Oral administration of metal chelator ameliorates motor dysfunction after a small hemorrhage near the internal capsule in rat.

Cerebral hemorrhage leads to local production of free iron, radicals, cytokines, etc. To investigate whether a decrease of iron-mediated radical production influences functional recovery after intracerebral hemorrhage (ICH), a modified ICH rat model with a small hemorrhage near the internal capsule (IC) accompanied with relatively severe motor dysfunction was first developed. Then clioquinol (CQ), an iron chelator that reduces hydroxyl radical production, was orally administrated.

Neurodegeneration of substantia nigra accompanied with macrophage/microglia infiltration after intrastriatal hemorrhage.

Intrastriatal hemorrhage in rats causes neurodegenaration of the substantia nigra (SN) followed by the appearance of ED1(+) cells (macrophage/microglia). ED1(+) cells were observed for at least 8 weeks after hemorrhage. Phosphorylation of p38 mitogen-activated protein kinase (MAPK) was shown in ED1(+) cells with the expression of both brain-derived neurotrophic factor (BDNF) mRNA and BDNF, suggesting that activated-p38 MAPK(+)/ED1(+) cells would produce BDNF and may exhibit trophic effect on the degenerating neurons in the SN.

Hemodynamic flow patterns evaluated by transcranial color-coded duplex sonography after STA-MCA bypass for internal carotid artery occlusion.

Extracranial-intracranial (EC-IC) bypass surgery had been widely performed for the treatment of internal carotid artery occlusion. However, it is presently difficult to predict how the bypass flow will contribute to intracranial circulation. We examined intracranial hemodynamics by transcranial color-coded duplex sonography (TCCD) after superficial temporal artery (STA)-middle cerebral artery (MCA) bypass and retrospectively studied the relationship between the postoperative contribution of the bypass flow and the preoperative collateral circulation and cerebrovascular perfusion status in 10 patients.