Emergent surgical embolectomy for middle cerebral artery occlusion due to carotid plaque rupture followed by elective carotid endarterectomy

2014 ◽  
Vol 121 (3) ◽  
pp. 631-636 ◽  
Author(s):  
Satoshi Kiyofuji ◽  
Tomohiro Inoue ◽  
Hirotaka Hasegawa ◽  
Akira Tamura ◽  
Isamu Saito
Keyword(s):  
Middle Cerebral Artery ◽  
Carotid Endarterectomy ◽  
Cerebral Artery ◽  
Vulnerable Plaque ◽  
Carotid Plaque ◽  
Plaque Rupture ◽  
Artery Occlusion ◽  
Large Artery ◽  
Mca Occlusion ◽  
Surgical Embolectomy

Embolic intracranial large artery occlusion with severe neurological deficit is associated with an extremely poor prognosis. The safest and most effective treatment strategy has not yet been determined when such emboli are associated with unstable proximal carotid plaque. The authors performed emergent surgical embolectomy for left middle cerebral artery (MCA) occlusion, and the patient experienced marked neurological recovery without focal deficit and regained premorbid activity. Postoperative investigation revealed “vulnerable plaque” of the left internal carotid artery without apparent evidence of cardiac embolism, such as would be seen with atrial fibrillation. Specimens from subsequent elective carotid endarterectomy (CEA) showed ruptured vulnerable plaque that was histologically consistent as a source of the intracranial embolic specimen. Surgical embolectomy for MCA occlusion due to carotid plaque rupture followed by CEA could be a safer and more effective alternative to endovascular treatment from the standpoint of obviating the risk of secondary embolism that could otherwise occur as a result of the manipulation of devices through an extremely unstable portion of plaque. Further, this strategy is associated with a high probability of complete recanalization with direct removal of hard and large, though fragile, emboli.

Acute Middle Cerebral Artery Occlusion: Experience with Volume Expansion Therapy

Neurosurgery ◽  
1986 ◽  
Vol 18 (4) ◽  
pp. 397-401 ◽  
Author(s):  
Bruce I. Tranmer ◽  
Cordell E. Gross ◽  
Ted S. Keller ◽  
Glenn W. Kindt
Keyword(s):  
Cardiac Output ◽  
Middle Cerebral Artery ◽  
Cerebral Artery ◽  
Volume Expansion ◽  
Artery Occlusion ◽  
Neurological Deficits ◽  
Life Styles ◽  
Arterial Blood ◽  
Mca Occlusion ◽  
The Mean

Abstract Five consecutive patients with acute neurological deficits after middle cerebral artery (MCA) occlusion were given emergency treatment with colloidal volume expansion. In each case, the diagnosis was confirmed promptly by computed tomography and cerebral angiography. Aggressive volume expansion therapy was started 2 to 18 hours (mean, 11 hr) after the onset of the neurological deficit. The mean colloidal volume used was 920 ml/day for an average of 4 days. During volume expansion, the mean cardiac output increased 57% from 4.6 + 0.6 to 7.2 + 1.9 litres/min (P < 0.05). The mean hematocrit decreased 19% from 46 + 3% to 37 + 4% (P < 0.01). The mean arterial blood pressure remained stable, and the pulmonary artery wedge pressure was maintained at < 15 mm Hg. Three patients improved dramatically with volume expansion therapy and have returned to their previous life-styles. Two patients made partial recoveries and manage at home with nursing care. The three patients who improved dramatically were young (aged <34) and, when compared to the older patients, they had greater increases in cardiac output (67% vs. 19%). No major complications or deaths were attributed to the volume expansion therapy. We propose that intravascular volume expansion and its concomitant augmentation of the cardiovascular dynamics may be effective in the treatment of acute neurological deficits after acute MCA occlusion.

scholarly journals ARL 17477, a Potent and Selective Neuronal NOS Inhibitor Decreases Infarct Volume after Transient Middle Cerebral Artery Occlusion in Rats

1996 ◽  
Vol 16 (4) ◽  
pp. 599-604 ◽  
Author(s):  
Zheng G. Zhang ◽  
David Reif ◽  
James Macdonald ◽  
Wen Xue Tang ◽  
Dietgard K. Kamp ◽  
...  
Keyword(s):  
Middle Cerebral Artery ◽  
Cerebral Artery ◽  
Cell Damage ◽  
Infarct Volume ◽  
Artery Occlusion ◽  
Arterial Blood ◽  
Mca Occlusion ◽  
Nos Inhibitor ◽  
Oxide Synthase ◽  
Cerebral Artery Occlusion

We tested the effects of administration of a selective neuronal nitric oxide synthase (nNOS) inhibitor, ARL 17477, on ischemic cell damage and regional cerebral blood flow (rCBF), in rats subjected to transient (2 h) middle cerebral artery (MCA) occlusion and 166 h of reperfusion (n = 48) and in rats without MCA occlusion (n = 25), respectively. Animals were administered ARL 17477 (i.v.): 10 mg/kg; 3 mg/kg; 1 mg/kg; N-nitro-L-arginine (L-NA) 10 mg/kg L-NA 1 mg/kg; and Vehicle. Administration of ARL 17477 1 mg/kg, 3 mg/kg and 10 mg/kg reduced ischemic infarct volume by 53 (p < 0.05), 23, and 6.5%, respectively. L-NA 1 mg/kg and 10 mg/kg increased infarct volume by 2 and 15%, respectively (p > 0.05). Administration of ARL 17477 (10 mg/kg) significantly (p < 0.05) decreased rCBF by 27 ± 5.3 and 24 ± 14.08% and cortical NOS activity by 86 ± 14.9 and 91 ± 8.9% at 10 min or 3 h, respectively, and did not alter mean arterial blood pressure (MABP). L-NA (10 mg/kg) significantly reduced rCBF by 23 ± 9.8% and NOS activity by 81 ± 7% and significantly (p < 0.05) increased MABP. Treatment with 3 mg/kg and 1 mg/kg ARL 17477 reduced rCBF by only 2.4 ± 4.5 and 0%, respectively, even when NOS activity was reduced by 63 ± 13.4 and 45 ± 15.7% at 3 h, respectively, (p < 0.05). The data demonstrate that ARL 17477 inhibits nNOS in the rat brain and causes a dose-dependent reduction in infarct volume after transient MCA occlusion.

scholarly journals Periinfarct and Remote Excitability Changes after Transient Middle Cerebral Artery Occlusion

2000 ◽  
Vol 20 (1) ◽  
pp. 45-52 ◽  
Author(s):  
Tobias Neumann-Haefelin ◽  
Otto W. Witte
Keyword(s):  
Middle Cerebral Artery ◽  
Cerebral Artery ◽  
Field Potential ◽  
Extracellular Recording ◽  
Artery Occlusion ◽  
Early Reperfusion ◽  
Paired Pulse ◽  
Mca Occlusion ◽  
Cortical Regions

Transient middle cerebral artery (MCA) occlusion results in substantially smaller cortical infarcts than permanent MCA occlusion if reperfusion is initiated within the first few hours. Only little information is available on the long-term functional outcome of the cortical regions “salvaged” by early reperfusion. To address this issue we examined basic electrophysiologic parameters in vitro using standard extracellular recording techniques at 7 and 28 days after transient MCA occlusion (1- and 2-hour ischemia) in rats. Both neocortical areas ipsi- and contralateral to MCA occlusion were systematically mapped to delineate the extent of periinfarct and remote alterations. In the periinfarct region we found a significant reduction of field potential amplitudes up to 3 mm when measuring from the infarct border at 7 days and up to 7 mm at 28 days. Paired-pulse inhibition, an indicator of GABAergic transmission, was only moderately impaired in this region at 7 days and not significantly different from control at 28 days. Remote effects were observed both ipsi- and contralaterally. Ipsilaterally they were restricted to a region close to the midline (presumably motor cortex) and were most likely attributable to the degeneration of corticostriatal connections. The extent of the contralateral excitability changes was clearly related to the size of the neocortical infarcts with large infarcts resulting in the widespread reduction of field potential amplitudes and an impairment of paired-pulse inhibition. The results show that there is a relatively large periinfarct region with decreased overall excitability after transient MCA occlusion which is likely to have a profound effect on perilesional processes involved in functional recovery. Remote excitability changes may contribute to the functional deficit and are probably related to deafferentation.

Neuroprotective effects of erythropoietin pretreatment in a rodent model of transient middle cerebral artery occlusion

2014 ◽  
Vol 121 (1) ◽  
pp. 55-62 ◽  
Author(s):  
Bernardo Oliveira Ratilal ◽  
Mariana Moreira Coutinho Arroja ◽  
Joao Pedro Fidalgo Rocha ◽  
Adelaide Maria Afonso Fernandes ◽  
Andreia Pereira Barateiro ◽  
...  
Keyword(s):  
Treatment Group ◽  
Middle Cerebral Artery ◽  
Brain Edema ◽  
Cerebral Artery ◽  
Plasma Levels ◽  
Infarct Volume ◽  
Neuron Specific Enolase ◽  
Artery Occlusion ◽  
Mca Occlusion ◽  
Cerebral Artery Occlusion

Object There is an unmet clinical need to develop neuroprotective agents for neurosurgical and endovascular procedures that require transient cerebral artery occlusion. The aim in this study was to explore the effects of a single dose of recombinant human erythropoietin (rhEPO) before middle cerebral artery (MCA) occlusion in a focal cerebral ischemia/reperfusion model. Methods Twenty-eight adult male Wistar rats were subjected to right MCA occlusion via the intraluminal thread technique for 60 minutes under continuous cortical perfusion monitoring by laser Doppler flowmetry. Rats were divided into 2 groups: control and treatment. In the treated group, rhEPO (1000 IU/kg intravenously) was administered 10 minutes before the onset of the MCA ischemia. At 24-hour reperfusion, animals were examined for neurological deficits, blood samples were collected, and animals were killed. The following parameters were evaluated: brain infarct volume, ipsilateral hemispheric edema, neuron-specific enolase plasma levels, parenchyma histological features (H & E staining), Fluoro-Jade–positive neurons, p-Akt and total Akt expression by Western blot analysis, and p-Akt–positive nuclei by immunohistochemical investigation. Results Infarct volume and Fluoro-Jade staining of degenerating neurons in the infarct area did not vary between groups. The severity of neurological deficit (p < 0.001), amount of brain edema (78% reduction in treatment group, p < 0.001), and neuron-specific enolase plasma levels (p < 0.001) were reduced in the treatment group. Perivascular edema was histologically less marked in the treatment group. No variations in the expression or localization of p-Akt were seen. Conclusions Administration of rhEPO before the onset of 60-minute transient MCA ischemia protected the brain from this insult. It is unlikely that rhEPO pretreatment leads to direct neuronal antiapoptotic effects, as supported by the lack of Akt activation, and its benefits are most probably related to an indirect effect on brain edema as a consequence of blood-brain barrier preservation. Although research on EPO derivatives is increasing, rhEPO acts through distinct neuroprotective pathways and its clinical safety profile is well known. Clinically available rhEPO is a potential therapy for prevention of neuronal injury induced by transitory artery occlusion during neurovascular procedures.

scholarly journals Reduction of Infarct Volume by Magnesium after Middle Cerebral Artery Occlusion in Rats

1991 ◽  
Vol 11 (6) ◽  
pp. 1025-1030 ◽  
Author(s):  
Yoshio Izumi ◽  
Simon Roussel ◽  
Elisabeth Pinard ◽  
Jacques Seylaz
Keyword(s):  
Middle Cerebral Artery ◽  
Cerebral Artery ◽  
Focal Cerebral Ischemia ◽  
Infarct Volume ◽  
Artery Occlusion ◽  
Triphenyltetrazolium Chloride ◽  
Ischemic Brain ◽  
Mca Occlusion ◽  
Cerebral Artery Occlusion ◽  
Hyperglycemic Effect

The effects of magnesium, an endogenous inhibitor of calcium entry into neurons, upon ischemic brain damage were investigated using a well-characterized model of focal cerebral ischemia in rats. Infarct volumes were determined by 2,3,5-triphenyltetrazolium chloride transcardiac perfusion 48 h after middle cerebral artery (MCA) occlusion. The area of ischemic damage was quantified by image analysis in coronal sections taken every 0.5 mm. MgCl2 (1 mmol/kg) was injected intraperitoneally just after MCA occlusion and again 1 h later. Posttreatment with MgCl2 (16 control and 16 treated rats) significantly reduced the cortical infarct volume. Compensation for the hyperglycemic effect of MgCl2 with insulin (17 rats) further reduced the infarct volume in the neocortex. No systemic effects of either treatment could account for the observed neuroprotection.

scholarly journals Redox Control of Neuronal Damage during Brain Ischemia after Middle Cerebral Artery Occlusion in the Rat: Immunohistochemical and Hybridization Studies of Thioredoxin

1998 ◽  
Vol 18 (2) ◽  
pp. 206-214 ◽  
Author(s):  
Yasushi Takagi ◽  
Tomoo Tokime ◽  
Kazuhiko Nozaki ◽  
Yasuhiro Gon ◽  
Haruhiko Kikuchi ◽  
...  
Keyword(s):  
Middle Cerebral Artery ◽  
Cerebral Artery ◽  
Brain Ischemia ◽  
Neuronal Damage ◽  
Artery Occlusion ◽  
Oxygen Intermediates ◽  
Ischemic Region ◽  
Mca Occlusion ◽  
Frontoparietal Cortex

Thioredoxin (TRX) is a small, multifunctional protein with a redox-active site and multiple biological functions that include reducing activity for reactive oxygen intermediates. We assayed TRX and TRX mRNA by immunohistochemical methods and hybridization experiments in the rat brain after middle cerebral artery (MCA) occlusion. During ischemia, the immunoreactivity for TRX decreased; it disappeared after MCA occlusion in the ischemic regions. It rapidly decreased and nearly disappeared at 4 and 16 hours after MCA occlusion in the lateral striatum and frontoparietal cortex, respectively. On the other hand, in the perifocal ischemic region, the penumbra, TRX immunoreactivity began to increase 4 hours after MCA occlusion and continued to increase until 24 hours after occlusion. In hybridization experiments, TRX mRNA decreased and nearly disappeared 4 hours after MCA occlusion in the lateral striatum. In the frontoparietal cortex, it decreased until 24 hours after MCA occlusion. In the perifocal ischemic region, TRX mRNA began to increase 4 hours after MCA occlusion and continued to increase until 24 hours. Northern blot analysis showed that total TRX mRNA in the operated hemispheres was induced from 8 hours and increased until 24 hours after the surgical procedures. We previously reported that recombinant TRX promotes the in vitro survival of primary cultured neurons. We now suggest that TRX in the penumbra has neuroprotective functions and that decreased levels of TRX in the ischemic core modify neuronal damage during focal brain ischemia.

scholarly journals 19F Imaging of Cerebral Blood Oxygenation in Experimental Middle Cerebral Artery Occlusion: Preliminary Results

1988 ◽  
Vol 8 (2) ◽  
pp. 276-281 ◽  
Author(s):  
D. Eidelberg ◽  
G. Johnson ◽  
P. S. Tofts ◽  
J. Dobbin ◽  
H. A. Crockard ◽  
...  
Keyword(s):  
Middle Cerebral Artery ◽  
Cerebral Artery ◽  
Perfusion Defect ◽  
Relaxation Times ◽  
Artery Occlusion ◽  
Blood Substitutes ◽  
Blood Oxygenation ◽  
Relative Reduction ◽  
Mca Occlusion

Fluorine (19F) nuclear magnetic resonance may be used to image cerebral perfusion in cats receiving perfluorocarbon blood substitutes. 19F relaxation times in these blood substitutes are dependent on oxygen tension (Po2) and may be used to calculate and spatially map cerebrovascular Po2 values in vivo. We have applied this noninvasive method to experimental middle cerebral artery (MCA) occlusion. Following MCA occlusion a perfusion defect is evident in the sylvian region, followed by the appearance of collaterals. Signal from the ipsilateral rete mirabilis is increased. Calculated cortical vascular Po2 values indicate a relative reduction in oxygenation in the ischaemic hemisphere. Po2 maps show a perfused hypoxaemic zone adjacent to the perfusion defect. These changes are partly reversed with reperfusion.

Somatosensory Evoked Potential Monitoring of Temporary Middle Cerebral Artery Occlusion during Aneurysm Operation

Neurosurgery ◽  
1987 ◽  
Vol 21 (4) ◽  
pp. 492-496 ◽  
Author(s):  
Jan J. A. Mooij ◽  
Anna Buchthal ◽  
Milan Belopavlovic
Keyword(s):  
Middle Cerebral Artery ◽  
Cerebral Artery ◽  
Artery Occlusion ◽  
Moderate Hypothermia ◽  
Cortical Function ◽  
Mca Occlusion ◽  
Median Nerve Stimulation ◽  
Temporary Occlusion ◽  
Evoked Potential Monitoring ◽  
Cerebral Artery Occlusion

Abstract Somatosensory evoked potentials (SEPs) in response to median nerve stimulation were used as a guide to cortical function during temporary occlusion of the distal M1 segment of the middle cerebral artery (MCA) in the surgical treatment of five large aneurysms of the MCA bifurcation. MCA occlusion times ranged from 8 to 19 minutes under moderate hypothermia at 28.8° to 30.3°C. SEPs were preserved for variable times during MCA occlusion, ranging from no increase in latency after 13 minutes of occlusion to severe deterioration after 6 minutes. In no case was MCA occlusion maintained for longer than 3 minutes in the presence of a severely disturbed SEP. Recovery of the SEP to its preoperative relationship with that of the nonoperated hemisphere was seen in all cases before the end of operation. All patients were awake after rewarming at the end of operation without any neurological deficit. Monitoring the SEP pertaining to the territory of a cerebral artery during its temporary occlusion can help avoid ischemic damage and will allow the surgeon to take advantage of the several benefits of this technique in aneurysm surgery. (Neurosurgery 21:492-496, 1987)

Distal versus Proximal Middle Cerebral Artery Occlusion: Different Mechanisms

2019 ◽  
Vol 47 (5-6) ◽  
pp. 238-244
Author(s):  
Young Seo Kim ◽  
Bum Joon Kim ◽  
Kyung Chul Noh ◽  
Kyung Mi Lee ◽  
Sung Hyuk Heo ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Middle Cerebral Artery ◽  
Cerebral Artery ◽  
Artery Occlusion ◽  
High Rate ◽  
Collateral Flow ◽  
Large Artery ◽  
Factors Associated ◽  
Imaging Characteristics ◽  
Distal Migration

Background: Clinical and radiological characteristics of middle cerebral artery (MCA) infarction may differ according to the location of occlusion. Objectives: We investigated the difference between proximal and distal symptomatic MCA occlusion (MCAO) in patients with ischemic stroke. The factors associated with the imaging characteristics were also analyzed. Methods: Patients with ischemic stroke due to MCAO were consecutively enrolled. The location of MCAO was determined by the ratio of the length of the ipsilesional MCA to that of the contralateral MCA and dichotomized to proximal and distal MCAO. Clinical and radiological characteristics were compared between patients with proximal and distal MCAO. Factors associated with the basal ganglia (BG) involvement, hemorrhagic transformation (HT), and neurological change during admission were investigated. Results: Among 181 included patients, MCAO location showed a bimodal peak (at the proximal [n = 99] and distal MCA [n = 82]). Proximal MCAO was more frequently associated with hyperlipidemia and large artery atherosclerosis, whereas distal MCAO was more frequently associated with hypertension, atrial fibrillation, and cardioembolic stroke. BG involvement was similar between the 2 groups (48 vs. 39%; p = 0.21), whereas HT was more frequent in distal MCAO (10 vs. 23%; p = 0.02). Among patients with proximal MCAO, hyperintense vessel sign was less frequently observed in those with a BG involvement than those without (38 vs. 60%; p = 0.03). Among those without BG involvement, the presence of HT was very low and similar between patients with proximal and distal MCAOs (1.9 vs. 2.0%). However, in patients with BG involvement, HT was more frequently observed in those with distal MCAO than in those with proximal MCAO (54.8 vs. 15.7%; p < 0.001). The presence of hyperintense vessel sign (OR 0.172, 95% CI 0.051–0.586; p = 0.005) and distal MCAO (OR 0.200, 95% CI 0.059–0.683; p = 0.011) was independently associated with improvement during admission. Conclusion: Proximal MCAO is more frequently associated with atherosclerosis, whereas distal MCAO is more frequently associated with cardioembolism. In proximal MCAO, the status of collateral flow presented by hyperintense vessel sign may affect the involvement of BG. In distal MCAO, distal migration of the embolus, which first impacted at the proximal MCA causing BG ischemia, may explain the high rate of HT by reperfusion injury. Hyperintense vessel sign and distal MCAO were independently associated with neurological improvement during admission.

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