Tolosa-Hunt syndrome with reversible dissection aneurysm.

A 49-year-old female presented with recurrent intolerable right retro-orbital pain, ptosis and diplopia for 4 months. Neurological evaluation revealed right oculomotor nerve and abducent nerve injuries. Neuroimaging found enlarged right cavernous sinus, right intracavernous carotid dissection aneurysm and a stenosis proximal to it. Tolosa-Hunt syndrome (THS) was suggested and treated with steroid. The clinical symptoms were alleviated after the treatment. After 3 months of follow-up cerebral angiography showed the lesions of the right intracavernous carotid stenosis and the dissection almost disappeared. Therefore, we proposed that the dissection and the stenosis are directly induced by the inflammation of THS.

Montelukast inhibits matrix metalloproteinases expression in atherosclerotic rabbits.

BACKGROUND: Matrix metalloproteinases (MMPs) play important roles in the development and destabilization of atherosclerotic plaques. It is known that montelukast inhibits neointimal hyperplasia. However, the underlying mechanisms for the inhibitory effects of montelukast on neointimal formation have been poorly defined. METHODS: Thirty-six male New Zealand White rabbits were randomized as normal control, placebo (0.9% NaCl, 1.5 ml/kg/day, via intraperitoneal injection), atorvastatin (atorvastatin, 1.5 mg/kg/day, orally) and montelukast groups (montelukast, 1.5 mg/kg/day, via intraperitoneal injection). Atherosclerosis was induced by balloon-injury and high-cholesterol (HC) diet. Serum lipids were measured at 0, 8 and 12 weeks. After 12 weeks, the rabbits were sacrificed and histopathological changes examined. Immunohistochemistry and reverse transcription-polymerase chain reaction were used to measure the expression of MMP-2 and MMP-9 in the plaques. RESULTS: It was found that montelukast reduced neointimal formation, decreased macrophage accumulation, and increased smooth muscle cells. It also attenuated the expression of MMP-2 and MMP-9 in atherosclerotic plaques, but it had no effect on plasma lipid levels. CONCLUSION: These data indicate that montelukast inhibits neointimal hyperplasia in association with decreased expression of MMP-2 and MMP-9 independent of plasma lipid levels in atherosclerotic plaques after vascular injury in hyperlipidemic rabbits.

[Effects of montelukast on atherosclerosis and monocyte chemoattractant protein-1 expression in ahypercholesterolemic rabbit model.].

OBJECTIVE: To investigate the effects of montelukast on atherosclerosis and monocyte chemoattractant protein-1 expression in a hypercholesterolemic rabbit model. METHODS: Thirty four male New Zealand white rabbits were randomized into four groups including normal control group (n = 6), placebo group (n = 8), atorvastatin group (1.5 mgxkg(-1)xd(-1), beginning at 8(th) weeks for 4 weeks, n = 10) and montelukast group (1 mgxkg(-1)xd(-1), beginning at 8(th) weeks for 4 weeks, n = 10). Rabbits except those in normal control group were fed a high cholesterol diet for 12 weeks. Serum lipids were measured at 0, 8 and 12 weeks after intervention. The intima/media ratio, percentages of macrophages or smooth muscle cells in intima and the expression of MCP-1 mRNA were examined. RESULTS: Atherosclerosis was evidenced in placebo group and atorvastatin or montelukast treatment significantly reduced neointima (0.32 +/- 0.12 and 0.34 +/- 0.10 vs. 1.12 +/- 0.36, P < 0.05) and macrophage content [(9.8 +/- 4.6)% and (11.2 +/- 3.7)% vs. (34.6 +/- 8.8)%, P < 0.05], increased SMC content [(18.6 +/- 6.9)% and (19.2 +/- 8.6)% vs. (5.2 +/- 2.3)%, P < 0.05] and inhibited expression of MCP-1 mRNA (0.42 +/- 0.08 and 0.40 +/- 0.06 vs. 2.36 +/- 0.48, P < 0.01). Montelukast had similar anti-atherogenetic effects as atorvastatin but had no influence on plasma lipids. CONCLUSIONS: Montelukast could attenuate atherosclerosis in this hypercholesterolemic rabbit model which might be attributed to its anti-inflammatory effects.

IL-18 accelerates the cell apoptosis by up-regulating cysteinyl leukotriene 2 receptor expression in human umbilical vein endothelial cells at the early stage of administration.

The purpose of the present study is to identify whether interleukin (IL)-18 can modulate cysteinyl leukotriene 2 receptor (CysLT2R) expression in Human Umbilical Vein Endothelial Cells (HUVECs) and how it influences the cell death. According to the results from real-time reverse transcription PCR, confocal laser scanning microscopy, and western blotting, a dose-dependent augmentation of CysLT2R protein expression in HUVECs was triggered by IL-18 for the first 2 h followed by down-regulation within the next 22 h after IL-18 administration. The flow cytometry showed that non-selective CysLT1R and CysLT2R antagonist BAY-u9773 could attenuate the early stage apoptosis mediated by IL-18 whereas CysLT1R antagonist Montelukast couldn't. Also, pretreatment with BAY-u9773 suppressed calcium influx of HUVECs induced by IL-18 whereas Montelukast didn't work. The observation that progression of cell death aggravated by IL-18 could be attenuated by BAY-u9773 may offer a chance to develop a novel way to treat arteriosclerosis.

Posterior circulation hyperperfusion syndrome after bilateral vertebral artery intracranial stenting.

Hyperperfusion syndrome is a well-documented clinical complication after endarterectomy and carotid stenting. However, little is known about this complication immediately after vertebral artery stenting. A 51-year-old woman who had repeated episodes of dizziness, nausea, and vomiting was diagnosed with vertebrobasilar insufficiency. Diffusion-weighted magnetic resonance imaging showed a lesion in the posterior inferior cerebellar artery territory. The patient underwent bilateral vertebral stenting due to severe stenosis in both intracranial segments of the vertebral arteries. Three hours after the procedure, she had severe headache with vomiting and gradually went into a coma. An urgent brain computed tomographic scan showed hemorrhage in the right cerebellum and subarachnoid region. Also, transcranial Doppler revealed approximate doubling of blood flow velocity in vertebral artery area compared with her baseline value. Cerebral blood flow and blood pressure monitoring, together with intensive antihypertensive therapy, are necessary to reduce the risk of hyperperfusion syndrome after vertebral stenting. Moreover, the safety and efficacy of intracranial vertebral stenting should be further reevaluated by large-scale randomized trials.