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OBJECTIVE AND IMPORTANCE: Cerebral venous and dural sinus thrombosis is a rare cause of stroke. Although morbidity and mortality have greatly decreased in recent years as a result of early diagnosis and timely medical treatment, when coma occurs the prognosis remains poor. We evaluated whether emergent decompressive craniectomy has a role in the treatment of patients with brain herniation from dural sinus thrombosis and hemorrhagic infarct. CLINICAL PRESENTATION: Three patients developed large hemorrhagic infarct with coma and bilaterally fixed and dilated pupils resulting from aseptic dural sinus thrombosis. INTERVENTION: Two patients underwent emergent surgical decompression as soon as brain herniation developed, and these patients had complete functional recovery. One underwent delayed surgical decompression and remained severely disabled. CONCLUSION: Our results provide preliminary evidence that emergent decompressive craniectomy is effective in patients with brain herniation from dural sinus thrombosis, provided that the clinical onset is recent. We therefore recommend consideration of this aggressive surgical technique for such patients, who may survive with good outcomes.

TO CLARIFY THE efficacy and limitations of the intra-arterial local infusion of a high-dose fibrinolytic agent for acute embolic stroke, we analyzed the results of 44 patients and compared them with those of 51 patients treated with intracarotid (18 patients) or intravenous (33 patients) inf

Objective The pathogenesis of pituitary apoplexy and the role of precipitating factors in pituitary apoplexy are poorly understood. Most of the published cases are in the form of case reports. We assessed the presumed precipitating factors in a series of patients treated surgically for pituitary apoplexy and reviewed the contemporary published literature. Method Thirty-eight consecutive patients with pituitary apoplexy were treated surgically by the Department of Neurosurgery at the University of Virginia, Charlottesville, VA, between January 1996 and March 2006. Their medical records were retrospectively reviewed. Contemporary published cases from 1990 to 2006 were also reviewed. Results Nine patients (24%) were identified as having precipitating factors for pituitary apoplexy. The factors identified were coronary artery surgery (two patients), other major surgery (two patients), pregnancy (two patients), gamma knife irradiation, anticoagulant therapy, and coagulopathy secondary to liver failure. The presentation, histology, and outcome were compared between those patients with a precipitating factor and those in whom none was identified. A review of the published literature showed that coronary artery surgery, pituitary stimulation, and coagulopathy were the most common precipitating factors. Conclusion A minority of patients with pituitary apoplexy will have precipitating factors. The majority of patients with precipitating factors will have histopathology showing hemorrhagic infarction or hemorrhage. The most common precipitating factors are pituitary stimulation, surgery, particularly coronary artery surgery, and coagulopathy. Caution in doing endocrine investigation, surgery, or anticoagulation in patients with a known pituitary tumor is advised. Patients with no diagnosed pituitary tumor but with a known precipitating factor who have neuro-ophthalmological deterioration or endocrine failure should undergo prompt magnetic resonance image scans and endocrine investigation and endocrine replacement as indicated.

OBJECTIVE: Hemorrhagic complications were analyzed in 106 procedures of 99 patients treated with percutaneous transluminal angioplasty (PTA) or stenting for intracranial arterial stenoses. METHODS: Ninety-nine patients with intracranial arterial stenosis were treated with PTA or stenting 106 times from January 1995 to December 2003. Fifty-seven patients had intracranial internal carotid artery stenosis, 23 had middle cerebral artery stenosis, and 19 had vertebrobasilar stenosis. Evaluation of hemodynamic compromise via single-photon emission computed tomography was performed 50 times for 50 patients before the treatment. RESULTS: Four hemorrhagic complications occurred in 106 procedures. Two of these cases involved intracerebral hemorrhage after PTA or stenting in the treated vascular territory 30 minutes and 16 hours after the treatment, respectively. One case showed subarachnoid hemorrhage, which appeared 6 hours after treatment. Hemodynamic compromise was found on single-photon emission computed tomography in these three cases. The last case with a hemorrhagic complication was a hemorrhagic infarction after recanalization of stent thrombosis, which appeared 3 days after stenting. Hyperperfusion syndrome was strongly suggested as the cause of hemorrhage in the two cases associated with intracerebral hemorrhage. CONCLUSION: The rate of hemorrhagic complication directly related to the procedure of PTA or stenting was 3%, and hyperperfusion syndrome was suggested as the cause of hemorrhage in two cases (2%), from the perspective of clinical characteristics and single-photon emission computed tomographic findings.

The authors report a case of cortical vein and sagittal sinus thrombosis after a transcallosal removal of a colloid cyst of the third ventricle. Thirty-six hours after the operation, the patient developed focal seizures; after progressive deterioration, he died on the sixth postoperative day. At the autopsy, a venous hemorrhagic infarct in the right frontoparietal area and fresh thrombus occluding the sagittal sinus and cortical veins were found. The mechanism of cortical vein and sinus thrombosis subsequent to this procedure is discussed, and suggestions are made to prevent this serious complication.

Hemorrhagic infarction after vasospasm is a rare condition in patients with aneurysmal subarachnoid hemorrhage (SAH). Induced hypertensive therapy is used for patients with vasospasm, but this treatment has a risk of inducing hemorrhagic infarction. A total of 221 patients whose first computed tomographic (CT) scans were examined within 2 weeks after SAH were investigated for this study. There was symptomatic vasospasm in 99 (45%), cerebral infarction in 37 (17%), and hemorrhagic infarction in 13 (6%). Hemorrhagic infarction usually occurred 20 to 30 days after aneurysmal rupture; this period corresponds with the remission stage of the vasospasm. On CT scans, the hemorrhagic infarction was revealed as a leaky hemorrhage in a low density area in 11 cases, and a massive hemorrhage with mass effect was seen in 2 cases. These findings suggest that hemorrhagic infarction after vasospasm may sometimes be fatal. Cerebral blood flow autoregulation in patients with vasospasm was normal or of a hypertensive type during the remission stage of vasospasm, when hemorrhagic infarction usually appeared. This finding shows that induced hypertension therapy is ineffective during this stage; it should be stopped by this stage because it is ineffective and also may aggravate hemorrhagic infarction.

Background and importance High-grade cavernous sinus (CS) dural arteriovenous fistulae with cortical venous drainage often have a malignant presentation requiring urgent treatment. In the absence of a venous access to the lesion, transarterial embolization can potentially cure these lesions; however, the high concentration of eloquent arterial territories adjacent to the fistula creates a precarious risk of arterial-arterial reflux. In such cases, a combined surgical and endovascular approach may provide the least invasive option. Clinical presentation We describe a patient presenting with a venous hemorrhagic infarct caused by a high-grade CS dural arteriovenous fistula (Barrow type D caroticocavernous fistula) with isolated drainage via the superficial middle cerebral vein into engorged perisylvian cortical veins. No transfemoral or ophthalmic strategy was angiographically apparent, and the posterior location of the involved CS compartment mitigated a direct puncture. The patient underwent direct puncture of the superficial middle cerebral vein via an orbitozygomatic craniotomy and the CS was catheterized under fluoroscopic guidance. The CS was coil-embolized back into the distal superficial middle cerebral vein with complete obliteration of the fistula. The patient did well with no new deficits and made an uneventful recovery. Conclusion This novel combined open surgical and endovascular approach enables obliteration of a CS dural arteriovenous fistula with isolated cortical venous drainage and avoids the additional manipulation with direct dissection and puncture of the CS itself.