Biomedical subjects
Publications and source records attributed to K TerBrugge.
Isolated dissecting aneurysms of the posterior cerebral artery are not as rare as previously reported. Affecting primarily a younger population, this condition can be recognized by angiographic patterns, the most common being a "pearl and string" morphology. We reviewed the literature and present a series of six cases, discussing management strategies.
BACKGROUND: Bilateral carotid cavernous fistulas may complicate head injury. Spontaneous resolution of post-traumatic direct carotid cavernous fistula is rare. CASE DESCRIPTION We present a case of a 42-year-old female who developed post-traumatic high flow bilateral carotid cavernous fistulas with cortical and deep venous drainage, who had a spontaneous resolution with thrombosis of the cavernous sinus outlets bilaterally and development of a trans-sellar intercarotid vascular communication. To our knowledge this is the first reported case in the literature describing such a phenomenon. CONCLUSION Bilateral direct carotid cavernous fistulas may undergo spontaneous resolution and form a benign trans-sellar intercarotid vascular communication.
OBJECT: To describe the clinical and angiographic results of endovascular occlusion of basilar bifurcation aneurysms with electrolytically detachable coils, and to identify factors which should be considered in deciding upon surgical or endovascular treatment. METHODS: We report our experience with 40 patients in whom occlusion of basilar bifurcation aneurysms with electrolytically detachable coils was attempted. All patients underwent superselective angiography and attempted embolization with Guglielmi detachable coils (GDCs). Angiographic and clinical results were prospectively recorded. Twenty-eight aneurysms presented with subarachnoid hemorrhage (SAH), 2 were symptomatic and 10 were incidental. RESULTS: Coils were not placed in 10 patients (25%) because of unfavorable anatomy. Complete aneurysm occlusion was achieved at the time of the initial procedure in 13 (32.5%), small neck remnants were present in 13 (32.5%), and in 4 (10.0%) there was obvious residual contrast filling of the aneurysm body. Of 23 patients successfully coiled after SAH, 20 were Grade 1 to 3 and 3 were grade 4 or 5 at the time of treatment. Eighteen (78%) made a good recovery. Procedural mortality was 2.5% and permanent morbidity was 7.5%. There were no permanent complications in patients with unruptured aneurysms. Complete aneurysm occlusion was possible in 10 (56%) of 18 aneurysms with small necks and 3 (14%) of 22 with large necks. Follow-up angiography in 25 of 28 surviving patients (mean, 12 months) demonstrated stability of all completely occluded aneurysms. Incompletely coiled aneurysms had variable results on follow-up angiograms: 15.4% improved, 69.2% worsened, and 15.4% were stable. No aneurysm bled after treatment during clinical follow-up averaging 22 months. CONCLUSIONS: Endovascular treatment of basilar bifurcation aneurysms appears to prevent early aneurysm rebleeding with acceptable rates of morbidity and mortality, but long-term follow-up is required.
OBJECTIVE AND IMPORTANCE: Vertebrobasilar dissecting aneurysms are an uncommon but increasingly recognized cause of subarachnoid hemorrhage (SAH). We describe a patient with SAH caused by a dissecting aneurysm involving both vertebral arteries as well as the basilar trunk. The patient was treated successfully with proximal occlusion of the vertebral arteries using endovascular balloon occlusion in two stages. The importance of early follow-up angiography to document progression or resolution of untreated dissections is emphasized. This approach is suggested as definitive treatment for vertebrobasilar dissection in appropriate circumstances. CLINICAL PRESENTATION: A 41-year-old man presented with SAH from spontaneous vertebrobasilar dissection. Angiography revealed aneurysmal dilation of the right vertebral artery and basilar trunk and occlusion of the left vertebral artery. INTERVENTION: The dissecting aneurysm was treated with balloon occlusion of the right vertebral artery. Repeat angiography 2 weeks later demonstrated resolution of the left vertebral occlusion, with restoration of antegrade flow in the basilar trunk and increased filling of the right vertebral and basilar dissecting aneurysms. Balloon occlusion of the left vertebral artery led to aneurysm thrombosis and excellent clinical outcome. CONCLUSION: Bilateral vertebrobasilar dissecting aneurysms are an uncommon cause of SAH. If unilateral proximal vertebral artery occlusion is chosen as the initial treatment, it is essential to document the status of the contralateral vessel using follow-up angiography. Staged bilateral vertebral artery occlusion should be considered in the event of recurrent or progressive aneurysm enlargement. Endovascular balloon occlusion has advantages over proximal clipping of the parent vessel: cranial nerve manipulation is avoided, test occlusion in the awake patient can be performed at the site of permanent occlusion, and therapeutic levels of anticoagulation can be maintained throughout and after the procedure, thus diminishing the likelihood of thromboembolic complications.
OBJECT: The goal of this study was to develop a classification system for aneurysms associated with arteriovenous malformations (AVMs) based on their anatomical and pathophysiological relationships and to determine the incidence and bleeding rates for these aneurysms as well as the effects of AVM treatment on their natural history. METHODS: Of 632 patients with AVMs, intranidal aneurysms were found in 35 (5.5%) and flow-related aneurysms in 71 (11.2%). Patients with intranidal aneurysms presented more frequently with hemorrhage (72% compared with 40%, p < 0.001) and had a 9.8% per year risk rate of bleeding during follow-up review. Twelve (17%) of the patients with flow-related aneurysms associated with an AVM presented with hemorrhage from an aneurysm, whereas 15 (21%) bled from their AVM. Seventeen patients underwent angiography after AVM treatment (mean 2.25 years). Of 23 proximal aneurysms, 18 (78.3%) were unchanged, four (17.4%) were smaller, and one (4.3%) had disappeared, whereas four (80%) of five distal aneurysms regressed completely and one was unchanged. Sixteen patients underwent angiography after partial AVM treatment (mean 3.8 years). In cases with less than a 50% reduction in the AVM, no aneurysms regressed, although two enlarged and bled. In cases with greater than a 50% reduction in the AVM, two of three distal aneurysms disappeared and five proximal aneurysms were unchanged. CONCLUSIONS: Arterial aneurysms associated with cerebral AVMs may be classified as intranidal, flow-related, or unrelated to the AVM nidus. Intranidal aneurysms have a high correlation with hemorrhagic clinical presentation and a risk of bleeding during the follow-up period that considerably exceeds that which would be expected in their absence. Patients with flow-related aneurysms in association with an AVM may present with hemorrhage from either lesion. Aneurysms that arise on distal feeding arteries near the nidus have a high probability of regressing with substantial or curative AVM therapy.
A number of classification schemes for intracranial dural arteriovenous fistulas (AVFs) have been published that claim to predict which lesions will present in a benign or aggressive fashion based on radiological anatomy. We have tested the validity of two proposed classification schemes for the first time in a large single-institution study. A series of 102 intracranial dural AVFs in 98 patients assessed at a single institution was analyzed. All patients were classified according to two grading scales: the more descriptive schema of Cognard, et al. (Cognard) and that recently proposed by Borden, et al. (Borden). According to the Borden classification, 55 patients were Type I, 18 Type II, and 29 Type III. Using the Cognard classification, 40 patients were Type I, 15 Type IIA, eight Type IIB, 10 Type IIA+B, 13 Type III, 12 Type IV, and four Type V. Intracranial hemorrhage (ICH) or nonhemorrhagic neurological deficit was considered an aggressive presenting clinical feature. A total of 16 (16%) of 102 intracranial dural AVFs presented with hemorrhage. Eleven of these hemorrhages (69%) occurred in either anterior cranial fossa or tentorial lesions. When analyzed according to the Borden classification, none (0%) of 55 Type I intracranial dural AVFs, two (11%) of 18 Type II, and 14 (48%) of 29 Type III intracranial dural AVFs presented with hemorrhage (p < 0.0001). After exclusion of visual or cranial nerve deficits that were clearly related to cavernous sinus intracranial dural AVFs, nonhemorrhagic neurological deficits were a feature of presentation in one (2%) of 55 Type I, five (28%) of 18 Type II, and nine (31%) of 29 Type III patients (p < 0.0001). When combined, an aggressive clinical presentation (ICH or nonhemorrhagic neurological deficit) was seen most commonly in intracranial dural AVFs located in the tentorium (11 (79%) of 14) and the anterior cranial fossa (three (75%) of four), but this simply reflected the number of higher grade lesions in these locations. Aggressive clinical presentation strongly correlated with Borden types: one (2%) of 55 Type I, seven (39%) of 18 Type II, and 23 (79%) of 29 Type III patients (p < 0.0001). A similar correlation with aggressive presentation was seen with the Cognard classification: none (0%) of 40 Type I, one (7%) of 15 Type IIA, three (38%) of eight Type IIB, four (40%) of 10 Type IIA+B, nine (69%) of 13 Type III, 10 (83%) of 12 Type IV, and four (100%) of four Type V (p < 0.0001). No location is immune from harboring lesions capable of an aggressive presentation. Location itself only raises the index of suspicion for dangerous venous anatomy in some intracranial dural AVFs. The configuration of venous anatomy as reflected by both the Cognard and Borden classifications strongly predicts intracranial dural AVFs that will present with ICH or nonhemorrhagic neurological deficit.
We reviewed the clinical and radiological features of ten patients with small arteriovenous malformations that caused intracerebral hematomas. In six patients, angiography showed a small nidus (less than 1 cm in diameter) with a shunt at the site of the hematoma, and in four only an early-filling vein was evident. Six patients had only delayed angiography (4 weeks or more after the ictus). In three, angiography within 2 days of the ictus failed to reveal the cause of the bleed, but repeat angiography showed an early-filling vein in two, and a nidus with shunting in one. In only one patient did early angiography reveal the malformation. MRI was obtained in eight patients, and in two prominent vessels were evident in the wall of the hematoma cavity. In investigation of an unexplained intracerebral hematoma, MRI may be useful to exclude a neoplasm or cavernoma, although the latter may be not be evident in the presence of a recent hematoma. We suggest early MRI and angiography for investigation of an unexplained, nonhypertensive intracerebral bleed, with follow-up MRI and delayed angiography if the initial studies fail to reveal the cause.
Large hemangioblastomas can be difficult to resect because of excessive bleeding. We report our experience with two patients whose large hemangioblastomas were embolized preoperatively and were totally resected with minimal blood loss and satisfactory postoperative outcome. Embolizations were carried out within 3 days of surgery, with the patient under general anesthesia, with 150- to 250-microns Contour emboli. A 65-year-old woman with progressive, severe myelopathy from a 4.5 x 2.1 x 1.4 cm intramedullary hemangioblastoma at T4 underwent embolization of the left T2 and T3 intercostal arteries; a 29-year-old man with Lindau's syndrome and posterior fossa hemorrhage from a 3.8 x 1.8 x 1.8 cm right cerebellar hemangioblastoma underwent embolization of the right posterior inferior cerebellar artery, two right anterior inferior cerebellar arteries, and a dural branch of the right vertebral artery. Embolization led to the complete obliteration of the tumoral blush without neurological sequelae. Both lesions were completely resected with a blood loss of 50 to 100 ml, with bleeding occurring mainly from the pseudocapsule of the lesion. Preoperative embolization of hemangioblastomas is a useful and relatively safe procedure that reduces blood loss at the time of surgery and allows complete resection.
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The authors present two patients who had dissecting aneurysms of the petrocavernous segment of the internal carotid artery. They successfully treated the condition with balloon embolization of the artery proximal to the aneurysm.
The authors reviewed four patients with dural arteriovenous malformations in the upper spinal axis. Two were at the foramen magnum and two were lower cervical. The patients presented with subarachnoid hemorrhage, a slowly progressive cervical myelopathy, a rapidly progressive thoracic myelopathy, and tinnitus with a sixth nerve palsy. This report emphasizes the importance of studying both the intracranial dural vessels as well as the supply to the cervical spine in searching for a spinal arteriovenous malformation. Subarachnoid hemorrhage with negative cerebral angiography requires spinal angiography if there are any signs or symptoms suggesting cord or nerve root dysfunction. Embolization by an endovascular approach resulted in an angiographic cure in two patients. A combination of embolization and surgery resulted in obliteration of the arteriovenous malformation in one patient. Embolization achieved a clinical cure in one patient, and clinical improvement in two patients.
The common vascular anomalies of cerebral aneurysm and arteriovenous malformation may exist independently, or together as part of a closely related hemodynamic pairing. Resection or embolization of an AVM may be followed by a decrease in local blood flow, and lead to regression of a suitably situated proximal aneurysm. However, aneurysms located outside the angioarchitecture of the AVM, which remain flow-unrelated to the malformation, will likely not regress, and may in fact enlarge. Two cases are presented which demonstrate these vascular relationships, in order to better understand the regional hemodynamics of these anomalies prior to surgical or endovascular treatment planning.
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The authors report an adult patient with a symptomatic interhemispheric cyst demonstrated by computerized tomography (CT), angiography, and at surgery. Choroid plexus epithelium was identified arising from the inner aspect of the cyst wall. Partial agenesis of the corpus callosum is postulated on the basis of the CT findings and the presence of choroid plexus in the interhemispheric cyst.
PURPOSE: We assessed the usefulness of superselective angiography in patients with micro-arteriovenous malformations. PATIENTS AND METHODS: Five patients had superselective angiography for either diagnosis or treatment of brain arteriovenous malformations having a nidus of less than 1 cm. All patients presented with an intracerebral hematoma. RESULTS: In one patient superselective angiography confirmed the presence of a shunt that was suspected due to visualization of an early vein on the follow-up angiogram; in another patient superselective angiography was helpful in defining the topography of the malformation; in the remaining three patients, superselective angiography was used for embolization of the malformation. We were unsuccessful in achieving a complete angiographic cure in these 3; however, superselective angiography revealed an aneurysm in one that was obliterated by the liquid adhesive embolic agent. CONCLUSION: With the recent advances in microcatheters, superselective angiography has a promising role in defining the topography and angioarchitecture of micro-arteriovenous malformations. Micro-arteriovenous malformations may not be angiographically evident at the time of initial hemorrhage due to the hematoma. With future technical advances it may be possible to completely obliterate these malformations by embolization alone.
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