Association of Internal Border Zone Infarction with Middle Cerebral Artery Steno-Occlusion

Background: Demonstrating the precise anatomical area of the internal border zone (IB) by brain imaging has been unclear, and it is not well known which relevant arteries are associated with IB infarction. Methods: Patients with IB infarctions were selected from 748 consecutive patients with acute ischemic stroke. The IB infarctions were identified by coronal diffusion-weighted imaging, excluding lesions over the upper pole of the lateral ventricle. The angiographic findings of the internal carotid artery (ICA) and middle cerebral artery (MCA), on contrast-enhanced MRA, were evaluated in the patients with and without IB infarction. Results: Thirty patients met the criteria for an IB infarction: 7 had MCA steno-occlusion without ICA disease, and 23 had ICA steno-occlusion. Sixty-one patients had ICA steno-occlusion without IB infarction. The multiple logistic regression analysis showed that a more than moderate degree of steno-occlusion of the MCA was a significant factor (OR, 11.32; p = 0.006) associated with IB infarction; whereas that of the ICA was not significant (OR, 2.19; p = 0.298). Conclusion: The results of this study suggest that IB infarctions were associated with MCA steno-occlusion. ICA disease resulting in IB infarctions would be expected to have significant MCA steno-occlusion causing hemodynamic compromise. Copyright (c) 2010 S. Karger AG, BaselThis study was supported by a grant (A060171) from the Korea Health 21 R&D Project, Ministry of Health, Welfare, and Family Affairs, Republic of Korea.Ay H, 2005, ANN NEUROL, V58, P688, DOI 10.1002/ana.20617Lee PH, 2004, J NEUROL NEUROSUR PS, V75, P727, DOI 10.1136/jnnp.2003.022574Lee PH, 2004, NEUROLOGY, V62, P1291Lee PH, 2003, STROKE, V34, P2630, DOI 10.1161/01.STR.0000097609.66185.05Arakawa S, 2003, AM J NEURORADIOL, V24, P427Kang DW, 2002, ARCH NEUROL-CHICAGO, V59, P1577Wong KS, 2002, ANN NEUROL, V52, P74, DOI 10.1002/ana.10250Ogasawara K, 2002, STROKE, V33, P1857, DOI 10.1161/33Hendrikse J, 2001, STROKE, V32, P2768Del Sette M, 2000, STROKE, V31, P631Read SJ, 1998, CEREBROVASC DIS, V8, P289Gandolfo C, 1998, CEREBROVASC DIS, V8, P255Wong KS, 1998, NEUROLOGY, V50, P812Moriwaki H, 1997, J NUCL MED, V38, P1556Hupperts RMM, 1997, J NEUROL, V244, P45Hupperts RMM, 1996, CEREBROVASC DIS, V6, P294MOUNIERVEHIER F, 1994, EUR NEUROL, V34, P11BLADIN CF, 1993, STROKE, V24, P1925DONNAN GA, 1993, CEREBROVASC DIS, V3, P248HUPPERTS RMM, 1993, CEREBROVASC DIS, V3, P231LEUNG SY, 1993, STROKE, V24, P779BOGOUSSLAVSKY J, 1992, NEUROLOGY, V42, P1992ANGELONI U, 1990, NEUROLOGY, V40, P1196BOGOUSSLAVSKY J, 1986, STROKE, V17, P1112BOGOUSSLAVSKY J, 1986, ANN NEUROL, V20, P346CAPLAN LR, 1986, STROKE, V17, P648WODARZ R, 1980, NEURORADIOLOGY, V19, P245

Phosphatidylinositol 3-kinase activator reduces motor neuronal cell death induced by G93A or A4V mutant SOD1 gene

The primary pathogenic mechanism of amyotrophic lateral sclerosis (ALS) remains largely unclear. We recently observed that motoneuron cell death mediated by G93A or A4V mutant SOD1, causing familial ALS, was related with decrease of survival signals, such as phosphatidylinositol 3-kinase (PI3-K) and Akt, which play a pivotal role in neuronal survival. Using a G93A or A4V mutant SOD1 transfected VSC4.1 motoneuron cells (G93A or A4V cells, respectively), we presently investigated whether PI3-K activator could reduce mutant SOD1-mediated motoneuron cell death. To investigate the effect of PI3-K activator on viability of G93A and A4V cells, these cells were treated with 10, 50 or 100ng/ml PI3-K activator for 24h and viability and intracellular signals, including Akt, glycogen synthase kinase-3 (GSK-3), heat shock transcription factor-1 (HSTF-1), cytosolic cytochrome c, caspase-3 and poly(ADP-ribose) polymerase (PARP), were compared with those without treatment (control). Compared with non-treated control G93A or A4V cells, the PI3-K activator treatment increased their viability by enhancing the survival signals, including pAkt, pGSK-3, and by inhibiting the death signals, including caspase-3 activation and PARP cleavage. These results suggest that PI3-K activator protects G93A or A4V cells from mutant SOD1-mediated motoneuron cell death by both activating survival signals and inactivating death signals