Clinical History
77-year-old man attended the ER due to prolonged intense headaches and decreased mental state. Relevant medical history includes chronic anticoagulant therapy due to atrial fibrillation.
A non-enhanced cranial CT was indicated (NECT).
Imaging Findings
NECT demonstrated bithalamic hypodensity of indistinct margins (Fig. 1)
A computed tomography (CT) venography was performed to rule out vascular implication (Fig. 2). It demonstrated an absence of deep cerebral venous system opacification (including straight sinus, superior sagittal sinus, Galen's vein and internal cerebral veins). Correct opacification of superior sagittal, transverse and cavernous sinuses is observed.
2 weeks later a follow-up magnetic resonance (MRI) scan was performed. Bithalamic affected areas correlated with FLAIR and T2WI hyperintensity, with multiple foci of microhaemorrhage in bilateral basal ganglia, without frank diffusion restriction. Angio MRI confirmed persistent lack of blood flow in the deep cerebral venous system.
Discussion
A. Background
Cerebral venous thrombosis is a relatively frequent entity with a relatively nonspecific clinical presentation, and therefore imaging techniques are key for diagnosis. Venous thrombosis comprises 1-2% of strokes, and of these 10% compromise the internal cerebral venous system [1].
The causes have been described as secondary to multiple, namely: trauma, hypercoagulative states such as coagulopathies (V Leiden factor, protein C resistance, protein S deficiency), pregnancy, contraceptives, illicit drug abuse, vasculitides, infection, and many others. Nevertheless, in up to 25% of cases no clear cause is identified [1].
B. Clinical Perspective
Clinical presentation is non-specific. Symptoms often include headache, nausea, decreased mental status and seizures. Due to the nonspecificity of symptoms, the diagnosis is often a primary imaging diagnosis.
C. Imaging Perspective
NECT typically demonstrates bithalamic hypodensity, due to vasogenic oedema (may be reversible) or cytotoxic oedema (established venous infarction). Spontaneously hyperdense venous sinuses suggests thrombosis [2, 3].
CT venography will demonstrate lack of opacification of the thrombosed sinuses. Sagittal and coronal reconstructions with maximum intensity projection (MIP) images are useful for visualization [3, 4].
In MRI acquisition, FLAIR and T2WI will best demonstrate areas of oedema and infarction, with prominent hyperintensity. T2*WI and SWI may often demonstrate multiple basal ganglia petechial foci. Spectroscopy may help differentiate from tumoral causes.
DWI is variable. Some lesions may restrict initially and normalize later on. Nevertheless, restriction is associated to established infarction. On the other hand, non-restriction may imply posterior normalization, suggesting venous congestion without infarction [2-3, 5].
D. Outcome
Outcome and prognosis is very variable, from asymptomatic cases to neurologic impairment or death. Most cases are asymptomatic after 16 months. Predictors of poor prognosis include haemorrhagic conversion and restriction of DWI [5].
Treatment is based on anticoagulation with or without thrombolysis [6].
E. Teaching Points
- Deep cerebral venous thrombosis is clinically a nonspecific entity, in which imaging has an important initial diagnostic role.
- Key features on NECT include bilateral bithalamic hypodensity and spontaneous hyperdensity of straight sinus and deep sinsuses.
- Key features on MRI are bithalamic intense FLAIR and T2SE hyperintensity with possible associated microhaemorrhagic foci on T2GE. DWI will help discern congestive from infarcted components.
- CT or MRI venography is useful in demonstrating the absence of venous blood flow.
- Treatment includes heparin with or without thrombolysis.
- Outcome is variable from asymptomatic to fatal. Haemorrhage and DWI restriction are important prognostic factors.
Differential Diagnosis List
Deep cerebral venous thrombosis with bithalamic infarction.
Glioma
Primary CNS lymphoma
Percheron artery infarction
Final Diagnosis
Deep cerebral venous thrombosis with bithalamic infarction.
