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

view similar cases:

Wednesday, 30 May 2012

Multiple Sclerosis

Mid Sagittal T2 wt image: Ill defined linear mild hyperintensity in the cervical cord at the level of C2.
A small well defined hyperintensity in the body of corpus callosum.

Parasagittal T2 wt image: well defined hyperintensity in fronto parietal
periventricular location, perpendicular to the ventricle.

Parasagittal T2 wt image: Oval hyperintensity in posterior parietal
periventricular white matter, oriented perpendicular to ventricle


  • Multiple sclerosis is considered an inflammatory, autoimmune neurologic disease that is characterised by demyelination and axonal injury.
  • Although MS lesion plaques can be found throughout the brain, they have a predilection for periventricular white matter and tend to have an ovoid configuration with the major axes perpendicular to the ventricular surface.
  • At the initial stage, the lesions are typically thin and appear to be linear (Dawson’s fingers),which is probably associated with the inflammatory changes around the long axis of the medullary vein that create the dilated perivenular space.
  • In addition to the periventricular region, the corpus callosum,subcortical region, brain stem, U-fibers, optic nerves, and visual pathway are also regions where lesions are frequently located.
  • The abnormalities of the corpus callosum, U-fibers, and optic nerves, however, may allow for the differentiation of MS from cerebrovascular disease.
  • Although MS is a disease that predominantly affects white matter, lesions can and do occur in gray matter and are better detected on FLAIR imaging.
  • Optic neuritis, which appears early and may be the only presentation in the initial stage of MS, can be detected by using a fat-suppression technique combined with contrast-enhanced imaging or by using long-echo short-tau inversion recovery (STIR) imaging.
  • The accumulation of hypointense lesions on T1(so-called black holes) may correlate with disease progression and disability.
  • In the acute inflammatory phase, the lesion may disrupt the BBB, leading to gadolinium enhancement that is believed to be the first detectable event on conventional MR imaging and may last from days to weeks.
  • Enhancing lesions, which may vary in shape and size, usually start as homogeneous enhancing nodules and subsequently progress to ringlike enhancements.
  • Contrast-enhanced T1WI is now routinely used in the study of MS and provides one in vivo measure of inflammatory activity. It is able to detect disease activity 5–10 times more frequently than the clinical evaluation of relapses  which suggests that most of the enhancing lesions are clinically silent.
  • Overall, T2 lesion load is significantly higher and enhancing T1 lesion load is lower in Secondary Progressive MS than in Relapsing Remitting MS.
  • Another imaging hallmark of MS is brain atrophy, which is considered to be a net accumulative disease burden as the ultimate consequence of all types of pathologic processes found in the brain.
  • Brain atrophy in MS usually appears as enlarged ventricles and the reduced size of the corpus callosum.
Reference: AJNR Am J Neuroradiol 27:1165–76 u Jun-Jul 2006

Monday, 28 May 2012

Neurogenic Heterotopic Ossification

Heterotopic ossification is defined as the formation within the soft tissues of abnormal, ectopic lamellar bone containing bone marrow.

Extensive ossification in the soft tissues around both shoulders in a patient with head injury an year ago
however the underlying bones are un affected.  

It has 3 etiologies:
Trauma (fractures, dislocations, post-surgery, burns)
Genetic (fibrodysplasia ossificans progressiva)
Neurogenic (mainly spinal cord injury and traumatic brain injury)

In a patient with such soft tissue ossification, ask for history of either a direct trauma to that site or trauma/surgery to brain/ spinal cord, one of which is the etiology in most of the cases.