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C Agbi

Publications and source records attributed to C Agbi.

3 recordsLinked to original sources

Primary primitive neuroectodermal tumor of the cauda equina.

Primitive neuroectodermal tumors (PNETs) are aggressive neoplasms composed predominantly of undifferentiated cells that show evidence of neural differentiation. Although their classification has been controversial, PNETs are well recognized primary tumors of both central and peripheral nervous systems. PNETs must be distinguished from other round-cell tumors, including Ewing's sarcoma, lymphoma, rhabdomyosarcoma, and small cell carcinoma. Intraspinal PNETs are rare neoplasms that are usually metastatic in origin. We describe the eighth reported primary PNET of the cauda equina that developed in a 52-year-old man with no significant medical history. The tumor was characterized by Homer-Wright rosettes and immunoreactivity for CD99, glial fibrillary acidic protein, neuron-specific enolase S100, and synaptophysin. The anatomic location of primary intrathecal PNETs is important as those arising in the spinal cord develop in the central nervous system, whereas those arising in the cauda equina develop in the peripheral nervous system. The histogenesis of intrathecal PNETs may be multifactorial.

Cauda Equina↗

Intracranial hemorrhage after stenting and angioplasty of extracranial carotid stenosis.

BACKGROUND AND PURPOSE: The transluminal angioplasty and stenting procedure has been recently advocated as a potential alternative to surgical endarterectomy for the treatment of severe extracranial carotid stenosis. This study assesses the incidence and significance of intracranial hemorrhage occurring after this procedure. METHODS: We retrospectively reviewed 104 carotid arteries (96 internal, two external, and six common) in 90 patients (63 male; mean age, 69.4 years; range, 48-88 years) who underwent primary stenting and angioplasty by use of Wallstents (103/104) at three centers between January 1996 and January 1999. Seventy-five (83%) patients were referred by neurosurgery departments. Seventy-one (68%) arteries were symptomatic; the mean stenosis percentage was 85% (range, 40-99%). RESULTS: Four intraparenchymal hemorrhages occurred, representing 4.4% of patients and 3.8% of vessels, after angioplasty and stent placement. The mean preoperative stenosis percentage was 95% (range, 90-99%). One hemorrhage occurred immediately after stent placement, whereas the three other hemorrhages occurred in a delayed fashion (mean, 2.8 days). The mean hematoma size was 4.8 cm (range, 2-8 cm). Three patients had associated subarachnoid or intraventricular bleeding; the fourth had associated subdural hemorrhage. Three hemorrhages were fatal; the fourth experienced two seizures only. No acute neurologic symptoms were present prior to hemorrhages, and there was no postprocedural hypertension in these patients. All had been receiving antiplatelet agents as well as intraprocedural IV heparin. CONCLUSION: Intracranial hemorrhage can occur after carotid angioplasty and stenting. We speculate that this represents cerebral hyperperfusion injury. The 3.8% incidence of cerebral hemorrhage observed is approximately sixfold greater than that reported post endarterectomy (0.6%) (95% CI, 0.2-8.7%). This is not statistically significant in this small study group. This trend may reflect patient selection, different anticoagulation protocols, and/or study population size. Additional data are needed to determine the safety and efficiency of carotid stenting as a treatment for carotid stenosis.

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