In this report, three operations for thalamic arteriovenous malformation (AVM) are discussed, mainly from the viewpoint of surgical approach and technique.
Case 1 was a 20-year-old male with a history of three episodes of intracranial hemorrhage. Angiogram demonstrated a nidus 2cm in diameter at the anterior inferior site of the left thalamus. The malformation was fed by anterior and posterior choroidal arteries and the anterior thalamoperforating artery. First surgery was performed using a subtemporal approach. The left posterior communicating artery which mainly fed the nidus was trapped. Second surgery was performed via a bifrontal craniotomy. An anterior transcallosal approach was used to expose the AVM. Nidus was totally excised via the left lateral ventricle. Postoperatively, no new neurological deficit appeared.
Case 2 was a 36-year-old female who experienced a sudden intraventricular hemorrhage. Angiogram demonstrated a nidus 2cm in diameter at the posterior superior site of the left thalamus. The malformation was fed by the anterior and posterior choroidal arteries. Surgery was performed via a left parietal craniotomy. A transparietal approach was used to expose the AVM and the nidus was totally excised. Although the patient exhibited Gerstmann syndrome and right homonymous hemianopsia, they were transient, and the patient was discharged with no deficit.
Case 3 was a 51-year-old female with a history of three episodes of intracranial hemorrhage. Angiogram demonstrated a nidus 4cm in diameter at the right thalamus. The malformation was fed by the anterior and posterior choroidal arteries, the anterior thalamoperforating artery and the thalamogeniculate artery. Surgery was performed via a right fronto-temporo-parietal craniotomy. At first, the feeder was clipped using a subtemporal approach. And then the nidus was totally excised using a transparietal and transventricle approach. Postoperatively, impairment of consciousness appeared.
It appeared to be important in surgery for AVM's in a critical area like the thalamus that management of the feeder be performed first, bleeding should be avoided as much as possible, and the normal brain tissue should not be damaged. Although the border between the nidus and the normal brain tissue should be ascertained, MRI was considered to be useful in determining these relationships. While it is reasonable to excise the thalamic AVM via the lateral ventricle, it is difficult to manage the feeder at first. Previous feeder clipping was useful in two cases. The trans parietal approach was used in two cases. Even at the dominant hemisphere, neurological deficit associated with this approach did not remain. Monitoring of SEP and using doppler sonography were also useful.

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We measured the flow velocity (FV) of the middle cerebral artery (MCA) using the transcranial Doppler sonography and the diameter of the MCA (R) from the angiography and calculated the blood flow (BF) by FV×πR² in 7 normal persons and 15 AVM patients. FV and BF of the common carotid artery (CCA) were also measured using the QFM-2000XA. FV and BF of MCA increased proportional to the size of the nidus of the AVMs, but BF showed a steeper increase than FV, because of the dilatation of the feeding artery of MCA especially in large AVMs. BF of CCA showed more increase than FV in large AVMs but no or little increase in medium and small AVMs; and the increase of FV and BF of CCA was much less than that of FV and BF of MCA in AVM patients. From the steep increase of BF in large AVMs, normal perfusion pressure breakthrough occurs because of hemodynamic stress as a result of the sudden increase of blood flow of the distal cerebral arteries after excision of the AVM.

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The authors planned a retrospective analysis of the outcome of surgery for large and giant arteriovenous malformations (AVMs), and a clarification of the risk factors affecting the outcome.
Thirty-five cases having AVMs larger than 4 cm in diameter were subjected to the present study. Of this series, 74% had a favorable outcome, but in 26% the result was unfavorable.
The risk factors giving rise to unfavorable outcome were as follows. 1) Giant AVM larger than 6cm in diameter, 2) Poorly demarcated AVM, in other words, diffuse AVM, and 3) AVM fed by deep feeders, such as lenticulostriate artery, thalamoperforating artery, and anterior/posterior choroidal artery. Fifteen out of 17 operations on patients who had no risk factors resulted in a favorable outcome. However, only one out of 6 patients having all of the 3 risk factors had a favorable outcome. These differences were statistically significant (p<0.01).
Six out of 9 patients having severe morbidity and mortality suffered from intraoperative or postoperative intracranial hemorrhage. Massive postoperative hemorrhage, which accounted for most of the unfavorable outcome, was related to a small residual nidus. One half of the postoperative bleeding due to residual AVM occurred within 24 hours after surgery. Therefore, postoperative angiography and emergent excision of the residual nidus must be made immediately after surgery to improve the surgical outcome of large and giant AVMs.

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Surgical problems of large high-flow AVMs were studied based on our own experiences with 5 patients undergoing staged operations. All patients had supratentorial large AVMs of Spetzler's grade IV. Three patients had histories of intracerebral hemorrhage and 2 complained of headache and general seizures. The ages of the patients ranged from 31 to 50 years. All but one patient (Case 4) underwent staged surgical treatment including feeder clipping, embolization or partial excision of the nidus. The AVMs were totally excised in 4 patients (Case 1, 2, 3, 4). Postoperative hemorrhagic complication occurred in 2 patients (Case 4, 5) following one-stage excision of the nidus and clipping of the main feeding vessels, respectively. In these two patients, preoperative angiographical steal was more remarkable and the sum of the diameters of the feeding vessels was larger than those in other patients without postoperative hemorrhage. The feeders were clipped adjacent to the nidus at 45% of the sum of the diameters of all feeding vessels on preoperative angiogram in Case 5. This resulted in severe intracerebral hemorrhage. The feeder clipping near the nidus and obliteration of a large amount of blood flow through feeding vessels thus carries a risk of hemorrhagic complication. Staged operation is preferable for large high-flow AVMs but careful selection of the feeders to be clipped and their sites is quite important to prevent hemorrhagic complication when AVMs have marked preoperative angiographical steal and large feeding vessels.

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Intracranial CBF monitoring was performed by either the laser Doppler or the heat pump method in five patients with intracranial arteriovenous malformations (AVMs). The size of the nidus was classified into two groups; large size (4-6cm·2 cases) and moderate size (2-4cm·3 cases). CBF was measured around the nidus before and after removal of the AVMs; adjacent to the feeding artery, draining vein, and normal cortex. The main feeding artery was temporarily clipped and the dynamic change of CBF was observed.
The CBF values were reduced in all of the large size group and one of the moderate size group in the areas adjacent to the proxymal site of feeding arteries before removal of the AVMs. Those areas were hyperperfused after removal of the AVMs and small hemorrhages occurred in those areas after surgery.
Those facts indicate that hypoperfusion (steal) around AVMs may cause the evolution of NPPB after surgery.

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The treatment of large high flow AVM's is one of the most difficult operations not only because of the operative technique but also due to the postoperative NPPB. Pre and postoperative cerebral blood circulatory changes in 10 cases of large high flow AVM were evaluated by SPECT study, angiography and CT studies. Preoperative SPECT showed a misery perfusion area (decreased CBF, increased CBV) around the nidus in 4 cases.
In these cases a postoperative 1st day dynamic scan showed remarkable hyperperfusion areas around the former nidus. But these hyperperfusion areas normalized 7 days after the operation.
Nidal volume of these 4 cases was over 70 cu cm. Local CBF during operation increased suddenly after application of temporary clips on the main feeders. An angiogram taken one or two weeks after the operation showed remarkable stagnating artery, fragile vessels and prolonged circulation time.
In conclusion, these cases were expected to develop postoperative NPPB. Pre and postoperative SPECT study, especially a postoperative dynamic SPECT study done after the 1st day, was the most useful examination for ascertaining the postoperative NPPB.

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The authors proposed a new technique for excision of a large high flow arteriovenous malformation to prevent normal perfusion pressure breakthrough. Selverstone carotid clamps was applied intra- and postoperatively to regulate cerebral blood flow. This procedure was combined with intraoperative cortical blood flow measurement.
According to the follow-up result of our 106 surgical cases, surgical risks were analized by an angiographical grading. The mechanism of normal perfusion pressure breakthrough was also discussed from our experience and literature. Criteria to apply this technique was also discussed. The authors present a case in which a large, high flow arteriovenous malformation was totally excised using this technique. Preoperative, intraoperative and postoperative cerebral blood flow measurement strongly suggested the usefulness of this technique for the safe excision of a large high-flow arteriovenous malformation.

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Normal perfusion pressure breakthrough phenomenon is a serious complication in surgery for AVMs. In this report, we studied capillary vessels of the brain adjacent to the nidus of arteriovenous malformations. We analyzed surgical specimens of 8 patients with large AVMs with a nidus of more than 4 cm and 10 patients with medium sized AVMs (4>nidus>2cm) histopathologically. The results indicate that the capillary vessels of almost all cases were stained well by the factor VIII related antigen immunohistochemically, no matter how large they were. The capillary vessels in patients with large AVMs could be stained positively with factor VIII related antigen at sites much farther from the nidus than could the vessels in patients with smaller AVMs. One patient developed postoperative intracerebral hemorrhage because of perfusion breakthrough syndrome. In this case, the capillary vessels were stained poorly with factor VIII related antigen, and astrocytes were stained by GFAP around the capillary vessels. Therefore, we must be careful with cases where capillary vessels stain poorly because the capillaries adjacent to the nidus are severely injured by ischemia, which is most probably the cause of breakthrough hemorrhage.

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There has been a common belief that arteriovenous malformation (AVM) has a zone of gliosis between the nidus and the surrounding brain tissue, and that the AVM can be removed at this line without additional neurological deficits. To assess the propriety of this theory, gliosis, axonal changes, and demyelination were examined with immunohistochemical techniques at the brain tissue adjacent to the AVM.
Of 82 histologically verified AVMs, 18 were large AVMs with a diameter of more than 4cm, and 36 were medium-sized AVMs with a diameter of 2 to 4cm. Another 28 were small AVMs, with a diameter of less than 2cm. Formalin of ethanol fixed, paraffin embedded surgical specimens of these AVMs were thin sliced and used for immunohistochemical staining. We used anti-glial fibrillary acidic protein (GFAP) antibody for detection of gliosis, anti-myelin basic protein (MBP) antibody for demyelination and anti-200kD neurofilament antibody for neuronal changes.
In the brain tissue facing the small AVM, no definite changes or reactions were identified. The axons abruptly ended at the wall of the AVM, and these axons were myelinated well as shown by MBP immunostaining. There were no reactive astrocytes detectable by GFAP immunostaining in the brain tissue facing the small AVM. This staining clearly indicated that the brain tissue facing the small AVM was normal. The brain tissue adjacent to the medium-sized AVM had similar properties to those facing the small AVM. The only difference between small and medium-sized AVMs was a few reactive astrocytes detectable in the brain tissue close to the AVM. However, this reaction was mild, and axons and myelin appeared normal. In the large AVMs, however, several reactive changes were observed. The axonal density was reduced in the brain tissue within 500μm from the edge of the AVM.The axons were thick and tortuous in this zone. These axonal changes were observed typically at the brain tissue facing the large draining veins. In some neurons, soma and dendrites were also stained by the anti-NF antibody, which normally stains only axons. The MBP staining was correlated to the NF staining, i. e., demyelination was especially observed at the tissue adjacent to the large draining veins. There was a zone of gliosis in the issue facing the large AVMs. The reactive astrocytes and glial fibers were observed in this zone. However, this zone was not more than 1mm from the edge of the AVM in the non-hemorrhagic cases.
In cases presenting intracerebral hemorrhage, a definite zone of gliosis was observed in the tissue facing the hematoma in even small or medium-sized AVMs. The brain tissue obtained from patients who underwent multi-staged surgery showed a gliotic layer at the surgical site. In those hemorrhagic cases and multi-staged surgical cases, a useful dissecting plane could be present and might be useful in surgery.
In summary, the brain tissue facing the small or medium-sized AVMs was histologically normal, whereas brain tissue facing the large AVMs had a small zone of gliosis. The zone was however, not more than 1mm. Therefore, surgery for AVMs located in functionally important areas must be based on the present data.

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MRI findings of thirteen outpatients with AVMs in the cerebral cortical area who, for various reasons, had undergone on surgical procedures were studied in respect to the relationship between frequency of the convulsive attacks and cerebral cortical findings around the AVM. Regarding the initial symptoms, eight patients were diagnosed as having AVMs with convulsions and five were found to have had subarachnoid hemorrhage. These patients were divided into two groups, that is to say, the frequent group, in which patients had had more than four convulsive attacks during the previous two months, and the rare group, in which patients had had less than two attacks. The former contained seven patients and the latter six. In the group with many convulsive attacks, the deposition of hemosiderin, degenerative changes (edema, gliosis, atrophy and so on) of cerebral cortex around the AVM and adhesions of subarachnoid spaces over the AVM were seen with high frequency especially in the T-2 weighted images. These MRI findings suggest that convulsive attacks in AVM patients are significantly influenced and increased by bleeding from the AVM.

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Using N-isopropyl-I-123-p-iodoamphetamine (IMP) and SPECT with acetazolamide (DIAMOX) activation test, the present study attempts to assess the regional cerebral perfusion and vasodilatory capacity in perifocal tissue of cerebral A-V malformation (AVM). Sixteen patients with cerebral AVM were studied, 10 males and 6 females, having an average age of 32. The AVM-nidus were mainly fed by cortical arteries. The angiographic diameter of AVM-nidus was classified as follows: less than 2 cm in 1 case, 2 to 2.5 cm in 6, 2.5 to 3 cm in 5, and 4.0 to 5 cm in 4. Their clinical features were divided as follows; 5 cases of hemorrhagic type (3 with a nidus of 2.0-2.5 cm in diameter, 2 with 3.0-3.5 cm), 9 cases of epileptic type and 2 cases of asymptomatic type. Regional cerebral perfusion in the perifocal area was assessed by the resting IMP SPECT in 13 patients and cerebral vasodilatory capacity was assessed by the DIAMOX-activated IMP SPECT in 12 patients.
Perifocal hypoperfusion areas were observed in 11 patients but were absent in 2 cases (one with a nidus of less than 2 cm in diameter, the other with 2 cm). The incidence of the perifocal hypoperfusion was as follows: 80% in AVM nidus of 2.0 to 2.5 cm in diameter, 100% in AVM nidus of more than 3cm. The limitation of cerebral vasodilatory capacity in perifocal tissue was observed in 7 patients (1 with a nidus of 2 cm in diameter, 3 with 3.0-3.5cm, 3 with 4.0-5.0cm). In 6 of these 7 patients, a past history of seizure attack was noted. The incidence of the limitation of perifocal vasodilatory capacity was as follows: 25% in AVM nidus of 2.0-2.5cm in diameter, 60% in AVM nidus of 3.0-3.5cm, 100% in AVM nidus of 4.0-5.0cm. Preoperative limitation of cerebral vasodilatory capacity in perifocal tissue was reversed by total removal of the AVM in 2 patients. It seems likely that the perifocal hypoperfusion area is caused by both the deactivation of perifocal tissue and intracerebral steal, because the perifocal hypoperfusion is not necessarily associated with the limitation of cerebral vasodilatory capacity. The limitation of cerebral vasodilatory capacity is probably caused by reduction of cerebral perfusion pressure due to intracerebral steal, because it is more apparent in patients with larger AVMs, and can be reversed by total removal of the AVM. Assessment of vascular reactivity in perifocal tissue of cerebral AVMs using ¹²³I-IMP SPECT activated by DIAMOX, might be a useful tool for the management of cerebral AVMs.

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Cerebral hemodynamics and metabolism of six men (mean age: 51 years) with arteriovenous malformation (AVM) of the brain were studied using the 150-labelled gas steady state method and positron emission tomography (PET). The AVMs were identified by X-ray CT and angiography as five non-hemorrhagic (retrosylvian-Rolandic, frontal, cerebellar regions on the right, and occipital dural, frontal ones on the left) and one hemorrhagic (right occipital). The duration from the onset or the last episode to the study was 22 days to three years. Neurologic abnormalities at the time of the study were found in two of patients; one with horizontal nystagmus and the other with light sensory aphasia (dysphasia).
The affected hemisphere was covered with tortuous enraged vessels in one patient with a large frontal AVM and could hardly be evaluated quantitatively due to the partial volume effect. Expect for this case, values were acceptable when the regions of interest (ROIs) were placed properly so as not to cover the component of the AVM.
The CBF and cerebral oxygen metabolism (CMRO₂) of the whole brain was decreased in the patient with a hematoma in spite of having no neurologic deterioration. The patient with dysphasia presented low CBF and CMRO₂ with increased cerebral blood volume (CBV) on the affected side.
In every case, the flow and oxygen metabolism was decreased in various degrees in the distant area with the same arterial supply and/or venous drainages as the AVM (“non-Nidus”), and the surrounding part of the nidus (“peri-Nidus”).
While cerebral blood volume (CBV) increased significantly, uncoupling between flow and metabolism could not be observed in those parts.
Vasoactivities to changes of PaCO₂ and blood pressure were further studied in one case using the H₂¹⁵O bolus injection method. In regions adjacent to the nidus (peri-Nidus), CO₂-reactivities were good to the hypercapnia, while less to hypocapnia. On the other hand, opposite corelations were documented at the distant area (non-Nidus). Autoregulation indices were all below 0.3%, which are considered to be well reserved autoregulatory changes.
Our results suggest that AVMs can bring hemodynamic and metabolic chages not only to the neighboring structures, but also their distant areas with the same vascular supply and/or drainage.

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In 10 cases of supratentorial AVM, hemodynamic characteristics of the cerebral circulation in the nidus itself, adjacent brain tissue, and on the area distant from the nidus were evaluated with HEADTOME SET-031 SPECT. The following results were obtained:
1. In 5 cases of high flow type AVM with a maximal nidus diameter over 3.7 cm, the steal phenomenon was detected by SPECT using IMP and ¹³³Xe.
2. The use of IMP for SPECT allowed the best visualization of the nidus, while the lesion observed with PAO-SPECT was narrower and poorly demarcated.
3.¹³³Xe was not suitable for visualization of lesions, although it was useful in detecting steal phenomenon in the remote region if Diamox was administered for CO₂ loading.
4. In one case of large AVM, excessive reaction to Diamox was observed, extending from the affected hemisphere to the opposite hemisphere. This reaction was improved by surgical embolization.

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Evaluation of preoperative hemodynamics and vascular reactivity of arteriovenous malformations supplying arteries (feeders), namely the middle Cerebral artery and dilated cerebral basal arteries such as the anterior choroidal artery and perforating arteries, was performed using transcranial Doppler ultrasound. Twenty normal subjects and 10 patients with angiographically proven cerebral arteriovenous malformations (AVM) were studied. Time mean velocity (Vm), peak systolic velocity (Vs) and end diastolic velosity (Vd) were measured by transcranial Doppler ultrasound (TC2-64, EME Co.) at bitemporal portions. The pulsatility index [PI=(S-D)/M] and the Resistance index [R=(S-D)/S] were calculated. To see pCO₂ reactivity, hyperventilation was done (deep breath: twice/5 sec. for 30 sec.). In patients with AVMs, blood velocity of feeders increased remarkably up to 150cm/sec (Vm) and 190 cm/sec (Vs) individually, which were more than two times the velocities measured for normal subjects. Both PI and R decreased significantly. Reactivity against hypocapnia also showed significant decrease. V(D) (velocity at sick side)/V(N) (velocity at normal side), Vd/Vs revealed that hemodynamic changes more clearly. These changes seemed to be more remarkable in patients with high blood flow velocity. According to the relationship between the artery and the nidus, cases were divided into three groups, namely mainly (Group A), partially (Group B) and poorly (Group C) angioma supplying arteries. These hemodynamic changes were remarkable in Group A. Postoperatively, these changes, including pCO₂ reactivity, recovered to the normal range.
Moreover, wave forms were analysed by FFT analyser (FAE 2000, Kikusui Elect. Comp.) in 40 normal subjects and in 5 patients with AVMs. Analysis of the wave forms revealed characteristic findings in all of the patients, namely disappearance of the groove which is commonly seen at 3 to 7 KHz range in normal adults. These wave forms resembled those of a child.
As a conclusion, characteristic changes were recognized in hemodynamics and pCO₂ reactivity of feeders, especially on mainly angioma supplying arteries. In such cases, care should be taken to guard against the normal perfusion pressure breakthrough phenomenon during surgery. Analysis of the wave forms of patients revealed characteristic changes; thus such analysis seems useful for diagnosis and analysis of the hemodynamics of AVMs.

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Long-term follow-up results were analysed in 29 cases of spontaneous carotid-cavernous fistulas. All were low flow type of spontaneous carotid-cavernous fistulas, and were treated with conservative therapy.
A complete regression of symptoms was noted in 25 cases, and a moderate regression in 4 cases. The regression of symptoms was usually delayed in patients less than 59 years old, and in cases with multiple draining veins.
Conjunctival injection was usually recognized within one month after the onset and disappeared more than one year later. Diplopia and blepharoptosis were usually recognized within one month after the onset and disappeared in 6-12 months. Exophthalmos and tinnitus were usually recognized within one year after the onset and disappeared within one year. Visual disturbance was usually recognized more than one year after the onset and disappeared within one year after the appearance.
From these results, it is seen that spontaneous carotid-cavernous fistulas show a very high incidence of spontaneous regression of symptoms, and conservative treatment is initially recommended.

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Three cases of dural arteriovenous malformation (AVM) in the cavernous region were treated by a direct surgical approach. Dural AVMs in these areas are supplied by meningeal branches of both the internal and external carotid arteries. Cavernous sinuses were incised at the lateral wall and packed with oxidized cellulose and EDH adhesive. Hypotension, hypothermia, and temporary clipping of the cervical ICA, were not required during surgery. In one patient packing was not complete, but symptoms improved after 6 months. In the other two cases, dural AVMs were occluded completely; and patency of the internal carotid artery was preserved in all cases.

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We treated 12 cases of carotid cavernous sinus fistula (CCF) by copper wire insertion into the cavernous sinus through a frontotemporal craniotomy. Five or six copper wires (0.5 mm thick and 10 mm long) were inserted into the Parkinson's Triangle through a 19 gauge spinal tap needle used as a guide needle under microscopical control. The closure of the fistula was verified in 11 cases by postoperative angiography. In one case, the CCF was partially closed. Postoperative intracerebral hematoma in one case and insertion of the wire into the pons in one case were observed. The third or sixth cranial nerve palsy temporarily worsened in 5 cases. But all patients showed full recovery from these complications. The surgical results in these 12 cases suggest that intracavernous thrombosis by copper wire insertion may prove to be the treatment of choice in CCF.

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Six cases of spontaneous carotid-cavernous fistulas of the dural arteriovenous malformation type were treated with the transvenous approach via the inferior petrosal sinus. Copper coils were mainly used as the embolic agent, but in two cases platinum coils were also tried. Catheterization through the inferior petrosal sinus into the cavernous sinus was successful in all cases, including a case in which the sinus was not opacified by the angiogram.
Immediate disappearance of fistulas was angiographically demonstrated in all cases. Bruit and exophthalmos disappeared immediately. Temporal aggravation of chemosis was observed in three cases after the embolization but disappeared within two weeks. Visual symptoms caused by the cranial nerve paresis gradually improved. No severe complications were observed, but pains around the retro-orbital and the fronto-temporal region were aggravated in all, which were controllable with medications and disappeared within 2 weeks. No recurrence was observed during an average follow-up period of 10.3 months. This method is considered to be a promising treatment for spontaneous carotid-cavernous fistulas of the dural arteriovenous malformation type.

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Experiences with transvenous embolization for 22 cases of cavernous dural arteriovenous shunts are reported. All cases showed clinical symptoms related to their abnormal AV shunts. Among 25 sides of AV shunts, 3 cases showed bilateral AV shunts, 9 sides presented with bilateral external carotid (EC) and bilateral internal carotid (IC) arterial supply, 9 sides were fed by unilateral EC and unilateral IC arterial supply, 4 sides were fed by bilateral EC and unilateral IC supply, 2 sides showed unilateral EC and 1 side was supplied by unilateral IC. Anterior venous drainage was prominent in 16 sides which were treated by superior ophthalmic vein approach. Posterior drainage was prominent in other instances those were embolized via inferior petrosal vein approach. All procedures were carried out under local anesthesia using DSA monitoring. Copper wires were mainly used as embolic materials, while platinum coils and/or silk sutures served as adjunctive materials. Angiographical complete cure was achieved in 12 sides (48%) immediately, and in 19 sides (76%) at follow up ranging from 1 to 20 months after the embolization. Clinical symptoms were cleared or significantly reduced in all cases. Transarterial embolization, radiation or carotid compression therapy were required in one case each. Repeated transvenous embolization was performed in one case. Transient cavernous sinus syndrome were noted in 5 cases, posterior ischemic optic neuropathy due to diabetes mellitus, cerebral embolism after transarterial embolization were observed in one case each.
With modern technologies in mini-catheters and embolic materials, transvenous embolization should be considered as one of the most definite and safest method for the closure of cavernous dural arteriovenous shunts.

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In this paper, we reported that a carotid-cavernous fistulae (CCF) and a dural arteriovenous malformation (dAVM) were treated by intravascular surgery via the intra-arterial and transvenous routes.
Case 1 A 2-month-old male presented exophthalmos and chemosis of the right eye, and bruit was detected. Ophthalmological findings included proptosis, conjuntival hyperemia, and pulsating exophalmos of the right eye.
Selective external carotid angiography revealed a high flow CCF supplied by an enlarged middle meningeal artery. Drainage from the cavernous sinus to the internal jugular vein was via a distended superior petrosal sinus.
We performed intra-arterial embolization (platinum spring coil ad 4-0 silk thread were used as embolic agents). The symptoms disappeared without complication.
Case 2 A 74-year-old female presented proptosis of the left eye and palsy of the left fourth and sixth cranial nerves.
Bilateral carotid angiography revealed a low flow dAVM in the bilateral cavernous sinuses (CS) supplied by each menigohypophyseal trunk. Drainage from the cavernous sinuses was via the inferior petrosal sinuses (IPS). To facilitate transvenous placement of emboli, catheters were placed in each paired IPS and paired CS via the femoral vein.
Emboli were positioned in each paired CS. The embolic agents used were platinum spring coil and 4-0 silk thread. The neurological deficits disappeared after the operation.
We believe that a high flow external carotid cavernous fistula (Case 1) can be corrected by the intra-arterial route, and also that transvenous embolization of dAVM (Case 2) can be performed safely and with certainty to reduce the risk of arterial embolization.

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