Embolic Hemiplegia following Blunt Thoraco-Cervical Trauma

A 21-year-old man became hemiplegic 36 hours after being assaulted on the neck and chest. A carotid angiogram showed middle cerebral artery branch occlusion. He died 5 days after the assault. Post mortem examination showed infarction of the brain. This infarction is attributed to an embolus that could have arisen either in the internal carotid artery or a tributary of the pulmonary vein.

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Nasopharyngeal Carcinoma Presenting as a Dual Territory Stroke: The Hyperdense Artery Sign

Philippine Journal of Otolaryngology Head and Neck Surgery ◽

10.32412/pjohns.v26i2.583 ◽

2011 ◽

Vol 26 (2) ◽

pp. 37-38

Author(s):

Ian C. Bickle

Keyword(s):

Carotid Artery ◽

Internal Carotid Artery ◽

Cerebral Infarction ◽

Middle Cerebral Artery ◽

Cerebral Artery ◽

Internal Carotid ◽

Ct Imaging ◽

The Body ◽

Attenuation Value ◽

The Brain

This 63 year-old chinese female, with both diabetes and hypertension, underwent CT imaging of the brain after presenting with a progressive left sided hemiplegia. The ‘hyperdense artery sign’ is a generic description that can be evident in any artery of the body on unenhanced CT, occurring due to the presence of intraluminal thrombosis (Figure 1). It is a well-established sign, most commonly described in CT imaging of the brain, where it is visualised in the vast majority of cases in the middle cerebral artery in the context of an acute cerebral infarction.1 It occurs uncommonly elsewhere, with the internal carotid artery (ICA) and basilar artery being other clinically significant sites. The ‘hyperdense ICA’ sign has been reported to be a reliable and highly specific marker of thromboembolic occlusion of the internal carotid artery.2 The ‘hyperdense artery sign’ is related to the attenuation value of intraluminal thrombus. The CT attenuation value (Hounsfield unit or HU) of normal blood is dependent on the haematocrit, ranging from 20 to 30 HU. As the process of thrombus retraction occurs, its water content decreases, increasing the concentration of haemoglobin within the clot. As a result this raises the attenuation value of the thrombus to 50–80 H. So the term ‘hyperdense’ is given.3 In this case, it proved to be the presenting symptom for an undiagnosed nasopharyngeal tumour, the thrombus likely developing as a complication of the surrounding tumour within the nasopharyngeal recess. The resultant outcome was a dual territory cerebral infarction of the anterior and middle cerebral artery territories, both supplied by branches of the internal carotid artery (Figures 2a & 2b).

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Response of canine internal carotid system to acetylcholine

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1991.261.5.h1392 ◽

1991 ◽

Vol 261 (5) ◽

pp. H1392-H1396

Author(s):

G. Dieguez ◽

E. Nava-Hernandez ◽

J. Valle ◽

A. L. Garcia-Villalon ◽

J. L. Garcia ◽

...

Keyword(s):

Carotid Artery ◽

Internal Carotid Artery ◽

Middle Cerebral Artery ◽

Cerebral Artery ◽

Internal Carotid ◽

Arterial System ◽

Low Concentrations ◽

Cervical Portion ◽

The Brain

The reactivity of the canine internal carotid system to acetylcholine (10(-8)-10(-4) M) was studied isometrically with 4-mm cylindrical segments from cervical and cavernous portions of the internal carotid artery and from the middle cerebral artery. Under control conditions, the cervical portion relaxed to every dose, the cavernous portion relaxed at low concentrations (10(-8)-10(-6) M) and contracted at higher concentrations (10(-5)-10(-4) M), whereas the middle cerebral artery contracted to every dose of acetylcholine. These responses were blocked by atropine (10(-6) M). Without endothelium, the cervical portion exhibited a lower relaxation, the cavernous portion contracted, and the middle cerebral artery was practically unresponsive to acetylcholine. These responses were also blocked by atropine. It suggests that the reactivity of the internal carotid system to acetylcholine 1) is endothelium dependent and 2) changes as it courses toward the brain, and this could be related to different embryological origin of the components of this arterial system.

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Rapid identification of a major diffusion/perfusion mismatch in distal internal carotid artery or middle cerebral artery ischemic stroke

BMC Neurology ◽

10.1186/1471-2377-12-132 ◽

2012 ◽

Vol 12 (1) ◽

Cited By ~ 16

Author(s):

Reza Hakimelahi ◽

Albert J Yoo ◽

Julian He ◽

Lee H Schwamm ◽

Michael H Lev ◽

...

Keyword(s):

Ischemic Stroke ◽

Carotid Artery ◽

Internal Carotid Artery ◽

Middle Cerebral Artery ◽

Cerebral Artery ◽

Internal Carotid ◽

Rapid Identification ◽

Distal Internal Carotid Artery

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Trapping, dome puncture, and direct suction decompression in conjunction with assistant superficial temporal artery- middle cerebral artery bypass to clip giant internal carotid artery bifurcation aneurysm

Surgical Neurology International ◽

10.25259/sni_462_2019 ◽

2019 ◽

Vol 10 ◽

pp. 205

Author(s):

Seiei Torazawa ◽

Hideaki Ono ◽

Tomohiro Inoue ◽

Takeo Tanishima ◽

Akira Tamura ◽

...

Keyword(s):

Carotid Artery ◽

Internal Carotid Artery ◽

Middle Cerebral Artery ◽

Cerebral Artery ◽

Internal Carotid ◽

Superficial Temporal Artery ◽

Temporal Artery ◽

Optimal Treatment ◽

Aneurysm Neck ◽

Bifurcation Aneurysm

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.

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Blister Aneurysms of the Internal Carotid Artery: Microsurgical Results and Management Strategy

Neurosurgery ◽

10.1227/neu.0000000000001259 ◽

2017 ◽

Vol 80 (2) ◽

pp. 235-247 ◽

Cited By ~ 27

Author(s):

Christopher M. Owen ◽

Nicola Montemurro ◽

Michael T. Lawton

Keyword(s):

Carotid Artery ◽

Internal Carotid Artery ◽

Middle Cerebral Artery ◽

Cerebral Artery ◽

Treatment Strategy ◽

Internal Carotid ◽

Artery Bypass ◽

External Carotid ◽

Parent Artery ◽

Intraoperative Rupture

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.

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Middle cerebral artery dissections: Differences between isolated and extended dissections of internal carotid artery

Journal of the Neurological Sciences ◽

10.1016/j.jns.2005.03.047 ◽

2005 ◽

Vol 235 (1-2) ◽

pp. 37-44 ◽

Cited By ~ 29

Author(s):

Chin-Hsien Lin ◽

Jiann-Shing Jeng ◽

Ping-Keung Yip

Keyword(s):

Carotid Artery ◽

Internal Carotid Artery ◽

Middle Cerebral Artery ◽

Cerebral Artery ◽

Internal Carotid

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Critical neurovascular brain anatomy

The Neurosurgeon's Handbook ◽

10.1093/med/9780198570677.003.0390 ◽

2010 ◽

pp. 504-517

Author(s):

George Samandouras

Keyword(s):

Carotid Artery ◽

Internal Carotid Artery ◽

Middle Cerebral Artery ◽

Cerebral Artery ◽

Basilar Artery ◽

Internal Carotid ◽

Anterior Cerebral Artery ◽

Brain Anatomy ◽

Vertebral Arteries ◽

System P

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.

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Origins and Pathways of Cerebrovascular Vasoactive Intestinal Polypeptide-Positive Nerves in Rat

Journal of Cerebral Blood Flow & Metabolism ◽

10.1038/jcbfm.1988.117 ◽

1988 ◽

Vol 8 (5) ◽

pp. 697-712 ◽

Cited By ~ 182

Author(s):

Norihiro Suzuki ◽

Jan Erik Hardebo ◽

Christer Owman

Keyword(s):

Carotid Artery ◽

Internal Carotid Artery ◽

Middle Cerebral Artery ◽

Cerebral Artery ◽

Vasoactive Intestinal Polypeptide ◽

Basilar Artery ◽

Internal Carotid ◽

Sphenopalatine Ganglion ◽

Cerebral Blood Vessels ◽

Carotid Canal

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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