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1/92. adenosine-induced cardiac pause for endovascular embolization of cerebral arteriovenous malformations: technical case report.

    OBJECTIVE: Extremely high flow through arteriovenous malformations (AVMs) may limit the safety and effectiveness of endovascular glue therapy. To achieve a more controlled deposition of glue, we used transient but profound systemic hypotension afforded by an intravenously administered bolus of adenosine to induce rapidly reversible high-degree atrioventricular block. methods AND CASE REPORT: A patient with a large high-flow occipital AVM fed primarily by the posterior cerebral artery underwent n-butyl cyanoacrylate glue embolization. nitroprusside-induced systemic hypotension did not adequately reduce flow through the nidus, as determined by contrast injection in the feeding artery. In a dose-escalation fashion, boluses of adenosine were administered to optimize the dose and verify that there was no flow reversal in the AVM and no other unexpected hemodynamic abnormalities by arterial pressure measurements and transcranial Doppler monitoring of the posterior cerebral artery feeding the AVM. Thereafter, 64 mg of adenosine was rapidly injected as a bolus to provide 10 to 15 seconds of systemic hypotension (approximately 20 mm Hg). Although there were conducted beats and some residual forward flow through the AVM during this time, the mean systemic and feeding artery pressures were roughly similar and remained relatively constant. A slow controlled injection of n-butyl cyanoacrylate glue was then performed, with excellent filling of the nidus. CONCLUSION: adenosine-induced cardiac pause may be a viable method of partial flow arrest in the treatment of cerebral AVMs. Safe, deep, and complete embolization with a permanent agent may increase the likelihood of endovascular therapy's being curative or may further improve the safety of microsurgical resection.
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2/92. Stereotactic radiosurgery. VIII. The classification of postradiation reactions.

    Postradiation reactions in the CNS are well described and catalogued in the conventional radiotherapy literature; acute, subacute and late CNS reactions are recognized. Tumours predispose to these normal tissue reactions by the oedema and pressure epiphenomena that occur in their environs, and probably by other mechanisms associated with tissue breakdown. That late normal tissue reactions (particularly permanent late sequelae--universally referred to as 'necrosis') occur in the normal nervous system is in the complication list of every radiosurgery centre. This article, for the first time, places postradiosurgery observations within or without the existing classification of reactions, and draws attention to the fact that previous 'radiosurgery risk factor' papers in the literature may be wrong to pool different 'reactions' in the formulation of risk formulae for normal brain damage following single shot radiotherapy. Acute reactions occur in the same manner as described for conventional radiotherapy, being a transient swelling phenomenon that occurs 12-48 h after therapy; they are fully reversible and do not usually augur late problems; routine administration of short duration steroids around the time of radiosurgery may prevent or delay the clinical signs. Subacute reactions occur 3-10 months later (a later time than the subacute reactions following conventionally fractionated radiotherapy), and may prove fully or partially reversible, or progress to permanent sequelae; the difference between these and late sequelae (which tend to be permanent themselves) then becomes blurred. That tumour swelling occurs in the subacute phase and is associated with oedema in the surrounding normal brain is an interesting observation (occurring in extra- and intra axial slow-growing tumours); it denotes tumour damage and has not been encountered in the conventionally-fractionated radiotherapy literature. Tumour shrinkage occurs later, with subsidence of the surrounding oedema, and this phenomenon may therefore be regarded (paradoxically) as a good prognostic sign, a point about which the referring clinician should be made aware. Similarly, contrast enhancement in the tumour perimeter at this time reflects a host reactive response and not tumour activity. Persistent clinical neurological signs and MRI changes (best seen on the T2 weighted sequences) beyond 2 years, indicate late damage or reaction. Usually, this represents scarring or coagulative necrosis without mass effect, but if there is a low signal area with mass effect and considerable surrounding oedema, liquefactive necrosis has occurred and (as in the brachytherapy literature) surgical decompression is very occasionally needed.
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3/92. Combination of intraoperative embolisation with surgical resection for treatment of giant cerebral arteriovenous malformations.

    Objective: To reduce the risk of surgical resection of giant arteriovenous malformation (AVM) and prevent normal perfusion pressure breakthrough (NPPB) and thus to lower postoperative mortality.methods: During the operation, which was carried out under general anaesthesia, the proximal ends of the feeding arteries were first ligated and 0.5 ml IBCA mixed with 0.5 ml of 5% glucose was injected into the vessels towards the AVM, then the malformed vessels were totally resected. Postoperative digital subtraction angiography (DSA) of the four vessels was performed in all patients.Results: Fifty patients with giant AVMs survived after operation, only 6 (12.0%) had transient neurological dysfunction and 44 (88.0%) recovered after a follow-up of 6-36 months. No patient suffered from NPPB.Conclusions: The embolisation could block the arteriovenous shunts sufficiently to decrease the blood flow away from the normal areas of the brain so as to prevent the incidence of intra- and post-operative rebleeding, especially in NPPB. Therefore, the combination of intraoperative embolisation with surgical resection is an effective strategy in the treatment of giant cerebral AVMs, which makes it possible to operate on patients who used to be regarded as inoperable cases.
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4/92. Haemorrhagic complication after total extirpation of huge arteriovenous malformations.

    Two cases with huge arteriovenous malformations (AVMs) who developed haemorrhagic complications after surgery are described. The cause of the postoperative haemorrhage was considered to be the normal perfusion pressure breakthrough phenomenon and/or occlusive hyperaemia. These two haemodynamic insults possibly occur simultaneously and induce life-threatening haemorrhage. It was concluded that a huge high-flow AVM with a large venous ampulla in its deep drainers has a high risk of a postoperative intravenous thrombosis, resulting in haemorrhage together with normal perfusion pressure breakthrough phenomenon.
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5/92. Surgical resection of cerebral arteriovenous malformation combined with pre-operative embolisation.

    To assess the importance of pre-operative embolisation, 27 cases of cerebral artriovenous malformation (AVM) treated in this institute between July 1994 and October 1998 were analysed. The patients' ages ranged from 3 to 70 years (average 36.9) with a follow-up period of 1-41 months (average 19.2). The patient presented with haemorrhage in 21 cases and seizure in five. In 21 of 27 cases, surgical resection of a nidus was performed, gamma knife therapy was applied in three and conservative therapy was chosen in three. Of 21 cases treated surgically, total removal was achieved in 19 cases and a residual nidus was seen in one (a large basal ganglia AVM). In the remaining case, postoperative angiography was not available. Pre-operative embolisation followed by surgical resection of the nidus was performed in seven cases in which there was a large AVM. A volume index was calculated to indicate the size of the nidus using X x Y x Z, where X is the maximum diameter (cm) of the nidus on the lateral angiogram, Y is the diameter (cm) perpendicular to X and Z is the maximum diameter (cm) on the anteroposter or angiogram. The index averaged 45.9 for the cases in which pre-operative embolisation was performed, while it was 5.6 in the cases without embolisation. Pre-operative embolisation was performed to reduce the nidus flow as much as possible, to prevent overload to the surrounding structures. At surgery, the nidus was resected from the surrounding tissue and care was taken not to enter the nidus. Postoperatively, the systolic blood pressure was maintained at 90-100 mmHg for several days in the intensive care unit. The results were excellent in 15 cases, good in three (hemiparesis due to the initial haemorrhage remained in all three), fair in one (a patient with a severe subarachnoid haemorrhage). Two patients died (acute pulmonary oedema and severe meningitis). Minor postoperative bleeding or oozing was seen in three cases. In conclusion, reducing the shunt flow through a nidus in a step-wise fashion with pre-operative embolisation of a large AVM seems to be quite helpful in preventing postoperative haemodynamic overload to the surrounding brain. It is also important not to enter the nidus when it is removed at surgery. This helps to prevent intraoperative and/or postoperative bleeding, and led to successful total removal of the nidus with a good postoperative course.
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6/92. Unilateral proptosis and chemosis caused by dural arteriovenous malformation of the superior sagittal sinus.

    We describe a patient with unilateral proptosis and chemosis resulting from a dural arteriovenous malformation (AVM) of the superior sagittal sinus (SSS) fed mainly by branches of both external carotid arteries. The symptoms may have been caused by increased SSS pressure and disturbance of venous flow by the dural AVM.
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7/92. Headaches and papilledema secondary to dural arteriovenous malformation.

    A 21-year-old developed progressive headaches and pulsatile tinnitus. He was found to have papilledema and a pulsatile bruit. A dural arteriovenous malformation was not recognized on brain CT or MRI, but was well documented on magnetic resonance angiography and cerebral angiography. Dural malformations draining into the superior sagittal sinus can cause increased intracranial venous pressure and secondarily increase intracranial pressure even without a mass effect.
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8/92. Dural arteriovenous malformation associated with recurrent subdural haematoma and intracranial hypertension.

    An unusual case of intracranial hypertension and symptoms of a left parieto-occipital mass lesion due to a dural arteriovenous malformation (AVM) with a large and dilated draining vein is reported. The patient also had a history of homolateral recurrent subdural haematoma, 11 years before. Subdural haematoma is rarely associated to a dural AVM. We suggest that the recurrent subdural haematoma was due to the very slow and intermittent venous bleeding from the preexisting dural malformation, which progressively enlarged in the following years to become very large. The symptoms of intracranial hypertension and papilloedema may be explained by the increased pressure in the dural sinus and the cerebral venous system. On the other hand, focal neurological symptoms in our case resulted from the mass effect due to an aneurysmally dilated draining vein in the left parieto-occipital region.
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9/92. Bilateral sixth-nerve palsy associated with dural arteriovenous malformation.

    A fifty-two year old postmenopausal woman was admitted to the hospital with complaints of diplopia, headache, humming over the head, and pain over the left eye. Neurological examination showed right abducens nerve palsy. In a few days, she also developed left abducens nerve palsy and chemosis, exophthalmos, and proptosis of both eyes. There was pulsation over the left eye. intraocular pressure was found to be elevated bilaterally. Selective carotid angiograms showed the presence of bilateral dural arteriovenous malformations (AVM) supplied by the external carotid arteries. Two months after the embolisation of the AVMs, eye movements improved. Repeat angiograms showed the absence of flow into the previously embolised AVMs.
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10/92. Combination of intraoperative embolization with surgical resection for treatment of giant cerebral arteriovenous malformation.

    OBJECTIVE: To reduce the risk of surgical resection of giant arteriovenous malformation (AVM) (> 6.0 cm) and prevent normal perfusion pressure breakthrough (NPPB) for lowering the postoperative mortality. methods: During the operation under barbiturate anesthesia, the proximal end of the feeding arteries were ligated at first, and 0.5 ml isobutyl 12-cyanoacrylate (IBCA) with 0.5 ml 5% glucose was injected into the vessels towards the AVM, then the malformed vessels were resected totally. Postoperative digital subtraction angiography of the four vessels was performed in all patients. RESULTS: 50 patients with giant AVM survived after operation, only 6 (12.0%) had transient neurological dysfunction and 44 (88.0%) recovered after a follow-up of 6-36 months. No patient suffered from normal perfusion pressure breakthrough (NPPB). CONCLUSIONS: The embolization could block the arteriovenous shunts sufficiently to decrease the blood flow away from the normal areas of the brain so as to prevent the incidence of intra- and postoperative rebleeding, especially in NPPB. Therefore, the combination of intraoperative embolization with surgical resection is an effective strategy in the treatment of giant cerebral AVMs, which make it operable for those used to be regarded as inoperable cases.
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