Joseph A. Horton

Aneurysms of the Intracavernous Carotid Artery: Natural History and Indications for Treatment

Of 37 patients with 44 intracavernous carotid artery aneurysms (ICCAAns) diagnosed between 1976 and 1988, patients with 20 aneurysms were followed without treatment for 5 months to 13 years (median, 2.4 years). Ten of the 20 ICCAAns were asymptomatic at diagnosis, and 10 were symptomatic. Three of the asymptomatic ICCAAns were symptomatic at follow-up. One of these required clipping because of a progressing cavernous sinus syndrome; the other 2 were minimally symptomatic and have not required treatment. Of the 10 initially symptomatic ICCAAns, 2 had not changed, 4 became more symptomatic, and 4 had symptomatically improved by follow-up. One patient with an ICCAAn that had not changed clinically was lost to follow-up 6 months after diagnosis. Of the 4 ICCAAns that became more symptomatic, 2 continue to be monitored, and 2 required intervention: one with detachable balloon occlusion of the aneurysm with preservation of the internal carotid artery lumen, and the other with gradual cervical internal carotid artery occlusion. The clinical course of this selected group of patients with ICCAAns suggests that the natural history of ICCAAns can be quite variable. Although clinical progression does occur, symptomatic ICCAAns also can improve spontaneously. Therapeutic intervention for asymptomatic ICCAAns should be reserved for patients with aneurysms arising at the anterior genu of the carotid siphon and/or extending into the subarachnoid space, where subarachnoid hemorrhage is most likely. Intervention for symptomatic ICCAAns should be reserved for patients with subarachnoid hemorrhage, epistaxis, severe facial or orbital pain, evidence of radiographic enlargement, progressive ophthalmoplegia, or progressive visual loss.

Operative exposure and management of the petrous and upper cervical internal carotid artery.

The exposure and operative management of the petrous and upper cervical internal carotid artery (ICA) in 29 patients is detailed. Twenty-seven of these patients had extensive cranial base neoplasms (benign or malignant), 1 had an inflammatory cholesteatoma, and 1 had an aneurysm of the upper cervical ICA immediately proximal to the carotid canal. Preoperative studies useful in the evaluation of these patients included computed tomography, magnetic resonance imaging, cerebral and cervical angiography, and a balloon occlusion test of the ICA with evaluation of neurological status and of cerebral blood flow. The exposure of the upper cervical and petrous ICA was useful to obtain proximal control of the cavernous ICA, aided in the operative approach to extensive petroclival, intracavernous, and parapharyngeal neoplasms, and enabled the total resection of 23 of 27 such tumors. A subtemporal and preauricular infratemporal fossa approach was most commonly used for the exposure of the artery. Intraoperative arterial management consisted of exposure and decompression only, dissection from encasing neoplasm, resection of the invaded arterial segment and vein graft reconstruction, or intentional arterial occlusion. Vascular complications included 1 stroke due to delayed arterial occlusion, 1 stroke and death due to infection spreading from the nasopharynx with bilateral ICA rupture, and 1 pseudoaneurysm formation secondary to wound infection necessitating postoperative balloon occlusion of the ICA. Nonvascular complications included facial nerve paralysis in 10 patients (usually temporary), glossopharyngeal and vagal paralysis in 13 patients requiring Teflon injection of the vocal cord in 9, temporary difficulties with mastication in 9 patients, and wound infection in 3. The surgical exposure and management of the upper cervical and petrous ICA may permit a total operative resection of extensive cranial base neoplasms and is also an alternative for the management of vascular lesions involving these segments of the artery. With malignant neoplasms extending from the nasopharynx, postoperative infection remains a problem and may best be resolved by the use of a vascularized rectus abdominis muscle flap to reconstruct defects of the nasopharynx. Bilateral ICA encasement by neoplasms is also a major problem to be solved. The value of such an aggressive approach to the management of malignant neoplasms remains to be proven.

A new method to predict safe resection of the internal carotid artery

A patent internal carotid artery (ICA) is essential in most patients. Management of skull base lesions often requires translocation, Balloon embolization, or resection of this vessel. Preoperative tests to assess the availability of collateral flow have not been uniformly accurate. A new test that significantly increases the safety of surgical removal of the ICA is described.

Lysis of intraventricular blood clot with urokinase in a canine model: Part 1. Canine intraventricular blood cast model.

To test the safety and feasibility of using direct instillation of urokinase to induce rapid lysis of intraventricular clots, an animal model of intraventricular blood cast is required. Injections of 11 ml of fresh, unclotted autologous blood into the ventricles of adult mongrel dogs did not produce a solid blood cast in the ventricular system, suggesting that the adult dogs have an unusual ability to clear uncoagulated whole blood from the ventricles and subarachnoid space. Injection of 9 ml of preclotted blood resulted in a subtotal cast of the ventricles, leaving only portions of the occipital horns free of solid clots. This volume of injected clots incurred no mortality and minimal morbidity, whereas injection of 10 to 12 ml resulted in a mortality of 42% and formidable morbidity. The technique of producing this intraventricular blood cast model, as well as that of implanting an indwelling ventricular catheter-reservoir system useful in chronic urokinase administration, is described.

Lysis of intraventricular blood clot with urokinase in a canine model: Part 2. In vivo safety study of intraventricular urokinase

It was determined from in vitro experiments that the minimal dose of urokinase required to lyse 10 ml of clotted canine blood within a closed space must exceed 10,000 IU. We empirically doubled this minimum effective dose and tested the in vivo safety of injecting 20,000 IU of urokinase every 12 hours for 4 days into the ventricles of six adult mongrel dogs through an implanted catheter-reservoir system. The animals were monitored carefully for local and systemic bleeding by neurological and clinical examination, hematological tests reflecting systemic fibrinolytic status, serial computed tomography, and postmortem histological examinations of the brain, meninges, and peripheral organs. It was found that this intraventricular dose regimen of urokinase did not cause intracranial hemorrhage even though the dogs had recent brain wounds related to transcerebral ventricular catheterization. Mild activation of systemic fibrinolysis, implying passage of the enzyme from ventricle to blood, occurred 4 to 6 hours after each intraventricular injection, but no systemic hemorrhages were seen. This dose regimen also did not cause acute or chronic inflammatory changes in the brain or meninges and did not disturb cerebrospinal fluid circulation.

Clinical observations on the effect of carotid artery occlusion on cerebral blood flow mapped by xenon computed tomography and its correlation with carotid artery back pressure

Xenon computed tomographic cerebral blood flow mapping was correlated with internal carotid artery stump pressures and clinical neurologic assessment during temporary internal carotid artery occlusion. One hundred fourteen patients with skull base tumors or intracranial aneurysms potentially requiring carotid resection or ligation underwent angiography, xenon CT cerebral blood flow mapping, and internal carotid artery blood pressure monitoring. The internal carotid artery was then temporarily occluded with a balloon catheter, stump pressure was measured through the catheter, and the xenon CT cerebral blood flow mapping was repeated. Adequate xenon CT cerebral blood flow was defined as greater than 30 cc/100 gm/min. All patients had normal xenon CT cerebral blood flow before internal carotid artery occlusion. During internal carotid artery occlusion, xenon CT cerebral blood flow was found to be normal (group I, 40 patients), globally reduced but still within the normal range (group II, 50 patients), or low in the distribution of the ipsilateral middle cerebral artery (group III, 13 patients). With balloon occlusion, an immediate neurologic deficit developed in 11 patients (9%) requiring deflation of the balloon preceding xenon CT cerebral blood flow measurement (group IV). In group I internal carotid artery blood pressure was 128 mm Hg. (range 85 to 171 mm Hg) with stump pressure 86 mm Hg (range 46 to 125 mm Hg). In group II internal carotid artery blood pressure was 130 mm Hg. (range 78 to 199 mm Hg), with stump pressure 86 mm Hg (range 31 to 150 mm Hg).(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Stroke Intervention with Intraarterial Urokinase Infusion

PURPOSE A preliminary evaluation of the efficacy and safety of treating patients with acute stroke with intraarterial urokinase infusions was performed. PATIENTS AND METHODS Twelve patients with acute stroke were treated within 8 hours of symptom onset (average, 5 hours). Thrombolysis was performed within the middle cerebral (n = 10), internal carotid (n = 1), and basilar (n = 1) arteries. Urokinase (160,000-500,000 IU) was infused through microcatheters placed into or adjacent to the thrombi. RESULTS Thrombolysis was angiographically successful in nine patients (75%), all of whom had long-term neurologic improvement. No or minimal neurologic deficits were present in six patients (50%). Thrombolysis failed in three patients (25%); one patient died and two developed severe permanent neurologic deficits. No hemorrhagic complications occurred. CONCLUSION Preliminary results suggest that intraarterial urokinase infusion may be effective and safe for treating patients with acute stroke. Potentially devastating neurologic damage was averted or lessened in nine patients (75%). No additional neurologic damage was caused by intervention in the remaining three patients (25%).

Elective resection of the internal carotid artery without reconstruction

Curability of skull base tumors is related to the ability to achieve a complete resection. Resection of the internal carotid artery with the tumor puts the patient at risk for catastrophic cerebral injury. Autogenous vein grafting is not always technically or physiologically possible.

Middle Cerebral Artery Blood Flow Velocity and Stable Xenon-Enhanced Computed Tomographic Blood Flow During Balloon Test Occlusion of the Internal Carotid Artery

BACKGROUND AND PURPOSE Transcranial Doppler ultrasonography has been reported to reflect changes in cerebral blood flow (CBF) with the use of radioactive tracer techniques, which are weighted to measure primarily cortical structures. We tested the hypothesis that changes in transcranial Doppler ultrasonography would reflect changes in CBF in the middle cerebral artery vascular territory with the use of stable xenon-enhanced CT to assess CBF during carotid occlusion. METHODS Thirty-one conscious patients underwent balloon test occlusion of the internal carotid artery and transcranial Doppler ultrasonography and xenon-enhanced CT assessment of blood flow velocity and CBF, respectively, of the middle cerebral artery and its distribution during balloon test occlusion. RESULTS A significant correlation was seen between the change in CBF and the change in blood flow velocity for both brain levels at which CBF was determined (P < .0001). The average change in blood flow velocity was -13.4%, and the change in CBF was -15.1% and -17.7% at the two anatomic levels examined. CONCLUSIONS The data indicate that changes in blood flow velocity generally reflect changes in CBF throughout the middle cerebral artery vascular territory with abrupt occlusion of the internal carotid artery in unanesthetized humans.

Intracranial thrombolysis via a catheter embedded in the clot.

We treated a patient with acute stroke by clot lysis with urokinase. The drug was administered via an arterial catheter that had been positioned in the middle cerebral artery with the catheter tip embedded in the thrombus. The use of a microcatheter that is not flow-directed was essential to performing this procedure. Thrombolysis was successful, but an underlying high-grade vascular stenosis caused rethrombosis. Nevertheless, the techniques used in treating this patient are relatively uncomplicated. They make intracranial arterial thrombolytic drug infusions practical and are an important subject for further clinical evaluation.