Intracranial aneurysm (IA) is a socially important disease as a major cause of subarachnoid hemorrhage. Recent experimental studies mainly using animal models have revealed a crucial role of macrophage-mediated chronic inflammatory responses in its pathogenesis. However, as findings from comprehensive analysis of unruptured human IAs are limited, factors regulating progression and rupture of IAs in humans remain unclear. Using surgically dissected human unruptured IA lesions and control arterial walls, gene expression profiles were obtained by RNA sequence analysis. RNA sequencing analysis was done with read count about 60~100 million which yielded 6~10 billion bases per sample. 79 over-expressed and 329 under-expressed genes in IA lesions were identified. Through Gene Ontology analysis, ‘chemokine activity’, ‘defense response’ and ‘extracellular region’ were picked up as over-represented terms which included CCL3 and CCL4 in common. Among these genes, quantitative RT-PCR analysis using another set of samples reproduced the above result. Finally, increase of CCL3 protein compared with that in control arterial walls was clarified in IA lesions. Findings of the present study again highlight importance of macrophage recruitment via CCL3 in the pathogenesis of IA progression.
Two patients underwent uneventful total removal of convexity or trigone meningioma, but subsequently edema enlarged causing symptoms 3-4 weeks later. Gradual improvement was obtained by steroid administration in 1 patient and re-craniotomy in 1 patient. The histological findings in Case 1 were not confirmed, but inflammatory reaction against residual microfibrillar collagen hemostat (MCH) may have developed. The specimen from around the cyst in Case 2 showed moderate staining for vascular endothelial growth factor (VEGF). VEGF secreted by the tumor might have resulted in spread of inflammation due to MCH in the brain parenchyma. Furthermore, inflammatory reactions may have obstructed or formed a one-way communication in the inferior horn and residual cavity, resulting in malabsorption of cerebrospinal fluid. Postoperative edema with the timing in these cases is difficult to anticipate. However, the risk of this phenomenon can probably be minimized by ensuring that MCH is removed as effectively as possible after use, or by refraining from use in the brain parenchyma and by taking care to connect the residual cavity to the ventricular system, particularly if the tumor contacts a cerebral ventricle.
A 65-year-old woman presented with a sudden onset of diplopia and left periorbital pain. Her symptoms resolved spontaneously 2 months later without any treatment. Five months thereafter, her symptoms recurred, and then again subsided spontaneously. One year after the second episode of disease, she developed left total ophthalomoplegia, and left periorbotal severe pain. She was seen in our clinic for further evaluation. Her neurological examination revealed complete paralysis of the left oculomotor, trochlear, and abducens nerves and dysesthesia in the left ophthalmic nerve area. Contrast-enhanced computed tomography (Picture 1A, black arrow) and contrast-enhanced magnetic resonance imaging showed an enhanced lesion in the left cavernous sinus (Picture 1B, white arrow). An endonasal transsphenoidal biopsy revealed a capillary hemangioma. Immunohistochemical studies for CD34 showed the strongly immunoreactive endothelium (Picture 1C: original magnification ×40). It is noteworthy that symptoms of capillary hemangioma may fluctuate because of spontaneous regression. Histopathological diagnosis is very important for subsequent treatment. Radiosurgery is quite effective for such lesions (1).The authors state that they have no Conflict of Interest (COI).
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