Cerebral Venous Thrombosis (CVT): Causes, Pathophysiology, Clinical Presentation, Imaging, Treatment, and Prognosis

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Cerebral Venous Thrombosis (CVT): Causes, Pathophysiology, Clinical Presentation, Imaging, Treatment, and Prognosis

Introduction

Cerebral venous thrombosis (CVT) is an uncommon yet potentially life-threatening cerebrovascular disorder characterized by thrombotic occlusion of cortical veins and/or dural venous sinuses. Its protean clinical manifestations, diverse precipitating factors, and imaging variability frequently delay diagnosis, underscoring the need for a systematic, up-to-date approach to recognition and management. This expert guide synthesizes pathobiology, epidemiology, clinical features, imaging strategy, treatment, and prognosis—and anchors these principles with a real-world case to illustrate decision-making pitfalls and pearls.

Case Vignette (Index Case)

A 78-year-old man presented with altered mental status and a new-onset seizure occurring one week after a fall. An initial non-contrast head CT was performed on arrival. Subsequent MRI sequences—including susceptibility-weighted imaging (SWI), fluid-attenuated inversion recovery (FLAIR), T2-weighted post-contrast, diffusion-weighted imaging (DWI), apparent diffusion coefficient (ADC), and T1-weighted post-contrast—were obtained within 24 hours. Imaging ultimately supported the diagnosis of dural sinus thrombosis, leading to hemorrhagic venous infarction.

Why CVT Matters

  • It can mimic a wide spectrum of neurologic diseases—from benign primary headaches to malignant intracranial hypertension or even tumor-like processes—leading to delays and misdiagnosis.
  • Timely anticoagulation improves outcomes—even in the presence of intracerebral hemorrhage related to venous infarction—highlighting the unique therapeutic logic compared with arterial stroke.

Etiology and Risk Factors (Causes)

CVT arises from a multifactorial interplay of systemic and local prothrombotic drivers. In about one-third of cases, no clear cause is identified (idiopathic). Recognized contributors include:

  • Inherited thrombophilias (e.g., protein S deficiency)
  • Hormonal states (pregnancy, puerperium, combined oral contraceptives)
  • Malignancy
  • Local head/neck infections or trauma
  • Systemic inflammatory or autoimmune conditions
  • Iatrogenic factors (e.g., dehydration, certain medications) 

While CVT tends to affect young to middle-aged adults and is approximately three times more common in women, it can occur in older adults, as in the presented case, often with more ambiguous presentations and higher comorbidity burdens. 

Pathophysiology

Two interrelated venous compartments are implicated:

  • Cortical veins
  • Dural venous sinuses

Thrombosis in cortical veins impedes venous drainage, leading to elevated venous and capillary hydrostatic pressure, venous congestion, and eventual breakdown of the blood–brain barrier with resultant vasogenic edema, cytotoxic injury, and venous infarction that may become hemorrhagic.

Thrombosis in the dural sinuses shares this pathophysiology but adds impaired cerebrospinal fluid (CSF) outflow dynamics, contributing to intracranial hypertension (e.g., papilledema, visual symptoms, pulsatile tinnitus, diffuse headache).

Collateral venous pathways can partially compensate, modulating the extent and tempo of parenchymal injury.

Epidemiology

  • Incidence: approximately 1.3 per 100,000 person-years.
  • Sex distribution: about threefold higher in women (hormonal factors and pregnancy/puerperium are important contributors).
  • Age: predominantly young to middle-aged adults, but can occur at any age, including the elderly.

Clinical Presentation

CVT is notorious for its heterogeneity:

  • Headache is the most common symptom, reported in roughly 90% of patients. Quality ranges from dull, subacute progression to thunderclap onset in some cases.
  • Focal neurological deficits (e.g., motor weakness, aphasia, visual changes) vary by the cortical territory involved.
  • Seizures occur in approximately 40% of cases and may be the presenting feature, especially when cortical veins are involved.
  • Features of elevated intracranial pressure (papilledema, transient visual obscurations, sixth nerve palsy) are common in sinus-dominant thrombosis.
  • Compared with arterial ischemic stroke, venous infarction often evolves over days rather than minutes to hours, sometimes misleading clinicians toward non-vascular diagnoses.

In the index case, the combination of altered mental status and a new seizure in an older adult following a recent fall initially broadened the differential (e.g., subdural hematoma), but the evolution and subsequent MRI clarified CVT with hemorrhagic venous infarction.

Imaging Strategy and Key Features

Imaging is central to diagnosis, staging, and management planning. A pragmatic sequence is as follows:

  1. Non-contrast CT (NCCT)
  • Utility: Rapid triage to exclude emergent mass effect, herniation, or large hemorrhage; may show indirect signs of venous infarction (cortical/subcortical hypodensity, sulcal effacement) or direct signs like hyperdense sinus (dense triangle or cord sign), though sensitivity is variable.
  • Pitfall: A normal NCCT does not exclude CVT; subtle findings can be overlooked, especially early.
  1. MRI brain with MR venography (MRV)
  • Sequences: SWI (or GRE), FLAIR, DWI/ADC, T1/T2 with and without contrast are complementary.
  • SWI (and GRE) are particularly valuable: they accentuate magnetic susceptibility from deoxyhemoglobin/hemosiderin and intraluminal thrombus, displaying “blooming” that flags both thrombosed venous structures and parenchymal microhemorrhage/macroscopic hemorrhage. 
  • FLAIR: highlights edema and subarachnoid/cortical signal changes; venous congestion may appear as cortical/subcortical hyperintensity.
  • DWI/ADC: typically shows mixed patterns; cytotoxic edema (restricted diffusion) within venous infarcts may coexist with vasogenic components (facilitated diffusion).
  • Post-contrast T1/T2: can reveal enhancement patterns, indirectly suggesting dural sinus involvement and venous congestion.
  1. CT venography or MR venography
  • Helps directly visualize filling defects in the dural sinuses and major cortical veins, delineating the extent of thrombosis and collateral channels.
  • The index case demonstrated near-occlusive filling defects in the superior sagittal sinus and occlusive defects in the right transverse and sigmoid sinuses, along with widespread cortical/dural venous changes—findings consistent with extensive dural sinus thrombosis.
  1. Angiographic considerations
  • Endovascular evaluation is generally reserved for select cases (e.g., clinical deterioration despite anticoagulation, or uncertain diagnosis when noninvasive studies are inconclusive).

Imaging synthesis for the case:

  • The imaging constellation supports dural sinus thrombosis with hemorrhagic venous infarction—explaining the acute seizure and subacute encephalopathy.

Differential Diagnosis

  • Hemorrhagic transformation of arterial ischemic stroke
  • Venous sinus thrombosis with hemorrhagic venous infarction (the correct diagnosis in this case)
  • Neoplasm with associated hemorrhage
  • Vascular malformation
  • Cerebral amyloid angiopathy

Clinical and imaging context—especially sinus/cortical venous filling defects plus SWI/GRE “blooming” in venous structures—discriminates CVT-associated hemorrhagic venous infarcts from arterial stroke or tumor.

Treatment

Principles

  • The cornerstone of acute management is therapeutic anticoagulation—even in the presence of venous hemorrhagic infarction—unless there is a compelling contraindication. 
  • Acute phase: parenteral anticoagulation with unfractionated heparin or low-molecular-weight heparin.
  • Subacute/chronic phase: transition to oral anticoagulants. The optimal duration is not definitively established but generally ranges from 3 to 12 months, individualized by provoking factors and recurrence risk. 
  • Search for and treat reversible precipitants (e.g., infection, dehydration, endocrine or hormonal contributors, prothrombotic iatrogenesis).
  • Endovascular thrombolysis/mechanical thrombectomy: reserved for deteriorating patients or those failing anticoagulation; decisions are case-by-case in specialized centers. 

Supportive Care

  • Control of intracranial pressure (elevate head of bed, hyperosmolar therapy in select cases)
  • Seizure management with antiepileptic drugs in those with seizures or cortical venous involvement
  • Management of severe intracranial hypertension may require CSF diversion or decompressive strategies in exceptional cases.
  • Multidisciplinary coordination (neurology, neuroradiology, neurocritical care) is often beneficial.

Prognosis

Outcomes vary with age, clot burden, presence of parenchymal lesions (especially hemorrhagic infarcts), delays in diagnosis, and underlying etiologies. Many patients recover substantially with timely anticoagulation, though a subset experiences persistent headaches, visual sequelae from intracranial hypertension, cognitive deficits, or epilepsy. Early identification and treatment of precipitating factors, as well as vigilant imaging follow-up, improve the odds of a favorable recovery. 

Figures

Figure 1. Axial non-contrast CT at presentation. Caption: Initial NCCT for triage in an elderly patient with altered mental status and new-onset seizure one week post-fall; CT is often non-specific in early CVT and may under-represent the extent of venous pathology. 

Figure 2. Axial susceptibility-weighted imaging (SWI). Caption: SWI accentuates susceptibility from intraluminal thrombus and parenchymal blood products, aiding detection of venous thrombosis and hemorrhagic components (“blooming” effect).  

Figure 3. Axial fluid-attenuated inversion recovery (FLAIR). Caption: FLAIR demonstrates edema and cortical/subcortical signal abnormalities consistent with venous congestion/infarction. 

Figure 4. Axial T2-weighted post-contrast. Caption: Post-contrast sequences support the assessment of dural sinus involvement and venous congestion patterns in CVT. 

Figure 5. Diffusion-weighted imaging (DWI). Caption: Venous infarction may show restricted diffusion (cytotoxic edema) intermingled with vasogenic components; patterns can be heterogeneous. 

Figure 6. Apparent diffusion coefficient (ADC). Caption: ADC maps contextualize DWI findings, distinguishing cytotoxic from vasogenic components in venous injury. 

Figure 7. Axial T1-weighted post-contrast. Caption: Post-contrast T1 images can highlight sinus-related abnormalities and parenchymal enhancement associated with venous infarction
Note: Venous phase angiographic imaging (CT/MR venography) in this case demonstrated near-occlusive filling defects in the superior sagittal sinus and occlusive defects in the right transverse/sigmoid sinuses, consistent with extensive dural sinus thrombosis. 

Quiz


1. A 78-year-old man develops altered mental status and a new-onset seizure one week after a fall. A non-contrast head CT is obtained. What does the CT show?
a) Normal exam
b) Diffuse cerebral edema
c) Subdural hematoma
d) Right frontal lobe hypodensity with mild sulcal effacement

  • Answer: d) Right frontal lobe hypodensity with mild sulcal effacement. Explanation: Early venous pathology on non-contrast CT can be subtle. Compared with the crescentic extra-axial hyperdensity seen in subdural hematoma, a cortical/subcortical hypodensity with mild sulcal effacement favors early venous congestion/edema from suspected CVT. The appropriate next step is a brain MRI with venous evaluation (MRV or CTV) to characterize parenchymal injury and confirm sinus thrombosis. 


2. What is the next best step?

a) Neurosurgical consultation
b) Repeat head CT in 12 hours
c) Brain MRI

  • Answer: c) Brain MRI. Explanation: When CVT is suspected, prompt MRI with SWI/GRE, FLAIR, DWI/ADC plus venographic imaging is key to confirm thrombus, map its extent, and guide urgent management. A normal or nonspecific CT does not exclude CVT.

3. Within 24 hours, brain MRI sequences (SWI, FLAIR, T2 post-contrast, DWI, ADC, T1 post-contrast) are obtained. Which of the following is absent?
(1) Intraparenchymal hematoma
(2) Cortical/subcortical edema
(3) Leptomeningeal and dural enhancement
(4) Restricted-diffusion intra-axial abscess
(5) Increased susceptibility within a right frontal cortical vein  

  • Answer: (4) Restricted-diffusion intra-axial abscess. Explanation: In CVT with hemorrhagic venous infarction, cortical/subcortical edema is common, leptomeningeal/dural enhancement can accompany venous congestion, and SWI frequently shows susceptibility within thrombosed cortical veins and parenchymal blood products. Intraparenchymal hemorrhage is also frequent when venous infarction is hemorrhagic. Restricted-diffusion intra-axial abscess is not a typical feature of CVT and is therefore the absent finding among the listed options. 

Practical Diagnostic Algorithm

  • Suspect CVT in subacute headache, new-onset seizures, focal deficits, or signs of intracranial hypertension—especially when demographics or risk factors align (hormonal state, thrombophilia, malignancy, infection, recent trauma).
  • Start with NCCT for safety triage; do not be reassured by a normal CT if suspicion remains.
  • Proceed promptly to MRI with SWI/GRE, FLAIR, DWI/ADC, and MRV, or obtain CT venography to confirm thrombosis and map its extent. 
  • Initiate therapeutic anticoagulation once CVT is diagnosed, even if venous hemorrhagic infarction is present, unless contraindicated. 
  • Investigate triggers (infection, hormonal therapies, dehydration, thrombophilia) and tailor anticoagulation duration (typically 3–12 months).

Key Take-Home Messages

  • CVT is a chameleon; think broadly, image early, and pursue venous-phase evaluation if the clinical picture does not fit an arterial paradigm.
  • SWI/GRE adds unique value by lighting up both clot and blood products—do not skip them.
  • Anticoagulation is the treatment backbone across phases; individualized duration and precipitant management are crucial.

References

[1] Case study materials: Non-contrast CT presentation and clinical setup.

[2] Case study materials: Brain MRI sequences (SWI, FLAIR, T2 post-contrast, DWI, ADC, T1 post-contrast).

[3] Case study materials: Utility of GRE/SWI; treatment with heparin acutely, oral anticoagulation chronically; typical 3–12 months duration; endovascular therapy is rare and case-by-case.

[4] Case study materials: Venous phase imaging with near-occlusive and occlusive sinus filling defects; diagnosis of dural sinus thrombosis with hemorrhagic venous infarction; differential diagnosis.

[5] Case study materials: Pathophysiology, epidemiology (incidence ~1.3 per 100,000 person-years; 3× more common in women), clinical presentation (headache ~90%, seizures ~40%), time course.

[6] J. M. Coutinho, R. Zuurbier, and J. Stam, “Cerebral venous thrombosis: An update,” Lancet Neurol., vol. 11, no. 10, pp. 957–968, 2012.

[7] S. M. Saposnik et al., “Diagnosis and management of cerebral venous thrombosis,” Stroke, vol. 42, no. 4, pp. 1158–1192, 2011.

[8] J. Stam, “Thrombosis of the cerebral veins and sinuses,” N. Engl. J. Med., vol. 352, no. 17, pp. 1791–1798, 2005.

[9] A. Ferro and D. Aguiar de Sousa, “Cerebral venous thrombosis: An update,” Curr. Neurol. Neurosci. Rep., vol. 19, no. 10, p. 74, 2019.

[10] F. Bonneville, “Imaging of cerebral venous thrombosis,” Diagn. Interv. Imaging, vol. 95, no. 12, pp. 1145–1150, 2014.

[11] A. Ghoneim, J. Straiton, C. Pollard, K. Macdonald, and R. Jampana, “Imaging of cerebral venous thrombosis,” Clin. Radiol., vol. 75, no. 4, pp. 254–264, 2020.

[12] S. M. Zuurbier and J. M. Coutinho, “Cerebral venous thrombosis,” Adv. Exp. Med. Biol., vol. 906, pp. 183–193, 2017.

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