Giant aneurysm of the middle cerebral artery containing an important blood channel

1972 ◽  
Vol 37 (3) ◽  
pp. 352-356 ◽  
Author(s):  
Hideo Terao ◽  
Isao Muraoka
Keyword(s):  
Cerebral Infarction ◽  
Middle Cerebral Artery ◽  
Cerebral Artery ◽  
Giant Aneurysm ◽  
Content Type ◽  
The Right ◽  
Fine Print

✓ An enormous globoid aneurysm arising from the right middle cerebral artery is reported. A functioning blood channel ran through the laminated thrombus within the aneurysm, and operative injury to this blood channel caused serious cerebral infarction.

Traumatic occlusion of the middle cerebral artery

1973 ◽  
Vol 39 (6) ◽  
pp. 753-756 ◽  
Author(s):  
Charles R. Loar ◽  
William M. Chadduck ◽  
G. Robert Nugent
Keyword(s):  
Middle Cerebral Artery ◽  
Cerebral Artery ◽  
Content Type ◽  
Complete Occlusion ◽  
Motorcycle Accident ◽  
The Right ◽  
Fine Print

✓ A case is reported of a patient rendered unconscious in a motorcycle accident. After a 6-hour lucid interval, he became unconscious again, and a left hemiplegia was noted. Arteriography demonstrated complete occlusion of the right middle cerebral artery. Comparable reported cases and theories of pathogenesis are discussed.

Comparison of middle cerebral artery trunk occlusion by silicone cylinder embolization and by trapping

1983 ◽  
Vol 58 (4) ◽  
pp. 492-499 ◽  
Author(s):  
Yoshikazu Okada ◽  
Takeshi Shima ◽  
Noboru Yokoyama ◽  
Tohru Uozumi
Keyword(s):  
Cerebral Infarction ◽  
Middle Cerebral Artery ◽  
Cerebral Artery ◽  
Clinicopathological Features ◽  
Neurological Deficits ◽  
Midline Shift ◽  
Content Type ◽  
Chronic Stage ◽  
The Brain ◽  
Fine Print

✓ The authors produced occlusion of the middle cerebral artery (MCA) trunk in dogs by two methods: silicone cylinder embolization and trapping. Comparative analyses of the clinicopathological features in these models, extending from the acute to chronic stage, were performed. Within 24 hours after embolization, the brain exhibited swelling without macroscopic infarction. Microangiograms revealed impaired filling in the deep areas of the brain with midline shift. At 4 to 7 days after embolization, the animals showed major neurological deficits, evident deep cerebral infarction, and poorly perfused areas in the deep cerebrum with prominent midline shift. At 3 to 4 weeks after embolization, the neurological deficits improved and the affected regions showed cavities or localized lesions. Microangiograms demonstrated hypervascular areas with abnormal vessels in the affected cerebrum. On the other hand, trapping of the MCA trunk produced mild neurological deficits, although there was no evidence of macroscopic lesions or impairment of filling. This study shows that silicone cylinder embolization in the MCA trunk produces a reliable and reproducible deep cerebral infarction in dogs.

Dissecting aneurysms of the anterior circle of Willis arteries

1987 ◽  
Vol 67 (2) ◽  
pp. 296-300 ◽  
Author(s):  
Ryuichi Kitani ◽  
Tooru Itouji ◽  
Yatsugi Noda ◽  
Makoto Kimura ◽  
Satoshi Uchida
Keyword(s):  
Cerebral Infarction ◽  
Middle Cerebral Artery ◽  
Cerebral Artery ◽  
Superficial Temporal Artery ◽  
Temporal Artery ◽  
Dissecting Aneurysm ◽  
Collateral Flow ◽  
Content Type ◽  
Initial Symptoms ◽  
The Right

✓ Two cases of spontaneous dissecting aneurysm extending from the supraclinoid portion of the internal carotid artery to the middle cerebral artery are reported in two teenaged patients. Both patients collapsed with a headache on the right side, left hemiparesis, and altered consciousness due to cerebral ischemia. One patient became alert in 2 days; however, his condition rapidly deteriorated 4 days later and he died on the 8th day from massive cerebral infarction. The other patient received a right superficial temporal artery (STA)-middle cerebral artery (MCA) anastomosis 50 hours after his initial symptoms. He improved gradually and is able to walk without help. Cerebral angiograms 3 months after the operation disclosed progressive attenuation of the MCA and dilatation of the anastomosed STA. Artificial collateral flow demonstrated in the postoperative angiogram may have been useful in preventing massive cerebral infarction.

Effect of opiate antagonists on middle cerebral artery occlusion infarct in the rat

1988 ◽  
Vol 69 (1) ◽  
pp. 98-103 ◽  
Author(s):  
William G. Obana ◽  
Lawrence H. Pitts ◽  
Merry C. Nishimura
Keyword(s):  
Cerebral Ischemia ◽  
Cerebral Infarction ◽  
Middle Cerebral Artery ◽  
Continuous Infusion ◽  
Cerebral Artery ◽  
Normal Saline ◽  
Focal Cerebral Ischemia ◽  
Content Type ◽  
Opiate Antagonists ◽  
Fine Print

✓ The authors examined the effect of the opiate antagonists naloxone and thyrotropin-releasing hormone (TRH) on neurological outcome and the size of areas of cerebral infarction in a rat model of focal cerebral ischemia. The middle cerebral artery (MCA) was permanently occluded in 66 adult Sprague-Dawley rats. The rats were randomly divided into three groups. In 20 Group I rats, TRH in normal saline was administered initially as a 2-mg/kg bolus followed by continuous infusion of 2 mg/kg/hr for 4 hours. In 20 Group II rats, naloxone in normal saline was administered initially as a 2-mg/kg bolus followed by continuous infusion of 2 mg/kg/hr for 4 hours. In 26 Group III rats, physiological saline was administered as an initial 0.5-cc bolus followed by continuous infusion of 0.5 cc/hr for 4 hours. All solutions were given in volumes of 0.5 cc for the bolus and 0.5 cc/hr for continuous infusion, and all infusions were begun within 10 minutes of MCA occlusion. Twenty-four hours after treatment, the rats underwent a careful neurological examination and were then sacrificed immediately. The size of areas of cerebral infarction was evaluated using 2,3,5-triphenyltetrazolium chloride staining techniques. The neurological grade of the rats correlated with the size of infarcted areas among all grades, irrespective of treatment (p < 0.01). Neither naloxone nor TRH improved neurological function or reduced the size of infarction compared to saline-treated control rats. Treatment with TRH caused a significant increase in mean arterial blood pressure during infusion, but naloxone had no effect. These results suggest that neither TRH nor naloxone are effective in the treatment of acute focal cerebral ischemia.

Middle cerebral artery embolectomy

1976 ◽  
Vol 44 (4) ◽  
pp. 517-521 ◽  
Author(s):  
Eddy Garrido ◽  
Bennett M. Stein
Keyword(s):  
Middle Cerebral Artery ◽  
Cerebral Artery ◽  
Content Type ◽  
Neurological Condition ◽  
Surgical Microscope ◽  
The Right ◽  
Fine Print

✓ A patient who developed an embolic occlusion of the right middle cerebral artery while undergoing a cerebral arteriogram was successfully operated on by removal of the embolus under the surgical microscope. Early postoperative cerebrovascular spasm was a factor in the transient deterioration of the patient's neurological condition. When the patient was last seen 2 ½ months after surgery she was almost intact neurologically with only a mild right parietal dysfunction but with total resolution of the left hemiplegia. The literature is reviewed.

MRI demonstration of clot in a small unruptured aneurysm causing stroke

1986 ◽  
Vol 65 (3) ◽  
pp. 411-412 ◽  
Author(s):  
Theodore W. Eller
Keyword(s):  
Magnetic Resonance Imaging ◽  
Magnetic Resonance ◽  
Middle Cerebral Artery ◽  
Computerized Tomography ◽  
Cerebral Artery ◽  
Unruptured Aneurysm ◽  
Resonance Imaging ◽  
Content Type ◽  
The Right ◽  
Fine Print

✓ The case is reported of a 69-year-old woman with an 18-mm unruptured aneurysm of the right middle cerebral artery which caused a moderate stroke. Magnetic resonance imaging revealed a clot inside the aneurysm that was not visible on computerized tomography scans. The danger of embolism from the clot prompted clipping of the aneurysm.

Surgical manipulation of primate cerebral arteries in established vasospasm

1991 ◽  
Vol 75 (3) ◽  
pp. 425-432 ◽  
Author(s):  
J. Max Findlay ◽  
R. Loch Macdonald ◽  
Bryce K. A. Weir ◽  
Michael G. A. Grace
Keyword(s):  
Cerebral Ischemia ◽  
Middle Cerebral Artery ◽  
Cerebral Artery ◽  
Cerebral Arteries ◽  
Circle Of Willis ◽  
Content Type ◽  
Increased Risk ◽  
The Right ◽  
Surgical Manipulation ◽  
Fine Print

✓ It is generally believed that surgery in the face of angiographic vasospasm is dangerous due to an increased incidence of postoperative cerebral ischemia. One theory is that arterial narrowing is exacerbated by surgical manipulation of vasospastic vessels during aneurysm dissection and clipping. This theory was tested in a primate model of cerebral vasospasm and the results reported. Six monkeys underwent baseline cerebral angiography, followed by induction of subarachnoid hemorrhage (SAH) on both sides of the circle of Willis. An equal amount of fresh autologous blood clot was placed around each internal carotid, anterior cerebral, and middle cerebral artery. Six days later, angiography was repeated and the right craniectomy was reopened for clot evacuation and surgical manipulation of the right cerebral arteries, including placement of a temporary aneurysm clip on the right middle cerebral artery. The left cerebral arteries were not exposed or manipulated, and served as controls. Twenty-four hours later angiography was repeated, then the animals were killed. Equal and significant vasospasm (> 40% reduction in vessel caliber compared to baseline, p < 0.05) was seen in the middle cerebral arteries on both sides of the circle of Willis in all animals 6 and 7 days after SAH. There was no significant change in the severity of vasospasm on Day 7 compared with Day 6 in the right cerebral arteries. Increased risk of postoperative cerebral ischemia for surgery in the peak vasospasm period may be due to mechanisms other than increased arterial narrowing precipitated by surgical manipulation.

Heparin reduces proliferative angiopathy following subarachnoid hemorrhage in cats

1985 ◽  
Vol 62 (4) ◽  
pp. 570-575 ◽  
Author(s):  
John P. Kapp ◽  
Ben R. Clower ◽  
Frederick M. Azar ◽  
Nobuyoshi Yabuno ◽  
Robert R. Smith
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Growth Factor ◽  
Middle Cerebral Artery ◽  
Cerebral Artery ◽  
Cerebral Arteries ◽  
Platelet Derived Growth Factor ◽  
Platelet Factor ◽  
Content Type ◽  
The Right ◽  
Fine Print

✓ Subarachnoid hemorrhage (SAH) was produced in cats by transorbital rupture of the right middle cerebral artery (MCA). In untreated cats, widespread proliferative angiopathy occurred in both MCA's by 16 days after SAH. In cats that received systemic heparin, the pathological events following SAH were clearly reduced in the ruptured artery, and were not present in the contralateral left MCA. Platelets are known to adhere to the subintimal surface of cerebral arteries after SAH. The authors suggest that platelet-derived growth factor released from the intimal platelet carpet following SAH may be the stimulus for the development of proliferative angiopathy, and that this platelet factor is inhibited by heparin.

Middle meningeal to middle cerebral arterial bypass for cerebral revascularization

1979 ◽  
Vol 50 (6) ◽  
pp. 802-804 ◽  
Author(s):  
Clinton F. Miller ◽  
Robert F. Spetzler ◽  
Dennis J. Kopaniky
Keyword(s):  
Middle Cerebral Artery ◽  
Cerebral Artery ◽  
Middle Meningeal Artery ◽  
Cerebral Revascularization ◽  
Content Type ◽  
Arterial Bypass ◽  
Meningeal Artery ◽  
Fine Print

✓ A case is reported of successful anastomosis of the middle meningeal artery to a cortical branch of the middle cerebral artery. Based on the analyses of 50 random angiograms, the authors discuss the circumstances in which such an anastomosis might be practical and indicated.

Posttraumatic bilateral middle cerebral artery occlusion

1975 ◽  
Vol 42 (2) ◽  
pp. 217-221 ◽  
Author(s):  
Skip Jacques ◽  
C. Hunter Shelden ◽  
D. Thomas Rogers ◽  
Anthony C. Trippi
Keyword(s):  
Middle Cerebral Artery ◽  
Middle Cerebral Artery Occlusion ◽  
Cerebral Artery ◽  
Artery Occlusion ◽  
Content Type ◽  
Pathophysiological Mechanisms ◽  
Cerebral Artery Occlusion ◽  
Fine Print

✓ The authors report a case of bilateral posttraumatic middle cerebral artery occlusion. Previously reported unilateral cases are reviewed and possible pathophysiological mechanisms disscussed.

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