Occlusion Of Ipsilateral Middle Cerebral Artery Research Articles

Metagenomics Analysis of Thrombus Samples Retrieved from Mechanical Thrombectomy.

PurposeThe purpose of this study was to assess the microbiota in middle cerebral artery thrombi retrieved in mechanical thrombectomy arising out of symptomatic carotid plaque within 6 hours of acute ischemic stroke. Thrombi were subjected to next-generation sequencing for a bacterial signature to determine their role in atherosclerosis.Materials and MethodsWe included 4 human middle cerebral artery thrombus samples (all patients were male). The median age for the patients was 51±13.6 years. Patients enrolled in the study from Pacific Medical University and Hospital underwent mechanical thrombectomy in the stroke window period. All patients underwent brain magnetic resonance angiography (MRA) and circle of Willis and neck vessel MRA along with the standard stroke workup to establish stroke etiology. Only patients with symptomatic carotid stenosis and tandem lesions with ipsilateral middle cerebral artery occlusion were included in the study. Thrombus samples were collected, stored at –80 degrees, and subjected to metagenomics analysis.ResultsOf the 4 patients undergoing thrombectomy for diagnosis with ischemic stroke, all thrombi recovered for bacterial DNA in qPCR were positive. More than 27 bacteria were present in the 4 thrombus samples. The majority of bacteria were Lactobacillus, Stenotrophomonas, Pseudomonas, Staphylococcus, and Finegoldia.ConclusionGenesis of symptomatic atherosclerotic carotid plaque leading to thromboembolism could be either due to direct mechanisms like acidification and local inflammation of plaque milieu with lactobacillus, biofilm dispersion leading to inflammation like with pseudomonas fluorescence, or enterococci or indirect mechanisms like Toll 2 like signaling by gut microbiota.

Successful mechanical thrombectomy for repeated ipsilateral middle cerebral artery occlusion in a patient with Trousseau syndrome: A case report

Successful mechanical thrombectomy for repeated ipsilateral middle cerebral artery occlusion in a patient with Trousseau syndrome: A case report

Early diagnosis of acute ischemic stroke and observation of thrombolytic therapy by 7.0T magnetic resonance

Objective To investigate the early diagnosis of acute ischemic stroke, and to evaluate the effect of early thrombolytic therapy. Methods 70 male C57BL/6J mice were stratified in group , sham group (n=6), non-thrombolytic therapy group (n=15), thrombolytic therapy group (n=49). The models of focal cerebral ischemia was induced via photothrombosis, the Magnetic resonance angiography (MRA) and apparent diffusion coefficient (ADC) of the magnetic resonance were used as criteria for successful modeling. The mice were treated with urokinase as a thrombolytic drug, then behavioral scores were observed. Acquisition of Diffusion-weighted imaging (DWI), ADC, Three-dimensional fast low angle shot (3D-Flash) and T2 signal by Magnetic resonance (MRI). Results In the fast-moving test of the balance beam, the speed of sham mice (30.97±7.32)×0.01 m/s was significantly faster than that of thrombolytic mice (15.39±8.82)×0.01 m/s and mice without thrombolytic therapy (2.56±2.80)×0.01 m/s. The modified neurological deficits scores (mNSS) of sham group (0.50±0.54) was significantly lower than that of thrombolytic mice (4.87±2.34) and non-thrombolytic mice (9.83±1.59). The ADC score of ipsilateral cerebrum (0.62±0.13)×0.001 mm2/sec of the model mice was lower than that of the contralateral ADC (0.43±0.07)×0.001 mm2/sec. After the completion of the model, the contralateral middle cerebral artery was still smooth and the ipsilateral middle cerebral artery occlusion. According to different treatment, a part of the ipsilateral middle cerebral artery were opened, the rate of the middle cerebral artery occlusion were opened is about 61.2%, non-thrombotic mice obstruction of the middle cerebral artery opening rate is about 6.67%. The infarct size (10.52±4.41) mm2 in the thrombolytic therapy group was significantly smaller than that in the untreated mice (23.38±1.66) mm2. Conclusion 7.0T MRI can be used as a criteria for the early diagnosis of acute ischemic stroke, to evaluate the effect of middle cerebral artery occlusion and recanalization. Key words: Ischemic stroke; Urokinase; Behavioral analysis; Magnetic resonance imaging

Intracarotid Sodium Nitroprusside on Fifth Post Ischemic Stroke Day in Middle Cerebral Artery Occlusion Rat Model.

Ischemic stroke at later stages (>4.5 hour) have very few treatment options left. In those cases Nitric Oxide (NO) may provide promising results. NO is active in signaling pathways. Sodium Nitroprusside (SNP), a NO donor was tested earlier in rat Middle Cerebral Artery Occlusion (MCAO) model in early stages (5-60 minutes) and found useful but in delayed stroke cases (60-120 minutes) found useless. This was due to local inducible Nitric Oxide Synthase Enzyme (iNOS) and superoxide (causes destructive effect) formation which was skipped. To evaluate the effect of Intracarotid Sodium Nitroprusside (ICSNP) in MCAO rat model of ischemic stroke (I/R model) fifth post ischemic stroke day. A total of 24 Sprague Dawley rats, weighing 250 gm to 280 gm, at CDRI-Lucknow, India were used. Rats were divided in three groups. Group A (n=4) were taken as sham with standard procedure but without any injection on fifth day, Group B (n=8) as control with injection of saline on fifth day and Group C (n=12) received SNP at dose of 3 mcg/kg/minute given directly in internal carotid artery via External Carotid Artery (ECA) with a modified intraluminal stump technique as Ischemia/Reperfusion (I/R) in ipsilateral MCAO at intracarotid artery region as a single dose therapy on fifth day and then wound was closed. Waited for full recovery for two hours, then neurobehavioural assessment scores were noted. Thereafter, the brains were quickly removed and sliced at 2 mm intervals. Animals showing no sign of neurological deficit, were excluded from the study. Tested animals were compared with control animals for neurological deficit, percentage of infarction by 2,3,5-Triphenyl Tetrazolium Chloride (TTC) staining, nNOS expression and scores were summed up. The statistical analysis was done by Newman-Keuls test, Graph Pad prism (version.5.0) and p<0.05 was considered statistically significant. ICSNP group (Group C) showed a good reduction in the cerebral infarction of 53.42% as compared to control (Group B). Group A mean change in Newman-Keuls test and Graph Pad prism (version.5.0) was showing increase of 1.44 points/6.55%, compared to Group B decrease of 0.7 points. A 60% decrease in ischemic zone noted in Group A. The use of single dose ICSNP is beneficial (53.42%) in fifth post stroke day.

Percutaneous Mechanical Thrombectomy in a Patient with Symptomatic Carotid Stenosis and Ipsilateral Middle Cerebral Artery Occlusion

Percutaneous Mechanical Thrombectomy in a Patient with Symptomatic Carotid Stenosis and Ipsilateral Middle Cerebral Artery Occlusion

Acute Ischemic Stroke in a 12-Year-Old Successfully Treated With Mechanical Thrombectomy

We report the case of a healthy 12-year-old girl with an acute ischemic stroke successfully treated with mechanical thrombectomy. The child was referred to our hospital 6 hours after sudden onset of severe headache and left hemiparesis. Cerebral angiography findings were consistent with right distal internal carotid artery occlusion in addition to ipsilateral middle cerebral artery occlusion. Subsequent mechanical thrombectomy with Solitaire AB device resulted in complete vessel recanalization. The patient experienced progressive neurologic improvement with good clinical recovery at the 3-month follow-up. To our knowledge, only 3 cases of primary mechanical thrombectomy in children have been previously reported in the literature. Safety and efficacy data for endovascular therapies in pediatric acute ischemic stroke are lacking. We propose mechanical thrombectomy as an option in children with significant neurologic deficits and proven arterial occlusion, especially when the therapeutic window for intravenous thrombolysis has been exceeded.

Granulocyte Colony-Stimulating Factor Enhances Arteriogenesis and Ameliorates Cerebral Damage in a Mouse Model of Ischemic Stroke

Enhancing collateral artery growth is a potent therapeutic approach to treat cardiovascular ischemic disease from occlusive artery. Granulocyte-macrophage colony-stimulating factor (GM-CSF) has gained attention for its ability to promote arteriogenesis, ameliorating brain damage, by the mechanisms involving monocyte upregulation. However, the recent clinical study testing its efficacy in myocardial ischemia has raised the question about its safety. We tested alternative colony-stimulating factors for their effects on collateral artery growth and brain protection. Brain hypoperfusion was produced by occluding the left common carotid artery in C57/BL6 mice. After the surgery, granulocyte colony-stimulating factor, macrophage colony-stimulating factor, or GM-CSF (100 μg/kg/day) was administered daily for 5 days. The angioarchitecture for leptomeningeal anastomoses and the circle of Willis were visualized after the colony-stimulating factor treatment. Circulating blood monocytes and Mac-2-positive cells in the dorsal surface of the brain were determined. A set of animals underwent subsequent ipsilateral middle cerebral artery occlusion and infarct volume was assessed. Granulocyte colony-stimulating factor as well as GM-CSF promoted leptomeningeal collateral growth after common carotid artery occlusion. Both granulocyte colony-stimulating factor and GM-CSF increased circulating blood monocytes and Mac-2-positive cells in the dorsal brain surface, suggesting the mechanisms coupled to monocyte upregulation might be shared. Infarct volume after middle cerebral artery occlusion was reduced by granulocyte colony-stimulating factor, similarly to GM-CSF. Macrophage colony-stimulating factor showed none of theses effects. Granulocyte colony-stimulating factor enhances collateral artery growth and reduces infarct volume in a mouse model of brain ischemia, similarly to GM-CSF.

Endovascular Coil Embolization of a Ruptured Distal Anterior Choroidal Artery Aneurysm Associated With Ipsilateral Middle Cerebral Artery Occlusion -Case Report-

An 84-year-old woman with a history of hypertension and a brain infarction presented with a rare distal anterior choroidal artery (AChoA) aneurysm not associated with moyamoya disease manifesting as sudden onset of headache caused by intraventricular hemorrhage. Digital subtraction angiography revealed a peripheral aneurysm in the left AChoA located distal to the plexal point and steno-occlusive changes of the proximal left middle cerebral artery (MCA) and the left posterior cerebral artery (PCA). Collateral arterial channels to the left MCA and left PCA territories were observed along the left AChoA. No neuroimaging findings were compatible with moyamoya disease. Since the aneurysm did not shrink at 2 months after the onset, endovascular treatment was indicated. Under local anesthesia, a microcatheter was placed into the AChoA proximal to the aneurysm with the aid of a 0.008-inch microguidewire. After a provocation test, three detachable platinum coils were delivered into the aneurysm and the parent artery. Complete obliteration of the aneurysm was achieved without additional neurological sequelae. Successful treatment of a ruptured distal AChoA aneurysm associated with atherosclerotic changes of the intracranial arteries was achieved using a meticulous endovascular technique.

Spontaneous recanalization of a middle cerebral artery occlusion with subsequent carotid endarterectomy

We report the case of a 55-year-old man who presented with a left hemisphere stroke. The initial computed tomography scan demonstrated a cerebral infarct in association with a left middle cerebral artery occlusion. Carotid duplex ultrasound imaging revealed a surgical grade stenosis of the proximal left internal carotid artery; however, in view of the uncertain benefits of internal carotid endarterectomy in the face of ipsilateral middle cerebral artery occlusion, surgery was deferred. Subsequent surveillance by transcranial Doppler imaging and repeat computed tomography demonstrated spontaneous recanalization. The patient proceeded to carotid endarterectomy with no complications.

Endovascular Treatment of a Lenticulostriate Artery Aneurysm with N-butyl Cyanoacrylate

Aneurysms arising from lenticulostriate artery branches in moyamoya-type disease are challenging lesions to treat, due to their fragility and deep location. Surgery is difficult and endovascular options may be limited. A 57-year-old woman presented with a right ganglionic parenchymal hemorrhage due to a ruptured lenticulostriate artery aneurysm associated with ipsilateral middle cerebral artery occlusion. The aneurysm and parent feeding artery were occluded using endovascular injection of N-butyl cyanoacrylate. The aneurysm was successfully obliterated and although some glue did enter the more distal middle cerebral artery, there was no change in the patient's neurologic status. In highly selected cases where lenticulostriate aneurysms cannot be directly accessed for surgery or endovascular coiling, obliteration with liquid acrylic glue may be considered as a therapeutic option.

DNA fragmentation and HSP70 protein induction in hippocampus and cortex occurs in separate neurons following permanent middle cerebral artery occlusions.

DNA nick end-labeling (TUNEL) and heat shock protein (HSP)70 immunocytochemistry were performed on the same brain sections 1 (n = 6), 3 (n = 12), and 7 (n = 7) days following permanent middle cerebral artery (MCA) occlusions produced in adult rats using the endovascular carotid suture method. In the cortex at 1 and 3 days following MCA occlusions, HSP70 immunoreactive neurons were located outside areas of infarction and showed little evidence of DNA fragmentation. HSP70-stained cortical neurons were intermingled with TUNEL cells near the infarct, but extended for greater distances away from the infarct. DNA fragmentation occurred in CA1 hippocampal neurons in 39% of the animals at 1 and 3 days following ipsilateral MCA occlusion. Bilateral DNA fragmentation occurred in CA1 neurons in one subject. HSP70 protein was expressed in CA1 hippocampal neurons in nine of 18 (50%) animals at 1 and 3 days following MCA occlusions, including all animals that exhibited hippocampal DNA fragmentation. Three animals had bilateral expression of HSP70 in CA1 neurons. Cells that stained for either HSP70 protein or DNA fragmentation existed in close proximity to one another. Approximately 5-7% of HSP70-stained cells were TUNEL stained and 3% of TUNEL-positive cells also stained for HSP70. There was no HSP70 staining or DNA fragmentation in the brains of sham-operated controls (n = 4) or in the brains of animals 7 days following MCA occlusions. These data suggest that ischemic cells capable of translating HSP70 protein generally do not undergo DNA fragmentation. These data support the concept that most HSP70 protein-containing neurons in the cortical "penumbra" and hippocampus survive ischemic injury and are "reversibly injured." It is shown that CA1 hippocampal pyramidal neurons die or are reversibly injured in approximately 50% of animals following permanent MCA occlusions. Although the mechanism of this hippocampal injury is unknown, it could relate to transynaptic activation of N-methyl-D-aspartate (NMDA) receptors that mediate induction of early genes in hippocampus.

Contribution of cerebrovascular parasympathetic and sensory innervation to the development of cerebral edema in rat focal ischemia and reperfusion

The purpose of this study was to investigate the contribution of cerebrovascular parasympathetic and sensory innervation to the development of ischemic brain edema. We measured the cerebral water content in rat focal ischemia and reperfusion model. A chronic transection of neither parasympathetic fiber nor sensory fiber (nasociliary nerve) modified the cerebral water content after 2 h ipsilateral middle cerebral artery (MCA) occlusion. However, a chronic transection of sensory fiber, but not the parasympathetic fiber, significantly attenuated the increase of the cerebral water content after 2 h occlusion of ipsilateral MCA followed by 2 h reperfusion. This result indicates that the cerebrovascular sensory innervation contributes to the development of cerebral edema in the postischemic reperfusion.

Middle cerebral artery occlusion in presence of low perfusion pressure increases infarct size in rats.

A model was set up in order to evaluate the importance of hemispheric perfusion pressure when the middle cerebral artery (MCA) is occluded in anaesthetized rats. In 6 animals the internal carotid artery (ICA) was occluded prior to ipsilateral MCA occlusion; in 17 animals the MCA only was occluded; 6 animals underwent the same preparation, but the vessels were left unoccluded. Four days after surgery the infarct volume was measured with a computerized image analyser. The infarcted areas were significantly larger in the ICA + MCA occluded group compared with the MCA occluded group (p less than 0.005), which in turn had larger infarcts than the sham-operated animals (p less than 0.001). These results indicate that patients with hypoperfusion, due to severe ICA stenosis and impaired collateral blood supply, are at higher risk of developing major stroke, when embolism into a cerebral artery occurs, as compared to patients with no, or only minor, reduction in hemispheric perfusion pressure.