Imminent occlusion of the superior sagittal sinus by compression from an interhemispheric empyema

This 23 year old male patient was receiving medical treatment for frontal sinusitis when he developed severe headache with nausea, vomiting and fever. At physical examination he presented with signs of meningeal irritation.
Bilateral frontal lesions, interpreted as cerebritis, were found on the subsequent emergency CT scan as well as the suggestion of an interhemispheric fluid collection. Analysis of the CSF after lumbar puncture showed abnormalities consistent with bacterial meningitis.
The patient was treated with broad spectrum antibiotics, however his clinical status continued to deteriorate. On the third day of hospitalization he developed repeated generalized seizures followed by coma.
Conventional MRI demonstrated a frank right frontal abscess and an apparently compressive interhemispheric empyema. In order to assess the patency of the superior sagittal sinus a complementary MRA examination was also performed.

(Compression of the superior sagittal sinus, 0.5 T)
Examination 1
Fig.1 Sagittal T1-weighted spin-echo images. The right frontal abscess is seen a slightly hypointense rounded lesion surrounded by an isointense rim (capsule) and a hypointense halo (edema). Diffuse filling of the interhemispheric fissure with effacement of the gyral pattern is also detected.
Fig.2 Transverse T2-weighted fast spin-echo images. The chronic frontal sinusitis and the concomitant right frontobasal abscess are clearly seen. Discrete widening of the subdural space on the right side of the falx in the occipital region is also noted.
Fig.3 Transverse T2-weighted fast spin-echo images of the cerebral vertex. The abnormal widening of the interhemispheric subdural space on the right side is more prominent on these images (subdural empyema).
Fig.4 Transverse Gadolinium-enhanced T1-weighted spin-echo images of the cerebral vertex. Leptomeningeal enhancement over the right cerebral hemisphere is seen. The superior sagittal sinus appears to be patent (signal void) on these images.
Fig.5 Sagittal thin section "anatomical" averaged modulus type source images from a 3D PC MRA acquisition. The interhemispheric empyema is well demonstrated.
Fig.6 Sagittal averaged modulus type source image from the 3D PC MRA acquisition and a midsagittal 2D PC MR angiogram (Venc: 30 cm/s). The superior sagittal sinus appears to be patent on the survey MRA image.
Fig.7 Targeted MIP reconstructions with angular differences from the 3D PC MRA acquisition (Venc: 30 cm/s) data set, showing an approximately 2 cm long abnormal segment of the superior sagittal sinus in the parietal region. The ascending parietal cortical veins appear to be more enlarged than usual (venous congestion?). However, because these afferent cortical veins, draining into the affected dural sinus segment are still visible, the segmental intravascular signal loss of the superior sagittal sinus was interpreted as a "flow gap", reflecting hemodynamically significant stenosis.
The patient underwent surgical intervention (evacuation of the frontal abscess and drainage of the empyema) which was followed by immediate clinical improvement. A follow-up MRI-MRA examination was performed on the second postoperative day.

Examination 2 (2nd day post-operative follow up)
Fig.8 Sagittal thin section "anatomical" averaged modulus type source images from a 3D PC MRA acquisition. The interhemispheric empyema does not show detectable interval changes despite the surgical evacuation.
Fig.9 Targeted MIP reconstructions with angular differences from the 3D PC MRA acquisition (Venc: 30 cm/s) data set. The "flow gap" at the abnormal segment of the superior sagittal sinus has almost disappeared, however the lumen of the sinus still appears to be stenosed.
One month postoperative follow-up was also performed by MRA.

Examination 3 (one-month post-operative follow-up)
Fig.10 Targeted MIP reconstructions with angular differences from the 3D PC MRA acquisition (Venc: 30 cm/s) data set. Almost complete normalization of the superior sagittal sinus is demonstrated. A moderate stenosis is still seen in the previously affected area, however the afferent cortical veins have also regained their normal size, suggesting disappearance of the venous congestion.

N.B. This patient was investigated entirely non-invasively throughout his clinical course. Diagnosis of the imminent occlusion of the superior sagittal sinus, the indication for surgical decompression and the postoperative evaluation were all based on MRA. The patient made a full clinical recovery.

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