Cerebral venous thrombosis associated with tentorial subdural hematoma during oxymetholone therapy

Androgen was reported to cause cerebral venous thrombosis (CVT) during replacement therapy for aplastic anemia. Oxymetholone, a synthetic androgen analogue, has been widely used in the treatment of aplastic anemia. A 40-year-old woman with aplastic anemia visited our hospital because of severe headache, nausea, vomiting, blurred vision and diplopia for a period of 1 month. She had taken oxymetholone for 2 years. Neurological examination revealed bilateral papilledema and bilateral sixth nerve palsies. Brain magnetic resonance imaging (MRI), performed at the time of admission, demonstrated left-sided tentorial SDH, and focal cerebral thrombosis of the left superficial sylvian vein and sigmoid sinus. MR venography revealed multiple irregularities in the superior sagittal sinus and left transverse sinus. CVT with tentorial subdural hematoma (SDH) caused by oxymetholone was strongly suggested. Oxymetholone was immediately discontinued, and her symptoms and signs disappeared. Because of the thrombocytopenia, anticoagulation was not started. She was discharged and visited the outpatient clinic without neurological symptoms for 6 months. This report supports the cautions given about the risk of CVT with oxymetholone supplementation in aplastic anemia. To the best of our knowledge, this is the first report of CVT associated with tentorial SDH that was probably caused by oxymetholone.     

Cerebral venous thrombosis associated with oligodendroglioma and pregnancy

Until now, cerebral venous sinus thrombosis (CVST) was principally an autopsy diagnosis; however, with the introduction of MRI and angiography, as well as enhanced clinical attentiveness, it is now reliably diagnosed during life. Herein, we describe a case of CVST accompanied by oligodendroglioma and pregnancy. In our patient, the following factors contributed to the formation of CVST: First, the pregnancy state, which is a known risk factor for developing venous thrombosis; and secondly, the oligodendroglioma could have changed the architecture of adjacent sinus (right lateral sinus) and provocation of the development of clot in the sinus.     

Cerebral venous thrombosis associated with recurrent epilepsy-like attacks

A 9-year-old girl with recurrent episodes of unconsciousness, with or without convulsions, was reported. The episodes, which have been observed 9 times over the last 6 years, were characterized by generalized or hemi-convulsions, associated features of headache and vomiting, disturbance of consciousness lasting for a few days, slow activity on EEG continuing for a few weeks after the episodes and no prophylactic effect of anticonvulsants. Repeated EEG examinations revealed no epileptic discharges. Cerebral angiography showed corkscrew-like veins in the frontal region. Cerebral venous thrombosis is strongly suggested as the underlying cause of her episodes.     

Cerebral venous thrombosis

Cerebral vein and dural sinus thromboses (CVT) appear to be rare, but their identification has increased in recent year, due to the increased use of MRI and to a better knowledge of the variable clinical presentation of CVT.CVT can be diagnosed by MR and MR-angiography. Catheter angiography is reserved for cases whose diagnosis remains uncertain with MR. The individual risk for CVT is determined by genetic factors, but may be increased by numerous predisposing conditions and precipitating factors. In recent CVT series death rate is below 10% and about 80% of patients make a complete recovery. The treatment of CVT includes etiological and symptomatic treatment, antithrombotic therapy (anticoagulants, local thrombolysis) and the treatment of intracranial hypertension. There are few randomized trials upon which to base treatment recommendations.     

Cerebral venous sinus thrombosis associated with factor V gene mutation.

The sex prevalence of idiopathic focal dystonia is reported from a data base review of all patients seen at the National Hospital of Neurology, Queen Square and King's College, London up to 1993. There was a higher prevalence of females to males in all categories of focal dystonia involving the craniocervical region. The female to male ratio for cranial dystonia was 1.92:1 (P < 0.01) and 1.6:1 (P < 0.001) for spasmodic torticollis. On the other hand, twice as many men than women had writer's cramp (M:F = 2.0:1, P < 0.01). At present, there is no clear explanation to account for this differences in the sex prevalence of different types of focal dystonia.     

Cerebral venous thrombosis with plasminogen deficiency

We describe a patient with inherited plasminogen deficiency who developed extensive cerebral venous thrombosis. Several other conditions that might have contributed to a hypercoagulable state, including mild thrombocytosis, thyrotoxicosis, and a chronic inflammatory lung disorder, were present. We also discuss the evidence linking plasminogen deficiency with a thrombophilic state. The diagnosis of cerebral venous thrombosis in this case was readily established by nuclear magnetic resonance imaging, a technique that is ideally suited for the evaluation and follow-up of patients with this condition.     

Cerebral venous thrombosis.

Cerebral venous thrombosis is an infrequent condition characterized by extreme variability in its clinical presentation and mode of onset. The combination of magnetic resonance imaging and magnetic resonance angiography is currently the best method for diagnosis. The proportion of cases of unknown etiology remains high. The prognosis, although better than previously thought, remains unpredictable. Treatment, which should be started as soon as the diagnosis is established, consists of reversing the underlying cause when known, control of seizures and intracranial hypertension, and the use of antithrombotics. Heparin should be the first-line antithrombotic agent. Recent studies have confirmed its safety even in patients with hemorrhagic parenchymal lesions. Local thrombolysis is indicated in the very rare cases that deteriorate despite adequate anticoagulation. Cerebrospinal fluid diversion or optic nerve fenestration is used for vision-threatening papilledema when intracranial pressure control is difficult.     

Cerebral venous thrombosis.

Neuroimagining facilities allow early recognition of cerebral venous thrombosis (CVT), which now appears far more common than previously assumed. The diagnosis remains difficult because of a wide spectrum of clinical presentation and a highly variable mode of onset. Numerous conditions (presently mostly noninfectious) can cause or predispose to CVT, which therefore requires an extensive etiologic work-up. The functional and vital prognosis is much better than classically thought with, in noninfectious CVT, a fatality rate of less than 10% and a complete recovery in over 70%. Although spontaneous recovery is possible, the efficacy of heparin is now well established.     

颅内静脉窦血栓形成的诊治(附9例报告)

目的探讨颅内静脉窦血栓形成(CVST)临床表现、诊断及治疗。方法回顾性分析9例经影像学诊断为CVST的患者,行抗凝及血管内介入溶栓治疗。结果9例患者均有颅内压增高表现;3例癫痫发作;2例颅内出血;2例出现意识障碍;1例偏瘫。头部CT、MRI、MRV、DSA为诊断提供依据。8例应用低分子肝素治疗,1例进行血管内介入尿激酶溶栓治疗,同时进行肝素抗凝治疗。治疗后9例患者中7例症状完全缓解,2例症状明显好转。随访6例患者半年至2年,疗效稳定,无1例复发。结论CVST患者多有颅内压增高表现,及时行MRI、MRV及DSA检查,以明确诊断。抗凝治疗为首选治疗方法,血管内介入溶栓治疗协同抗凝治疗可提高疗效。     

Cerebral venous and sinus thrombosis

Introduction: Although anticoagulation (AC) reduces the risk of a fatal outcome or severe disability in patients with cerebral venous and sinus thrombosis (CVST), prognosis of severe cases is still difficult to predict. The authors studied the clinical course of patients with CVST who died despite AC therapy to look for clinical features that might explain the lethal course of these patients. Materials and Methods: Retrospective analysis of a series of 79 consecutive patients with CVST who were treated with a standard regimen of dose-adjusted iv heparin. Case histories of patients with a fatal outcome are presented. Results: The authors identified eight patients with a fatal outcome. All patients were stuporous or comatose at the start of AC, and four patients showed markedly delayed intracranial circulation times, indicating extensive venous thrombosis. Two patients improved, but deteriorated secondarily after reduction or discontinuation of AC. Sufficient activated partial thromboplastin time levels were reached only after a delay in three patients, and critical deterioration occurred in two of them during this time. Conclusion: Although inadequate AC may have contributed to the fatal outcome, some patients with extensive venous thrombosis who are stuporous or comatose at the start of AC may carry an increased risk of death, despite heparin therapy. More aggressive treatment approaches, such as endovascular thrombolysis, may be needed for this subgroup of patients with CVST.     

Cerebral venous and sinus thrombosis

Abstract. Cerebral venous and sinus thrombosis (CVST) can present with a variety of clinical symptoms ranging from isolated headache to deep coma. Prognosis is better than previously thought and prospective studies have reported an independent survival of more than 80% of patients. Although it may be difficult to predict recovery in an individual patient, clinical presentation on hospital admission and the results of neuroimaging investigations are—apart from the underlying condition—the most important prognostic factors. Comatose patients with intracranial haemorrhage (ICH) on admission brain scan carry the highest risk of a fatal outcome. Available treatment data from controlled trials favour the use of anticoagulation (AC) as the first-line therapy of CVST because it may reduce the risk of a fatal outcome and severe disability and does not promote ICH. A few patients deteriorate despise adequate AC which may warrant the use of more aggressive treatment modalities such as local thrombolysis. The risk of recurrence is low (< 10%) and most relapses occur within the first 12 months. Analogous to patients with extracerebral venous thrombosis, oral AC is usually continued for 3 months after idiopathic CVST and for 6–12 months in patients with inherited or acquired thrombophilia but controlled data proving the benefit of long-term AC in patients with CVST are not available.Abbreviations CVST cerebral venous and sinus thrombosis - aPTT activated partial thromboplastin time - IU international units - INR international normalized ratio - AED antiepileptic drug - ICP intracranial pressure - mOsm/kg milliosmole per kilogram     

Cerebral venous thrombosis in children

Cerebral venous thrombosis is an important cause of stroke in children. Understanding the natural history of the disease is essential for rational application of new interventions. We retrospectively identified 31 children with cerebral venous thrombosis confirmed by head computed tomography (4 patients) or by magnetic resonance imaging (27 patients). Risk factors, clinical and radiographic features, and neurologic outcomes were analyzed. There were 21 males and 10 females aged 1 day to 13 years (median 14 days). Nineteen (61%) were neonates. The most common risk factors included mastoiditis, persistent pulmonary hypertension, cardiac malformation, and dehydration. The chief clinical features were seizures, fever, respiratory distress, and lethargy. Fifteen patients had infarctions (8 hemorrhagic, 7 ischemic). Protein C and antithrombin III deficiency were the most common coagulopathies among 14 tested patients. On discharge, 11 patients were normal, 17 had residual deficits, and 2 patients died. Twenty-seven patients were followed from 1 month to 12 years (mean 22 months). At follow-up, 11 patients were normal, and 13 patients had development delay. One had residual hemiparesis and cortical visual impairment. Two had other deficits. Neonatal cerebral venous thrombosis is probably more common than previously thought, and outcomes are worse in this group. All children with cerebral venous thrombosis should be tested for coagulation disorders.     

Cerebral venous thrombosis with familial antithrombin III deficiency

A case of cerebral venous thrombosis with familial antithrombin III (AT III) deficiency was reported and we discussed the anticoagulant therapy of cerebral venous thrombosis from the viewpoint of AT III. The patient, a 17-year-old boy, was admitted to our clinic with severe bifrontal headache, generalized convulsions and progressive disturbance of consciousness. He developed deep vein thrombosis in his right leg and pulmonary emboli two years earlier when he was placed on heparin and so forth, followed by warfarin sodium. Warfarin was terminated 9 months prior to his recent illness. On neurological examination on admission, he was semicomatous with blurred disc margins, roving eye movements with right abducens nerve palsy, nuchal stiffness and right flaccid hemiplegia. Left carotid angiogram and CT scan revealed extensive superior sagittal sinus thrombosis, complicated with hemorrhagic infarcts in bilateral frontal lobes. When examined for coagulation studies, the patient and his father had decrease in AT III activity and antigen levels. He was treated successfully with antiedematous agents and anticonvulsants during acute phase of illness. He was thereafter placed on warfarin 5-6 mg/day with no further clinical thromboembolic event for 2 years 9 months. There was no neurological abnormality when he was last examined, although he was treated with valproic acid 1,200 mg/day and phenytoin 250 mg/day to control occasional adversive seizures. A coagulation study following infusion of 5,000 units of AT III was carried out. Warfarin was discontinued the day before the study. 0.64 U/kg of AT III administration resulted in a 1% increase in AT III level after the infusion. The biological half life of AT III was 14.4 hours.(ABSTRACT TRUNCATED AT 250 WORDS)