Yasuyuki Nomoto

Expression of Nuclear Factor κB and Tumor Necrosis Factor α in the Mouse Brain after Experimental Thermal Ablation Injury

OBJECTIVE Nuclear factor kappa B (NFkappaB) participates in the regulation of a diverse range of genes involved in inflammation and acute phase responses. We investigated the expression of the activated form of NFkappaB and tumor necrosis factor alpha (TNFalpha), an inflammatory cytokine, in experimental brain injury. METHODS We generated focal brain injury in mice using radiofrequency thermal ablation at the caudate putamen in mice. Intracerebral expression of TNFalpha and the p50 and p65 subunits of NFkappaB were studied using immunohistochemistry at 1, 4, and 8 hours and at 1, 2, 4, 8, 14, and 28 days postinjury. RESULTS Coagulative necrosis approximately 2 mm in diameter was produced at the site of injury. No immunoreactivity for TNFalpha, NFkappaB p50, or NFkappaB p65 was detected in the injured area in the early phase postinjury. On posttrauma Day 2, however, weak expression of TNFalpha, NFkappaB p50, and NFkappaB p65 was detected in mononuclear cells that infiltrated edematous tissue surrounding the lesion. On posttrauma Days 4 to 8, the expression of TNFalpha, NFkappaB p50, and NFkappaB p65 was prominently increased in infiltrating and proliferating mononuclear cells (macrophages and microglia) and in proliferating reactive astrocytes surrounding the lesion. Nuclear subcellular localization of the expression of NFkappaB p50 and p65 was observed, which indicated that these subunits might be activated in these cells. On posttrauma Day 14, the expression of TNFalpha, NFkappaB p50, and NFkappaB p65 decreased and was limited to mononuclear cells, and it finally disappeared on Day 28. The temporal profiles of TNFalpha, NFkappaB p50, and NFkappaB p65 were closely associated with the occurrence of secondary insults and the tissue-remodeling process in wound healing. CONCLUSION These results suggest that TNFalpha, NFkappaB p50, and NFkappaB p65 may play a central role in the injury-induced immune response that leads to secondary insults or wound healing after brain injury. Inappropriate and deregulated activation of NFkappaB in injured brain tissue may be implicated in the development of secondary brain damage.

Traumatic middle meningeal artery pseudoaneurysm and subsequent fistula formation with the cavernous sinus: case report.

BACKGROUND A combination of pseudoaneurysm and arteriovenous fistula of the middle meningeal artery is rare. We describe a case of traumatic pseudoaneurysm of the middle meningeal artery, which subsequently formed a fistula with the cavernous sinus. CASE DESCRIPTION A 23-year-old man suffered from blunt head trauma and skull fractures. Sixteen days later, he suddenly experienced headache and a bruit was auscultated over the left ear. Three-dimensional computed tomographic angiography revealed dilatation of the left middle meningeal artery. The dilation proved to be a pseudoaneurysm on cerebral angiograms and it was also found to have formed a fistula with the cavernous sinus. Both lesions were successfully obliterated by endovascular embolization using microcoils. CONCLUSION Head injury may lead to asymptomatic pseudoaneurysm or dural arteriovenous fistula. Neurosurgeons should always bear in mind the possibility of such vascular injuries after blunt head trauma to prevent any hemorrhagic complications.

Intracerebral cyst associated with meningioma

A 27-year-old male had experienced an episode of severe headache and nausea, sometimes accompanied by an inability to name objects. Magnetic resonance imaging showed a huge cyst within the left temporal lobe and a high degree of brain shift by it. A small round mass, which appeared to be a mural nodule, was located in the tip of left middle fossa. It was highly enhancing together with its attached dura mater, but the cyst wall was not enhanced. Sphenoid ridge meningioma with an associated intracerebral cyst or cystic glioma invading the dura mater was suspected. During surgery the small tumor was found to be arising from the sphenoid ridge and evaginating into the tip of the temporal lobe. The intracerebral cyst had a smooth surface and the tumor was visible outside the cyst through its wall. The tumor was totally removed, but the cyst wall was left without excision. Postoperatively he had no symptoms. Histological examination showed a microcystic meningioma. It is stressed that differentiations of cystic meningiomas from other cystic tumors and, of intratumoral from extratumoral cystic meningiomas using radiological, operative or histological findings are important.