A 38 year old female presented with a sudden onset, severe occipital headache with vomiting, dizziness and blurred vision. The patient had just finished steroid treatment for a chest infection and was on the combined oral contraceptive pill. The patient demonstrated no focal neurology with normal visual acuity/fundoscopy.
The un-enhanced CT, performed 10 hours after the initial symptoms, demonstrates increased attenuation within the straight sinus, vein of Galen [Figure 1a], superior sagittal sinus [Figure 2a] and left transverse sinus [Figure 3a]. There was no evidence of a sub-arachnoid or cerebral haemorrhage. A CT venogram was subsequently performed, which demonstrated corresponding filling defects in the vein of Galen and straight sinus [Figure 1b], superior sagittal sinus [Figure 2b] and left transverse sinus [Figure 3b]. Figure 4 demonstrates the filling defects within the vein of Galen (white arrow), straight sinus and superior sagittal sinus on a CT venogram sagittal reconstruction. A follow up MRI at 6 months demonstrated re-canalisation of all sinuses and deep cerebral veins [Figure 5].
This patient was female, had just finished steroid treatment after a chest infection and was on the combined oral contraceptive pill, all risk factors for venous sinus thrombosis.  Venous sinus thrombosis has an estimated annual incidence of 3-4 cases per million per year.  The clinical presentation is variable which can make diagnosis difficult, but headache is the most common symptom.
The appearance of venous sinus thrombosis on un-enhanced CT is high attenuation secondary to thrombus formation, with corresponding filling defects on CT venogram as demonstrated in this case.
A differential for hyper-attenuation of the un-enhanced venous sinuses is elevated levels of haematocrit (secondary to polycythaemia for example). Children also have higher haematocrit levels and a lower brain density often causing a hyper-dense appearance of the sinuses.  Another differential is partial volume effects due to the proximity of the cerebral venous sinuses to bony structures. For both of these differentials, there should not be a corresponding filling defect on a CT venogram.
The venous sinuses can be separated into the deep cerebral veins comprising the straight sinus, internal cerebral veins and the vein of Galen, and the cerebral venous sinuses comprising the sigmoid, transverse and superior sagittal sinuses. High attenuation in the deep cerebral veins on un-enhanced CT has been shown to be 100% sensitive and 99.4% specific for deep venous sinus thrombosis. This compares with a sensitivity and specificity of only 64.6% and 97.2% respectively for cerebral venous sinus thrombosis. 
Deep venous sinus thrombosis is not always considered in the differential diagnosis of acute headache, but has been associated with increased mortality compared with cerebral venous sinus thrombosis, including a more rapidly decreasing time course, altered consciousness and long tract signs.  If present on imaging, deep venous sinus thrombosis requires prompt management given the increased risk of morbidity.
Therefore given its high sensitivity, un-enhanced CT is of significant value in detecting deep venous involvement and a CT venogram should subsequently be performed to increase the sensitivity for detecting cerebral venous sinus thrombosis.
Follow up in this instance was with an MR venogram after 6 months [Figure 5] which demonstrated re-canalisation of the venous sinuses after anticoagulant therapy. The patient also underwent a thrombophilia screen which was negative.
Differential Diagnosis List
Deep venous sinus thrombosis.
Partial Volume Effects
Deep venous sinus thrombosis.