Revascularization of occluded internal carotid arteries by hypertrophied vasa vasorum: report of four cases.

OBJECTIVE AND IMPORTANCE: The vasa vasorum are involved in the pathophysiological development of carotid artery atherosclerosis, providing vascular support to the thickened intima and plaque. When advanced atherosclerosis causes carotid artery occlusion, the vasa vasorum may serve as a means of revascularization. CLINICAL PRESENTATION: We studied four patients with internal carotid artery occlusion who exhibited revascularization, distal to the occlusion, by small vascular channels that were inconsistent with recanalization through the thrombus. The channels had an angiographic appearance consistent with their being hypertrophied vasa vasorum. Significant collateral circulation was provided by the revascularization. INTERVENTION: All four patients exhibited adequate collateral circulation and were treated with antiplatelet or anticoagulation medication. CONCLUSION: The vasa vasorum have not been previously reported to contribute to the revascularization of occluded arteries. The four cases presented in this report suggest that the vasa vasorum can be a source of collateral circulation after carotid artery occlusion secondary to atherosclerotic disease.

Magnetic resonance evaluation of ventrolateral medullary compression in essential hypertension.

OBJECT: The authors designed a blinded prospective study comparing patients with essential hypertension to patients without hypertension in which magnetic resonance (MR) imaging was used to evaluate the role of lateral medullary compression by adjacent vascular structures as a cause of neurogenic hypertension. METHODS: Patients with documented essential hypertension were recruited to undergo thin-slice axial brainstem MR imaging evaluation. Nonhypertensive (control) patients scheduled to undergo MR imaging for other reasons also underwent thin-slice MR imaging to form a basis for comparison. Magnetic resonance images obtained in patients from the hypertensive (30 patients) and the control (45 patients) groups were then compared by four independent reviewers (two neuroradiologists and two neurosurgeons) who were blinded to the patients' diagnosis and hypertensive status. Images were reviewed with regard to left versus right vertebral artery (VA) dominance, compression of the medulla on the left and/or right side, and brainstem rotation. Medullary compression was graded as either vessel contact without associated brainstem deformity or vessel contact with associated brainstem deformity. CONCLUSIONS: There was a tendency toward left VA dominance in the hypertensive group compared with the control group, although a significant difference was shown by only one of the four reviewers. There were no differences in brainstem compression or rotation between the hypertensive and nonhypertensive groups. These results are contrary to those of recently published studies in which MR imaging and/or MR angiography revealed lateral brainstem vascular compression in hypertensive patients but not in nonhypertensive (control) patients. Reasons for this discrepancy are discussed. On the basis of their own experience and that of others, the authors believe that neurogenic hypertension does exist. However, thin-slice MR imaging may not be a reliable method for detecting neurovascularly induced essential hypertension and the prevalence of neurovascular compression as the source of hypertension may be overestimated when using current imaging techniques.

Sequential outer table craniotomy a in hyperossified meningioma. Technical note.

A hyperossified meningioma with significant calvarial thickening is fairly common. Craniectomy of the involved region followed by cranioplasty is usually required to resect the bone overgrowth. However, in some cases, the hyperossified calvaria is too thick to allow safe penetration with a craniotome or trephine. In this report, the authors present a technique for preserving the outer calvaria while still resecting the majority of the underlying tumor mass. The key is to perform a craniotomy in a region adjacent to the hyperossified bone and to remove the tumorous, ossified inner table through this "window" by means of a high-speed drill. A second craniotomy can then be performed over the undermined area; this maneuver can be advanced and repeated until the tumor is resected. Frameless stereotactic guidance and microplates are useful in performing this procedure.

Thrombin-soaked gelatin sponge and brain edema in rats.

Previous work from this laboratory has shown that injection of thrombin into rat basal ganglia causes brain edema. This study investigates the effect on rat brain of thrombin-soaked gelatin sponge (used for intraoperative hemostasis in clinical situations) at a concentration similar to that used in humans. Three models were developed to evaluate this effect. In the first model, a gelatin sponge soaked with vehicle or thrombin (100 U/cm3) was placed on the intact pia of the right frontal lobe in rats without cortical lesions. In the second model, frontal cortex was excised (3 mm3) and the exposed brain was cauterized with electrocoagulation. Gelatin sponge was soaked with vehicle or thrombin (1000, 100, 10, or 1 U/cm3) and placed in the lesion site. In the third model, hirudin, a specific thrombin antagonist, was added to the thrombin-soaked gelatin sponge and placed in a similar cortical lesion to determine if the observed effects were specific to thrombin. The dose-response range for thrombin was determined qualitatively by magnetic resonance (MR) imaging and quantitatively by brain edema formation 24 hours after exposure. We found no edema in the cortically intact rats. The rats given cortical lesions developed significant edema when subjected to 1000, 100, and 10 U/cm3 thrombin as seen on MR imaging and at 100 and 10 U/cm3 thrombin as revealed by wet/dry weight and ion studies of brain tissue. Topical hirudin prevented thrombin-induced edema. It is concluded that thrombin-soaked gelatin sponges cause or enhance significant brain edema in rats at concentrations typically used for human neurosurgery.

Edema from intracerebral hemorrhage: the role of thrombin.

The mechanism by which intracerebral hemorrhage leads to the formation of brain edema is unknown. This study assesses the components of blood to determine if any are toxic to surrounding brain. Various solutions were infused stereotactically into the right basal ganglia of rats. The animals were sacrificed 24 hours later; brain edema and ion contents were measured. Whole blood caused an increase in brain water content and ion changes consistent with brain edema. Concentrated blood cells, serum from clotted blood, and plasma from unclotted blood all failed to provoke edema formation when infused directly into the brain. On the other hand, activation of the coagulation cascade by adding prothrombinase to plasma did produce brain edema. The edema response to whole blood could be prevented by adding a specific thrombin inhibitor, hirudin, to the injected blood. This study indicates that thrombin plays an important role in edema formation from an intracerebral blood clot.

Vertebral artery dissection related to basilar impression: case report.

A 50-year-old man with myelopathy secondary to basilar impression developed bilateral vertebral artery dissection after undergoing treatment with 8 pounds of cervical traction. The vertebral artery dissection resulted in vertebrobasilar insufficiency and posterior circulation stroke. In this report, the current management philosophies in the treatment of basilar impression are discussed, and the pertinent neurovascular anatomy is illustrated. This report suggests that vertebral artery injury may result from attempted reduction of severe basilar impression. Regardless of the cause of cranial settling, the risk of vertebral artery injury with cervical traction should be considered in patients with severe basilar impression.