Clinical presentation of CVT patients largely depends on location and extent of thrombosis and possibly hemorrhagic infarction. Furthermore, symptom onset may be acute (< 48 hours; 37%), subacute (> 48 hours but < 30 days; 56%) or chronic (> 30 days; 7%) [1].

Most symptoms observed in CVT patients either correspond to intracranial hypertension, focal neurological deficits, seizures or encephalopathy [7].

• CVT interferes with blood drainage and causes an increase in venular, capillary and finally arterial blood pressure. Therefore, CVT patients may experience intense headaches that may aggravate or ease with posture changes. In fact, headaches are the most frequent cause of initial presentation. Elevated intracranial blood pressure may also provoke papilledema, visual impairment and disturb awareness.
• Focal neurological anomalies may comprise motor deficits and aphasia. Sensory malfunctions have been reported but are less common.
• Seizures are as common as neurological deficits and may be observed in about one out of three patients. Both focal and generalized seizures have been reported in CVT and patients may enter status epilepticus.
• Mental status changes are the main manifestation of encephalopathy.

• Weakness

  While the first patient presented with severe unremitting headache with papilledema due to raised intracranial pressure, the second patient presented with seizures and focal weakness due to parenchymal hemorrhage. [neurology.org]

  Possible neurological signs include hemiparesis, weakness of the lower limbs, sometimes bilaterally, aphasia, ataxia, chorea and hemianopia. [patient.info]

  Symptoms may include headache, abnormal vision, any of the symptoms of stroke such as weakness of the face and limbs on one side of the body, and seizures. [en.wikipedia.org]

  In addition, one patient developed unilateral weakness and parasthesias, whereas a second patient developed a partial seizure. [ajnr.org]

  Seventy-three patients had limb weakness with 68 having hemiplegia (right side 40; left side 28) and five had quadriplegia without difference between the groups. Two patients had isolated aphasia and three had ataxia. [jscisociety.com]

• Epilepsy

  They both presented with intracranial hypertension syndrome and symptomatic focal epilepsy. CVT was diagnosed with MRI and MR venography. Hypothyroidism was diagnosed in the acute phase of CVT. Both had an autoimmune thyroiditis. [ncbi.nlm.nih.gov]

  The spectrum of adverse outcomes in CVT includes the following: Death Temporary or permanent neurologic impairment and disability Epilepsy Hydrocephalus Chronic venous outflow obstruction resulting in chronic headache and/or pseudotumor cerebri Vision [clinicaladvisor.com]

  Epilepsy was noticed in a case stabilized using carbamazepin; ophtalmoplegia after a cavernous sinus thrombosis; pyramidal hypertonia in the newborn of 18 days. [panafrican-med-journal.com]

  Chronic granulomatous meningitis with multiple cranial nerve lesions hydrocephalus, stroke, sinus thrombosis, and epilepsy. South Med J. 2000;93:1108-1111. R obson SC, White NW, Aronson I, Woollgar R, GoodmanH, Jacobs P. [casereports.in]

  Complications include seizures, hydrocephalus, intracranial hypertension and neurological deterioration. [ 10 ] Prognosis Long-term follow-up suggests a generally good prognosis but there may be residual pyramidal symptoms, epilepsy, visual field defects [patient.info]

• Inflammation

  Cerebral sinus venous thrombosis may be due to local inflammation or to acquired or genetic thrombophilia including hyperhomocysteinemia. [ncbi.nlm.nih.gov]

  Malignant otitis media, mastoiditis and sinusitis may compromise cerebral veins; although inflammation is less identified as the cause of CVT. [symptoma.com]

  Inflammation and coagulation in inflammatory bowel disease: the clot thickens. Am J Gastroenterol 2007;102:174-86. DOI PubMed 9. van Bodegraven AA, Schoorl M, Baak JP, Linskens RK, Bartels PC, Tuynman HA. [nnjournal.net]

  This is probably related to inflammation and stretching of sigmoid sinus walls due to thrombus. Overall, unilateral headache was twice more common than diffuse or localized headache but unilateral pain had no association with site of thrombosis. [link.springer.com]

  Vasculitis (3%) Polycythaemia or thrombocytosis (2.8%) Surgery (2.7%) Vascular anomaly in the CNS like dural fistula, AVM, etc (1.9%) Dehydration (1.9%) If all the possible risk factors were piled into one big table, it would look like this: Local inflammation [derangedphysiology.com]

• Unconsciousness

  Family and friends can describe the symptoms they saw, especially if the person who had the stroke is unconscious. The final diagnosis, however, is usually made based on how the blood is flowing in the brain. Imaging tests show areas of blood flow. [hopkinsmedicine.org]

  Family and friends can describe the symptoms they saw, especially if the person who had the stroke is unconscious. But the final diagnosis is often made based on how the blood is flowing in the brain. Imaging tests show areas of blood flow. [cedars-sinai.edu]

  The presence of fever, deep venous thrombosis, seizures, focal neurological deficits, and unconsciousness were predictors of a poor outcome. [10] » References 1. Ribes MF. [neurologyindia.com]

  Given the frequency of epileptic seizures in children with an acute CVT, continuous electroencephalography monitoring may be considered for individuals who are unconscious or mechanically ventilated (Class IIb; Level of Evidence C). [stroke.ahajournals.org]

• Falling

  In severely raised intracranial pressure, the level of consciousness is decreased, the blood pressure rises, the heart rate falls and the patient assumes an abnormal posture. [2] Causes [ edit ] Cerebral venous sinus thrombosis is more common in particular [en.wikipedia.org]

  […] approximately 4 persons per year among the 52% of yearly US deliveries who receive epidural anesthesia for delivery. 34 Four of the 16 pregnant and 1 of the nonpregnant cases cited in tables 1 and 2 who had dural punctures with large-bore needles may fall [anesthesiology.pubs.asahq.org]

  Clinical findings in CVT fall into two major categories: Those related to increased intracranial pressure due to impaired venous drainage; and, those related to focal brain injury from venous ischemia/infarction or hemorrhage. [neurologyindia.com]

  Clinical findings in CVT usually fall into 2 major categories, depending on the mechanism of neurological dysfunction: (1) Those that are related to increased intracranial pressure attributable to impaired venous drainage and (2) those related to focal [stroke.ahajournals.org]

• Vomiting

  A 48-year-old female suffered from two episodes of severe headache and vomiting 7 days before and on the day of admission. She was deeply somnolent with mild paresis of her right leg. [ncbi.nlm.nih.gov]

  On 17 th April he continued to suffer from the headache with one episode of vomiting. He then went to one government hospital and was admitted there. [pubs.sciepub.com]

  […] infection of the lateral sinuses (transverse/sigmoid sinuses) or mastoiditis Rhinogenic (e.g., after sinusitis ) Through facial infections Meningitis References: [3] [4] [5] Pathophysiology Clinical features Headache (acute, subacute, or chronic) Nausea, vomiting [amboss.com]

  Headache is one of the usual symptoms along with nausea, vomiting and seizures which are lesser common. Focal neurological deficits may also occur. Both genetic and acquired conditions may predispose to cerebral venous thrombosis. [omicsonline.org]

  Nausea and vomiting. Difficulty speaking, seeing or hearing. Inability to move one side of your face or one arm. Confusion or diminished alertness. Fainting, loss of consciousness or coma. [elcaminohospital.org]

• Nausea

  […] generally infection of the lateral sinuses (transverse/sigmoid sinuses) or mastoiditis Rhinogenic (e.g., after sinusitis ) Through facial infections Meningitis References: [3] [4] [5] Pathophysiology Clinical features Headache (acute, subacute, or chronic) Nausea [amboss.com]

  Headache is one of the usual symptoms along with nausea, vomiting and seizures which are lesser common. Focal neurological deficits may also occur. Both genetic and acquired conditions may predispose to cerebral venous thrombosis. [omicsonline.org]

  It was associated with nausea but not with vomiting, photophobia and phonophobia. The patient stated that he never had headache of such nature & severity in his life. [pubs.sciepub.com]

  But then in a few days things got even worse, with symptoms such as blurred vision, nausea and a sensitivity to light. It was finally a magnetic resonance imaging along with magnetic resonance angiography that identified the problem. [relieve-migraine-headache.com]

  Nausea and vomiting. Difficulty speaking, seeing or hearing. Inability to move one side of your face or one arm. Confusion or diminished alertness. Fainting, loss of consciousness or coma. [elcaminohospital.org]

• Thrombosis

  No recurrent thrombosis or bleeding episodes were observed. [ncbi.nlm.nih.gov]

  When to think of venous thrombosis Venous thrombosis has a nonspecific presentation and therefore it is important to recognize subtle imaging findings and indirect signs that may indicate the presence of thrombosis. [radiologyassistant.nl]

• Headache

  We retrieved 100 patients with isolated headache, 52 patients with early CVT diagnosis (early isolated headache) and 48 with late CVT diagnosis (late isolated headache). [ncbi.nlm.nih.gov]

  The presentation of headache could mimic thunderclap headache [ 5 ], migraine [ 6 ], orthostatic headache [ 7 ], cluster headache [ 8 ], headache related to increased intracranial pressure, and diffuse tension type headache. [link.springer.com]

  As public awareness grows, more people are concerned about headache in cerebral venous thrombosis. If there is headache involved, you have a better chance of being diagnosed, but there are some things you need to know. [relieve-migraine-headache.com]

• Stroke

  Diagnosis and management of cerebral venous thrombosis: a statement for healthcare professionals from the American Heart Association/American Stroke Association. Stroke 2011;42:1158-1192. 5. [j-stroke.org]

  Has been member of editorial board in Stroke, Journal of Stroke and cerebrovascular diseases and cerebrovascular Diseases. [singer-polignac.org]

  Although the association between PFO and cryptogenic stroke is well shown in young adults, the causality is still unclear. The pathogenetic mechanism of ischemic stroke related to PFO is not entirely understood. [ncbi.nlm.nih.gov]

  J Stroke Cerebrovasc Dis. 2008;17:49-54. [physiciansweekly.com]

  This chain of events is part of a stroke that can occur in adults and children. It can occur even in newborns and babies in the womb. A stroke can damage the brain and central nervous system. [hopkinsmedicine.org]

• Seizure

  Mortality and residual disability are relevant in patients presenting with intracranial hemorrhage or with epileptic seizures. [ncbi.nlm.nih.gov]

  If a seizure does not occur, seizure prophylaxis is not necessary. 1,2,11,39 Further testing for underlying etiology is recommended, including thrombophilia. 1,2,3,6 Follow up imaging at 3-6 months is required to assess for recanalization of the affected [emdocs.net]

  Seizures, including focal, generalized, and status epilepticus, are seen in 30–40% of patients [7,11]. As seizures are rare in strokes, CVT should be considered in any patient with a focal neurologic deficit and seizure [1,2]. [epmonthly.com]

  Sagittal sinus thrombosis: motor deficits, bilateral deficits, seizures Lateral sinus thrombosis: isolated intracranial hypertension Left transverse sinus thrombosis: Aphasia Deep venous sinus (straight) thrombosis: behavioural symptoms (thalamic lesions [lifeinthefastlane.com]

• Papilledema

  Check for papilledema in cases presenting with headache. Look for potential risk factors of CVT. [pedemmorsels.com]

  and hypertensive encephalopathy (altered mental status with papilledema and end‐organ damage in the setting of severe hypertension) 10 serious causes of headache to consider for every ED patient with headache Lesion on CT scan (blood, pus or tumor): [emergencymedicinecases.com]

  While the first patient presented with severe unremitting headache with papilledema due to raised intracranial pressure, the second patient presented with seizures and focal weakness due to parenchymal hemorrhage. [neurology.org]

  […] sigmoid sinuses) or mastoiditis Rhinogenic (e.g., after sinusitis ) Through facial infections Meningitis References: [3] [4] [5] Pathophysiology Clinical features Headache (acute, subacute, or chronic) Nausea, vomiting, vision impairment ; ), bilateral papilledema [amboss.com]

  The cranial nerves examination revealed no abnormality except papilledema. There was no other focal deficit. [pubs.sciepub.com]

• Meningism

  Other rare cause of CVT with lymphocytic meningitis is neurobrucellosis [ 3 ]. [casereports.in]

  […] infections (e.g.sinusitis, otitis media, meningitis, head and neck infections) mechanical injury to the sinuses or jugular veins (e.g. trauma, venous catheterisation, neurosurgical procedures) drugs (e.g. androgens, IV immunoglobulin) haematological [lifeinthefastlane.com]

  The specific causes include meningitis and otitis media, head injury, instrumentation (such as jugular central venous catheter), surgery and drugs. Cerebral vein thrombosis can be asymptomatic or symptomatic. [angiologist.com]

  […] cell disease ) Nephrotic syndrome Dehydration Infectious Otogenic (e.g., after acute otitis media ) → generally infection of the lateral sinuses (transverse/sigmoid sinuses) or mastoiditis Rhinogenic (e.g., after sinusitis ) Through facial infections Meningitis [amboss.com]

  There are numerous connections between the cortical veins and dural sinuses, and also with the venous system of the meninges, scalp and nasal sinuses. [jpma.org.pk]

Diagnostic imaging is applied to confirm a tentative diagnosis of CVT, to locate the thrombus (or thrombi) and to assess brain damage. Magnetic resonance flow imaging and contrast-enhanced computed tomography scans are most commonly carried out to this end, with the former being more sensitive than the latter. As time elapses after thrombus formation, findings vary [1]:

• Initially, thrombi may be depicted as isointense areas in T1-weighted images and hypointense spots in T2-weighted images. Several days later, thrombi appear hyperintense in both weightings.
• In images obtained by contrast-enhanced computed tomography, filling defects indicate thrombi in veins or sinuses. Central, hypodense areas may be surrounded by hyperdense borders. Such findings are not to be expected during the first days after symptom onset, which is why magnetic resonance imaging has a higher sensitivity in cases of acute CVT.
• Brain edema and hemorrhages can be visualized by both techniques.

It is of utmost importance to determine whether a CVT patient is suffering from any systemic prothrombotic condition since such disorders also favor thrombus formation within other vessels. Consequently, affected individuals present increased risks of ischemic stroke, myocardial or renal infarction, and other thrombosis-related diseases. A screen for systemic hypercoagulability may comprise laboratory analysis of blood samples (hemogram, blood biochemistry and coagulation tests), diagnostic imaging (applying those techniques described for diagnosis of CVT itself) and genetic testing [8].

If no risk factor can be identified, repeated analysis after a few weeks is recommended. Certain malignancies, for instance, may cause hypercoagulability. If they are not detected during initial exams but during follow-ups, treatment may still be initialized in a timely manner.

Of note, recovery (principally recanalization and development of collaterals) and possible recurrence should also be monitored in follow-ups, ideally by means of magnetic resonance imaging.

• Colitis

  […] mainly associated during episodes of relapse of ulcerative colitis. [nnjournal.net]

  […] or factor V Leiden mutation Cancer Collagen vascular diseases like lupus, Wegener’s granulomatosis, and Behcet syndrome Obesity Low blood pressure in the brain (intracranial hypotension) Inflammatory bowel disease like Crohn’s disease or ulcerative colitis [hopkinsmedicine.org]

  Leiden mutation Cancer Collagen vascular diseases such as lupus, granulomatosis with polyangiitis, and Behcet syndrome Obesity Low blood pressure in the brain (intracranial hypotension) Inflammatory bowel disease such as Crohn’s disease or ulcerative colitis [cedars-sinai.edu]

  Cerebral venous sinus thrombosis as presenting feature of ulcerative colitis. Acta Gastroenterol Belg. 2009 Jul-Sep. 72(3):350-3. [Medline]. Towbin A. [emedicine.medscape.com]

  Crohn's disease and ulcerative colitis increase the risk, as does the use of steroids to treat them. [patient.info]

Thrombolysis is the mainstay of CVT treatment. For a long time, it has been a matter of debate whether patients who are presenting with intracranial hemorrhage due to CVT should receive heparin and/or fibrinolytics. This therapeutic approach continues to rise significant concern, but available data emphasize the importance of an early thrombolytic therapy in all patients [9]. As has been mentioned above, mortality is significantly higher in those patients who do not receive thrombolytic therapy [1].

Chemical and/or mechanical thrombectomy should be considered in patients who deteriorate under standard therapy or who are moribund on presentation [9]. These patients should nevertheless receive anticoagulants.

Additionally, supportive measures may be provided to relieve symptoms associated with CVT. For instance, patients who suffer from seizures may benefit from anti-epileptic drugs like sodium valproate or phenytoin. Benzodiazepines are generally administered to terminate status epilepticus [10].

Availability, sensitivity and specificity of modern imaging techniques have significantly decreased CVT-associated mortality. A large retrospective study based on data obtained in more than 600 cases diagnosed in nearly two dozen countries yielded the following results: about 80% of all CVT patients recovered completely, 10% remained mild to moderately disabled, 2% remained severely disabled and 8% died [4].

Early initiation of thrombolytic therapy considerably improves the outcome and if thrombolysis is not carried out, mortality rises to more than 60% [1]. Unfavorable prognostic parameters are decreased awareness, cerebral hemorrhages, status epilepticus and paralysis. These symptoms are often associated with hemorrhagic infarctions visible in images obtained by magnetic resonance imaging or computed tomography scans..

A plethora of congenital and acquired conditions may incline the balance between coagulation and fibrinolysis towards the former.

With regards to congenital diseases, a variety of genetic disorders may cause a systemic prothrombotic condition. Prothrombin G20210A and factor V Leiden mutation as well as deficiencies in protein C, protein S or antithrombin III shall be mentioned as examples for hereditary diseases associated with an increased risk of CVT [2] [3]. Mutations of the gene encoding for methylenetetrahydrofolate reductase have also been proposed as possible triggers of CVT [2]. Such mutations are commonly associated with thrombosis.

More commonly, CVT is caused by acquired disturbances of hemostasis. Such disorders may provoke thrombi formation in distinct vessels of the whole body or be restricted to determined intracranial areas. Dehydration, use of oral contraceptives, pregnancy and puerperium as well as antiphospholipid syndrome and hypercoagulability due to malignancies are related to an overall increased risk of vein thrombosis. This also applies for pathologies causing polycythemia or thrombocytosis. Head trauma, intracranial neoplasms or inflammatory processes affecting either the brain itself or adjacent tissues are possible local causes of CVT. Malignant otitis media, mastoiditis and sinusitis may compromise cerebral veins; although inflammation is less identified as the cause of CVT.

In the majority of cases, at least one of the aforementioned risk factors is identified in patients presenting with CVT. This particularly applies to pediatric patients and young adults. In the elderly, the proportion of cases that cannot be ascribed to any underlying disease is more prominent.

In general, CVT is an uncommon disease. It is also a rare cause of cerebral infarction. The annual incidence of CVT has been repeatedly estimated to be less than 1 per 100,000 inhabitants. Incidence rates don't seem to vary among different age groups, but the likelihood of suffering CVT is significantly increased in patients pertaining to the above mentioned risk groups. Pregnancy, for instance, causes a 10-fold increase in the risk of CVT.

In general, most patients are diagnosed with CVT during their fourth and fifth decade of life, but young children account for considerable shares of CVT patients too.

Women are affected three times more often than men [4]. Pregnancy, puerperium and the use of oral contraceptives have been identified as gender-specific risk factors and may partially explain the observed female predilection, which is less marked in children and elder women than in young adults. Women tend to suffer from CVT at younger ages and have a better prognosis than men.

Endothelial lesions, blood stasis and alterations of blood composition - commonly known as Virchow's triad - are the main triggers of thrombosis and CVT is no exception to this rule [5]. As indicated in the Etiology section of this article, many conditions may evoke one of those states and since they are mutually dependent, this may lead into a self-perpetuating cycle. Endothelial lesions, for instance, may result from local inflammatory processes. They cause formation of white thrombi, i.e., of blood clots that mainly consist of thrombocytes. However, local disturbances of blood flow cause blood stasis and formation of secondary red thrombi. Consequently, the thrombus grows and blood drainage decreases further.

Reduction of venous drainage due to CVT causes cerebral blood flow to decrease. Those brain regions that are drained by the affected vessel are not supplied with oxygen and nutrients; the patient sustains cerebral infarction. Because vessels passing through the infarct core are filled with blood, CVT triggers hemorrhagic infarction not ischemic stroke. Pathophysiological events following infarction and blood-brain barrier breakdown are neuronal death, cytotoxic and vasogenic edema, hemorrhages, hematoma, microgliosis and astrogliosis. Persistent neuroinflammation may significantly contribute to CVT-associated morbidity and mortality.

Additionally, thrombi may exert a local mass effect and compress adjacent tissues. Cavernous sinus syndrome, for instance, is associated with neurological symptoms due to compression of the oculomotor, trochlear, trigeminal and/or abducens nerves (cranial nerves III, IV, V and VI, respectively). It is caused by space-occupying processes taking place in the cavernous sinus - by CVT, for instance [6].

Appropriate hydration is an important preventive measure against CVT. This applies particularly to patients pertaining to any of the above described risk groups, e.g., pregnant women, women who take oral contraceptives, anyone suffering from a systemic illness or a disease affecting the head and neck region.

Patients diagnosed with inherited thrombophilia should receive prophylactic treatment against CVT.

Cerebral vein thrombosis (CVT) refers to the formation of a blood clot in intracranial veins and most commonly, this condition affects more than one vessel.

Of note, physicians often use the term cerebral thrombosis in a broader sense and may not only refer to thrombus formation within a cerebral vessel, but also to vessel occlusion due to thromboembolism. The former more frequently occurs in veins and vein sinus and is the topic of this article. Emboli, in contrast, tend to lodge in arteries. They block arterial blood supply to dependent tissues and cause ischemic infarction. Thromboembolism is the most common cause of stroke and incidence rates are much higher than those of CVT.

Thrombus formation may be triggered by a variety of local and systemic diseases that provoke endothelial damage or that interfere with the equilibrium between pro- and anticoagulatory factors. And although small thrombi may not significantly diminish blood drainage, they do constitute obstacles that alter fluid mechanics locally. This contributes to the formation of secondary red thrombi and further reduction of venous outflow. In severe cases, the affected vein or vein sinus may become occluded.

The above described events may lead to hemorrhagic infarction of the area drained by the affected vessel and trigger symptoms of stroke. Contrary to thromboembolic stroke, symptom onset is not necessarily acute. Indeed, subacute or chronic onset of symptoms is observed in two out of three patients presenting with CVT [1]. Clinical presentation varies largely and complaints range from headaches, visual impairment and dysarthria to hemiparesis and coma.

CVT is diagnosed by means of neuroimaging and treatment generally consists of thrombolysis.

Cerebral vein thrombosis (CVT) is the medical term for the formation of a blood clot within an intracranial vein. Thrombi may interfere with blood drainage, cause an increase in venular, capillary and finally arterial blood pressure and thus reduce cerebral blood flow. This may lead to hemorrhagic infarction and stroke.

Of note, CVT is an uncommon trigger of stroke. Most cases of cerebral infarction are provoked by thromboembolism, i.e., blood clots form within any vessel and are carried away into cerebral arteries.

Causes

Any condition provoking endothelial damage or blood stasis in cerebral vessels as well as pathologies that incline the balance between coagulation and fibrinolysis towards the former may cause CVT. The following shall be mentioned as examples:

• Genetic disorders like prothrombin G20210A and factor V Leiden mutation, deficiencies in protein C, protein S or antithrombin III
• Head trauma or surgery
• Inflammation of brain, meninges or adjacent tissues
• Pregnancy, puerperium
• Use of oral contraceptives

Symptoms

The most common symptom of CVT are headaches. Symptom onset may be acute, subacute or chronic and patients may claim headaches to intensify within hours, days or weeks. Possibly, headaches aggravate when adopting certain postures.

Further symptoms of CVT are:

• Visual impairment
• Diminished awareness, loss of consciousness
• Motor deficits like hemiplegia
• Aphasia
• Seizures
• Altered mental status

Diagnosis

In order to confirm a tentative diagnosis of CVT, magnetic resonance imaging or computed tomography scans will be applied. By means of these techniques, the affected vein and the thrombus lodged within it can be visualized. They also allow for an evaluation of concomitant brain damage.

As has been indicated above, CVT may be triggered by a variety of conditions. Laboratory analyses of blood samples and genetic tests may be carried out to identify the cause of CVT in an individual case.

Treatment

In most cases, drug-mediated thrombolysis is indicated. Patients receive heparin and/or fibrinolytics that dissolve the thrombus and facilitate recanalization. In severe cases, surgery may be necessary to mechanically remove the blood clot.

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2. Marjot T, Yadav S, Hasan N, et al. Genes associated with adult cerebral venous thrombosis. Stroke. 2011; 42(4):913-918.
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