The common imaging feature that results from occlusion of the superior sagittal sinus is of bilateral superficial paramedian parietal or frontal hemorrhagic infarctions or edematous venous congestion. In the case of CT with contrast infusion in axial images, a lack of dye opacification in the posterior sagittal sinus can be observed with careful adjustment of the viewing window (“empty delta sign”). The spinal fluid pressure is increased, and the fluid may be slightly sanguinous. Transverse sinus thrombosis causes hemorrhagic infarction of the temporal lobe convexity, usually with considerable vasogenic edema. The enhanced CT, arteriography (venous phase), and MRV (Fig. 33-39) facilitate diagnosis by directly visualizing the venous occlusion by showing an absence of opacification of a sinus or, at times, a clot within a vein. Once a venous thrombosis becomes established for several days or longer, the tributary surface veins take on a “corkscrew” appearance that is appreciated on the venous phase of an angiogram.
Chaps. 12 and 13, in cases of cavernous sinus thrombosis there may be marked chemosis and proptosis, corresponding to a clot in the anterior portion of the sinus and there may be disordered function of cranial nerves III, IV, VI, and the ophthalmic division of V when the posterior portion is affected. If there is spread of the clot to the inferior petrosal sinus, palsies of cranial nerves VI, IX, X, and XI may result. Also involvement of the superior petrosal sinus may be accompanied by a fifth nerve palsy.
Thrombosis of the venous sinuses in neonates presents special problems in diagnosis. In the series reported by deVeber and colleagues, various perinatal complications, including systemic illness such as severe dehydration or infection were common precedents; the outcome was poor. In young children the risk factors differed, in that connective tissue and prothrombotic disorders and head and neck infections were more common.
Occlusion of the vein of Galen and of the internal cerebral veins is the least common and clinically most obscure of the venous syndromes.
From the few cases that have been studied, a picture of bithalamic infarction emerges, sometimes reversible, and consisting mainly of inattention, spatial neglect, and amnesia in the case reported by Benabdeljili and colleagues, and of akinetic mutism and apathy as in the case reported by Gladstone and associates. The case series of van den Bergh and colleagues emphasizes the difficulty in diagnosis of partial syndromes of this nature. In most reports of this condition, it is the neuropsychologic aspects that are emphasized. Other cases have manifested coma and pupillary changes referable to the ischemic diencephalon and rostral midbrain. Perhaps most striking is the MRI, with a large bilobular region of signal change that encompasses the thalami. Much of the signal change probably represents reversible edema and venous congestion, because substantial clinical improvement may occur. Angiography is needed to confirm the diagnosis, most often a magnetic resonance venogram.
Treatment of Cerebral Venous Thrombosis