We investigated a treatment strategy for arteriovenous malformations (AVMs) of the brain based on results of 107 patients treated with Gamma Knife (GK) surgery between 1991 and 1995. Total obliteration was obtained in 80.5%. The obliteration rate was 82.1% in Grade 3 of Spetzler-Martin scale, 75.0% in Grade 4, 50.0% in Grade 5, and 66.7% in Grade 6. The obliteration rate of slow and low flow AVMs (moya type) within 12 months (65.5%) was significantly higher than that of rapid and/or high flow AVMs (shunt, mixed type). Six patients had bleeding 7 to 42 months after GK surgery. The annual rate of bleeding in accumulated years was 2.3%. Adverse effects appeared in 2 (1.9%) of 107 patients, and both patients had AVMs in the internal capsule. We concluded that microsurgery is recommended for AVMs operable without morbidity, and GK surgery is recommended for AVMs in functional areas, and that intravascular embolization is required for large, rapid and/or high flow AVMs, especially those with hemorrhagic risk factors.
We investigated the methods for treating arteriovenous malformations (AVMs) based on the clinical data and questionnaires sent to affiliated hospitals over 9 years. In 27 institutes, there were twice as many embolizations in the second half (5 years) than in the first half, and the overall clinical results improved especially in the latter half. Responses to a questionnaire on treatment strategy for 62 patterns of virtual AVMs simulating various types and situations were obtained from 17 institutes. There were three general strategies showing more than 70% consensus: 1) radiosurgery for small AVMs without bleeding; 2) embolization plus radiosurgery for large AVMs with ischemic events, and for large, eloquent ones and deep-seated ones with minor hemorrhage; 3) surgical removal for small, middle-sized AVMs with large hematoma except for middle-sized eloquent and deep-seated ones. The strategy used for high-grade AVMs with large hematoma was very different among the institutes. Generally, there is less aggressive surgical extirpation for difficult AVMs, and the dependence on radiosurgery with or without embolization seem to have become greater. The significance of embolization is that it makes the following treatments easier and more effective. Although the indication of radiosurgery is expanding based on its excellent results, embolization still plays a role to reduce the size and hemorrhagic risks and to eliminate factors unfavorable for radiosurgery.
We retrospectively analyzed clinical courses and outcomes of cerebral arteriovenous malformations in 214 patients (3-79 years old) admitted to our institute between January 1987 and March 2000 in order to determine their natural history and therapeutic outcomes. The cerebral arteriovenous malformations were located in the cerebral hemisphere in 142, basal ganglia-thalamus in 19, cerebellum in 24, corpus callosum in 13, brainstem in 6, and others in 10 (Spetzler & Martin Grade I, 17; II, 44; III, 81; IV, 57; V, 13; and VI, 2). The initial presentation was hemorrhage in 121, seizure in 40, ischemia in 21, headache in 18, and asymptomatic in 14. The annual re-bleeding risk was 11.9% in 121 cases with hemorrhagic onset, and the annual bleeding risk was 3.2% in 93 cases with non-hemorrhagic onset. Bleeding risks between initial treatment and complete obliteration of the lesion were 9.7% and 11.4% in hemorrhagic and non-hemorrhagic groups. In 129 cases who suffered from hemorrhage, total extirpation was achieved in 97 and complete obliteration was obtained in 109 in combination with transarterial embolization and/or radiosurgery. In 85 cases without hemorrhage, complete obliteration was obtained in 55 cases. Surgical morbidity and mortality were 5.8% and 0.6%. Clinical outcome was excellent/good in 141 (92%) out of 154 cases who received surgical treatments, in 18 (86%) out of 21 cases who received radiosurgery, and in 23 (59%) out of 39 cases who received partial transarterial embolization or observation. Cerebral arteriovenous malformations should be treated considering their relatively high re-bleeding risks in hemorrhagic cases and treatment-related bleeding risks.
We examined the tissue characterization of carotid plaques using integrated backscatter (IB) and correlated it with the histological analysis in 15 patients who subsequently underwent carotid endarterectomy (CEA). All 15 patients, 11 male and 4 female, mean age 68 years, with carotid stenotic (70% or greater lumen reduction) atherosclerotic plaques verified by angiography and B-mode ultrasonography were included in this study. A 7.5 MHz probe was used to obtain IB value. The pathological examination (HE and Masson trichrome stains) was carried out at a similar level of the isonation. The IB value of normal carotid wall was －14.9±3.8 dB. The IB value of fatty tissue (－19.0±5.0 dB) was significantly lower than fibrotic (－14.0±6.2 dB) and calcific (＋2.1±6.3 dB) content (P<0.01). The intraplaque hemorrhage site exhibited very low backscatter value (－24.0±5.0 dB) which was even lower than the fatty tissue value. The integrated backscatter provides quantitative assessment of plaque structures. The IB value of the atherosclerotic plaque is useful in distinguishing lipidic, fibrotic, calcific, and hemorrhagic content.
Thirty patients with cerebral AVM (19 men and 11 women; 0-82 years old) underwent superselective angiography to evaluate the microvascular architecture before endovascular or surgical treatment. Of these 30 patients, 20 presented with intracranial hemorrhage and 10 with others. The nidus was located in the cerebral cortex in 20 patients, the cerebral subcortex in 7 and the cerebellum in 3. The nidus was classified into 3 types with superselective angiography: (1) type-RD nidus, which consisted of reticular and dense vessels, (2) type-RS consisted of reticular and scattered vessels, (3) type-F consisted of fistulous vessels. Twenty-four patients had a type-RD nidus, 1 had a combined type-RD and RS, 5 had a combined type-RD and F, and 1 had a pure type-F nidus. In 1 patient, the nidus seemed to be type-RD on the conventional angiogram, but superselective angiography revealed it to be a fistulous single cavity. As other findings, 6 venous varices on the draining route, 2 separated nidi connected with venous bridges, and an arterialized venous malformation were clarified with superselective angiography. Three transit arteries and 4 feeding perforating arteries were also detected. In 2 patients, the normal cortical artery distal to the nidus was reconstructed by the leptomeningeal collateral circulation in the retrograde fashion. In conclusion, superselective angiography provides new detailed information useful for both endovascular and surgical treatment.
Many asymptomatic non-ruptured intracranial aneurysms are detected by non-invasive radiological examinations. On the other hand, the question has arisen whether surgical treatment of them is justifiable or not because their natural history is not clear. Therefore, we should discuss with patients the possible risk of surgical treatment when they decide to undergo surgery. We retrospectively investigated treatment results and surgical complications involving asymptomatic non-ruptured intracranial aneurysms. From Jan. 1998 to Dec. 1999, we treated 151 patients (56 male, 95 female) aged 22-77 (mean 58.4), with 201 non-ruptured asymptomatic intracranial saccular aneurysms, excluding multiple aneurysms combined with subarachnoidal hemorrhage, within 6 months of onset. Our policy was that surgical treatment was indicated if the aneurismal size was over 3-4 mm, the patient’s age was under 70, and their general condition was satisfactory. Neck clipping was the first choice of the surgical treatment. Direct surgery was difficult for such aneurysms as internal carotid artery aneurysm arising near the dural ring, those involving posterior circulation and those of a large-size. Such aneurysms were treated with intravascular embolization if possible. We evaluated the surgical risk by the number of the operations (169 cases). Permanent morbidity resulted in 7 cases of the 112 direct surgery (6.3%) and 3 cases of the 56 cases of intravascular embolization (5.6%). No deaths resulted. The causes for the morbidity were brain damage or cranial nerve injury at the approach, a perforating artery injury or occlusion of the parent artery at the clipping in the direct surgery, and distal embolism and perforating artery occlusion in the intravascular embolization. The risk factor of the patients with postoperative neurological deficits was the aneurismal size (>10 mm, p<0.05) with no relation to the age over 70, preoperative ischemic complication of the brain, the triple major risk factors for arteriosclerosis (hypertension, diabetes mellitus, hyperlipidemia) or aneurysmal location. Transient or minor surgical complications were found in 58 cases (34.3%). The prognosis of severe subarachnoidal hemorrhage caused by the rupture of the aneurysm is poor, and surgical therapy for non-ruptured aneurysm over 10 mm in size is difficult. We have, therefore, decided not to change our treatment policy. However, even for transient or minor complications, surgical risk is accompanied with the treatment of cerebral aneurysm. We should seek to reduce such surgical complications by analyzing their causes.
We retrospectively analyzed treatment modalities and outcome in 26 patients with cerebral arteriovenous malformations (AVMs) since 1991, when endovascular treatment was introduced in our clinic. In treating AVM, it is our policy to: 1) Aim at surgical resection of AVMs except non-ruptured eloquent AVMs. 2) Resect AVM without endovascular embolization in emergent cases and AVMs with a small nidus fed by a few feeding cortical arteries. 3) Choose resection with preoperative indispensable embolization in AVMs with deep feeders or multiple feeders that hide behind the nidus at the surgery. 4) Choose radiosurgery or radiosurgery with endovascular embolization in non-ruptured eloquent AVMs. Fourteen of 17 patients (82.4%) had no complications after surgery. However, we could not avoid complication due to endovascular embolization in spite of careful procedure. Twenty of 24 patients (83.3%) had good recovery and moderate disability in Glasgow outcome scale three months after treatment. From these results, we conclude that our strategies for the treatment of AVMs are proper.
There are some problems in the surgery for the internal carotid artery bifurcation aneurysm (ICB-An). We present 16 cases diagnosed as ICB-An in our institute, and discuss the ICB-An with a review of previous reports. We experienced 16 cases of ICB-An (5 male and 11 female), 1-15 mm in a diameter. Eleven cases presented subarachnoid hemorrhage, and ICB-An was ruptured in 3 of 11. Five cases were all asymptomatic unruptured aneurysm, incidentally diagnosed. Nine of 11 SAH cases and 4 of 5 unruptured aneurysm cases demonstrated multiple aneurysms. We surgically treated 12 cases by direct clipping, and 1 by wrapping. Surgery-related deficits in neurology was not observed in any of the operated cases. In the surgery for the ICB-An, over-retraction of the frontal lobe results in premature rupture, because the aneurysmal dome, which is mostly projected upward at the ICB, adhered to the frontal base. Opening the sylvian fissure is the most important procedure to premature rupture and damage of the perforators form the A1 and M1. Endoscopic assistance is also helpful to confirm the clipping procedure.
A 48-year-old female presented with a subarachnoid hemorrhage (SAH) due to right vertebral dissecting aneurysm. Diagnosis was made with vertebral angiogram, magnetic resonance images (MRI) and three-dimensional CT angiography (3D-CTA). These studies showed that the posterior inferior cerebellar artery (PICA) originated from the dissecting aneurysm itself. She underwent proximal occlusion of the right vertebral artery using Guglielmi detachable coils on day 28. Six months later, however, a left vertebral angiogram revealed an enlargement of the dissecting aneurysm that expanded to the PICA. This time, she underwent right occipital artery(OA)-PICA anastomosis prior to the entrapment of the dissecting aneurysm. After the OA-PICA anastomosis, MRI revealed a complete thrombosis of the dissecting aneurysm. Thrombosis of the vertebral dissecting aneurysm after a revascularization of the PICA is rare. We discuss the mechanism of thrombosis and treatment for ruptured PICA-involved dissecting aneurysm of the vertebral artery.
We surgically treated a giant thrombosed fusiform middle cerebral aneurysm with dolichoectatic and tortuous (so-called “serpentine”) channel in a 55-year-old male. He showed mass signs progressively for over 4 years. We performed STA-MCA anastomosis and clipping and debulking of the aneurysm. His aphasia worsened and he developed right hemiparesis after operation. The natural history of the giant thrombosed fusiform aneurysms is not well known now. But many of the case will grow worse gradually without aggressive treatment. We recommend earlier diagnosis and earlier treatments for giant fusiform aneurysm.
A 59-year-old woman was admitted for a transient loss of consciousness, vomiting and severe headache. She was alert without neurological deficit then, and brain CT showed SAH (Fisher group 3). Angiography was performed on day 4 and showed left anterior cerebral artery aneurysm. Her previous history was as follows: She had undergone platelet transfusion after a myoma uteri operation when she was 37 years old. At 54 years old, she was diagnosed with idiopathic thrombocytopenic purpura (ITP), and had been receiving prednisolone since then. On admission, her platelet count was low (4.6×104/µl). We selected delayed surgery, and first γ-globulin and prednisolone were used to improve the platelet count. The patient developed a transient monoparesis in her right leg about 1 week after admission, but this gradually disappeared. The aneurysm was clipped 2 weeks after admission. The postoperative course was uneventful. We discuss the treatment of ruptured intracranial aneurysm with ITP.