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Magnetic resonance imaging has been reported to have advantages over conventional angiography in the diagnosis of dural sinus thrombosis. A case report is presented describing the application of MR techniques including MR angiography, to diagnose and monitor therapy for dural sinus thrombosis.
Lemierre's syndrome, a rare and almost forgotten cause of internal jugular vein thrombosis, is usually caused by an anaerobic head and neck infection. Left untreated, it can result in the release of septic emboli. We describe the case of a 42-year-old man who presented with fever and a tender, swollen neck mass. Computed tomography revealed an edematous parapharyngeal area and a compressed internal jugular vein. Despite antibiotic treatment, the patient's condition worsened, and a parapharyngeal fluid collection was drained 4 days later. Six weeks later, the patient returned to the outpatient department complaining of headaches, and he was found to have a tender, firm neck. He was readmitted, and magnetic resonance venography revealed a right internal jugular vein thrombosis that extended intracranially to the sigmoid sinus. He was anticoagulated for 6 months, and he remained well during outpatient follow-up. We examine the controversial roles that anticoagulation and thrombolysis play in Lemierre's syndrome and sigmoid sinus thrombosis, and we review the diagnostic options.
A 64-year-old man presented with symptoms of obstructive hydrocephalus secondary to a vein of Galen aneurysm associated with a dural arteriovenous malformation and straight sinus thrombosis. The interrelationship of these lesions and their clinical and radiological features are discussed. It is proposed that in this case sinus thrombosis was the primary event in the subsequent development of the other lesions.
Cerebral dural sinus thrombosis remains an uneasy clinical diagnosis because it may present with a spectrum of nonspecific manifestations. CT and MR findings have been described to help recognize this entity. We report here a case with different stages of thrombosed superior sagittal and right transverse dural sinuses demonstrated by CT and MR imaging.
Two patients with angiographically proven longitudinal sinus thrombosis were studied from a coagulation point of view. In the first case, marked primary thrombocytosis was found. This patient was treated with aspirin, dipyridamole and radioactive phosphorus. In the second case, fibrinogen and whole blood plasma viscosity were elevated. This patient developed deep vein thrombosis of the left leg a few weeks after the cerebral episode and was treated with coumarin drugs. The importance of a coagulation study in every patient with cerebral vein thrombosis is emphasized.
Dural sinus thrombosis (DST) is rarely associated with spontaneous intracranial hypotension (SIH). Engorgement of the venous system, caused by the CSF loss that occurs in SIH, is considered to favour the thrombosis, although signs of both SIH and DST are usually seen simultaneously at the first diagnostic MRI. We observed two patients with SIH and DST. Changes in pattern of headaches and MRI findings demonstrated that DST followed SIH. In SIH, the velocity of the blood flow in the dural sinuses may be reduced because of dilatation of the venous system which compensates the CSF loss. Other possible mechanisms seem unlikely on the grounds of both clinical presentation and MRI studies.
A 43-year-old woman was suffered from an increasing headache with nausea and vomiting for nine days. She had received danazol 400 mg daily for endometriosis last two months. CT scan and neurological examinations revealed no evidence of abnormality. MRI showed isosignal intensity on T1-weighted images and high signal intensity on T2-weighted images in the superior sagittal, right transverse, sigmoid and straight sinuses suggesting thrombosis. With angiography, we confirmed extensive dural sinus thrombosis in the superior sagittal, straight, right transverse and sigmoid sinuses. She, then, developed progressing neurological deterioration with dysarthria and drowsy. Microcatheter was placed directly into the thrombus at dural sinus via transfemoral route. Thrombolytic therapy with urokinase was performed in right transverse, confluens sinuum, superior sagittal and straight sinuses. Successful recanalization with remarkable improvement of symptoms was achieved except right transverse sinus. We believe danazol played a role in the occurrence of dural sinus thrombosis. MRI and MRV were noninvasive and useful for diagnosis and follow-up of dural sinus thrombosis. Direct thrombolysis should be considered for dural sinus thrombosis, especially when clinical symptoms are rapidly deterioration with conventional anticoagulant therapy.
Sinus-vein thrombosis is increasingly recognized as a much more frequent neurological disorder than was anticipated before. We examined the pathophysiology of superior sagittal sinus thrombosis (SSST) from 19 patients and a rat SSST model. We treated 19 cases with SSST who were diagnosed by angiography. The symptoms of nine patients, who suffered multiple intracerebral hemorrhage, were abrupt. In another ten patients who recovered satisfactorily, the condition progressed slowly and they were treated with heparin and urokinase. Multivariate analysis demonstrated that female, sudden onset (<24 hours) and posterior 1/3 occlusion are related to bad outcome. Experimentally, SSST was induced by ligation and slow injection of kaolin-cephalin suspension into SSS in rats. Regional cerebral blood flow (rCBF) and tissue hemoglobin oxygen saturation (Hb Sao(2)) using a "scanning" technique were measured at 48 locations, and fluorescence angiography was performed before and until 90 min after SSST induction. After 48 hours the animals were sacrificed for histological studies. Decrease of rCBF and tissue Hb SO(2) and brain damage were seen in group B (n = 10) with an extension of thrombosis from SSS into cortical veins. Brain injury was not observed in group A (n = 8) with SSS thrombus alone and sham-operated animals (n = 5). In conclusion, a brain with acute extension of thrombus from SSS into cortical veins becomes critical for cerebral blood supply and metabolism. CBF, tissue HbSO(2) and repeated angiography can be helpful monitors for the early detection of critical conditions after SSST. As to the therapy, restraint on the ongoing thrombus is essential to protect the brain with SSST, and we encourage the use of combination therapy of heparin and urokinase as early as possible in cases without intracerebral hemorrhage.
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We report an unusual case of fusobacterial infection with secondary intracranial invasion. The condition was complicated by a cavernous sinus thrombosis and ischemic stroke. The patient was a 63-year-old woman with no history of systemic disease who had undergone a tooth extraction before the onset of symptoms. She initially suffered from sphenomaxillary sinusitis and a cavernous sinus thrombosis, and subsequently developed meningitis. Cerebrospinal fluid examination suggested a pyogenic infection. Anaerobic culture revealed Fusobacterium nucleatum. However, despite immediate antibiotic therapy, her condition remained unstable over the next few days, and she eventually developed an ischemic stroke. We describe our experience in the management of this case of anaerobic meningitis and the unusual complication of ischemic stroke; this case suggests that more aggressive therapy in addition to empirical antibiotics may be warranted.
A case of superior sagittal sinus thrombosis after a closed head injury is presented along with a review of 11 other reported cases. Review of the literature indicates that this condition is rarely recognized and that further investigation is necessary to define the incidence, prognostic factors, and optimal therapy of this condition.
Inflammatory bowel disease (IBD) is an idiopathic inflammatory disease of the gastrointestinal tract. The pathophysiology of IBD is probably the result of the complex interaction of genetic susceptibility and environmental influences. There is a well-known risk of thrombosis in patients with IBD. We present the case of a 53-year-old man with ulcerative colitis, who spontaneously developed intracranial sinus thrombosis that was treated with low molecular weight heparin. Literature was searched to assess the frequency and characteristics of cerebral sinus thrombosis in IBD and the role of certain etiopathological factors in such thrombotic patients.
At Emory, six cases of lateral sinus thrombosis (LST) were seen over the last ten years--two children and four adults. The picture and bacteriology of LST have changed with the advent of antibiotics as has the usefulness of various diagnostic tests. Less is it a disease of children in association with acute otitis media. More often it is seen in the adult patient after a long history of chronic ear disease. Fever and mastoid and neck tenderness are still universal signs of the affliction. However, rarely patients do present with progressive anemia, emaciation and evidence of septic emboli. Since antibiotics are commonly used during the prodromal ear infection, cultures are often negative. If they do identify an organism, it is usually a mixed flora rather than beta hemolytic streptococcus. Spinal fluid results are variable and seldom is there evidence of increased spinal fluid pressure. Arteriography, venography, and digital subtraction venography are the most reliable tests to prove and delimit the thrombus. Early management involves high dose broad spectrum, intravenous antibiotics including chloramphenicol. Surgical intervention involves a mastoidectomy, exposure of the sinus, incision and drainage, but not necessarily removal of the thrombus. Internal jugular vein ligation should be reserved for those cases in which septicemia and embolization do not respond to initial surgery and intravenous antibiotics.
Lateral sinus thrombosis (LST) is an infrequent complication of otitis media and mastoiditis in the antibiotic era. A recent case of LST in a 7-year-old boy, the third such case at our institutions in the past 5 years, prompted a review of the modern day English literature concerning LST in pediatric patients. Our goal was to highlight the clinical findings suggestive of LST in the antibiotic era as well as to analyze retrospectively the diagnostic and therapeutic modalities of greatest benefit based on the outcomes reported in the reviewed studies.
Clinical manifestations of superior sagittal sinus (SSS) thrombosis are nonspecific but characterized by headache, papilledema, seizures, focal deficits, progressive coma and death. Recurrent transient focal neurologic deficit is an extremely rare manifestation in superior sagittal sinus thrombosis and the mechanism is unknown. A 45-year-old man presented with headache for two weeks and four episodes of transient (5-10 minutes) right or left hemiparesis for two days. Magnetic resonance image and transfemoral cerebral angiography revealed superior sagittal sinus thrombosis with numerous prominent collateral venous channels. There was no parenchymal lesion. After four days of heparinization, no further transient focal neurologic deficits developed. Follow-up angiography showed partial recanalization of the SSS. Possible mechanism of transient ischemic attacks in this patient is thought to be a transient functional disturbance due to a temporal reduction of tissue perfusion in the process of operating fully-enough collateral channels.
Superior sagittal sinus thrombosis (SSST) has been reported to be caused by coagulopathy following oral contraceptive therapy, DIC, infection around the sinus, compression from a tumor, infiltration of tumor, and an inherited deficiency of proteins C and S, but SSST associated with hematological malignancies and L-asparaginase (L-Asp) therapy is rare. We report a case of an adult patient with acute lymphoblastic leukemia (ALL) who developed SSST during the remission induction therapy. A 25-year-old man was admitted with left facial nerve palsy and, following bone marrow aspiration and lumbar puncture, he was diagnosed as having T-ALL with CNS involvement. He received a 1-AdVP regimen as remission induction therapy and intrathecal administration of methotrexate and cytarabine. On day 29, he had a generalized convulsion and SSST was demonstrated by imaging tests. Lymphoid malignancy (ALL in particular), the use of L-Asp, CNS involvement, and intrathecal chemotherapy might be risk factors for the occurrence SSST. When a patient with those factors develops any neurological symptoms, we should pay attention to the occurrence of SSST, as well as stroke or CNS involvement, though SSST is rare.
To call attention to complications of chronic otitis media, the case of a patient who simultaneously developed lateral sinus thrombosis and Bezold's abscess is reported. A 7 year old boy presented with fever, drowsiness, cervical mass and otorrhea not responding to medical management. Work-up revealed lateral sinus thrombosis and cervical abscess secondary to right ear cholesteatoma. After treatment with surgery and antibiotics, he had a favorable outcome. We review the literature regarding the diagnosis and management of these complications and concluded that although less frequent they remain a clinical challenge.
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