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Distal anterior inferior cerebellar artery (AICA) pseudoaneurysms are very rare lesions. Although cases have been previously reported, only a few have been reported as a result of vestibular schwannoma (VS) radiation, none have been reported as a result of VS resection, and only one has been reported as treated with parent vessel occlusion (PVO) with n-butyl cyanoacrylate (nBCA). We report a case of a 65-year-old man with a history of right-sided VS surgery and radiation who presented years later with a ruptured pseudoaneurysm of the distal right AICA and was treated with endovascular PVO using nBCA. The aneurysm was completely obliterated and the patient had no worsening of symptoms or neurological exam. The case illustrates a very rare complication of VS surgery and radiation as well as an effective treatment for distal AICA aneurysms.

Distal anterior inferior cerebellar artery (AICA) pseudoaneurysms are very rare lesions. Although cases have been previously reported, only a few have been reported as a result of vestibular schwannoma (VS) radiation, none have been reported as a result of VS resection, and only one has been reported as treated with parent vessel occlusion (PVO) with n-butyl cyanoacrylate (nBCA). We report a case of a 65-year-old man with a history of right-sided VS surgery and radiation who presented years later with a ruptured pseudoaneurysm of the distal right AICA and was treated with endovascular PVO using nBCA. The aneurysm was completely obliterated and the patient had no worsening of symptoms or neurological exam. The case illustrates a very rare complication of VS surgery and radiation as well as an effective treatment for distal AICA aneurysms.

BACKGROUND AND IMPORTANCE: The abuse of cocaine can lead to significant destruction of midline craniofacial structures. This process occurs secondary to myriad mechanisms, including ischemic necrosis, irritation by chemical adulterants, and direct trauma during its administration. Coupled with a prolonged chronic infection of intranasal and anterior skull base regions, an encephalocele can be formed. We report a case of an encephalocele secondary to cocaine use and its associated complications. CLINICAL PRESENTATION: A 56-year-old man presented with altered mental status and cerebritis secondary to the presence of an intranasal encephalocele. On computed tomography, extensive destruction of the anterior cranial fossa was observed. The patient had a 30-year history of intranasal cocaine abuse, and his urine tested positive for the presence of cocaine on admission. The patient was treated with intravenous antibiotics and underwent a repair of his cranial defect and resection of the encephalocele. The patient made a good recovery after treatment. CONCLUSION: Alternative causes of an encephalocele, including trauma, surgery, and congenital malformation, were ruled out in this patient. Histopathological analysis of the necrotic tissue and the absence of renal or pulmonary disease also indicated that the patient did not suffer from Wegener granulomatosis, a known cause of spontaneous intranasal lesions. To the best of our knowledge, this is the first report of an encephalocele likely induced solely by cocaine abuse.

Kaposi sarcoma (KS) is one of the most common tumors in patients with human immunodeficiency virus (HIV), which characteristically presents with cutaneous lesions. The authors report a rare case of spinal KS with no cutaneous manifestation in a 32-year-old man with the acquired immunodeficiency syndrome who presented with abdominal pain. A computed tomography scan revealed incidental lesions in his lumbar spine, and additional imaging studies revealed numerous lesions in the lumbosacral spine and pelvis. An open biopsy was performed, and histopathological examination of the lesion confirmed the diagnosis of KS. At the time of presentation, the patient had no skin lesion or any other manifestation indicative of KS. The authors suggest that in HIV-positive patients who present with spinal lesions, KS should be included in the differential diagnosis.

Gene expression profiling of metastatic brain tumors from primary lung adenocarcinoma, using a 17k-expression array, revealed that 1561 genes were consistently altered. Further functional classification placed the genes into seven categories: cell cycle and DNA damage repair, apoptosis, signal transduction molecules, transcription factors, invasion and metastasis, adhesion, and angiogenesis. Genes involved in apoptosis, such as caspase 2 (CASP2), transforming growth factor-beta inducible early gene (TIEG), and neuroprotective heat shock protein 70 (Hsp70) were underexpressed in metastatic brain tumors. Alterations in Rho GTPases (ARHGAP26, ARHGAP1), as well as down-regulation of the metastasis suppressor gene KiSS-1 were noted, which may contribute to tumor aggression. Overexpression of the invasion-related gene neurofibromatosis 1 (NF1), and angiogenesis-related genes vascular endothelial growth factor-B (VEGF-B) and placental growth factor (PGF) was also evidenced. Brain-specific angiogenesis inhibitors 1 and 3 (BAI1 and BAI3) were underexpressed as well. Examination of cell-adhesion and migration-related genes revealed an increased expression of integrins and extracellular matrices collagen and laminin. The study also showed alterations in p53 protein-associated genes, among these increased gene expression of p53, up-regulation of Reprimo or candidate mediator of the p53-dependent G2-arrest, down-regulation of p53-regulated apoptosis-inducing protein 1 (p53AIP1), decreased expression of tumor protein inducible nuclear protein 1 (p53DINP1), and down-regulation of Mdm4 (MDMX). The results demonstrated that genes involved in adhesion, motility, and angiogenesis were consistently up-regulated in metastatic brain tumors, while genes involved in apoptosis, neuroprotection, and suppression of angiogenesis were markedly down-regulated, collectively making these cancer cells prone to metastasis.

In the past several decades methods have been developed to stabilize the subaxial cervical spine both posteriorly and anteriorly. Methods of posterior stabilization have progressed from interspinous wiring, through facet wiring and sublaminar wiring, to the lateral mass screws with plates and rods that are in use today. Plates for anterior stabilization have evolved from rigid plates requiring bicortical screws through those used with unicortical locking screws, to dynamic load-sharing plates used with variable angle screws. The original description of spinous process wiring was published by Hadra in 1891. In 1942 Rogers described the interspinous wiring method used for trauma-induced cervical instability, which was modified by Bohlman in 1985 (triple wiring technique). Luque rods with sublaminar wires were introduced in the late 1970s to address multilevel and occipitocervical instability. Facet wiring was developed in 1977 by Callahan to address the problem of stabilization when laminae are not present. Wiring remained the method used until Roy-Camille introduced the lateral mass screw-plate construct in the 1980s. The first plate for anterior stabilization was designed by Orozco and Llovet in 1970 and was later refined by Caspar; this was a rigid plate with bicortical screws. Morscher devised unicortical locking screws in the 1980s. The latest concept of dynamic load-sharing plates with variable angle screws was developed in 2000. In this article historical landmarks in surgical methods for the stabilization of the subaxial cervical spine are reviewed.

OBJECT: Extensive invasion and angiogenesis are hallmark features of malignant gliomas. Communication between malignant glioma cells and surrounding astrocytes occurs, resulting in transformation of the astrocytic phenotype. In the present study, the authors examined whether malignant glioma cells and vascular endothelial cells (VECs) communicate through the formation of gap junctions and whether this communication influences angiogenesis. METHODS: Connexin43 (Cx43), a gap junction protein expressed in glioma cells, was identified in human umbilical VECs (HUVECs). Immunocytochemical staining for Cx43 demonstrated immunoreactive plaques at areas of cell-cell contact among HUVECs as well as between HUVECs and Cx43-expressing malignant glioma cells. Dye transfer, performed using the gap junction-permeable dye dicarboxy-dichlorofluorescein diacetate (CDCF), among these cocultures indicated that these were functional communications. Calcium signaling also occurred from malignant glioma cells to HUVECs. Tube formation by HUVECs cocultured with Cx43-transfected T98G malignant glioma cells (T98G-Cx43 cells) or with U87MG malignant glioma cells, which naturally express Cx43, was significantly increased compared with tube formation by HUVECs alone. The difference in tube formation by HUVECs cocultured with empty vector-transfected T98G glioma cells (T98G-mock cells) or with Cx43-deficient U373MG malignant glioma cells and tube formation by HUVECs alone was not statistically significant. Furthermore, the concentration of vascular endothelial growth factor (VEGF), an angiogenic factor important for the induction of angiogenesis and blood vessel formation, was significantly higher in medium harvested from cultures of T98G-Cx43 cells than in that harvested from cultures of control T98G-mock cells. Human malignant glioma U87MG cells also secreted increased concentrations of VEGF as compared with HUVECs alone. Nevertheless, there was no statistically significant difference in tube formation by HUVECs cultured in medium conditioned by either Cx43-expressing or Cx43-deficient glioma cells, suggesting that the direct gap junction communication between glioma cells and HUVECs may play a much more significant role than the increased VEGF secretion in vascular tube formation in this assay. CONCLUSIONS: These results indicate that functional gap junction formation between human malignant glioma cells and VECs occurs. This communication appears to influence tumor angiogenesis. Targeting gap junction signaling may offer a potential mechanism for therapy in patients with these tumors.