Thursday, 31 May 2012


Axial T1 wt image:  Linear hyperintensity in posterior interhemispheric fissure in straight sinus.
Mild hyperintensity seen in superior sagittal sinus- s/o sub acute thrombosis

Axial T1 wt image: Right transverse sinus is dilated with diffuse hyperintense signal
s/o sub acute thrombosis.

Axial T2 wt Image: Ill-defined T2 hyperintensity in anteromedial aspect of
left thalamus- vasogenic edema(normal ADC values with no blooming on GRE)

Causal factors:
1.   Local - sinus trauma, regional infection such as that in mastoiditis, and
      neoplastic invasion or compression.
2.   Systemic- protein S and protein C deficiencies, peripartum state,
      oral contraceptive use, and hypercoagulable states secondary to
3.   Unidentified – in 25%.

·    Focal neurologic symptoms are more often seen in patients with
      parenchymal changes observed at imaging than in those without such

·    The deep venous system drains the inferior frontal lobe, most of the deep
      white matter of the frontal, temporal and parietal lobes, corpus callosum,
      upper brainstem, basal ganglia and the thalamus.

·    Increased attenuation in the venous sinuses on CT also may be seen in
      patients with dehydration, an elevated hematocrit level, or a subjacent
      subarachnoid or subdural hemorrhage.

·    In most cases, a close comparison of sinus attenuation with arterial
      attenuation can help differentiate between a physiologic increase in sinus
      attenuation and increased attenuation due to thrombosis.

·    Empty Delta Sign

·    The signal intensity of venous thrombi on T1- and T2-weighted MR images
      varies according to the interval between the onset of thrombus formation
      and the time of imaging.
Stage of bleed/sequence

·    Organized thrombus with intrinsic vascularity in chronic CSVT can enhance
      with contrast.

·    GRE imaging sequences may be an important diagnostic aid in 
          acute-stage thrombosis, when the signal intensities on 
          T1- and T2-weighted images may be more subtle.

·    DWI allows subclassification of parenchymal abnormalities
      as either primarily vasogenic edema (with increased ADC values
      presumably related to venous congestion) or primarily cytotoxic edema
     (with decreased ADC values related to cellular energy disruption).

·    Patients with diminished ADC values more often have parenchymal sequelae,
      while those with normal or increased ADC values usually do not.

·    In contrast with arterial ischemic states, many parenchymal abnormalities
      secondary to venous occlusion are reversible.

·    Parenchymal swelling without abnormalities in attenuation or signal intensity
      on images may occur. Such patients typically have more prominent clinical
      symptoms than would be expected on the basis of imaging findings.

·    The enhancement is typically gyral in location and may extend into the white

·    Increased tentorial enhancement (likely related to dural venous collaterals),
      adjacent leptomeningeal enhancement, and prominent cortical venous
      enhancement (secondary to venous congestion) also may be visible.

·    Flame-shaped irregular zones of lobar hemorrhage in the parasagittal
      frontal and parietal lobes are typical findings in patients with
      superior sagittal sinus thrombosis.

·    Hemorrhage in the temporal or occipital lobes is more typical of transverse
      sinus occlusion.

·    Thalamic edema is the imaging hallmark of deep venous thrombosis  and it
      may extend into the caudate regions and deep white matter.

·    “Cord sign ”and  “Hyperintense vein sign ” are typically seen in isolated
      cortical venous thrombosis on CT and MRI respectively.

·    CSVT mimics
ü  Sinus hypoplasia
ü  Flow gaps
ü  Arachnoid granulations
ü  Thrombus shine signal

Ref: Imaging of Cerebral Venous Thrombosis: Current Techniques, Spectrum of Findings, and Diagnostic Pitfalls Radiographics
October 2006 26:suppl 1 S19-S41; doi:10.1148/rg.26si055174

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