Seizures after Onyx embolization for the treatment of cerebral arteriovenous malformation.

Onyx embolization of cerebral arteriovenous malformations (AVM) has become increasingly common. We explored the risk of seizures after Onyx use.A retrospective review was conducted of 20 patients with supratentorial brain arteriovenous malformation (AVM) who received Onyx embolization between 2006 and 2009. Baseline demographics, clinical history, seizure history, AVM characteristics and treatment were compared between those who developed post-onyx seizure and those who did not. MRIs were reviewed for edema following Onyx treatment.Of 20 patients who underwent Onyx embolization, the initial AVM presentation was hemorrhage in 40% (N=8). The median number of embolizations was two (range 1-4) and the median final obliteration amount was 90% (range 50-100%). A history of seizure was present in 50% (N=10) of patients pre-embolization and 12 (60%) patients received seizure medications (treatment or prophylaxis) prior to embolization. Seizur post-Onyx embolization occurred in 45% (N=9). The median time to seizur post-Onyx was seven days (range 0.3-210). Four patients (20%) with seizures post-Onyx had no seizure history. Two of these patients (10%) had no other identifiable cause for seizure other than recent Onyx embolization. Seizures in these two patients occurred within 24 hours of Onyx administration. Among patients with post-Onyx seizures, there was a trend toward larger AVM size (P=0.091) and lower percent obliteration (P=0.062). Peri-AVM edema was present in 75% of MRIs performed within one month of Onyx treatment and may represent a possible etiology for seizures.New onset seizures post-Onyx embolization are not uncommon. Further study of seizure prevention is warranted.

Reporting standards for endovascular repair of saccular intracranial cerebral aneurysms.

BACKGROUND AND PURPOSE: The goal of this article is to provide consensus recommendations for reporting standards, terminology, and written definitions when reporting on the radiological evaluation and endovascular treatment of intracranial, cerebral aneurysms. These criteria can be used to design clinical trials, to provide uniformity of definitions for appropriate selection and stratification of patients, and to allow analysis and meta-analysis of reported data. METHODS: This article was written under the auspices of the Joint Writing Group of the Technology Assessment Committee, Society of NeuroInterventional Surgery, Society of Interventional Radiology; Joint Section on Cerebrovascular Neurosurgery of the American Association of Neurological Surgeons and Congress of Neurological Surgeons; and Section of Stroke and Interventional Neurology of the American Academy of Neurology. A computerized search of the National Library of Medicine database of literature (PubMed) from January 1991 to December 2007 was conducted with the goal to identify published endovascular cerebrovascular interventional data about the assessment and endovascular treatment of cerebral aneurysms useful as benchmarks for quality assessment. We sought to identify those risk adjustment variables that affect the likelihood of success and complications. This article offers the rationale for different clinical and technical considerations that may be important during the design of clinical trials for endovascular treatment of cerebral aneurysms. Included in this guidance article are suggestions for uniform reporting standards for such trials. These definitions and standards are primarily intended for research purposes; however, they should also be helpful in clinical practice and applicable to all publications. CONCLUSIONS: The evaluation and treatment of brain aneurysms often involve multiple medical specialties. Recent reviews by the American Heart Association have surveyed the medical literature to develop guidelines for the clinical management of ruptured and unruptured cerebral aneurysms. Despite efforts to synthesize existing knowledge on cerebral aneurysm evaluation and treatment, significant inconsistencies remain in nomenclature and definition for research and reporting purposes. These operational definitions were selected by consensus of a multidisciplinary writing group to provide consistency for reporting on imaging in clinical trials and observational studies involving cerebral aneurysms. These definitions should help different groups to publish results that are directly comparable.

A rare spontaneous osteosarcoma of the calvarium in a patient with long-standing fibrous dysplasia: CT and MR findings.

A 52-year-old man with long-standing craniofacial polyostotic fibrous dysplasia (FD) and no history of prior radiation therapy developed a spontaneous right temporal bone osteosarcoma. Such spontaneous sarcomatous degeneration of FD is rare, particularly in the calvarium/skull, where, to our knowledge, only six prior cases have been reported in the literature. We report this case because it is a rare entity with well-documented CT and MR images, and to emphasize the importance of depicting imaging features of sarcomatous degeneration among the complex imaging findings of FD.

Clinical improvement related to thrombolysis of third ventricular blood clot in a patient with thalamic hemorrhage.

Intraventricular extension of hemorrhage after intraparenchymal hemorrhage is associated with significant morbidity and mortality. Clinical improvement is reported in a patient with thalamic hemorrhage with intraventricular extension after third and fourth ventricular blood clot resolution with instillation of urokinase intraventricularly. A 49-year-old man with hypertension collapsed while at work. A computed tomography (CT) scan of the head revealed a left thalamic hemorrhage with extension into the lateral, third, and fourth ventricles and associated hydrocephalus. A left frontal intraventricular catheter (IVC) was placed and intraventricular urokinase was administered at a dose of 25,000 U every 12 hours. The CT scan revealed resolution of the lateral ventricular dilatation and blood clot but no decrease in third or fourth ventricular hemorrhage. No clinical improvement was noted. The IVC was reinserted on the right side with the catheter tip placed through the foramen of Monroe into the third ventricle. Twelve hours after receiving the first dose of urokinase through the new catheter, the patient's condition improved. The CT scan showed a reduction in the volume of blood of the third and fourth ventricles. This case report shows that treatment of hydrocephalus with an IVC was not sufficient to provide a therapeutic effect. Substantial clinical improvement occurred only after the blood clot was cleared from the third and fourth ventricles.

Applications of fast-setting hydroxyapatite cement: cranioplasty.

A variety of autogenous and synthetic materials have been used to repair cranial defects resulting from traumatic and iatrogenic causes. In theory, the ideal material should be readily available and safe. It should adequately protect the underlying central nervous system, resist cerebrospinal fluid fistula formation, and be easily contoured. One promising synthetic biomaterial that has been used for cranioplasty is hydroxyapatite cement. This biomaterial has successfully restored cranial contour in most patients in whom it has been used; however, difficulties have arisen because of the material's prolonged water solubility. When exposed to cerebrospinal fluid or blood, inadequate setting of the cement occurs, resulting in loss of its structural integrity. This problem can be alleviated with the use of fast-setting hydroxyapatite cement, which hardens 6 to 12 times faster than the traditional cement. We present, to the best of our knowledge, the first series of the use of this material in 21 patients requiring cranioplasty. The advantages and limitations of fast-setting hydroxyapatite cement will be discussed.

Decreased nitric oxide availability contributes to acute cerebral ischemia after subarachnoid hemorrhage.

OBJECTIVE: Disturbances of the L-arginine-nitric oxide (NO) vasodilatory pathway have been implicated as a cause of acute vasoconstriction and ischemia after subarachnoid hemorrhage (SAH). Because NO-dependent vasodilatory mechanisms are still intact in this setting, acute vasoconstriction may be the result of limited NO availability after SAH. The present study examines this hypothesis by administration of the NO synthase inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME). METHODS: SAH was induced by the endovascular suture method in anesthetized rats. L-NAME (30 mg/kg intravenously) was injected 20 minutes before or 15, 30, or 60 minutes after SAH. Control rats received normal saline. Arterial and intracranial pressure and cerebral blood flow (CBF) were measured continuously for 60 minutes after SAH. RESULTS: L-NAME administration 20 minutes before SAH produced a significant decrease in resting CBF (29.4 +/- 3.4%; P < 0.05), but it had no effect on the acute decrease in CBF after SAH or on its early recovery up to 30 minutes after SAH. However, a significant decrease in CBF recovery was found in animals receiving L-NAME injections (28.7 +/- 9.4%; P < 0.05 versus controls) 60 minutes after SAH. Administration of L-NAME 15 or 30 minutes after SAH had no effect on CBF recovery, as compared with controls. However, when administered 60 minutes after SAH, L-NAME decreased CBF significantly (45.4 +/- 8.8%; P < 0.05 versus controls). CONCLUSION: These results indicate a biphasic pattern of NO availability after SAH. NO-mediated vasodilation is limited during the first 30 minutes of SAH and is restored 60 minutes after SAH.

Acute decrease in cerebral nitric oxide levels after subarachnoid hemorrhage.

Disturbances in the nitric oxide (NO) vasodilatory pathway have been implicated in acute vasoconstriction and ischemia after subarachnoid hemorrhage (SAH). The authors hypothesize that blood released during SAH leads to vasoconstriction by scavenging NO and limiting its availability. This was tested by measuring the major NO metabolites nitrite and nitrate in five different brain regions before and after experimental SAH. The basal NO metabolites levels were as follows (mean +/- SD, micromol/mg wet weight): brain stem, 0.14 +/- 0.07; cerebellum, 0.12 +/- 0.08; ventral convexity cortex, 0.22 +/- 0.15; dorsal convexity cortex, 0.16 +/- 0.11; and hippocampus, 0.26 +/- 0.17. In sham-operated animals, no effect of the nitric oxide synthase (NOS) inhibitor L(G)-nitro-L-arginine-methyl-ester (30 mg/kg) was found on NO metabolites 40 minutes after administration, but a significant decrease was seen after 120 minutes. The NO metabolites decreased significantly 10 minutes after SAH in all brain regions except for hippocampus, and recovered to control levels in cerebellum at 60 minutes and in brain stem and dorsal cerebral cortex 180 minutes after SAH, while remaining low in ventral convexity cortex. Nitrite recovered completely in all brain regions at 180 minutes after SAH, whereas nitrate remained decreased in brain stem and ventral convexity cortex. Our results indicate that SAH causes acute decreases in cerebral NO levels by a mechanism other than NOS inhibition and provide further support for the hypothesis that alterations in the NO vasodilatory pathway contribute directly to the ischemic insult after SAH.

Experimental models of subarachnoid hemorrhage in the rat: a refinement of the endovascular filament model.

The rat endovascular filament model has been utilized to study subarachnoid hemorrhage (SAH). Because the severity of the hemorrhage with this model has proven difficult to modulate, we attempted to vary the hemorrhage by modifying filament size, and compared this model to the blood injection method with regards to acute physiological responses and hemorrhage size. SAH was achieved using either a 3-0 or 4-0 filament, or by injecting 0.3 cc of autologous blood into the cisterna magna. Peak ICP elevations were lowest in the 4-0 filament group. CBF decreased acutely and rose from its nadir in all three models with the injection model demonstrating the earliest recovery. In the injection group, mean arterial blood pressure rose acutely and remained elevated, whereas in the 3-0 group, MABP rose transiently and in the 4-0 group it did not rise significantly. Histologically, there was less subarachnoid blood in the 4-0 group vs. the injection or 3-0 groups and a different distribution of blood in the two experimental models. Varying filament size provides a method to modulate the severity of SAH in the filament model. In addition, the rat endovascular filament and blood injection models produce different distribution of blood and physiological responses.

Adenosine-induced transient asystole for management of a basilar artery aneurysm. Case report.

Advances in anesthetic and surgical management, such as induced deep hypothermic circulatory arrest and application of temporary clips, have improved outcome for patients with basilar artery aneurysms. Nonetheless, these techniques are associated with significant risks. The authors report a case in which three transient periods of cardiac asystole were induced during basilar artery aneurysm surgery. Adenosine-induced asystole facilitated the safe clipping of the aneurysm by producing consistent periods of profound hypotension and collapse of the aneurysm without the need for temporary clipping. This technique provided unencumbered identification of perforating arteries, precise definition of the local anatomy, and an ideal environment for the safe placement of the aneurysm clip.

Effects of S-nitrosoglutathione on acute vasoconstriction and glutamate release after subarachnoid hemorrhage.

BACKGROUND AND PURPOSE: Subarachnoid hemorrhage (SAH) causes acute vasoconstriction that contributes to ischemic brain injury shortly after the initial bleed. It has been theorized that decreased availability of nitric oxide (NO) may contribute to acute vasoconstriction. Therefore we examined the effect of the NO donor N-nitroso glutathione (GSNO) on acute vasoconstriction and early ischemic glutamate release after experimental SAH. METHODS: SAH was induced by the endovascular suture method in anesthetized rats. GSNO (1 micromol/L/kg, n=31) or saline (n=21) was injected 5 minutes after SAH. Sham-operated rats received GSNO (1 micromol/L/kg, n=5) 5 minutes after sham surgery. Arterial and intracranial pressures, cerebral blood flow (CBF), and extracellular glutamate release were measured serially for 60 minutes after SAH. SAH size was determined, and vascular measurements were made histologically. RESULTS: GSNO had no effect on resting blood pressure, intracranial pressure, cerebral perfusion pressure, or CBF in sham-operated animals. However, administration of GSNO after SAH was associated with significantly increased CBF (161.6+/-26.6% versus saline 37.1+/-5.5%, 60 minutes after SAH, P<0.05), increased blood vessel diameter (internal carotid artery [ICA] 285.0+/-16.5 microm versus saline 149.2+/-14.1 microm, P<0.01), decreased vessel wall thickness (ICA12.9+/-0.7 microm versus saline 25.1+/-1.6 microm, P<0.01), and decreased extracellular glutamate levels (3315.6+/-1048.3% versus saline469. 7+/-134.3%, P<0.05). Blood pressure decreased transiently, whereas intracranial pressure, cerebral perfusion pressure, and SAH size were not affected. CONCLUSIONS: These results suggest that GSNO can reverse acute vasoconstriction and prevent ischemic brain injury after SAH. This further implies that acute vasoconstriction contributes significantly to ischemic brain injury after SAH and is mediated in part by decreased availability of NO.

Use of an acellular dermal allograft for dural replacement: an experimental study.

OBJECTIVE: In this study, a nonimmunogenic, acellular, dermal collagen matrix termed XenoDerm (LifeCell Corp., The Woodlands, TX) was examined for use as a dural replacement material in a porcine model. This model was used to investigate whether AlloDerm (LifeCell), an almost identical material made from human dermis, could be safely used in neurological surgery. METHODS: Bilateral temporoparietal dural defects were surgically created in 12 Yucatan minipigs. One side was repaired with autologous pericranium, and the other was repaired with XenoDerm. The pigs were killed after 1, 3, or 6 months, and the areas of dural repair were collected and examined macroscopically and histologically. XenoDerm is derived from porcine skin collected in thin sheets. It is processed so that the epidermis and all dermal cells are removed without disruption of the collagen matrix, rendering the material immunogenically inert and resistant to calcification. It is packaged as a freeze-dried sheet and is easily rehydrated at the time of surgery. RESULTS: There were no postoperative complications, and all pigs survived. Both grafts performed well as dural replacements in all cases. There was no macroscopic evidence of inflammation or cerebrospinal fluid leakage. The XenoDerm grafts were intact, retained their original dimensions, and resembled the surrounding dura. The autologous pericranial grafts, in contrast, were thicker than when implanted and had bony excrescences firmly adhering to their surfaces. Again, however, there was no evidence of cerebrospinal fluid fistulae. There was no gross adherence to the underlying meninges or brain tissue in any specimen. Repopulation by fibroblasts and neovascularization were evident in the XenoDerm grafts as early as 1 month after surgery; by 3 months, the XenoDerm had been remodeled to assume the connective tissue appearance of the surrounding dura. CONCLUSION: In this porcine model, an allograft of acellular dermis is a nearly ideal dural replacement. AlloDerm, the human equivalent of XenoDerm, would be an allograft of acellular dermis after implantation in human subjects. On the basis of this study and previous work with AlloDerm in other reconstructive applications, it is proposed that this material could be similarly used for duraplasty in human subjects.

Thyrocervical to vertebral artery transposition and ipsilateral carotid endarterectomy.

BACKGROUND: We report a new method for treating patients with symptomatic high-grade stenosis of the proximal vertebral artery associated with high-grade stenosis of the ipsilateral carotid artery. METHODS: Our patient had high-grade stenosis of the proximal right vertebral artery as well as high-grade stenosis of the ipsilateral carotid artery and suffered continued posterior circulation ischemic neurological deficits despite anticoagulation. RESULTS: The patient was successfully treated with a carotid endarterectomy and thyrocervical-to-vertebral artery transposition in a single operation. CONCLUSION: This procedure has the advantage in this setting of avoiding additional cross clamping on the diseased carotid artery that would normally be required for the vertebral-to-carotid artery transposition with carotid endarterectomy. Also, thrombosis at one anastamosis site would not endanger the other site as well.

Spontaneous caudate hemorrhage associated with ingestion of a decongestant containing phenylpropanolamine.

Intracerebral hemorrhage has been associated with phenylpropanolamine, a sympathomimetic agent contained in many over-the-counter medications. Caudate hemorrhage is infrequent, usually related to hypertension, and has not been reported following ingestion of medications containing phenylpropanolamine. We report an unusual case of caudate hemorrhage which developed in a patient taking an over-the-counter nasal decongestant containing phenylpropanolamine.

Acute vasoconstriction after subarachnoid hemorrhage.

OBJECTIVE: Decreased cerebral blood flow (CBF) and cerebral ischemia occurring immediately after subarachnoid hemorrhage (SAH) may be caused by acute microvascular constriction. However, CBF can also be influenced by changes in intracranial pressure (ICP) and cerebral perfusion pressure (CPP). The goal of these experiments was to assess the significance of acute vasoconstriction after SAH and its relationship to changes in CBF, ICP, CPP, and extracellular glutamate concentrations. METHODS: Three experiments were performed using the endovascular filament technique to produce SAH. In the first experiment, CBF, ICP, and CPP were measured for 60 minutes after SAH (n = 21) and were correlated with the 24-hour mortality rate. In the second experiment, rats undergoing SAH (n = 23) or a sham procedure (n = 7) were perfused 60 minutes after SAH for measurement of the circumference and wall thickness of the internal carotid and anterior cerebral arteries and correlation with CBF, ICP, and CPP. In the third experiment (n = 11), extracellular glutamate concentrations determined by hippocampal and cortical microdialysis and high performance liquid chromatography were correlated with physiological changes. RESULTS: CBF reductions to less than 40% of baseline for 60 minutes after SAH predicted 24-hour mortality with 100% accuracy and were used to define "lethal" SAH. In contrast, ICP and CPP 60 minutes after SAH were not correlated with the mortality rate. The vascular circumference was significantly smaller in lethal than in sublethal SAH or sham-operated rats (P < 0.001). Vessel measurements were correlated with both CBF and hemorrhage size (P < 0.01). Extracellular glutamate concentration increased to 600% of baseline after lethal SAH in both hippocampus and cortex and was inversely correlated with CBF (r = 0.9, P < 0.001) but did not increase after sublethal SAH. CONCLUSION: Acute vasoconstriction after SAH occurs independently of changes in ICP and CPP and is associated with decreased CBF, larger hemorrhage size, persistent elevations of extracellular glutamate, and poor outcome. Acute vasoconstriction seems to contribute directly to ischemic brain injury after SAH. Further evaluations of pharmacological agents with the potential to reverse acute vasoconstriction may increase CBF and improve outcome.

Effects of basic fibroblast growth factor on in vivo cerebral tumorigenesis in rats.

OBJECTIVE: In vitro evidence suggests that basic fibroblast growth factor (bFGF) promotes tumor cell proliferation and angiogenesis. In this study, we evaluated the early and delayed effects of recombinant human bFGF on the early and late phases of in vivo, in situ tumorigenesis in rats. METHODS: Brain tumors were induced by transplacentally exposing fetal rats to N-nitrosoethylurea on Day 17 of pregnancy. On postnatal (PN) Day 60 or 90, N-nitrosoethylurea-exposed rats underwent stereotactic intraventricular implantation of Gelfoam saturated with bFGF (60 micrograms) or vehicle; the rats were killed 4 days (early group) or 30 days (delayed group) later. The early and delayed effects of bFGF on the early phase of tumorigenesis (PN Day 60) were evaluated in 14 and 10 rats, respectively; early and delayed effects on the late phase of tumorigenesis (PN Day 90) were evaluated in 12 rats each. RESULTS: Histological examination 30 days after implantation showed a significantly higher tumor rate in rats that had been treated with bFGF on PN Day 90, compared with vehicle-treated control rats (P < 0.05); furthermore, in the bFGF-treated animals there was significantly greater intratumoral and periventricular glial fibrillary acidic protein expression, as determined immunohistochemically. Increased vascularity in the tumor ipsilateral to the implant was found in 2 of 14 rats that had been treated with bFGF on PN Day 60. CONCLUSION: These findings support in vitro evidence that bFGF and its receptor complex are implicated in the genesis and progression of N-nitrosoethylurea-induced brain tumors in this animal model.

Surgical management of subarachnoid hemorrhage.

Spontaneous subarachnoid hemorrhage is usually caused by a ruptured cerebral aneurysm. Aneurysmal rupture classically presents with sudden severe headache, often accompanied by an altered mental status. Diagnosis is made with computed tomography or lumbar puncture. Patients with ruptured cerebral aneurysms are at risk for rebleeding, cerebral artery vasospasm (and subsequent ischemia or stroke), and hydrocephalus. Early surgical clipping of the aneurysm under the microscope is usually the initial treatment of choice. This surgery prevents rebleeding and allows for safe use of pressors in the event that clinical vasospasm develops. Factors that would favor delayed surgery, "coiling" procedures, or conservative management include poor patient condition, basilar artery aneurysms, and unusually large or irregular aneurysms. Patients with ruptured aneurysms are treated with nimodipine, a calcium-channel blocker, to help prevent vasospasm-related ischemia. The degree of vasospasm that develops in the first 2 wks after aneurysmal rupture is assessed by transcranial Doppler sonography and cerebral angiography, in addition to the clinical examination. Patients with symptomatic vasospasm are kept well hydrated and treated with pressors (provided the aneurysm has been successfully clipped).

Intracerebral hemorrhage occurring remote from the craniotomy site.

OBJECTIVE: The purpose of this study was to analyze the available clinical data on postoperative intracerebral hemorrhages that occur in locations remote from the sites of craniotomy. METHODS: The findings of 37 cases of postoperative intracerebral hemorrhages occurring remote from the craniotomy sites were reviewed (5 from our records and 32 from the literature). RESULTS: Remote postoperative intracerebral hemorrhages presented within the first few hours postoperatively in 78% of the patients and were not related to the types of lesions for which the craniotomies were performed. Supratentorial procedures that produced infratentorial hemorrhages involved operations in the deep sylvian fissure and paraclinoid region in 81% of the patients and hemorrhages in the cerebellar vermis in 67% of the patients. Infratentorial procedures that produced supratentorial hemorrhages were performed with the patient in the sitting position for 87% of the patients. The remote supratentorial hemorrhages that occurred were superficial and lobar in 84% of the patients, as opposed to deep and basal ganglionic, which are classic locations for hypertensive hemorrhages. Remote intracerebral hemorrhages occurring after craniotomies were not associated with hypertension, coagulopathy, cerebrospinal fluid drainage, or underlying occult lesions. These hemorrhages commonly led to significant complications; 5 of 37 patients (14%) were left severely disabled, and 12 of 37 patients (32%) died. CONCLUSIONS: Remote intracerebral hemorrhage is a rare complication of craniotomy with significant morbidity and mortality. Such hemorrhages likely develop at or soon after surgery, tend to occur preferentially in certain locations, and can be related to the craniotomy site, operative positioning, and nonspecific mechanical factors. They do not seem to be related to hypertension, coagulopathy, cerebrospinal fluid drainage, or underlying pathological abnormalities.