Adam I. Lewis

Management of 100 consecutive direct carotid-cavernous fistulas: results of treatment with detachable balloons.

Direct carotid-cavernous fistulas are high-flow shunts with a direct connection between the internal carotid artery and the cavernous sinus. The goals of treatment are to eliminate the fistula and preserve carotid artery patency. The authors reviewed the outcome of 98 patients with 100 consecutive direct carotid-cavernous fistulas initially treated by transarterial embolization with detachable balloons (1979-1992) at the University of Cincinnati Medical Center to evaluate the merits of this technique and to provide a standard for comparison with future treatment alternatives. Among 100 fistulas, 76 were traumatic in origin, 22 resulted from a ruptured aneurysm, and 2 were iatrogenic. The most common presentations were orbital bruit (80%), proptosis (72%), chemosis (55%), abducens palsy (49%), and conjunctival injection (44%). Eighty-eight fistulas were successfully occluded in 86 patients with detachable balloon(s), and internal carotid blood flow was preserved in 66 patients (75%). Initial attempts at balloon occlusion failed in four patients in whom the fistula eventually closed spontaneously. Five patients required direct surgery to occlude the fistula, and two were treated with nondetachable balloons; one patient died from injuries sustained from trauma. The permanent neurological complication rate was 4%, including cerebral infarction in one patient, frontal intracerebral hemorrhage in one patient, and vision loss in another patient. One death occurred related to cerebral infarction from a balloon that shifted. Transient ischemia occurred in three patients. On the basis of these results, we conclude that transarterial embolization with detachable balloons provides a high rate of fistula obliteration with low morbidity and is the best initial procedure to treat direct carotid-cavernous fistulas.

Management strategies and surgical techniques for deep-seated supratentorial arteriovenous malformations.

The therapeutic options for arteriovenous malformations (AVMs) of the thalamus and the basal ganglia have expanded to include preoperative embolization, stereotactic radiation, and microsurgery. Adjuncts to surgery such as stereotactic guidance, electrophysiological monitoring, intraoperative ultrasound, intraoperative angiography, and induced hypotension have significantly reduced postoperative morbidity. We review the management and outcome of 65 consecutive patients who were treated for deep-seated supratentorial vascular malformations; 45 patients (69%) were treated surgically, 10 patients (15%) were treated conservatively, and 10 patients (15%) underwent radiosurgery. This retrospective study (1976-1993) includes 51 AVMs (78%), 14 cavernous angiomas (22%), and 10 associated vascular anomalies (15%). Initially, 59 (91%) of 65 patients presented with hemorrhage; 23 patients (39%) suffered recurrent hemorrhages. Malformations ranged in size from 1 to 7.5 cm (mean, 2.8 cm). AVMs were fed principally by the anterior and posterior choroidal, thalamoperforate, and lenticulostriate arteries. Venous drainage was uniform via the deep venous system. Among 39 patients who underwent surgery for AVMs, 26 (67%) improved, 7 (18%) remained unchanged, 5 (13%) worsened, and 1 (3%) died. Among six patients who underwent surgery for cavernous angiomas, four (66%) improved, one (17%) remained unchanged, and one (17%) worsened. Operative complications included transient neurological deficits in seven patients (16%), permanent neurological deficits in six patients (13%), and new bleeding from residual AVMs in four patients (9%). Among 10 patients treated conservatively, 3 (30%) had repeat hemorrhages, 2 (20%) had progressive neurological deficits, and 1 (10%) died.(ABSTRACT TRUNCATED AT 250 WORDS)

Relaxation of Subarachnoid HemorrhageInduced Spasm of Rabbit Basilar Artery by the K+ Channel Activator Cromakalim

BACKGROUND AND PURPOSE Cerebral vasospasm resulting from subarachnoid hemorrhage (SAH) is refractory to most vasodilators. However, despite evidence that a mechanism underlying the vasospasm may be smooth muscle cell membrane depolarization resulting from decreased K+ conductance, the ability of K+ channel activators to relax the spasm has not been thoroughly investigated. The purpose of this study, therefore, was to investigate whether K+ channel activation selectively relaxes SAH-induced vasospasm. METHODS Three days after SAH in the rabbit, relaxation of the basilar artery in response to the K+ channel activator cromakalim as well as to staurosporine (protein kinase C antagonist), forskolin (adenylate cyclase activator), and sodium nitroprusside (guanylate cyclase activator) was measured in situ with the use of a cranial window. Relaxation in response to these agents was also investigated in control vessels contracted with serotonin. Membrane potential of the smooth muscle cells of the basilar artery from SAH and control rabbit was measured in vitro with the use of intracellular microelectrodes. RESULTS Cromakalim completely relaxed the SAH-induced spastic basilar artery, while staurosporine, forskolin, and sodium nitroprusside were significantly less efficacious. In contrast, sodium nitroprusside and forskolin were more efficacious relaxants in serotonin-contracted control vessels than in SAH vessels. The K+ channel blocker glyburide and high [K+] prevented cromakalim-induced relaxation. Glyburide did not inhibit forskolin-induced relaxation of serotonin-contracted control vessels. Cromakalim concentration-dependently repolarized spastic basilar artery smooth muscle cells, and the repolarization was prevented by glyburide. CONCLUSIONS These results suggest that K+ channel activation selectively relaxes SAH-induced vasospasm. We speculate that the ability of K+ channel activators to selectively relax the spasm may be due, at least in part, to the underlying inhibition of K+ channels after SAH.

Endothelin ETA and ETB receptors in subarachnoid hemorrhage-induced cerebral vasospasm

The relative roles of endothelin ETA and ETB receptor activation in cerebral vasospasm following subarachnoid hemorrhage were investigated in the rabbit. The endothelin ETA receptor antagonist, BQ610 (1 microM; homopiperidinyl-CO-Leu-D-Trp(CHO)-D-Trp-OH), and the endothelin ETA/ETB receptor antagonist, PD145065 (1 microM; Ac-D-Bhg-L-Leu-L-Asp-L-Ile-L-Ile-L-Trp), relaxed the vasospastic basilar artery in situ by 45% and 87%, respectively. These results suggest that subarachnoid hemorrhage-induced vasospasm of the rabbit basilar artery is due to activation of both endothelin ETA and ETB receptors.

Dural Cavernous Angiomas Outside the Middle Cranial Fossa

Cavernous angiomas of the dura mater are clinically and radiographically distinct from parenchymal cavernous angiomas. In this report, we present two cases of dural cavernous angiomas located outside the middle cranial fossa. The first patient is a 36-year-old woman with two dural cavernous angiomas, including one that enlarged during a 2-year period of observation. The second patient is a 33-year-old man with medically intractable seizures from a dural cavernous angioma of the convexity, which was discovered at autopsy. From our experience and a review of the literature, we have identified two groups of dural cavernous angiomas that differ in incidence, natural history, and surgical management. Most dural cavernous angiomas arise from the middle fossa; in contrast, only 15 cases of dural cavernous angiomas outside the middle fossa have been reported. Those in the middle fossa are more clinically aggressive and more difficult to resect surgically, because they grow toward the cavernous sinus and the parasellar region. Most patients with dural cavernous angiomas outside the middle fossa present with headaches, whereas those patients with dural cavernous angiomas in the middle fossa present with ocular signs, visual field defects, endocrinopathy, and trigeminal symptoms. Radiographically, both of the angiomas resemble meningiomas. Because of their intimate association with the cavernous sinus, surgical resection of middle fossa cavernous angiomas often is incomplete and may require postoperative radiosurgery to control growth. In contrast, angiomas in other locations are easily and successfully resected with little blood loss. The location of dural cavernous angiomas is an important factor in making the surgical decision and in predicting the outcome.

Immunohistochemical localization of endothelial nitric oxide synthase in vessels of the dura mater of the Sprague-Dawley rat

Nitric oxide (NO) and the dura mater are implicated in the pathogenesis of vascular headache. Many studies have demonstrated the participation of NO in headache; however, few studies have identified NO in the dura mater. In this study, nine Sprague-Dawley rats were examined with immunohistochemistry using two different endothelial nitric oxide synthase (eNOS) monoclonal antibodies, H32 and ECNOS. eNOS was successfully localized to the endothelium of the middle meningeal artery. To the best of our knowledge, this is the first study to report NOS immunopositive endothelial cells in the blood vessels of the rat dura mater. The authors propose that NO plays an active role in dural vasodilation, contributing to the pathogenesis of vascular headache; in the future, NO inhibitors could serve as pharmacological agents to treat vascular headache.