Jugulotympanic paragangliomas: 75 years of evolution in understanding.

Jugulotympanic paragangliomas were first described approximately 75 years ago. Since that time, there has been considerable evolution in knowledge of tumor biology, methods of classification, and appropriate management strategies. This paper attempts to summarize these gains in information.

Pipeline Embolization Device for Treatment of Craniocervical Internal Carotid Artery Dissections: Report of 3 Cases.

BACKGROUND: Dissecting pseudoaneurysms of the craniocervical circulation are uncommon, accounting for only 3% of all cerebral aneurysms. These aneurysms pose a challenge due to their location and anatomic configuration. The Pipeline Embolization Device (PED) is a flow diversion technique that successfully treats aneurysms by diverting blood flow away from the aneurysm and reconstructing the diseased parent artery by altering its hemodynamics. CASE DESCRIPTION: We report 3 cases in which the PED was used to treat craniocervical carotid artery dissection with associated pseudoaneurysms. A single PED was used in the first case, 4 PEDs were used in the second case, and 3 PEDs and a PRECISE PRO RX carotid stent were placed in the third case. All 3 patients achieved full neurologic recovery postoperatively. Cerebral angiography performed postoperatively demonstrated revascularization, good laminar flow, and no in-stent or adjacent stenosis. CONCLUSIONS: PED placement offers a safe and effective method of treating spontaneous or traumatic craniocervical carotid artery dissections with excellent neurologic outcomes postoperatively and complete long-term aneurysmal occlusion.

Resolution of trigeminal neuralgia by coil embolization of a persistent primitive trigeminal artery aneurysm.

The persistent primitive trigeminal artery (PTA) is a rare anastomosis between the carotid artery and basilar artery. While most PTAs are asymptomatic, lateral variants can occasionally compress the trigeminal nerve and precipitate trigeminal neuralgia. Aneurysms of the PTA are exceptionally rare in the literature and have not previously been associated with trigeminal neuralgia. We present the first case of an aneurysm of the PTA causing trigeminal neuralgia. The patient underwent coil embolization of the aneurysm which relieved her symptoms. We propose embolization as a viable therapeutic option for the resolution of trigeminal neuralgia when the condition is secondary to irritation by the high velocity pulsatile flow of an aneurysm.

Resolution of trigeminal neuralgia by coil embolization of a persistent primitive trigeminal artery aneurysm.

The persistent primitive trigeminal artery (PTA) is a rare anastomosis between the carotid artery and basilar artery. While most PTAs are asymptomatic, lateral variants can occasionally compress the trigeminal nerve and precipitate trigeminal neuralgia. Aneurysms of the PTA are exceptionally rare in the literature and have not previously been associated with trigeminal neuralgia. We present the first case of an aneurysm of the PTA causing trigeminal neuralgia. The patient underwent coil embolization of the aneurysm which relieved her symptoms. We propose embolization as a viable therapeutic option for the resolution of trigeminal neuralgia when the condition is secondary to irritation by the high velocity pulsatile flow of an aneurysm.

Cauda equina syndrome secondary to an absent inferior vena cava managed with surgical decompression.

The authors report on the case of a 24-year-old man who presented with back pain and radiculopathy due to epidural venous engorgement in the setting of a congenitally absent inferior vena cava. Despite initial improvement after steroid administration, the patient's health ultimately declined over a period of weeks, and signs and symptoms of cauda equina syndrome manifested. Lumbar decompression was performed and involved coagulation and resection of the compressive epidural veins. No complications occurred, and the patient made a full neurological recovery.

Use of endovascular embolization to treat a ruptured arteriovenous malformation in a pregnant woman: a case report.

INTRODUCTION: Pregnancy has been linked to increased rates of arteriovenous malformation rupture. This link remains a matter of debate and very few studies have addressed the management of arteriovenous malformation in pregnancy. Unruptured arteriovenous malformations in pregnant woman generally warrant conservative management due to the low rupture risk. When pregnant women present with ruptured arteriovenous malformation, however, surgery is often indicated due to the increased risk of re-rupture and associated mortality. Endovascular embolization is widely accepted as an important component of contemporary, multimodal therapy for arteriovenous malformations. Although rarely curative, embolization can facilitate subsequent surgical resection or radiosurgery. No previous reports have been devoted to the endovascular management of an arteriovenous malformation in a pregnant woman. CASE PRESENTATION: A 23-year-old Caucasian woman presented with headache and visual disturbance after the rupture of a left parieto-occipital arteriovenous malformation in the 22nd week of her pregnancy. After involving high-risk obstetric consultants and taking precautions to shield the fetus from ionizing radiation, we proceeded with a single stage of endovascular embolization followed soon after by open surgical resection of the arteriovenous malformation. There were several goals for the angiography in this patient: to better understand the anatomy of the arteriovenous malformation, including the number and orientation of feeding arteries and draining veins; to look for associated pre-nidal or intra-nidal aneurysms; and to partially embolize the arteriovenous malformation via safely-accessible feeders to facilitate surgical resection and minimize blood loss and operative morbidity. CONCLUSION: From our experience and review of the literature, we maintain that ruptured arteriovenous malformations in pregnancy may be managed in a similar manner to those in non-gravid women. Precautions should be taken to reduce the operative time and exposure of the fetus to ionizing radiation and contrast agents.

The spectrum of management practices in nontraumatic subarachnoid hemorrhage: A survey of high-volume centers in the United States.

BACKGROUND: There is a considerable variety of management practices for nontraumatic subarachnoid hemorrhage (ntSAH) across high-volume centers in the United States. We sought to design a survey which would highlight areas of controversy in the modern management of ntSAH and identify specific areas of interest fo further study. METHODS: A questionnaire on management practices in ntSAH was formulated using a popular web-based survey tool (SurveyMonkey(™), Palo Alto, CA) and sent to endovascular neurointerventionists and cerebrovascular surgeons who manage a high volume of these patients annually. Two-hundred questionnaires were delivered electronically, and after a period of 2 months, the questionnaire was resent to nonresponders. RESULTS: Seventy-three physicians responded, representing a cross-section of academic and other high-volume centers of excellence from around the country. On average, the responding interventionists in this survey each manage approximately 100 patients with ntSAH annually. Over 57% reported using steroids to treat this patient population. Approximately 18% of the respondents use intrathecal thrombolytics in ntSAH. Over 90% of responding physicians administer nimodipine to all patients with ntSAH. Over 40% selectively administer antiepileptic drugs to patients with ntSAH. Several additional questions were posed regarding the methods of detecting and treating vasospasm, as well as the indications for CSF diversion in patients with ntSAH further demonstrating the great diversity in management. CONCLUSION: This survey illustrates the astonishing variety of treatment practices for patients with ntSAH and underscores the need for further study.

Detection of pre-neoplastic and neoplastic prostate disease by MALDI profiling of urine.

The heterogeneous progression to the development of prostate cancer (PCa) has precluded effective early detection screens. Existing prostate cancer screening paradigms have relatively poor specificity for cancer relative to other prostate diseases, commonly benign prostatic hyperplasia (BPH). A method for discrimination of BPH, HGPIN, and PCa urine proteome was developed through testing 407 patient samples using matrix assisted laser desorption-mass spectrometry time of flight (MALDI-TOF). Urine samples were adsorbed to reverse phase resin, washed, and the eluant spotted directly for MALDI-TOF analysis of peptides. The processing resolved over 130 verifiable signals of a mass range of 1000-5000 m/z to suggest 71.2% specificity and 67.4% sensitivity in discriminating PCa vs. BPH. Comparing BPH and HGPIN resulted in 73.6% specificity and 69.2% sensitivity. Comparing PCa and HGPIN resulted in 80.8% specificity and 81.0% sensitivity. The high throughput, low-cost assay method developed is amenable for large patient numbers required for supporting biomarker identification.

TGF-beta-induced RhoA and p160ROCK activation is involved in the inhibition of Cdc25A with resultant cell-cycle arrest.

The ability of the transforming growth factor beta (TGF-beta) signaling pathways to inhibit proliferation of most cells while stimulating proliferation of others remains a conundrum. In this article, we report that the absence of RhoA and p160ROCK activity in fibroblastic NIH 3T3 cells and its presence in epithelial NMuMG cells can at least partially explain the difference in the TGF-beta growth response. Further, evidence is presented for TGF-beta-stimulated p160ROCK translocation to the nucleus and inhibitory phosphorylation of the cyclin-dependent kinase-activating phosphatase, Cdc25A. The resultant suppression of Cdk2 activity contributes to G1/S inhibition in NMuMG cells. These data provide evidence that signaling through RhoA and p160ROCK is important in TGF-beta inhibition of cell proliferation and links signaling components for epithelial transdifferentiation with regulation of cell-cycle progression.

Transforming growth factor-beta-induced apoptosis is mediated by Smad-dependent expression of GADD45b through p38 activation.

Transforming growth factor-beta (TGF-beta)-dependent apoptosis is important in the elimination of damaged or abnormal cells from normal tissues in vivo. In this report, we identify GADD45b as an effector of TGF-beta-induced apoptosis. GADD45b has been shown to be a positive mediator of apoptosis induced by certain cytokines and oncogenes. We show that Gadd45b is an immediateearly response gene for TGF-beta and that the proximal Gadd45b promoter is activated by TGF-beta through the action of Smad2, Smad3, and Smad4. We show that ectopic expression of GADD45b in AML12 murine hepatocytes is sufficient to activate p38 and to trigger apoptotic cell death, whereas antisense inhibition of Gadd45b expression blocks TGF-beta-dependent p38 activation and apoptosis. Furthermore, we also show that TGF-beta can activate p38 and induce apoptosis in mouse primary hepatocytes from wild-type mice, but not from Gadd45b-/- mice. All of these findings suggest that GADD45b participates in TGF-beta-induced apoptosis by acting upstream of p38 activation.