Over the past 30 years, the development of diagnostic spinal angiography has led to effective endovascular techniques for treatment of spinal vascular malformations. Specific locations, size, rapidity of shunt, and clinical presentation determine the best treatment and prognosis.

Thallium imaging has been proposed as a noninvasive method to distinguish recurrent tumor from cerebral radiation necrosis in patients who have undergone radiation therapy. Previous reports have supported the intuitive hypothesis that metabolically active tumor tissue would accumulate Tl-201 to a much higher degree than nonviable necrotic tissue. A case of biopsy-proven cerebral radiation necrosis is presented demonstrating a degree of Tl-201 avidity previously thought to be diagnostic of recurrent tumor. Based on this finding, it is concluded that a high degree of Tl-201 uptake does not exclude the diagnosis of cerebral radiation necrosis.

Seventy-one intracranial aneurysms were treated by endovascular techniques, with the placement of minicoils inside the aneurysmal sac. Most aneurysms were manifest by hemorrhage (67 cases), and 43 of these were treated within the first 3 days after presentation. At the 1-year follow-up examination, the outcome was scored as good in 84.5% of cases, but the morbidity and mortality rates were 4.2% and 11.3%, respectively. Twenty-nine aneurysms in the anterior circulation and 42 in the posterior circulation were treated. In this series, 23 patients were classified as Hunt and Hess neurological Grade I, 27 as Grade II, 12 as Grade III, nine as Grade IV, and none as Grade V. Thirty-three aneurysms were less than 10 mm in diameter, 28 were 10 to 25 mm, and 10 were larger than 25 mm. The preliminary results from this study appear to justify the emergency treatment of aneurysms by this approach. Aneurysms in the posterior circulation are particularly well suited for this type of surgery.

PURPOSE To evaluate the nature of aneurysms of the spinal arteries, their relative frequency, and the risks associated with these lesions. METHODS We retrospectively reviewed the spinal angiographic studies of 186 patients with spinal cord vascular malformations--70 intramedullary AVMs, 44 extra (peri) medullary AV fistulas, and 72 dural AV fistulas. RESULTS Fifteen spinal artery aneurysms (SAs) in 14 out of 70 patients (20%) with an intramedullary AVM were discovered. No SAs were observed in the other types of spinal vascular malformations. The intramedullary AVMs with SAs were cervical in seven cases and thoracic in the other seven cases (one of the thoracic had two SAs). Fourteen SAs were located on a major feeding vessel to the associated intramedullary AVM (10 on the anterior spinal artery and four on a posterior spinal artery and only one SA was located remote from the AVM feeding vessels. This remote aneurysm was located on the intercostal artery feeding a vertebral angioma in a patient with metameric angiomatosis. Subarachnoid hemorrhage occurred in all cases of SA. The presence of a SA carried a statistically significant (P less than .05) increase in the risk of bleeding. CONCLUSIONS Although increased blood flow seems to be an important factor in formation of these SAs associated with intramedullary AVMs, the role of a developmental vascular anomaly must be stressed: metameric angiomatosis was found in six out of the 14 patients (43%).

PURPOSE:To evaluate the changes occurring in spinal aneurysm (SA) size related to modification of endovascularly treated AVMs.METHODS:Fourteen patients with an intramedullary AVM and associated SA underwent endovascular treatment of their AVM with particles. Embolization sessions numbered from one to 14 (mean five) in each patient.RESULTS:Four patients had SAs with size changes mirroring those of the AVM with embolization: these decreased in size or disappeared after AVM reduction or cure and increased or recurred after AVM recanalization. A second group of patients had SAs that remained unchanged despite AVM changes (six of seven of these were in patients with metameric angiomatosis).CONCLUSIONS:Results in the first group lend support to the hemodynamic theory of associated aneurysm formation. On the other hand, aneurysms that remained unchanged probably are not AVM flow-related and could be an expression of an extensive vascular disorder such as metameric angiomatosis; however, hemodynamic and developmental factors could be concurrent.

A simple, reliable and cheap device for intra-operative monitoring of the facial nerve during surgery for cerebellopontine angle tumours is presented. It consists of a single use tracheostomy tube with a low pressure air inflatable cuff placed in the mouth of the patient on the side of the tumour, connected by a pressure transducer to a monitoring unit. It records any pressure changes in the patient's mouth induced by muscular contractions as a result of excitation of the inferior parts of the facial nerve.

The authors describe a case of fusiform basilar artery aneurysm not amenable to surgical clipping or balloon occlusion with preservation of the parent artery. The aneurysm was treated by balloon occlusion (proximal basilar artery) after test occlusion was well-tolerated; 7-year follow-up showed good results.

Among 121 intracerebral aneurysms presenting at one institution between 1984 and 1989, 16 were treated by endovascular means. All 16 lesions were intradural and intracranial, and had failed either surgical or endovascular attempts at selective exclusion with parent vessel preservation. The lesions included four giant middle cerebral artery (MCA) aneurysms, one giant anterior communicating artery aneurysm, six giant posterior cerebral artery aneurysms, one posterior inferior cerebellar artery aneurysm, one giant mid-basilar artery aneurysm, two giant fusiform basilar artery aneurysms, and one dissecting vertebral artery aneurysm. One of the 16 patients failed an MCA test occlusion and was approached surgically after attempted endovascular selective occlusion. Treatment involved pretreatment evaluation of cerebral blood flow followed by a preliminary parent vessel test occlusion under neuroleptic analgesia with vigilant neurological monitoring. If the test occlusion was tolerated, it was immediately followed by permanent occlusion of the parent vessel with either detachable or nondetachable balloon or coils. The follow-up period ranged from 1 to 8 years. Excellent outcomes were obtained in 12 cases with complete angiographic obliteration of the aneurysm and no new neurological deficits and/or improvement of the preembolization symptoms. Four patients died: two related to the procedure, one secondary to rupture of another untreated aneurysm, and the fourth from a postoperative MCA thrombosis after having failed endovascular test occlusion. The angiographic, clinical, and cerebral blood flow criteria for occlusion tolerance are discussed.

Seven cases of vein of Galen aneurysms treated by percutaneous transvenous endovascular occlusion of the aneurysmal vein are presented. In one case, the approach was via the femoral vein, and in the other six cases, by the jugular vein. All of the malformations were multipedicular and, additionally, in six of the seven there was an intervening arterial-arterial network between the posterior thalamoperforating arteries and the wall of the venous aneurysm. This fistulous network was interpreted as purely arterial and not as an associated arteriovenous malformation. For this reason, the transvenous approach was considered justified, and was performed without risk of hemorrhage caused by retrograde venous hypertension. Measurement of intra-aneurysmal pressure during the course of treatment allowed better understanding of the hemodynamics of the lesions, guided the amount of occlusion to be accomplished during each treatment session, and thus may have prevented the phenomenon of normal perfusion pressure breakthrough. The percutaneous transvenous approach offers all the advantages of the transtorcular approach but avoids surgery. Because of our excellent angiographic and clinical results-five complete and two partial occlusions, with favorable outcomes and no major complications-we believe that this technique is better for the treatment of multipedicular vein of Galen aneurysms than transarterial embolization or surgery.

Twenty-one patients with aneurysms of the vertebrobasilar circulation underwent unilateral or bilateral endovascular occlusion of the vertebral artery. Six patients presented with subarachnoid hemorrhage (SAH), 10 with mass effect, four with mass effect and SAH, and one with ischemic symptoms. Thirteen patients had good outcomes with complete clinical and angiographic cure. Six patients had partial thrombosis of their aneurysms. There was one death and one treatment failure. One patient suffered transient stroke. It is concluded that endovascular occlusion of the vertebral artery following test occlusion is a safe and effective treatment for proximal aneurysms of the vertebrobasilar circulation.

Between 1980 and 1990, 150 patients with cervicofacial vascular malformations were studied at the authors' institution with computed tomography, plain radiography, and angiography. Since 1989, 34 of these patients have also undergone magnetic resonance (MR) imaging. Capillary-venous hemangiomas seem to be the best indication for the adjunctive use of MR imaging. The venous pouches, characteristic of this type of lesion, cause elevated signal intensity, well seen on the T2-weighted images. Excellent fat and muscle differentiation with MR imaging allows appreciation of the depth of extension of these lesions and their delimitation from normal tissue. Arteriovenous malformations (AVMs) are characterized by serpentine signal voids, indicative of the high flow rate of these lesions. Delimitation of the AVM nidus in the midst of the afferent and efferent dilated vessels is often difficult. Study of immature angiomas with MR imaging should be restricted to lesions in specific locations (eg, orbital, laryngeal). Lymphatic malformations showed either tissular or cystic signal intensity changes. MR imaging does not replace other studies but represents an important complementary study for the delineation and diagnosis of deep extensions of vascular malformations, allowing better planning of therapy.

Fifteen patients were observed between 1987 and 1990: there were six with angiographically confirmed vertebral artery dissection, and 9 with carotid artery dissection. Results showed concordance of MRI and angiographic findings, in all cases but one. The dissected portion consistently showed a semilunar hyperintensity narrowing the residual eccentric signal void of the lumen when the artery was not completely occluded. In one angiographically occluded vessel, MR detected a small signal void within the hyperintensity, indicating that the artery was not completely occluded. The length of the dissected portion was clearly demonstrated by MR. Follow up MR and angiographic studies confirmed the regression of the dissection, and also allowed examination of the cerebral parenchyma.

The indications, technique, and results of embolization of arteriovenous malformations with liquid adhesive agents delivered through the anterior choroidal artery are reported. Arteriovenous malformations of the temporal lobe were found in four patients with intracerebral bleeding and two with intractable epilepsy. In five of the six, the dominant arterial feeder was the anterior choroidal artery. All patients underwent superselective catheterization of the anterior choroidal artery and embolization of the arteriovenous malformation. Complications related to the anterior choroidal artery embolization developed after embolization in one patient, after which we changed our technique of embolizing arteriovenous malformations via this artery. A thorough understanding of the functional anatomic structures supplied by each segment of the artery is important. Guidelines for safe catheterization and embolization are given. Embolization of arteriovenous malformations fed predominantly by the anterior choroidal artery is difficult and dangerous. An understanding of the functional anatomy of this artery and proper technique can enable successful embolization of arteriovenous malformations via this route.

Three cases of direct arteriovenous fistulas of the scalp (two involving cirsoid aneurysms) are presented. All three patients were treated with direct puncture of the venous pouch and injection of absolute ethyl alcohol during compression of the venous outflow of the fistula. Two of the three patients were cured with this treatment alone. The third patient, with a very high-flow giant fistula, required injection of glue to close the fistula and subsequent surgical extirpation of the resulting hard mass lesion.

Three cases of complex aneurysms are presented in which balloon embolization therapy was associated with subsequent aneurysmal rupture, causing subarachnoid hemorrhage in two cases and a carotid-cavernous fistula in one. Two of these patients were treated directly by balloon embolization following surgical exploration. The third patient developed the fistula during postembolization volume expansion and heparinization.

To evaluate the long-term results of endovascular treatment with particles in the management of thoracic intramedullary arteriovenous malformations (AVMs), the authors retrospectively reviewed the angiographic and clinical findings in 35 patients. Follow-up was 1-15 years (mean, 6 years) in 28 patients and 6-10 months (mean, 7 months) in seven. A total of 158 embolization procedures were performed in 35 patients. Revascularization occurred frequently, necessitating multiple endovascular sessions. Long-term clinical evaluation showed clinical improvement, compared with the initial status before treatment, in 63% of the patients. Clinical aggravation due to embolization was observed in seven patients (20%) after 12 of the 158 endovascular sessions (8%). These results are better than those reported after surgery and indicate that embolization with particles is an efficient and safe tool in the treatment of thoracic intramedullary AVMs.

✓ Aneurysms of the intracavernous portion of the internal carotid artery may become very large, but they very rarely rupture. A case is described in which rupture of such a lesion resulted in a lethal massive subdural hematoma with transtentorial herniation. This is the second reported case of substantiated intracranial rupture from a wholly intracavernous carotid artery aneurysm.

One hundred fifty‐four patients with brain tumors of various types were given an intravenous infusion of the thymidine analogue bromodeoxyuridine (BUdR), 200 mg/m2, at the time of surgery but before biopsy of the tumor to label S‐phase cells. Excised tumor specimens were fixed, sectioned, and stained by immunoperoxidase methods to detect BUdR. The labelling index (LI), or percentage of BUdR‐labelled cells, was calculated for each tumor specimen. The LIs of glioblastomas, medulloblastomas, and most highly anaplastic astrocytomas were 5% to 20%. The majority of moderately anaplastic astrocytomas showed LIs of less than 1 %, but 30% of them had LIs similar to those of highly malignant gliomas. Most pituitary adenomas and neurinomas showed LIs of less than 1%. Non‐ malignant meningiomas had LIs of less than 1%, whereas malignant meningiomas had LIs higher than 2.7%. This is an important observation, because malignant meningiomas are not well‐defined histopathologically and their growth rate and rate of recurrence cannot be predicted by current diagnostic procedures. By estimating the proliferative potential of individual tumors more precisely, the BUdR LI supplements histopathological diagnosis, allowing a more accurate estimate of prognosis and facilitating the design of treatment regimens for individual patients.

Alterations in cerebral metabolic activity were measured after different doses of phenobarbital. Local cerebral glucose utilization was determined in 58 brain regions with the use of the [14C]deoxyglucose technique in 3-month-old Fischer 344 rats, at 1 h after the ip administration of saline or of phenobarbital. Whole brain glucose utilization declined in a dose-related manner by 4%, 13%, 33%, 35%, and 56% after phenobarbital 18, 60, 180, 300, and 600 mg/kg, respectively. The number of regions significantly affected (P less than 0.05) increased from 7 to 95% of the regions examined between doses of 18 to 600 mg/kg. Metabolism decreased in all significantly affected regions except the interpeduncular nucleus, where it was increased. In a separate group of rats, the number of falls per 5 min from a constantly rotating cylinder was measured at subanesthetic doses of phenobarbital. Doses of drug that affected performance on the rotating cylinder (18 and 60 mg/kg) reduced glucose utilization in brain regions involved with motor performance, including the red nucleus, vestibular nucleus, substantia nigra, and deep layers of the superior colliculus, whereas cerebral cortical regions were not altered significantly. The results demonstrate that phenobarbital reduces cerebral glucose utilization, in a dose-dependent manner, in most brain regions and affects subcortical regions of the motor system significantly before reducing metabolism in the cerebral cortex.