Infarct patterns in atherosclerotic middle cerebral artery versus internal carotid artery disease

Neurology ◽  
2004 ◽  
Vol 62 (8) ◽  
pp. 1291-1296 ◽  
Author(s):  
P. H. Lee ◽  
S. -H. Oh ◽  
O. Y. Bang ◽  
S. -Y. Joo ◽  
I. S. Joo ◽  
...  
PLoS ONE ◽  
2019 ◽  
Vol 14 (12) ◽  
pp. e0225906
Author(s):  
Changqing Zhang ◽  
Yilong Wang ◽  
Xingquan Zhao ◽  
Liping Liu ◽  
ChunXue Wang ◽  
...  

2020 ◽  
Vol 19 (4) ◽  
pp. 56-64
Author(s):  
L. Herasym ◽  
I. Tsumanets

Carotid artery disease leads to stroke in 30% of cases. The total frequency of carotid artery deformations varies from 10 to 40% depending on the results of angiographic and pathological examinations. Coiling of the internal carotid artery is associated with embryological pathology, and elongation and inflection are the result of fibromuscular dysplasia or changes that are accompanied by atherosclerotic damage to the arteries. Kinking – an artery bend at an acute angle. It can be congenital, when from early childhood there is a violation of cerebral circulation and develops over time from an elongated carotid artery. The formation of inflections contributes to hypertension, the progression of atherosclerosis. Coiling – the formation of a loop of an artery. Despite the smooth running of the loop, the changes in bleeding in it are significant. The nature of bends in coiling can vary depending on body position, blood pressure. The most common is the elongation of the internal carotid or spinal artery, which leads to the formation of smooth curves along the vessel. Elongation of the arteries is usually detected in random studies. The main etiological causes of pathological tortuosity of the internal carotid artery include: congenital deformation of the vascular wall, hypertension, osteochondrosis of the cervical vertebrae, compression of the bracheocephalic arteries, cranial nerves. The review article deals with anatomy and topography of the major vascular-nervous bundle components of the neck on the stages of early ontogenesis from the point of view of surgical correction of departures from their normal development in newborns and children of an early age. However, literary data are controversial and fragmentary concerning anatomical peculiarities of the carotid arteries, internal jugular vein, and vagus. The facts concerning synoptic correlation of the major vascular-nervous bundle components of the neck in fetuses and newborns are not systematized. Carotid artery disease leads to stroke in 30% of cases. The total frequency of carotid artery deformations varies from 10 to 40% depending on the results of angiographic and pathological examinations. 


2019 ◽  
Vol 10 ◽  
pp. 205
Author(s):  
Seiei Torazawa ◽  
Hideaki Ono ◽  
Tomohiro Inoue ◽  
Takeo Tanishima ◽  
Akira Tamura ◽  
...  

Background: Very large and giant aneurysms (≥20 mm) of the internal carotid artery (ICA) bifurcation (ICAbif) are definitely rare, and optimal treatment is not established. Endovascular treatments are reported as suboptimal due to difficulties of complete occlusion and tendencies to recanalization. Therefore, direct surgery remains an effective strategy if the clipping can be performed safely and reliably, although very difficult. Case Description: Two cases of ICAbif aneurysms (>20 mm) were treated. Prior assistant superficial temporal artery (STA)-middle cerebral artery (MCA) bypass was performed to avoid ischemic complications during prolonged temporary occlusion of the arteries in both cases. In Case 1 (22-mm aneurysm), the dome was inadvertently torn in applying the clip because trapping had resulted in insufficient decompression. Therefore, in Case 2 (28-mm aneurysm), almost complete trapping of the aneurysm and subsequent dome puncture was performed, and the aneurysm was totally deflated by suction from the incision. This complete aneurysm decompression allowed safe dissection and successful clipping. Conclusion: Trapping, deliberate aneurysm dome puncture, and suction decompression from the incision in conjunction with assistant STA-MCA bypass can achieve complete aneurysm deflation, and these techniques enable safe dissection of the aneurysm and direct clipping of the aneurysm neck. Direct clipping with this technique for very large and giant ICAbif aneurysms may be the optimal treatment choice with the acceptable outcome if endovascular treatment remains suboptimal.


Neurosurgery ◽  
2017 ◽  
Vol 80 (2) ◽  
pp. 235-247 ◽  
Author(s):  
Christopher M. Owen ◽  
Nicola Montemurro ◽  
Michael T. Lawton

Abstract BACKGROUND: Blister aneurysms of the supraclinoid internal carotid artery (ICA) are challenging lesions with high intraoperative rupture rates and significant morbidity. An optimal treatment strategy for these aneurysms has not been established. OBJECTIVE: To analyze treatment strategy, operative techniques, and outcomes in a consecutive 17-year series of ICA blister aneurysms treated microsurgically. METHODS: Seventeen patients underwent blister aneurysm treatment with direct clipping, bypass and trapping, or clip-reinforced wrapping. RESULTS: Twelve aneurysms (71%) were treated with direct surgical clipping. Three patients required bypass: 1 superficial temporal artery to middle cerebral artery bypass, 1 external carotid artery to middle cerebral artery bypass, and 1 ICA to middle cerebral artery bypass. One patient was treated with clip-reinforced wrapping. Initial treatment strategy was enacted 71% of the time. Intraoperative rupture occurred in 7 patients (41%), doubling the rate of a poor outcome (57% vs 30% for patients with and without intraoperative rupture, respectively). Severe vasospasm developed in 9 of 16 patients (56%). Twelve patients (65%) were improved or unchanged after treatment, and 10 patients (59%) had good outcomes (modified Rankin Scale scores of 1 or 2). CONCLUSION: ICA blister aneurysms can be cautiously explored and treated with direct clipping as the first-line technique in the majority of cases. Complete trapping of the parent artery with temporary clips and placing permanent clip blades along normal arterial walls enables clipping that avoids intraoperative aneurysm rupture. Trapping/bypass is used as the second-line treatment, maintaining a low threshold for bypass with extensive or friable pathology of the carotid wall and in patients with incomplete circles of Willis.


2010 ◽  
pp. 504-517
Author(s):  
George Samandouras

Chapter 9.1 covers critical neurovascular brain anatomy, including internal carotid artery, the middle cerebral artery, the anterior cerebral artery, the vertebral arteries (VAs), the basilar artery (BA), and the venous system.


1988 ◽  
Vol 8 (5) ◽  
pp. 697-712 ◽  
Author(s):  
Norihiro Suzuki ◽  
Jan Erik Hardebo ◽  
Christer Owman

In order to clarify the origins and pathways of vasoactive intestinal polypeptide (VlP)-containing nerve fibers in cerebral blood vessels of rat, denervation experiments and retrograde axonal tracing methods (true blue) were used. Numerous VIP-positive nerve cells were recognized in the sphenopalatine ganglion and in a mini-ganglion (internal carotid mini-ganglion) located on the internal carotid artery in the carotid canal, where the parasympathetic greater superficial petrosal nerve is joined by the sympathetic fibers from the internal carotid nerve, to form the Vidian nerve. VIP fiber bridges in the greater deep petrosal nerve and the internal carotid nerve reached the wall of the internal carotid artery. Two weeks after bilateral removal of the sphenopalatine ganglion or sectioning of the structures in the ethmoidal foramen, VIP fibers in the anterior part of the circle of Willis completely disappeared. Very few remained in the middle cerebral artery, the posterior cerebral artery, and rostral two-thirds of the basilar artery, whereas they remained in the caudal one-third of the basilar artery, the vertebral artery, and intracranial and carotid canal segments of the internal carotid artery. One week after application of true blue to the middle cerebral artery, dye accumulated in the ganglion cells in the sphenopalatine, otic and internal carotid mini-ganglion; some of the cells were positive for VIP. The results show that the VIP nerves in rat cerebral blood vessels originate: (a) in the sphenopalatine, and otic ganglion to innervate the circle of Willis and its branches from anterior and caudally and (b) from the internal carotid mini-ganglion to innervate the internal carotid artery at the level of the carotid canal and to some extent its intracranial extensions.


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