Cerebrovascular Disease 1: Vascular Territories (DRAFT)

2018 ◽  
Author(s):  
Tamara Kaplan ◽  
Tracey Milligan
Keyword(s):  
Cerebrovascular Disease ◽  
Middle Cerebral Artery ◽  
Cerebral Artery ◽  
Anterior Cerebral Artery ◽  
Posterior Cerebral Artery ◽  
Sensory Loss ◽  
Homonymous Hemianopia ◽  
Leg Weakness ◽  
Sensory Changes ◽  
The Brain

The video in this chapter explores cerebrovascular disease, and focuses on vascular territories. It discusses the middle cerebral artery (MCA), posterior cerebral artery (PCA), and anterior cerebral artery (ACA), along with the portions of the brain they supply, as well as the different presentations of stroke in the three territories - contralateral weakness, sensory loss, and aphasia in MCA stroke, contralateral homonymous hemianopia in PCA stroke, and contralateral leg weakness and sensory changes in ACA stroke.

Human fetal medial striate artery or artery of Heubner

2009 ◽  
Vol 3 (4) ◽  
pp. 296-301 ◽  
Author(s):  
Ljiljana Vasović ◽  
Sladjana Ugrenović ◽  
Ivan Jovanović
Keyword(s):  
Middle Cerebral Artery ◽  
Diagnostic Test ◽  
Cerebral Artery ◽  
Cerebral Circulation ◽  
Anterior Cerebral Artery ◽  
Anatomical Variations ◽  
Test Results ◽  
Terminal Part ◽  
The Brain

Object The authors describe some of the features of the medial striate branch or recurrent artery of Heubner (RAH). This structure has indisputable functional, neurological, and neurosurgical significance, and originates from the A1 and/or A2 segments of the anterior cerebral artery. Methods Microdissection of 94 human fetal specimens was performed. The RAH was observed in 97.3% (single in 71.6%, double in 25.1%, and triple in 3.3%) of the cases. Its origin was from A2 in 42.3% of specimens, from the A1–A2 junction in 25.7%, and from A1 in 20%. Results Five types and 14 subtypes of the RAH were identified, determined based on vessel origin and number. In its course, the RAH gave 1–12 branches, and the terminal part most frequently penetrated into the brain through the anterior perforated substance at the level of the sphenoid segment of the middle cerebral artery. The specimens with a single RAH fenestration, abnormal double RAH anastomosis, and unusual RAH origin and relationship to the surrounding vessels represented new data. Conclusions The authors' observations of common anatomical variations in the number and origin of the RAH, as well as its abnormalities, may assist neuroradiologists in the interpretation of diagnostic test results and neurosurgeons in performing procedures in the anterior cerebral circulation.

scholarly journals Hemispatial neglect in cerebrovascular disease involving the territory of the middle cerebral artery and posterior cerebral artery.

Nosotchu ◽  
1994 ◽  
Vol 16 (5) ◽  
pp. 348-353
Author(s):  
Kenichi Iijima ◽  
Shotai Kobayashi ◽  
Nobuo Suyama ◽  
Kazuya Yamashita ◽  
Shuhei Yamaguchi
Keyword(s):  
Cerebrovascular Disease ◽  
Middle Cerebral Artery ◽  
Cerebral Artery ◽  
Posterior Cerebral Artery ◽  
Hemispatial Neglect

Ruptured Aneurysm at the Origin of the Accessory Middle Cerebral Artery: Case Report

Neurosurgery ◽  
1990 ◽  
Vol 26 (2) ◽  
pp. 320-322 ◽  
Author(s):  
Satoshi Kuwabara ◽  
Hiroki Naitoh
Keyword(s):  
Middle Cerebral Artery ◽  
Cerebral Artery ◽  
Anterior Cerebral Artery ◽  
Relevant Literature ◽  
Vascular Anomaly ◽  
Ruptured Aneurysm ◽  
Accessory Middle Cerebral Artery ◽  
Horizontal Portion ◽  
The Brain ◽  
Perforating Arteries

Abstract The accessory middle cerebral artery is a rare vascular anomaly of the brain. We describe a case of a ruptured aneurysm at the junction of the accessory middle cerebral artery and the horizontal portion of the anterior cerebral artery. The lesion was demonstrated by angiography and confirmed at surgery. No perforating arteries arising from this accessory artery were found. There have been only four previous reports of aneurysms located at the origin of the accessory middle cerebral artery. The relevant literature is briefly reviewed.

Abstract WP285: Hemicraniectomy Outcomes in Patients with Malignant Middle Cerebral Artery Infarctions Plus

Stroke ◽  
2013 ◽  
Vol 44 (suppl_1) ◽  
Author(s):  
Navdeep S Sangha ◽  
Malcolm Irani ◽  
Hui Peng ◽  
Tzu-Ching Wu ◽  
Andrew D Barreto ◽  
...  
Keyword(s):  
Middle Cerebral Artery ◽  
Cerebral Artery ◽  
Anterior Cerebral Artery ◽  
Posterior Cerebral Artery ◽  
High Rate ◽  
Clinical Implications ◽  
Vascular Territory ◽  
Good Outcome ◽  
The Mean ◽  
One Year

Hemicraniectomy (HC) is a proven treatment to reduce mortality and improve outcomes in patients with malignant middle cerebral artery (MCA) infarction. The benefit of HC in patients with MCA strokes plus infarctions in other vascular territories has not been well defined. We hypothesized that there would be no difference in outcomes in patients with MCA strokes compared to those with MCA Plus infarctions. We retrospectively reviewed our registry from 07/2003 to 12/2011, and identified consecutive patients diagnosed with an ischemic stroke that underwent HC. Outcome measures included mRS at discharge, mRS at day 90 and death at one year. A good outcome was defined as mRS 0-4. The vascular territory of infarction was established by a vascular neurologist who reviewed the nearest CT scan prior to the procedure and compared it with the official interpretation of a neuroradiologist. The MCA Plus infarctions included MCA + anterior cerebral artery (ACA), MCA + posterior cerebral artery (PCA) and MCA + ACA + PCA. Ninety seven patients had a HC. Sixty four were MCA and 33 were MCA Plus. The mean MCA and MCA plus ages were 51.9 (± 14.2) and 51.3 (± 12.8) years respectively. Median NIHSS was 12.5 (IQR 10.0-15.0) in MCA vs. 12.2 (IQR 9.5-14.0) in MCA Plus. MCA group had a good outcome at discharge in 25% of subjects vs. 21% in the MCA Plus cohort, OR 0.72 (95% CI: 0.24-2.15). For patients with available data, 40% of MCA was dead at 90 days and 50% in MCA Plus, and for those who survived, 33% of MCA had a good outcome compared to 15% of the MCA Plus, OR 2.4 (95% CI: 0.45-7.61). Forty eight percent of MCA patients were dead at one year vs. 76% of the MCA Plus patients. We found no difference in good outcomes at discharge and 90 days in our cohort of patients who received a HC with MCA or MCA plus infarctions. Limitations include a high rate of missing data at day 90 and at one year, and poor standardization of HC timing. Further prospective studies are necessary to evaluate the clinical implications of HC in MCA Plus syndromes.

Compensatory Enlargement of the Posterior Communicating Artery Following Arterio-Sclerotic Changes of the Posterior Cerebral Artery

1940 ◽  
Vol 86 (365) ◽  
pp. 1086-1091 ◽  
Author(s):  
R. Klein
Keyword(s):  
Cerebral Artery ◽  
Anterior Cerebral Artery ◽  
Posterior Cerebral Artery ◽  
Anterior Communicating Artery ◽  
Brain Vessels ◽  
Anatomical Changes ◽  
Vast Literature ◽  
Compensatory Enlargement ◽  
The Brain ◽  
Circulatory Disturbances

While a vast literature refers to anomalies in various arteries of the brain, there are only a few reports concerning anatomical changes of vessels following altered circulatory conditions. Critchley mentions in his study of the anterior cerebral artery and its syndromes, an observation in which an arterio-sclerotic anterior cerebral artery of one side was so small as to be incapable of maintaining an adequate circulation, so that by way of an abnormally large anterior communicating artery the opposite anterior cerebral supplied both hemispheres. Critchley adds to that case several similar observations from the literature. The application of arteriography to circulatory disturbances has directed attention to analogous cases. Thus Moniz reported several observations in which a closure of the carotid artery of one side led to a distension of the anterior communicating in order to establish collateral circulation. The same mechanism appeared to be effective in the following two cases which we met in the course of our studies on brain vessels.

Cerebral hypoxia-ischemia and middle cerebral artery occlusion induce expression of the cannabinoid CB2 receptor in the brain

2007 ◽  
Vol 412 (2) ◽  
pp. 114-117 ◽  
Author(s):  
John C. Ashton ◽  
Rosanna M.A. Rahman ◽  
Shiva M. Nair ◽  
Brad A. Sutherland ◽  
Michelle Glass ◽  
...  
Keyword(s):  
Middle Cerebral Artery ◽  
Middle Cerebral Artery Occlusion ◽  
Cerebral Artery ◽  
Artery Occlusion ◽  
Cerebral Hypoxia ◽  
Cb2 Receptor ◽  
Hypoxia Ischemia ◽  
Cerebral Artery Occlusion ◽  
The Brain

Abstract 166: Endothelial Overexpression of LOX-1 Increases Stroke Size in vivo

2013 ◽  
Vol 113 (suppl_1) ◽  
Author(s):  
Alexander Akhmedov ◽  
Remo D Spescha ◽  
Francesco Paneni ◽  
Giovani G Camici ◽  
Thomas F Luescher
Keyword(s):  
Endothelial Cells ◽  
Ischemic Stroke ◽  
Endothelial Dysfunction ◽  
Middle Cerebral Artery ◽  
Middle Cerebral Artery Occlusion ◽  
Cerebral Artery ◽  
Oxidized Ldl ◽  
Artery Occlusion ◽  
Cerebral Artery Occlusion ◽  
The Brain

Background— Stroke is one of the most common causes of death and long term disability worldwide primarily affecting the elderly population. Lectin-like oxidized LDL receptor 1 (LOX-1) is the receptor for oxidized LDL identified in endothelial cells. Binding of OxLDL to LOX-1 induces several cellular events in endothelial cells, such as activation of transcription factor NF-kB, upregulation of MCP-1, and reduction in intracellular NO. Accumulating evidence suggests that LOX-1 is involved in endothelial dysfunction, inflammation, atherogenesis, myocardial infarction, and intimal thickening after balloon catheter injury. Interestingly, a recent study demonstrated that acetylsalicylic acid (aspirin), which could prevent ischemic stroke, inhibited Ox-LDL-mediated LOX-1 expression in human coronary endothelial cells. The expression of LOX-1 was increased at a transient ischemic core site in the rat middle cerebral artery occlusion model. These data suggest that LOX-1 expression induces atherosclerosis in the brain and is the precipitating cause of ischemic stroke. Therefore, the goal of the present study was to investigate the role of endothelial LOX-1 in stroke using experimental mouse model. Methods and Results— 12-week-old male LOX-1TG generated recently in our group and wild-type (WT) mice were applied for a transient middle cerebral artery occlusion (MCAO) model to induce ischemia/reperfusion (I/R) brain injury. LOX-1TG mice developed 24h post-MCAO significantly larger infarcts in the brain compared to WT (81.51±8.84 vs. 46.41±10.13, n=7, p < 0.05) as assessed morphologically using Triphenyltetrazolium chloride (TTC) staining. Moreover, LOX-1TG showed higher neurological deficit in RotaRod (35.57±8.92 vs. 66.14±10.63, n=7, p < 0.05) and Bederson tests (2.22±0.14 vs. 1.25±0.30, n=9-12, p < 0.05) - two experimental physiological tests for neurological function. Conclusions— Thus, our data suggest that LOX-1 plays a critical role in the ischemic stroke when expressed at unphysiological levels. Such LOX-1 -associated phenotype could be due to the endothelial dysfunction. Therefore, LOX-1 may represent novel therapeutic targets for preventing ischemic stroke.

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