The likelihood of rupture of unruptured intracranial aneurysms that were less than 10 mm in diameter was exceedingly low among patients in group 1 and was substantially higher among those in group 2. The risk of morbidity and mortality related to surgery greatly exceeded the 7.5-year risk of rupture among patients in group 1 with unruptured intracranial aneurysms smaller than 10 mm in diameter.

Background and Purpose— Dural arteriovenous shunts with cortical venous reflux or drainage may cause neurological symptoms and death with or without intracranial hemorrhage. Present knowledge about the natural history of these lesions is limited, however. We investigated the incidences of intracranial hemorrhage, progressive dementia syndrome, and death in patients diagnosed in our neurovascular center. Methods— We evaluated the records of 85 patients with dural arteriovenous shunts with cortical venous drainage or reflux hospitalized in our institution from 1978 to 2007. The annual incidences of intracranial hemorrhage, progressive dementia syndrome, and death were calculated. Results— Fifty-three patients did not have an intracranial hemorrhage as the presenting event. One of these patients bled after diagnosis. Thirty-two patients had an intracranial hemorrhage as the presenting event. Three patients bled after diagnosis. One of these patients died. Apart from deficits caused by hemorrhage, no patient reported adverse neurological symptoms. In patients presenting with an intracranial hemorrhage the annual risk for hemorrhage is approximately 7.4% and in those not presenting with a hemorrhage it is approximately 1.5%. Conclusion— The risk of intracranial hemorrhage from a dural arteriovenous shunt with cortical venous drainage is most likely smaller than previously proposed. Presentation with hemorrhage is a risk factor for hemorrhage. The risks of developing neurological symptoms not related to hemorrhage are also less than previously reported.

Subarachnoid hemorrhage (SAH) causes an inflammatory reaction and may lead to ischemic brain damage. Experimental ischemia has been shown to be connected with the alarm-reaction cytokines interleukin-1 receptor antagonist (IL-1Ra) and tumor necrosis factor-alpha (TNF alpha). Increased levels of these cytokines, however, have not been detected thus far in patients following an SAH event. For this reason daily cerebrospinal fluid (CSF) samples were collected from 22 consecutively enrolled patients with SAH and from 10 non-SAH patients (controls). The CSF samples were studied using immunoassays for IL-1Ra and TNF alpha to investigate whether an SAH caused increased cytokine levels. The mean IL-1Ra levels were significantly higher in patients with SAH who were in poor clinical condition on admission than in those who were in good condition (318 pg/ml vs. 82 pg/ml, p < 0.02). The IL-1Ra levels increased during delayed ischemic episodes and after surgery in patients who were in poor clinical condition. Significant increases in IL-1Ra and TNF alpha were detected during Days 4 through 10 in patients suffering from SAH who eventually had a poor outcome (p < 0.05). Patients with good outcomes and control patients had low levels of these cytokines. The levels of IL-1Ra increased after surgery in patients with Hunt and Hess Grades III through V, but not in those with Grade I or II. This finding indicates that patients in poor clinical condition have a labile biochemical state in the brain that is reflected in increased cytokine levels following the surgical trauma. Both IL-1Ra and TNF alpha are known to induce fever, malaise, leukocytosis, and nitric oxide synthesis and to mediate ischemic and traumatic brain injuries. The present study shows that levels of these cytokines increase after SAH occurs and that high cytokine levels correlate with brain damage. It is therefore likely that fever, leukocytosis, and nitric oxide synthesis are also mediated by IL-1 in patients suffering from SAH and it is probable that the inflammatory mediators contribute to brain damage.

Over the long term, outcomes were worse following conservative treatment or shunt insertion surgery than after microsurgery of symptomatic cavernomas. Incidental cavernomas carried a low risk of neurological deterioration. Surgery should follow generally accepted indications, but only with the confidence that total removal can be safely achieved. Surgery that is performed within 10 to 30 days following ictus may be preferable to delayed surgery.