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[Mono- or bilateral abducens paralysis as the initial symptom of sinus vein thrombosis].

BACKGROUND: Sinus vein thrombosis is a rare intracerebral complication of mastoiditis. We report on the clinical ophthalmologic symptomatology of this secondary illness. PATIENTS AND METHODS HISTORY: two young female patients, aged 14 and 3.5 years, presented at our pediatric ophthalmology section due to diplopia. Both girls had suffered 1-2 weeks earlier from otitis media, which had been treated with antibiotics. Other neurological symptoms were not reported. CLINICAL COURSE: Best corrected visual acuity was 20/20 OD/OS in both patients. Ocular alignment revealed a bilateral abduction deficit in the 14-year-old girl and a monolateral abduction deficit of the right eye in the younger patient. Ophthalmoscopic examination evidenced bilateral papilledema in both patients. Magnetic resonance tomography and magnetic resonance angiography showed mastoiditis and thrombosis of the sigmoid and transverse sinuses. THERAPY: Following mastoidectomy, high-dose antibiotic therapy, and full-dose heparin therapy, rapid improvement occurred. CONCLUSIONS: Thrombosis of the sigmoid sinus following mastoiditis is a rare but severe complication of middle ear inflammation. Immediate surgical and antibiotic therapy is necessary. Symptoms can possibly occur even when the primary focus seems to resolve.

Abducens Nerve Diseases↗

[Thrombus propagation and venous drainage disturbance in cerebral sinus-vein thrombosis--38 autopsied cerebral sinus-vein thrombosis].

38 autopsied cases of cerebral sinus-vein thrombosis (CSVT) in our institute were studied. In this study, special attention was paid for the evolution and fate of venous thrombus. 18 cases showed hemorrhagic infarction or intracerebral hematoma (group 1; G 1). In contrast, no cerebral parenchymal changes were observed in the other 20 cases (group 2; G 2). In 13 of 18 cases of G 1, superior sagittal sinus (SSS) were thrombosed. 10 of these 13 cases showed thrombosed cerebral cortical veins (CV) or deep cerebral veins (DV). In contrast, none of 16 cases of G 1 with thrombosed SSS showed thrombosed CV or DV. All cases of the solitary thrombosis of CV or DV (each 2 cases) belong to G 1. Venous thrombi were divided into three stages according to its process of organization; recent thrombus (R), hyalinized thrombus (H), organized thrombus (O). In the venous thrombi of G 1, 6 cases were R, 6 were partly H, 6 were partly 0. In addition to O, R and H were also observed in group O. Distribution of various stage of thrombus in same case suggested that gradual thrombus evolution had occurred before or after the clinical onset in CSVT. This study suggested: (1) CV or DV occlusion may play an important role for the advent of cerebral parenchymal changes in CSVT. (2) Gradual thrombus evolution after the onset is one of possible causes of slow clinical deteoration after the onset. Therefore, prevention of these thrombus propagation with anti-platelet drugs or fibrinolotic therapy should be recommended for the treatment of CSVT. On the contrary, hyperosmolar agents and diuretics may produce potential risk of dehydration, and as a result, accelerate secondary thrombus extension.

Adolescent↗

Magnetic resonance imaging in lateral sinus hypoplasia and thrombosis.

Lateral sinus thrombosis may be difficult to differentiate angiographically from lateral sinus hypoplasia, which mainly affects its proximal transverse portion. Using magnetic resonance imaging, we evaluated six patients who demonstrated poor filling or lack of filling of one or both lateral sinuses at angiography. In each patient, magnetic resonance imaging unambiguously demonstrated either lateral sinus thrombosis or lateral sinus hypoplasia. The latter was characterized by a frank asymmetry in size (surface of section) of the transverse portion of the lateral sinuses on parasagittal images without any abnormal signal in the course of the sinus. Lateral sinus thrombosis was indicated by increased intraluminal signal on all planes and with all pulse sequences. By virtue of its freedom from bone-related artifact, its multiplanar imaging capability, and its sensitivity to both blood flow and thrombus formation, magnetic resonance imaging is an excellent tool for the evaluation of lateral sinus thrombosis or hypoplasia.

Carotid Arteries↗

Septic thrombosis of the dural venous sinuses.

From 1940 to 1984, 19 cases of septic dural-sinus thrombosis have been diagnosed at the Massachusetts General Hospital, and some 136 cases have been reported from other institutions. Septic thrombosis most frequently involves the cavernous sinuses (96 cases). Facial or sphenoid air sinus infection often precede cavernous-sinus disease. In addition to the classical signs of proptosis, chemosis, and oculomotor paralysis, isolated sixth-nerve palsy and hypo- or hyperesthesia of the fifth nerve may be found. The major pathogens associated with cavernous-sinus infection include Staphylococcus aureus, other gram-positive organisms, and anaerobes. Septic lateral-sinus thrombosis (64 cases) is almost exclusively a complication of otitis media and/or mastoid infection. Organisms causing this infection include Proteus species, Escherichia coli, S. aureus, and anaerobes. Septic thrombosis of the superior sagittal sinus (23 cases) most frequently accompanies bacterial meningitis or air sinus infection. Causative organisms include Streptococcus pneumoniae, S. aureus, other streptococci, and Klebsiella species. Because septic dural-sinus thrombosis is rare, this disease is frequently misdiagnosed. Evaluation should include lumbar puncture, air sinus films, and computed tomographic scan with contrast. Other helpful diagnostic tests may include carotid angiography, and dynamic brain scan. Orbital venography is the most definitive study in cases of chronic cavernous-sinus thrombosis. Therapy should include intravenous antibiotics and early surgical drainage of purulent exudate in the air sinuses or mastoid regions. Retrospective analysis suggests that treatment with heparin may reduce mortality in carefully selected cases of septic cavernous-sinus thrombosis. Anticoagulation is not recommended in other forms of septic dural-sinus thrombosis. Mortality in the antibiotic-era remains high, particularly in patients with septic thrombosis of the cavernous (30%) and superior sagittal (78%) sinuses.

Adolescent↗

Occlusion of the pig superior sagittal sinus, bridging and cortical veins: multistep evolution of sinus-vein thrombosis.

Cerebral sinus-vein thrombosis may lead to severe hemodynamic changes, elevated intracranial pressure (ICP), and brain edema. It is supposed that progression of the thrombus from the sinus into bridging and cortical veins plays a key role in the development of these pathophysiological changes, but this hypothesis lacks experimental proof. The aim of this study, using a novel animal model of sinus-vein thrombosis, was to evaluate the effects of a standardized occlusion of the superior sagittal sinus and its bridging and cortical veins on hemodynamic alterations, on brain water content, and on ICP in domestic pigs. In 10 animals, the middle third of the superior sagittal sinus was occluded with a catheter-guided balloon. Five of these pigs received an additional injection of 1 ml fibrin glue into the superior sagittal sinus anterior to the inflated balloon, leading to an obstruction of bridging and cortical veins. In five control animals the balloon was inserted but not inflated. Five pigs underwent cerebral angiography. Four hours after occlusion, the brains were frozen in liquid nitrogen, and coronal slices were examined for Evans blue dye extravasation, regional water content, and histological changes. Occlusion of the superior sagittal sinus alone did not affect ICP or cerebral perfusion pressure (CPP). The additional injection of fibrin glue caused an obstruction of cortical and bridging veins as well as severe increases in mean (+/- standard deviation) ICP to 49.4 +/- 14.3 mm Hg, compared with 8.3 +/- 4.5 mm Hg in sham-treated controls and 7.1 +/- 3.9 mm Hg in animals with occlusion of the superior sagittal sinus alone. There was also a steep fall in the mean CPP to 34.2 +/- 19.6 mm Hg compared with 96.4 +/- 13.8 mm Hg in the control group. White-matter water content anterior to the occlusion site was elevated to 81.9 +/- 3.7 gm/100 gm frozen weight in the fibrin group as compared to 70.7 +/- 2.2 gm/100 gm in controls. Posterior to the occlusion site, water content did not differ among the three groups. Angiography demonstrated collateral flow via cortical and bridging veins in animals with occlusion of the superior sagittal sinus alone. Additional fibrin glue obstructed these collateral vessels. The data suggest a multistep process of pathophysiological alterations in patients with sinus-vein thrombosis and may explain why these patients present with a wide variety of symptoms: minor neurological deficits or headache might indicate thrombosis of the superior sagittal sinus and/or its bridging veins.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

[Anticoagulant treatment in hemorrhagic brains infarts due to large sinus venous thrombosis].

Cerebral venous and sinus thrombosis is an infrequent condition which presents with a wide spectrum of signs and a variable mode of onset. Sinus thrombosis may cause isolated intracranial hypertension but also may cause cerebral venous infarcts, which are frequently hemorrhagic. Treatment with antithrombotic agents is controversial because there is only one randomised controlled trial with unfractionated heparin. We report a 46- years-old man complaining of progressive headache, paraparesis and dysphasia. After admission, his neurological status worsened and he developed tetraparesis, depressed level of consciousness and seizures. A cranial computarized tomography (CT) scan showed multiple hyperdensities suggestive of hemorrhagic infarcts. Magnetic resonance imaging (MRI) study confirmed extensive cerebral venous thrombosis. Unfractionated heparin was administered for two weeks followed by acenocumarol. Within a few days his neurological status improved, and five weeks after admission the patient only hadd slight neurological deficit. After 11 years of follow-up, he has had a complete recovery. The G20210A mutation in the prothrombin gene was detected as a likely risk factor for venous thrombosis. Therapeutical and diagnosis aspects are discussed. We review the previous literature on the topic.

Anticoagulants↗

[Diagnosis of thrombosis of cavernous sinus in magnetic resonance imaging].

The diagnosis of the cavernous sinus thrombosis requires a careful clinical evaluation and appropriate radiological methods. In this report we describe the magnetic resonance imaging findings in a patient with the clinical diagnosis of cavernous sinus disorder and its correlation with orbital phlebography and histopathologic studies.

Candidiasis↗