was identified in more than 85% of patients with cerebral venous thrombosis, and multiple risk factors are found in more than 50% of patients with cerebral venous thrombosis ⁴⁹.

Acquired thrombophilia should be suspected in patients with a history of nephrotic syndrome (due to loss of antithrombin) or antiphospholipid antibodies ⁹. Additional causes and risk factors associated with cerebral venous thrombosis include chronic inflammatory disease states such as systemic lupus erythematosus (SLE), inflammatory bowel disease (Crohn’s disease and ulcerative colitis), cancer, and inflammation in blood vessels such as Wegener’s granulomatosis ⁹. Local infections such as otitis and mastoiditis, which can lead to thrombosis of the adjacent sigmoid and transverse sinuses, have also been implicated in developing cerebral venous thrombosis. Cerebral venous thrombosis may also be seen in a patient with a head injury, after certain neurosurgical procedures, direct injury to the sinuses or jugular veins, such as jugular vein catheterization, and even after a lumbar puncture ⁵⁰, ⁵¹.

Cortical vein thrombosis risk factors

Cortical vein thrombosis has multiple risk factors, which can be grouped into:

Transient risk factors:
- Oral contraceptive pills very common cause in female patients <50 years of age and other medications with prothrombotic effects e.g., steroids,
- Pregnancy and puerperium (the period after giving birth),
- Infections, especially those involving the central nervous system or the paranasal sinus, the ear and the mastoid sinus (dural sinus occlusive disease)
- Skull abnormalities or trauma
- Compressing mass: e.g. meningioma
- Systemic illness
  - Dehydration: e.g. gastroenteritis
  - Sepsis
  - Cancer
  - Connective tissue disorders
- Iatrogenic
  - COVID-19 vaccine, especially AstraZeneca ⁵²
Permanent risk factors:
- Prothrombotic medical conditions, including genetic thrombophilic diseases, antiphospholipid syndrome, myeloproliferative disorders and cancers.

In around 13% of adult cerebral venous thrombosis no risk factors are identified (idiopathic) ¹⁹.

Cortical vein thrombosis pathophysiology

The pathogenesis of isolated cortical venous thrombosis is similar to cerebral venous thrombosis in that the formation of thrombosis can occlude blood drainage from the cerebral cortex ¹. This lack of blood drainage can lead to increased venous or capillary pressure which leads to a decrease in cerebral perfusion, which can also increase intracranial pressure (ICP) resulting in vasogenic edema.

With increasing vasogenic edema and intravenous pressures, venous or capillaries vessels can rupture, leading to hemorrhage and dysfunction. If the dural sinuses are specifically occluded, it can decrease cerebrospinal fluid reabsorption, which also increases intracranial pressure (ICP) ⁴⁶. Any of these mechanisms that increase intracranial pressure within the rigid cranium can cause herniation syndrome.

Cortical vein thrombosis symptoms

Cerebral venous thrombosis symptoms include the following:

headaches (89-91%) ⁵³
decreased or altered conscious state
decreased or altered vision
nausea and vomiting

Cerebral venous thrombosis signs include the following:

papilledema
cranial nerve palsies
focal neurological deficits (52-68%) ⁵³
seizures (39-44%) ⁵³
coma

Signs and symptoms may be acute, subacute, or chronic, with the most common symptom in cerebral venous thrombosis being a headache. In patients with a past medical history of headaches or migraines with auras, it is important to compare the headache’s features with the previous presentations to determine a significant difference. Any new-onset headache with characteristics that differ from their previous headache pattern, new-onset seizures, rapid encephalopathy, or focal neurological symptoms that do not fit typical patterns of stroke should warrant further evaluation.isolated cortical venous thrombosis should be considered in the setting of motor and sensory deficits with a new-onset headache.

The absence of increased intracranial pressure with focal or generalized seizures associated with aphasia, hemiparesis, hemianopia, and other focal neurological abnormalities should prompt physicians to consider isolated cortical venous thrombosis as a diagnosis ³³. Typically the focal neurological findings involve motor and sensory deficits. Headache is the most common complaint and sometimes is the only presenting symptom. Headache onset varies as some patients present with a gradual increase in headache severity over several days, while others have a rapid and severe headache within minutes.

Cortical vein thrombosis diagnosis

Once a clinician suspects isolated cortical venous thrombosis per the history and physical examination, urgent neuroimaging (CT, MRI and MR venography of the brain) is warranted in the initial diagnostic workup ¹. Given cerebral venous thrombosis varied presentation and myriad of symptoms, one must have a high index of suspicion to identify and diagnose this rare and potentially life-threatening condition correctly. Cerebral venous thrombosis should be suspected in young and middle-aged patients, especially those with cerebral venous thrombosis risk factors, such as postpartum women, those with genetic or acquired thrombophilia, and patients with focal neurological findings. It should also be suspected in the following ⁹:

Under the age of 50
Who present with atypical headaches or those having multiple repeat evaluations for an unrelenting headaches
Focal neurological deficit
Stroke-like symptoms, especially in the absence of vascular risk factors that would predispose to cerebral vascular accidents (carotid atherosclerosis)
Seizures (focal, generalized, or status-epilepticus)
Intracranial hypertension or evidence of papilledema on funduscopic exam
Patients with CT evidence of hemorrhagic infarcts, particularly in the setting of multiple infarcts not confined to a single vascular territory

Some important clinical clues to the diagnosis include slow progression, bilateral involvement, and concurrent seizures ⁴⁹.

There are no pertinent laboratory tests that can evaluate for isolated cortical venous thrombosis, and the diagnosis is typically made with magnetic resonance imaging (MRI) and magnetic resonance venography (MRV) ¹. If the institution does not have MRI, then cranial computed tomography (CT) with CT venography (CTV) can also be an option ⁵⁴.

Neuroimaging

Non-contrast computed tomography (unenhanced CT) is usually the first imaging investigation performed, given the nonspecific clinical presentation in these cases. Unfortunately, CT is usually normal ⁵⁵, ¹⁶. Potential findings include ²:

Cord sign
Dense vein sign
Cortical edema
Cortical or peripheral venous hemorrhage (linear cortical density or gyriform heterogeneous hemorrhage)

Magnetic resonance imaging (MRI) with gradient-echo T2 susceptibility-weighted sequences with MR venography (MRV) is considered the most sensitive imaging modality for isolated cortical venous thrombosis ¹. Typically the blood clot (thrombus) will present as an area of hypointensity within the cortical vein only on MRI. If a blood clot (thrombus) is present within the sinuses, then a diagnosis of cerebral venous sinus thrombosis (CVST) should be considered. Regarding cortical venous thrombosis, one study recommended that ‘cord sign’ (see Figure 5) seen on non-contrast-enhanced brain CT can point to the diagnosis of cortical vein thrombosis ⁵. The cord sign refers to cordlike hyperattenuation within a dural venous sinus on non-contrast enhanced CT of the brain due to dural venous sinus thrombosis ¹⁵. The cord sign is pathognomonic of cortical vein thrombosis ⁵. The cord sign is most commonly seen in the transverse sinus because along the origin of the tentorium it runs approximately in the axial plane such that it is visible on one image. It is important to appreciate that normal blood within the dural sinuses is usually of slightly increased density relative to brain tissue and that true hyperdensity is the key to recognizing thrombosis ¹⁵. A false positive cord sign may also be seen in the setting of generalized cerebral edema when it is actually the brain which is of reduced density rather than the sinus being hyperdense ¹⁵. MRI equivalent of the cord sign can be difficult to identify, especially during the early phase as the blood clot (thrombus) tends to be isointense with brain on T1-weighted images and hypointense on T2-weighted images, appearing as flow void ⁴. From 3 to 7 days after thrombosis, the blood clot (thrombus) becomes hyperintense on both T1- and T2-weighted images and is therefore easier to identify ⁴. Occlusion involving small veins at the cortical level is difficult to identify ¹⁶.

MRI findings are dependent on the age of the thrombus, as signal intensities change depending on thrombus age. Therefore, MRI interpretation requires a detailed understanding of the evolutionary changes seen radiographically. An acutely formed thrombus (0 to 7 days) is harder to detect, but by week 2, abnormalities are easier to detect, with both T1 and T2-weighted images showing a hyperdense signal. The combination of an abnormal signal in a venous sinus combined with the absence of flow on MRV confirms the diagnosis of cerebral venous thrombosis. 2-dimensional lumen-based TOF showing the absence of a flow void in the dural sinus is the most sensitive imaging modality. Multiscale entropy (MSE) of hemoglobin products within the thrombus is of high diagnostic value ¹⁶. The presence of DWI abnormality within the involved veins or sinus indicates low chances of recanalization. The differentials include arachnoid granulations and fenestrations ⁵⁶.

Cerebral angiography: If the diagnosis is still in question after using MRI and magnetic resonance venography (MRV), then intra-arterial angiography is indicated. Angiography allows for superior visualization of the cerebral veins and helps identify anatomical variants of normal venous anatomy that mimic cerebral venous thrombosis. It is useful in rare cases of isolated cortical vein thrombosis without sinus thrombosis and may show indirect signs such as dilated and tortuous “corkscrew” collateral veins, evidence that there may be thrombosis further downstream of the sinuses. Superior sagittal sinus is most frequently involved, followed by transverse sinus ⁴⁹.

Laboratory tests

While laboratory tests alone are insufficient for diagnosis, some tests have significant prognostic value. Laboratory tests should include a complete blood count, coagulation panel, chemistry panel, as well as inflammatory markers such as a sedimentation rate (ESR) and C-reactive protein (CRP) to evaluate for proinflammatory states ⁹. A patient could benefit from a screening for protein C deficiency, protein S deficiency, antithrombin deficiency, G20210 prothrombin gene variant, and factor V Leiden thrombophilia. Evaluation for lupus anticoagulant and antiphospholipid syndrome should also be considered.

Ideally, a screening test that could effectively rule out the diagnosis without subjecting patients to neuroimaging when it is not necessary would be ideal and prove helpful to clinical practice. The D-dimer assay has been evaluated in this regard, and unfortunately, it has been shown to have an unacceptable false-negative rate of up to 26% in one study. This low sensitivity of the D-dimer assay is in contrast to the utility of the D-dimer in ruling out deep venous thrombosis, which may be due to the lower thrombotic burden of cerebral venous thrombosis compared to deep vein thrombosis (DVT) ⁵⁷, ⁵⁸.

Based on recent American Heart Associationand the American Stroke Association guidelines, a negative D-dimer does not effectively rule out cerebral venous thrombosis and should not preclude neuroimaging if there is clinical suspicion for cerebral venous thrombosis ⁵⁹, ⁶⁰. However, adding D-dimer (≥500 μg/L) to the clinical cerebral venous thrombosis score (comprising of variables such as seizure, known thrombophilia, oral contraceptive use, duration of symptoms for >6 days, worst headache ever, and focal neurologic deficits) has shown to improve its predictive value ⁶¹.

Cortical vein thrombosis differential diagnosis

Cortical vein thrombosis can initially present as a severe headache. Imaging is essential as it aids in differentiating isolated cortical venous thrombosis from subarachnoid hemorrhage, meningoencephalitis, or a space-occupying lesion such as a tumor. Ruling out any acute metabolic encephalopathies due to infection is important. Clinical suspicion for infection should be high in patients presenting with fevers, elevated white blood count with band neutrophils, and positive blood cultures ⁶².

Isolated cortical venous thrombosis can be the first sign of a prothrombotic state. Other potential causes that need to be considered or worked up are vasculitis syndromes, primary/secondary thrombocytosis, polycythemia vera, antiphospholipid syndrome, and systemic lupus erythematosus. If isolated cortical venous thrombosis is suspect or discovered, the patient could benefit from a screening for protein C deficiency, protein S deficiency, antithrombin deficiency, G20210 prothrombin gene variant, and factor V Leiden thrombophilia ¹.

Cortical vein thrombosis treatment

Anticoagulation

Anticoagulation medications also known as blood thinners or anticoagulants are medicines that prevent blood clots from forming. Anticoagulation medications do not break up clots that you already have. But they can stop those clots from getting bigger.

There are different types of blood thinners:

Anticoagulants, such as heparin or warfarin (also called Coumadin), slow down your body’s process of making clots.
Antiplatelets, such as aspirin and clopidogrel, prevent blood cells called platelets from clumping together to form a clot. Antiplatelets are mainly taken by people who have had a heart attack or stroke.

Anticoagulation has been a controversial topic due to the potential for hemorrhagic transformation of cerebral infarcts before administering anticoagulation. The goal of anticoagulation is to prevent thrombus propagation, help recanalize the lumen of occluded cerebral veins, and to prevent the complications of deep venous thrombosis and pulmonary embolism in patients who already have thrombus burden and are predisposed to forming additional thrombi. The results of two randomized controlled trials, which compared anticoagulation with placebo, although statistically insignificant, showed that anticoagulation had a favorable outcome more often than controls. They also showed that anticoagulation was safe and not contraindicated, even in patients with cerebral hemorrhage.

Based on these randomized controlled trials and other observational studies, anticoagulation is recommended as a safe and effective treatment of cerebral venous thrombosis. It should be initiated immediately upon diagnosis of cerebral venous thrombosis. Anticoagulation with intravenous unfractionated heparin or subcutaneously administered low-molecular-weight heparin is recommended as a bridge to oral anticoagulation with a vitamin K antagonist. There are no outcome differences while comparing unfractionated heparin (UFH) or low molecular weight heparin (LMWH). The European stroke organization guidelines advocate unfractionated heparin in patients with renal insufficiency or the probability of requiring emergent reversal ⁴⁹.

The target goal of treatment is an international normalized ratio (INR) of 2.0 to 3.0 cerebral venous thrombosis 3 to 6 months in patients with provoked cerebral venous thrombosis and 6 to 12 months in patients with unprovoked cerebral venous thrombosis ⁴⁹. Indefinite anticoagulation should be considered in patients with recurrent cerebral venous thrombosis, those who develop deep vein thrombosis and pulmonary embolism in addition to cerebral venous thrombosis, or those with first-time cerebral venous thrombosis in the setting of severe thrombophilia.

Thrombolysis (Thrombolytic Therapy)

Thrombolysis also called fibrinolytic therapy is the breakdown of blood clots formed in blood vessels using medications (thrombolytics) or a minimally invasive procedure to break up blood clots and prevent new clots from forming.

Although most patients see clinical improvement with anticoagulation therapy, a small subset of patients do not, and these individuals clinically deteriorate despite anticoagulation. In these cases, where the prognosis is poor, systemic and catheter-directed thrombolysis is indicated in patients with large and extensive cerebral venous thrombi who clinically deteriorate despite treatment with anticoagulation ⁹. As is the case, whenever fibrinolytics are used, there is an increased risk of intracranial hemorrhage ⁹. Based on a systemic review conducted in 2003 ⁴⁹, which looked at 72 studies and 169 patients with cerebral venous thrombosis, there seems to be a possible clinical benefit due to the use of fibrinolytics in patients with a severe presentation. Intracranial hemorrhage occurred in 17% of patients treated with fibrinolytics and was associated with clinical deterioration in 5% of cases. Overall, endovascular thrombolytics should be used at centers with staff experienced in interventional radiology and should be reserved for patients who are clinically deteriorating and despite treatment with anticoagulation. A systematic study has shown local thrombolysis to be beneficial only in patients with severe cerebral venous thrombosis, whereas the results are anecdotal for mechanical thrombectomy ⁴⁹.

Surgical Intervention

Surgical thrombectomy is reserved for cases of severe neurological deterioration despite maximal medical therapy. In the case of large venous infarcts and hemorrhages causing a mass effect with risk of herniation, decompressive surgery has been thought to improve clinical outcomes, especially if done early. Decompressive surgery is life-saving, with favorable outcomes observed in more than 50% of patients, with a mortality rate of approximately 20% ⁴⁹.

Supportive Care

It is important to find the underlying contributory factors of cerebral venous thrombosis and devise a treatment strategy to correct them. Women on hormonal contraceptive therapy should seek non-estrogen-based methods of contraception such as levonorgestrel and copper intrauterine devices or progestin-only pills. Further testing to identify the cause of all acquired and reversible thrombophilic states should be conducted and, when possible, corrected. In addition to clinical follow-up, the American Heart Association and American Stroke Association recommend follow-up imaging 3 to 6 months after diagnosis to assess for recanalization.

The risks for intracerebral hemorrhage following anticoagulation therapy ranged from zero to 5.4%. A systematic review has shown that the overall mortality was 9.4%, and dependency of 9.4% and 9.7%, respectively ⁶³, ⁶⁴.

Post-Stroke Rehabilitation

Stroke rehabilitation is vital to stroke recovery and can help you relearn skills you lost because of the brain damage. The goal is to help you become as independent as possible and to have the best possible quality of life.

Physical therapy is the main form of rehabilitation for most people with stroke. The aim of physical therapy is to help people relearn simple motor activities such as walking, sitting, standing, lying down, and the process of switching from one type of movement to another. To achieve this, physical therapists use training and exercises to restore movement, balance, and coordination. In one stroke rehabilitation study, researchers compared at home physical therapy to a locomotor training program using treadmill walking with body weight support followed by walking practice. The Locomotor Experience Applied Post-Stroke (LEAPS) trial found that people who had a stroke and had physical therapy at home improved their ability to walk just as well as those who were treated with the locomotor training program. Study investigators also found that patients continued to improve up to one year after stroke, defying conventional wisdom that recovery occurs early and largely ends at six months.
Occupational therapy helps people relearn the skills needed to perform everyday activities such as eating, drinking and swallowing, dressing, bathing, cooking, reading and writing, and toileting. This type also involves exercise and training. Occupational therapists can recommend home or workplace modifications to better help the person resume living an independent or semi-independent lifestyle.
Speech therapy helps people with stroke relearn language and speaking skills or learn other forms of communication. Speech therapy is appropriate for people who have no problems with cognition or thinking but have problems understanding speech or written words, or problems forming speech. Speech therapy also helps people develop coping skills to deal with the frustration of not being able to communicate fully. With time and patience, speech therapy can help a stroke survivor regain some, and sometimes all, language and speaking abilities.
Vocational therapy helps people return to the workforce. Approximately one-fourth of all strokes occur in people between the ages of 45 and 65. For most people in this age group, returning to work is a major concern. It may involve relearning the more complex skills that were performed on the job or learning new skills for a different job. Vocational therapists can help people with lasting disabilities identify job skills and strengths and look for new work opportunities if necessary.
Psychological or psychiatric therapy can assist many people as they recuperate from stroke. Depression, anxiety, frustration, and anger are common disabilities in people with stroke. Psychological or psychiatric therapy, along with medication, can help ease some of the mental and emotional problems that result from stroke. Sometimes it is useful for family members to seek psychological help for themselves, as well.
The U.S. Food and Drug Administration (FDA) approved the Neurolutions Upper Extremity Rehabilitation System for individuals age 18 and older with upper arm disability who are undergoing stroke rehabilitation to increase range of motion and grasping. The brain-computer interface uses non-invasive electroencephalography electrodes to record brain activity, which is then wirelessly conveyed to a tablet for the analysis of the intended muscle movement, and a signal is sent to a wireless electronic hand brace, which in turn moves the person’s hand.
The FDA approved the MicroTransponder Vivistim Paired VNS (vagus nerve stimulation) System, which is to be used along with stroke rehabilitation to help individuals who have moderate to severe impaired upper limb and extremity motor defects caused by a chronic ischemic stroke. The system electrically stimulates the vagus nerve, which runs from the brain down to the abdomen, to improve upper limb and extremity motor function and to improve an individual’s ability to move the arms and hands.

Cortical vein thrombosis prognosis

In general, cortical vein thrombosis or isolated cortical vein thrombosis has a good prognosis ¹. One systematic review of 325 cortical vein thrombosis cases found that more than 90% of patients had good outcomes upon discharge or follow-up within one year ³. This included complete recovery with a return to baseline status or partial recovery ³. It is also important to note that most patients had their clinical symptoms recovery earlier than their findings in the neuroimaging ³. In that systematic review study, the in-hospital mortality was 3.0% ³. Patients treated with long-term anticoagulation for up to 6 months do have complete or partial recovery of clinical symptoms ³.

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Cortical vein thrombosis

Cortical vein thrombosis

How common is isolated cortical venous thrombosis?

Venous Drainage of the Central Nervous System

Dural Venous Sinuses

Veins of the Cerebrum

Superficial veins of cerebrum

Deep veins of cerebrum

Veins of the Cerebellum

Veins of the Brainstem

Veins of the Spinal Cord

Cortical vein thrombosis causes

Cortical vein thrombosis risk factors

Cortical vein thrombosis pathophysiology

Cortical vein thrombosis symptoms

Cortical vein thrombosis diagnosis

Neuroimaging

Laboratory tests

Cortical vein thrombosis differential diagnosis

Cortical vein thrombosis treatment

Anticoagulation

Thrombolysis (Thrombolytic Therapy)

Surgical Intervention

Supportive Care

Post-Stroke Rehabilitation

Cortical vein thrombosis prognosis

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