Diagnostic Challenges in Cerebral Venous Thrombosis: Hemorrhagic Presentations and Differential Hypotheses

Abstract

Cerebral venous thrombosis (CVT) is a rare, often underdiagnosed condition marked by the formation of thrombi in the cerebral veins and sinuses, which can lead to various clinical symptoms, such as headaches, seizures, and, in some cases, intracranial hemorrhage. This case study presents a 35-year-old hypertensive woman with sudden headache, loss of consciousness, and seizures, who was subsequently diagnosed with CVT complicated by interhemispheric hemorrhage, a rare and challenging presentation. The initial imaging showed frontal interhemispheric hemorrhage and hypodensities, with no arterial abnormalities. Cerebral angiography confirmed CVT due to the absence of opacification in the sagittal sinuses. Treatment involved complete anticoagulation despite hemorrhage, following current guidelines to prevent further thrombotic events. The patient also received anticonvulsants and nimodipine to control seizures and prevent vasospasm, along with close neurological monitoring and blood pressure control. Pneumatic compression was applied to avoid venous thromboembolism due to immobility. This case highlights the diagnostic complexities of CVT, especially when hemorrhage is involved, emphasizing the importance of early, individualized treatment to improve patient outcomes.

Resumo

A trombose venosa cerebral (TVC) é uma condição rara, muitas vezes subdiagnosticada, marcada pela formação de trombos nas veias e seios da face cerebrais, que pode levar a diversos sintomas clínicos, como dores de cabeça, convulsões e, em alguns casos, hemorragia intracraniana. Este estudo de caso apresenta uma mulher hipertensa de 35 anos com cefaleia súbita, perda de consciência e convulsões, que posteriormente foi diagnosticada com TVC complicada por hemorragia inter-hemisférica, uma apresentação rara e desafiadora. A imagem inicial mostrou hemorragia inter-hemisférica frontal e hipodensidades, sem anormalidades arteriais. A angiografia cerebral confirmou a TVC pela ausência de opacificação nos seios sagitais. O tratamento envolveu anticoagulação completa, apesar da hemorragia, seguindo as diretrizes atuais para evitar novos eventos trombóticos. O paciente também recebeu anticonvulsivantes e nimodipina para controlar convulsões e prevenir vasoespasmo, juntamente com monitoramento neurológico rigoroso e controle da pressão arterial. A compressão pneumática foi aplicada para evitar tromboembolismo venoso devido à imobilidade. Este caso destaca as complexidades diagnósticas da TVC, especialmente quando a hemorragia está envolvida, enfatizando a importância do tratamento precoce e individualizado para melhorar os resultados dos pacientes.

Keywords

cerebral venous thrombosis - intracranial hemorrhages - thrombophilia - anticoagulants - seizures - neuroimaging

Palavras-chaves

trombose venosa cerebral - hemorragias intracranianas - trombofilia - anticoagulantes - convulsões - neuroimagem

Introduction

Studies indicate that CVT predominantly affects young adults and women, with an estimated annual incidence of 3 to 4 cases per million inhabitants, and is more common in patients with risk factors such as thrombophilia, use of oral contraceptives, and prothrombotic conditions, such as the puerperal period.[1] The diagnosis of CVT is particularly complex due to the variety of clinical presentations, and is often confused with other neurological conditions, which can delay appropriate treatment and increase the risk of serious complications such as intracerebral hemorrhage and cerebral edema.[2]

The pathophysiology of CVT involves occlusion of the cerebral veins, resulting in increased venous pressure, decreased cerebral perfusion, and ultimately hemorrhage due to rupture of small vessels.[3] The therapeutic management of this condition is equally challenging, especially when associated with hemorrhages. Anticoagulation is the standard treatment, even in the presence of hemorrhage, since it aims to prevent new thrombotic events, improve venous flow, and reduce intracranial pressure.[4] However, the presence of interhemispheric hemorrhage adds a layer of complexity to management, requiring a multidisciplinary and individualized approach.[5]

The present report describes a case of CVT with interhemispheric hemorrhage, highlighting the diagnostic and therapeutic challenges faced throughout clinical management, and reviews the main approaches based on the current literature.

Case Report

A 35-year-old hypertensive female patient presented with sudden headache and loss of consciousness, followed by seizures, and was admitted to a hospital. During the night, he had a feverish episode. At the initial examination, the patient was awake but sleepy, with slowed responses, partially time-oriented, isochoric and light-reactive pupils, with no apparent motor deficits, and showing signs of meningismus. Cranial tomography showed frontal interhemispheric hemorrhage and small right frontal intraparenchymal hemorrhage contiguous to the former. In addition, bilateral hypodensities were observed in the frontal regions, raising suspicions of subarachnoid hemorrhage (SAH), brain tumor, vasospasm, venous infarction or cerebitis. Arterial computed tomography angiography (CTA) showed no arterial abnormalities. The patient was admitted to the ICU for intensive neurological monitoring and clinical management. Cerebral angiography with right radial puncture was performed, demonstrating good opacification of the intracranial vessels and absence of arteriovenous malformations or aneurysms. However, there was a lack of opacification of the anterior and middle thirds of the upper sagittal sinus, in addition to the absence of opacification of the inferior sagittal sinus, compatible with cerebral venous thrombosis. The approach adopted included full anticoagulation, in addition to phenytoin to control seizures. The patient evolved hemodynamically stable, afebrile and without new acute neurological events. Therapeutic planning included strict neurological surveillance, blood pressure control with a systolic blood pressure target below 150 mm Hg, and venous thromboembolism prophylaxis with pneumatic compression.

Discussion

CVT presents a wide spectrum of signs and symptoms, often mimicking other neurological conditions, such as ischemic stroke or meningitis, which can delay proper diagnosis.[1] In this case, the patient presented with sudden headache, loss of consciousness and seizures, in addition to signs of meningismus, a clinical condition that could easily be confused with a subarachnoid hemorrhage or encephalitis. The presence of interhemispheric hemorrhage on initial imaging added complexity to the diagnosis, since this location is rare in CVT and could be associated with arteriovenous malformations or aneurysms ([Figs. 1] and [2]). However, cerebral angiography was fundamental for the definitive diagnosis, as it revealed failure of opacification of the upper and lower sagittal sinuses, compatible with CVT.[2] Although MRV or CTV are standard and less invasive methods for diagnosing CVT, digital subtraction angiography (DSA) was preferred here due to diagnostic uncertainty and the need to exclude arteriovenous malformations or subtle vascular anomalies not visible in non-invasive imaging.

Fig. 1 Cranial computed tomography, (A-B) Axial plane: Bilateral extensive hypodensities with poorly defined borders in the high frontal convexities, cortico-subcortical, and parasagittal regions, more pronounced on the right, potentially indicating recent ischemic lesions. Associated acute hemorrhagic foci in the right parasagittal region, measuring 2.2 cm and 2.9 cm.

Fig. 2 Digital subtraction angiography: (A) Sagittal plane; (B) Oblique plane. The images demonstrate absence of contrast opacification in the anterior and middle thirds of the superior sagittal sinus (blue arrow), along with complete lack of opacification in the inferior sagittal sinus, findings consistent with cerebral venous thrombosis.

Studies indicate that CVT predominantly affects young women, often associated with risk factors such as the use of oral contraceptives, the puerperal period, and thrombophilic conditions.[6] The patient in question had hypertension, a possible risk factor, which may have contributed to the development of CVT.

Intracranial hemorrhage in CVT occurs due to increased venous pressure resulting from venous occlusion, which leads to rupture of small cerebral vessels.[3] The literature most commonly describes parenchymal hemorrhages in cortical and subcortical regions in cases of CVT.[6] However, a hyperdense and rounded image with adjacent edema in the cerebral hemisphere, combined with sudden onset of symptoms, should prompt consideration of differential diagnoses such as subarachnoid hemorrhage (SAH), brain tumors, or infections. This is particularly important given that the typical presentation of CVT tends to be more prolonged or chronic, often featuring headache and progressively worsening neurological symptoms.

The management of CVT, especially in the presence of hemorrhage, remains a topic of debate. However, anticoagulation, even in cases with hemorrhage, is widely recommended to prevent new thrombotic events, improve venous flow, and reduce intracranial pressure.[3] [7] In this case, the patient was treated with full anticoagulation, despite interhemispheric hemorrhage, in accordance with the guidelines that recommend the use of anticoagulants to prevent thrombosis from worsening. The risk of exacerbation of hemorrhage is a constant challenge, but studies show that early anticoagulation tends to improve prognosis, as long as it is closely monitored.[7]

In addition to anticoagulation, anticonvulsants (phenytoin) were administered to control seizures and nimodipine to prevent vasospasm. These complementary interventions are essential to minimize neurological complications and ensure a stable recovery. Tight blood pressure control and intensive neurological surveillance were crucial to prevent thrombosis progression and worsening of bleeding, ensuring that the patient remained hemodynamically stable.[4] Although typically used in aneurysmal subarachnoid hemorrhage, its use was considered due to the suspicion of cortical SAH, where vasospasm may occur and exacerbate neurological injury.

The use of pneumatic compression for prophylaxis of venous thromboembolism was also appropriate, considering the risk of secondary thrombotic events due to prolonged immobilization of the patient.

Conclusion

This case illustrates the importance of detailed diagnostic work-up, including advanced neuroimaging, in patients with atypical intracranial hemorrhage and nonspecific neurological symptoms. CVT, although rare, should be considered in the differential diagnosis of atypical hemorrhages and seizures. Early and appropriate management can prevent serious complications and improve the prognosis of these patients.

Conflict of Interest

None.

• References

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• 3 Stam J. Thrombosis of the cerebral veins and sinuses. N Engl J Med 2005; 352 (17) 1791-1798
• 4 Coutinho JM, Ferro JM, Zuurbier SM. et al. Thrombolysis or anticoagulation for cerebral venous thrombosis: rationale and design of the TO-ACT trial. Int J Stroke 2013; 8 (02) 135-140
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• 6 Ferro JM, Canhão P, Stam J, Bousser MG, Barinagarrementeria F. ISCVT Investigators. Prognosis of cerebral vein and dural sinus thrombosis: results of the International Study on Cerebral Vein and Dural Sinus Thrombosis (ISCVT). Stroke 2004; 35 (03) 664-670
• 7 Saposnik G, Barinagarrementeria F, Brown Jr RD. et al; American Heart Association Stroke Council and the Council on Epidemiology and Prevention. Diagnosis and management of cerebral venous thrombosis: a statement for healthcare professionals from the American Heart Association/American Stroke Association. Stroke 2011; 42 (04) 1158-1192

Publikationsverlauf

Eingereicht: 29. Oktober 2024

Angenommen: 09. September 2025

Artikel online veröffentlicht:
29. Dezember 2025