Middle occlusion

Figure 9-6T. (Top) Cascade Mini-Ring, (metal and plastic). Originally used by permission of Mass Transfer, Inc., now, Glitsch, Inc. (middle and bottom) Elevation and plan views of Ballast rings (right) and Cascade Mini-Rings (left). Note how high aspect ratio of former permits occlusion of interior surfaces. Low aspect ratio of Cascade Mini-Rings, on the other hand, favors orientation that exposes internal surfaces for excellent film formation, intimate mixing, and gas-liquid contact. Used by permission of Glitsch, Inc. Bull. 345.

Occasionally, the diagnosis of acute ischemia can be established by NCCT because embohc material can be visualized directly, usually in the MCA or its branches. Emboli are often more radiodense than normal brain tissue, and therefore an affected proximal MCA may appear as a linear hyperdensity ( hyperdense middle cerebral artery sign or HMCA sign, Fig. 2.1c). One study found that the HMCA sign was 100% specific for MCA occlusion, but only 27% sensitive, probably because the density of embohc material is often indistinguishable from that of the normal MCA. ... 

Slivka A, Murphy E, Horrocks L. Cerebral edema after temporary and permanent middle cerebral artery occlusion in the rat. Stroke 1995 26 1061-1065. 

Middle Cerebral Artery Occlusion and the PROACT Trial The safety and efficacy of lAT in the anterior circulation have been evaluated in two randomized, multicenter, placebo-controlled trials. In the Prolyse in Acute Cerebral Thromboembolism (PROACT) 1 and 11 trials, patients with proximal MCA (Ml or M2 segment) occlusions within 6 hours of symptom onset were treated with recombinant prourokinase (r-pro-UK) or placebo. ... 

A significant neurologic deficit expected to result in long-term disability, and attributable to large vessel occlusion (basilar, vertebral, internal carotid, or middle cerebral artery M1 or M2 branches). 

Ueda T, Hatakeyama T, Kohno K, Kumon Y, Sakaki S. Endovascular treatment for acute thrombotic occlusion of the middle cerebral artery local intra-arterial thrombolysis combined with percutaneous transluminal angioplasty. Neuroradiology 1997 39 99-104. 

Nakano S, Iseda T, Yoneyama T, Kawano H, Wakisaka S. Direct percutaneous transluminal angioplasty for acute middle cerebral artery trunk occlusion an alternative option to intra-arterial thrombolysis. Stroke 2002 33 2872-2876. 

Izumi Y Roussel S, Pinard E, Seylaz J. Reduction of infarct volume by magnesium after middle cerebral artery occlusion in rats. J Cereb Blood Flow Metab 1991 11 1025-1030. 

Corbett D, Hamilton M, Colboume F. Persistent neuroprotection with prolonged postischemic h3fpothermia in adult rats subjected to transient middle cerebral artery occlusion. Exp Neurol 2000 163 200-206. 

Weinstein PR, Anderson GG, Telles DA. Results of h3fperbaric oxygen therapy during temporary middle cerebral artery occlusion in unanesthetized cats. Neurosurgery 1987 20 518-524. 

Meyer FB, Piepgras DG, Sundt TM, Yanagihara T. Emergency embolectomy for acute embolic occlusion of the middle cerebral artery. Clin Neurosurg 1985 32 155-173. 

In another study of 19 patients with complete or near-complete (TIMI grade 0 or 1) middle cerebral artery (MCA) occlusion, combination therapy with reduced-dose rt-PA and tirofiban infusion was associated with recanalization in 68% of patients, significant reductions of MRI ischemic lesion volumes, and substantial clinical improvement (median NIHSS change from 17 at baseline to 2 after treatment, p = 0.002). No cases of sICH occurred. 

Straub S, Junghans U, Jovanovic V, Wittsack HJ, Seitz RJ, Siebler M. Systemic thrombolysis with recombinant tissue plasminogen activator and tirofiban in acute middle cerebral artery occlusion. Stroke 2004 35 705-709. 

Kiening KL. Schneider GH, Unterherg AE, Lanksch WR. Effect of tromethamine (THAM) on infarct volume following permanent middle cerebral artery occlusion in rats. Acta Neurochir 1997 70 188-190. 

Table 5.1 Effects of compound 231617 on infarct volume in the middle cerebral occlusion model of focal stroke...

Martz, D., Rayos, G., Schielke, G.P. and Betz, A.L. (1989). Allopurinol and dimethylthiourea reduce brain infarction following middle cerebral artery occlusion in rats. Stroke 20, 488-494. 

N-Nitro-L-arginine methyl ester (L-NAME) is an inhibitor of NOS L-NAME reportedly reduces the volume of cortical and striatal infarct after middle cerebral artery occlusion in the rat. This protection can be reversed by co-injection of L-arginine. L-NAME also reduced the excitotoxic damage induced by NMDA injection. Finally, the authors showed that L-NAME reduced glutamate efflux produced by ischaemic injury in rats. The authors concluded that NOS induced by NMDA receptor overstimulation is a key event in the neuronal injury cascade (Buisson eta/., 1993). 

In contrast to the deleterious effects of arginine described by Buisson, L-arginine was shown to decrease infarct size caused by middle cerebral artery occlusion in spontaneously hypertensive rats. L-Arginine is a precursor for NO synthesis by NOS. The authors attributed the protection to dilation of cerebral blood vessels by NO (Morikawa et 1992). These examples illustrate the difficulty that the NO villain/protector paradox presents to us. 

Morikawa, E., Huang, Z. and Moskowitz, M.A. (1992). l-Aiginine decreases infarct size caused by middle cerebral arterial occlusion in SHR. Am. J. Physiol. 263, H1632-H1635. 

Although liver uptake of this compound is relatively high, the ischemic regions of the heart were visualized. SPECT images obtained from cats that were administered BMS-181321 one hour after middle cerebral artery occlusion (MCAO) showed selective brain retention in the ischemic territory of the MCA... 

T. Malinski, F. Bailey, Z.G. Zhang, and M. Chopp, Nitric-oxide measured by a porphyrinic microsensor in rat-brain after transient middle cerebral-artery occlusion. J. Cereb. Blood Flow Metab. 13, 355-358 (1993). 

Papadopoulos, C. M., Tsai, S-Y., Alsbiei, T., O Brien, T. E., Schwab, M. E. and Kartje, G. L. Functional recovery and neuroanatomical plasticity following middle cerebral artery occlusion and IN-1 antibody treatment in the adult rat. Ann. Neurol. 51 433-441, 2002. 

Since the early 1980s, much effort has focused on animal models of acute and chronic neurodegeneration in search of therapeutics for stroke. Neuronal cell death follows strokes, acute ischemic insults, and chronic neurodegeneration, such as Parkinson s disease, Alzheimer s disease (AD), epilepsy, and Huntington s disease. Up to 80% of all strokes result from focal infarcts and ischemia in the middle cerebral artery (MCA), so the commonly used animal models for neuroprotection are produced by temporary or permanent occlusion of the MCA.5 Lesions of the MCA include occlusion by electrocoagulation, intraluminal monofilaments, photochemical effects, thrombosis, and endothelin-1, but all of these models necessitate studying reperfusion events and validating MCA occlusion by behavioral assessments. 

Fig. 2.11 Effect of vigorous lifestyle and pharmacologic management on stopping progression of CAD. Top row PET scan a year after bypass surgery, showing a severe resting defect of the apex in the distribution of the initial LAD occlusion. Middle row Dipyridamole stress causes more...

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