Compression Of Internal Carotid Artery Research Articles

Abstract 018: External carotid artery Pseudo aneurysm induced Internal Carotid Artery compression causing acute ischemic stroke

Introduction Here, we describe a patient in whom ischemic stroke was caused by compression of the Internal Carotid Artery (ICA) by a Pseudoaneurysm (PSA) of the External Carotid Artery (ECA) after Gun Shot injury. Eventually, the PSA of the Internal maxillary artery (IMAX) was embolized, resulting in resolution of the patient's symptoms. Methods Case Report Results A 75‐year‐old male with a history of atrial fibrillation on Eliquis presented to the emergency department after sustaining a gunshot wound to the left face. He had extensive injuries through the left masticator and submandibular space with an inferior orbital wall fracture. A Computed Tomography Angiography (CTA) neck showed injuries to the left proximal IMAX with a small PSA. As the PSA was asymptomatic it was managed with observation. On HOD day 13, CTA was done for a brief period of unresponsiveness, which showed high‐grade narrowing of left cervical ICA due to extrinsic compression from PSA which was supplied by a branch of the left ECA with distal re‐constitution (image A). The next day, patient developed right sided plegia and aphasia with NIHSS of 17. A CT head showed no acute intracranial abnormality. The patient underwent emergent Digital Subtraction Angiography (DSA), which demonstrated occlusion of the left cervical ICA from compression from a left IMAX PSA which was treated with n‐butyl‐cyanoacrylate TRUFILL embolization with resolution of flow limitation in the left cervical ICA (Image B1,B2). After embolization, the patient was oriented and able to lift right arm and leg anti‐gravity. Magnetic Resonance Imaging (MRI) was contraindicated due to retained bullet fragments. Repeat CT head did not show stroke. Conclusion A Pseudo aneurysm is characterized by a rupture of the arterial wall and the formation of an aneurysmal sac by the adjacent structures while the sustaining artery remains intact. The most prevalent causes are penetrating or acute blunt neck trauma, hyperextension injury, and injury to the base of the skull (1). Predisposing factors for PSA include carotid endarterectomy or a late complication of carotid artery dissection, infection, radiotherapy, and malignancy (1‐2). Cox et al. reported 124 patients with significant neck and head penetrating injuries. Eleven patients were found to have thirteen head and neck PSA: two in the ICA, one in the vertebral artery, and ten involving branches of the ECA. Two of seven symptomatic PSAs manifested with episodes of massive hemorrhage (3). There have been case reports describing the consequences of an elongated styloid process causing an ischemic stroke due to subsequent dissection and PSA formation (4). According to our knowledge, this case report is one of the first to describe acute ischemic symptoms resulting from ECA PSA‐induced ICA compression, with resolution of symptoms following PSA embolization. The educational value of our case lies not only in the rarity of the condition but also in the uniqueness of its presentation. This case is a fundamental addition to the existing literature on rare neuro‐vascular anomalies leading to potential catastrophic outcomes.

Eagle Syndrome with Internal Carotid Artery Compression causing Recurred Syncope: A Case Report.

We herein report a 54-year-old man with eagle syndrome who presented with repeated episodes of syncope, especially after moving his head to a downward position. Computed tomography with contrast revealed a bilateral elongated styloid process. The left internal carotid artery was obviously compressed by the left elongated styloid processes. A transcranial Doppler examination detected a significantly decreased blood flow velocity in the left middle cerebral artery when the patient slightly lowered his head position. After surgery, the positional cerebral blood flow alteration disappeared. No further similar syncope episodes have been reported to date.

Pseudostroke as a manifestation of mediastinal choriocarcinoma in an elderly man

We describe a rare clinical case: onset of acute neurological symptoms suggestive of a pesudostroke, caused by an imbalance in cerebral blood flow as a result of internal carotid artery compression by an enlarged lymph node secondary to metastases from a disseminated non-gestational mediastinal choriocarcinoma. This was accompanied by decompensation due to paraneoplastic coagulopathy.

Recurrent Head and Neck Adenocarcinoma Presenting With a Pituitary Mass

Abstract Background: Metastasis to the pituitary gland is a rare condition. Only 1.8% of all surgically resected pituitary masses are metastases with the majority originating in the breast and lung (1). Salivary gland tumors rarely metastasize to the brain and only a few cases have been reported in the literature. Clinical Case: A 61 year-old woman presented to an outside emergency department with horizontal diplopia, blurry vision and left-sided sharp frontal headaches. MRI of the head showed a large, 2.0 x 4.6 x 1.8 cm sellar/suprasellar mass involving both cavernous sinuses, encasing the right internal carotid artery which was narrowed, and compressing the optic chiasm. Her past medical history was significant for adenocarcinoma of the left buccal mucosa and masseteric space, treated with resection in 2016, and a second resection in 2018 for recurrence followed by radiation therapy. Areas were identified where focal perineural invasion was present. She was referred to our institution for treatment recommendations for the sellar/suprasellar lesion. Laboratory testing revealed secondary hypothyroidism, adrenal insufficiency and partial diabetes insipidus, and she was started on replacement hormone therapy with levothyroxine and hydrocortisone. Neurosurgery and ENT evaluated patient and a surgical biopsy and subtotal resection via an endoscopic endonasal transsphenoidal approach was recommended for diagnosis and possible decompression of the optic chiasm. The final pathology was consistent with metastatic, high grade adenocarcinoma, supported by positive mucicarmine stain for mucin, positive immunohistochemical stain for CAM 5.2 and CK7 and negative immunohistochemical stains for the pituitary transcription factors, PIT-1 and SF-1. Conclusion: We report the second case in the literature of adenocarcinoma of the head and neck to the pituitary gland. In our case, radiological appearance of the tumor together with patient’s malignancy history led to the consideration of a pituitary metastasis. Tumors invading the cavernous sinus and causing internal carotid artery compression are rarely pituitary adenomas (2). Presence of these imaging features in patients with known risk factors for malignancy should raise suspicion for pituitary metastasis. The route of spread from the masseteric space to the sellar region remains unclear. Tumor metastasis can occur through direct invasion, hematogenous spread and perineural spread. Hematogenous spread and/or perineural spread along the trigeminal nerve are the most likely routes of metastasis in this case. Reference: (1)Javanbakht A, D’Apuzzo M, Badie B, Salehian B. Pituitary metastasis: A rare condition. Endocr Connect 2018; 7(10):1049-1057. PMID: 30139817. (2)Molitch ME et al (2012) Tumors invading the cavernous sinus that cause internal carotid artery compression are rarely pituitary adenomas. Pituitary 15(4):598–600

Imaging and Intervention in Internal Carotid Artery Pseudoaneurysm Secondary to Retropharyngeal Abscess.

Vascular complications secondary to retropharyngeal abscess are rarely encountered in the post antibiotic era and include compression of internal carotid artery (ICA), infective arteritis and pseudoaneurysm formation. Post infectious ICA pseudoaneurysm formation is reported predominantly in the paediatric age group and rare in adults. We report a case of retropharyngeal abscess complicated by ICA pseudoaneurysm in an adult successfully managed by endovascular approach.

Position-Related Subclavian and Internal Carotid Artery Compression During Robotic Thymectomy

Position-Related Subclavian and Internal Carotid Artery Compression During Robotic Thymectomy

Granulomatous hypophysitis causing compression of the internal carotid arteries reversible with azathioprine and rituximab treatment.

Compression of the internal carotid artery (ICA) in the cavernous sinus area is a rare event and is mostly associated with pituitary adenomas and meningiomas. Other causes of ICA compression are less well known. We present a rare case of granulomatous hypophysitis causing compression of the ICA, which was treated successfully with immune-suppressive agents. The electronic database MEDLINE (PubMed) was searched systematically and other cases with ICA compression were identified and analyzed. A female patient with a history of two previous transsphenoidal operations for suspected pituitary adenoma and post-operative complete pituitary insufficiency presented with severe headaches, nausea, fatigue, and diplopia. Pituitary MRI scan suggested relapse of the pituitary lesion with atypical bilateral infiltration of cavernous sinuses and compression of ICAs. After histological reevaluation of her previous pituitary operations, granulomatous hypophysitis was diagnosed. Treatment was started with high doses of prednisolone. With decreasing doses of prednisolone, symptoms recurred, and azathioprine was started, followed by administration of rituximab resulting in clinical recovery and regression of ICA compression. Literature analysis disclosed 36 case reports with ICA compression in the cavernous sinus region (12 pituitary adenoma, 6 meningioma, 7 hypophysitis, 5 other tumors, and 4 other etiologies). Two cases of hypophysitis recovered completely; five cases improved only partly. In the case of ICA compression, clinical signs, onset of symptoms, radiological findings and pituitary insufficiencies should be thoroughly evaluated, and hypophysitis should be considered as a possible cause. In our patient, treatment with azathioprine and, finally, rituximab was successful.

A Case of Internal Carotid Artery Compression With Mandible Depression

We report an unusual case of a 53-year-old female presenting with symptoms of transient ischemic attack secondary to compression of the left internal carotid artery with mandible depression. Duplex ultrasound examination confirmed compression of the left internal carotid artery with mouth opening. Normally, the posterior belly of the digastric muscle contracts to induce mandible depression and opens the mouth; however, this muscle contraction motion caused compression on her internal carotid artery resulting in her symptoms.

Transcranial Doppler for Eagle Syndrome: Rare Presentation of Unilateral Internal Carotid Artery Compression by the Stylohyoid Ligament With Provocative Maneuvers

Eagle syndrome is a rare condition caused by compression of the internal carotid artery (ICA) or cranial nerves by an elongated styloid process or calcified stylohyoid ligament. This patient is a 56 year-old woman who presented with episodes of positional syncope for 8 years. Transcranial Doppler (TCD) demonstrated abnormally decreased flow in the left middle cerebral artery (MCA) during the syncopal episodes. The patient was evaluated by TCD, transcranial imaging (TCI), and carotid duplex (CD). First, a baseline CD and TCI were performed with the patient in a neutral position. TCD was then used during symptomatic provocative maneuvers to monitor the bilateral MCAs. Intraoperative TCD monitoring was also done during bilateral stylohyoid ligament resection, and postoperatively during the same provocative maneuvers.The baseline CD examination revealed normal extracranial carotid anatomy; TCD and TCI showed normal mean velocities and a normal anatomic variant of fetal origin of the left posterior cerebral artery. During provocative maneuvers, TCD showed abnormally dampened to absent flow in the left MCA, consistent with compression of the left extracranial ICA. CT scan confirmed elongated stylohyoid ligaments bilaterally. The MCA mean velocities were monitored intraoperatively and postoperatively by TCD and showed no changes with head positioning immediately following resection of the stylohyoid ligaments. The patient reported no syncopal episodes at follow-up 6 days after surgery. Although rare, Eagle syndrome should be considered as a cause of positional syncope. TCD can serve as a diagnostic test, an intraoperative monitoring tool, and a method for documenting the surgical outcome.

Isolated third cranial nerve palsy from non-aneurysmal internal carotid artery compression

An 86 year-old-female, presented with a 6-day history of sudden onset of left-sided retro-orbital pain, ptosis and diplopia. On examination, her blood pressure was 190/90 and had a normal heart rate and temperature. Neurological examination revealed only complete left side oculomotor nerve—CN3 palsy with complete ptosis, mydriasis and with the eye looking down and out and unable to adduct the orbit. The pupillary reaction was sluggish. Her medical history included hypertension and chronic kidney failure but was not on …

Cerebral ischaemia in pituitary disorders—more common than previously thought: two case reports and literature review

Vasospasm and consequent cerebral ischaemia in aneurysmal subarachnoid haemorrhage are well-described. The development of cerebral ischaemia following pituitary tumour surgery is under-appreciated, and can be attributed to mainly cerebral vasospasm or internal carotid artery compression. We report on two patients with pituitary tumours who developed delayed cerebral ischaemia after transsphenoidal and transcranial pituitary macroadenoma decompression. The patients had vasospasm of intracranial vessels demonstrable on magnetic resonance angiogram. One recovered neurologically following nimodipine and hypertensive-hypervolaemia therapy while the other developed fulminant cerebral infarction. We discuss the complex multi-factorial mechanisms of cerebral ischaemia in pituitary disorders, as well as the management strategies and their limitations.

Recurrent syncope caused by compression of internal carotid artery by an anomalous hyoid bone

In rare cases a syncope can be caused by compression or irritation of the carotid artery and the carotid sinus due to congenital anatomical anomalies of cervical structures like the hyoid bone. We present the case a of 36 year old man with recurrent syncopes when turning his head. Clinical investigations revealed a hyoid bone anomaly with elongated lesser cornua, especially on the right symptomatic side. Surgical resection of the right lesser cornu led to complete resolution of symptoms over a two year follow-up. Syncope especially in younger subjects may be caused by congenital anomalies of the musculoskeletal system in the cervical region and should be considered in the differential diagnosis of syncope, transient cerebral ischemia and stroke.

Tumors invading the cavernous sinus that cause internal carotid artery compression are rarely pituitary adenomas

There is a clinical impression that when tumors invade the cavernous sinus, compression of the internal carotid artery is rare with pituitary adenomas and more common with other types of lesions but there are no actual data to support this impression. To confirm the impression that the finding of internal carotid artery compression by tumors invading the cavernous sinus is inconsistent with a diagnosis of a pituitary adenoma, we performed a retrospective analysis of MRI scans performed between 2000 and July 2009. An initial search of the radiology database was performed using the terms "invasive mass cavernous MRI" and subsequent refinement narrowed the evaluation to 141 patients with cavernous sinus invasion by sellar/parasellar tumors for whom there were clinical/pathological data to determine tumor type. 83 of the 141 patients with cavernous sinus invasion had carotid artery encasement; 58 were pituitary adenomas and 25 were other types of lesions. Eight of these 83 scans revealed compression of the internal carotid lumen, with only one being a pituitary adenoma and seven being other types of lesions. Therefore, only 1/58 (1.7%) of pituitary adenomas and 7/25 (28%) of non-pituitary adenoma lesions that encased the internal carotid artery caused compression of the artery (P = 0.0007). A mass lesion that invades the cavernous sinus and encases the internal carotid artery is very unlikely, therefore, to be a pituitary adenoma if it compresses the lumen of the internal carotid artery.

Unusual Positional Compression of the Internal Carotid Artery Causes Carotid Thrombosis and Cerebral Ischemia

This article reports an unusual case of positional compression of internal carotid artery resulting in carotid thrombosis and stroke in a 37-year-old man. A patient was operated urgently for a free-floating thrombotic mass in the internal carotid artery. Open thrombectomy was performed in acute phase of stroke for prevention of the recapitulative cerebral thromboembolism. Hemiplegia completely disappeared within 7 months.

Stent-Assisted Coil Trapping in a Manual Internal Carotid Artery Compression Test for the Treatment of a Fusiform Dissecting Aneurysm

Internal carotid artery (ICA) trapping can be used for the treatment of giant intracranial aneurysms, blood blister-like aneurysms, and fusiform dissecting aneurysms. Fusiform dissecting aneurysms are challenging to treat surgically and endovascularly because of no definite neck and critical perforators. Surgical or endovascular trapping of the ICA with or without an extracranial-intracranial bypass has commonly been used as an effective method to treat these lesions, but balloon test occlusion (BTO) must be performed. Here, we report a case of a ruptured fusiform dissecting aneurysm of the distal ICA, which was successfully treated using an endovascular ICA trapping with a manual ICA compression test instead of BTO.

Hyoid bone-related focal carotid vasculopathy

An 83-year-old sedentary man with hypertension, hypercholesterolemia, coronary insufficiency, and diabetes mellitus presented with an acute transient sensory right hand deficit while eating, without pain. There was no recent head or cervical trauma. Clinical examination was normal. Brain MRI showed a chronic (asymptomatic) watershed infarction between the left posterior and middle cerebral arteries, and no recent infarction. A diagnosis of a transient ischemic attack was made. Because of the co-existence of a chronic left-sided watershed infarction, an underlying left carotid artery pathology was suspected. Carotid duplex examination showed a large atheromatous plaque at the proximal internal carotid artery (ICA) with an irregular surface, associated with a 50% stenosis. Velocities did not change after head rotation. CT angiography confirmed focal vasculopathy (and the 50% stenosis) in the anteromedial side of the ICA, in near contact with the left-sided greater horn of the hyoid bone (Figs. 1, 2). Fat-saturation T1/T2 MRI, in search for ICA dissection, did not show intramural hematoma or ICA dilatation. Suspecting an artery-to-artery embolism, heparin treatment was given for 1 week, followed by oral anticoagulation, which was switched to acetylsalicylic acid after 3 months. Because of the patient’s age and associated co-morbidities, surgery (partial hyoid bone resection) was not performed. Rare cases of hyoid bone-related focal carotid pathology have been reported [1–5]. Two patients had a carotid pseudoaneurysm (probably related to earlier dissection), and three patients had a (non-atherosclerotic or atherosclerotic) vasculopathy (2 with a moderate and 1 with a 90% stenosis) explained by mechanical ICA compression. In two of these earlier reported patients, repetitive trauma seemed to play a role (playing golf, and carrying heavy weight on the shoulder) in the pathogenesis. Surgical partial hyoid bone resection has been performed in some of the earlier described patients without complications. Possible etiologies in hyoid bone-related carotid pathology include dissection, pseudoaneurysm, stenosis, or occlusion due to direct compression, and pressure-induced plaque formation (directly by hyoid bone compression leading to constructional changes in the carotid wall contour or indirectly by changes in blood flow and shear forces) and/or rupture. Each of these causes may potentially lead to stenosis, occlusion, or artery-to-artery embolism. Our patient had no high grade stenosis, no arguments on duplex examination for intermittent head position-related stenosis, and no excessive head rotation or external compression. Our patient had a sedentary lifestyle due to coronary insufficiency and no arguments in favor of ICA dissection. Repetitive head rotation in normal daily life (associated with mild carotid compression by the hyoid bone) seemed to have led to the formation of an atheromatous plaque and potentially also for mechanical plaque rupture, leading to artery-to-artery embolism. D. Renard (&) P. Labauge Department of Neurology, CHU Nimes, Hopital Caremeau, Place du Pr Debre, 30029 Nimes Cedex 4, France e-mail: dimitrirenard@hotmail.com

Compression of the cervical internal carotid artery by the stylopharyngeus muscle: an anatomical study with potential clinical significance

Occasionally, the internal carotid artery (ICA) may be symptomatically compressed in the neck by an elongated styloid process. The authors are unaware, however, of any study to date in which the aim was to describe the compression of this part of the ICA by surrounding muscles extending from the styloid process. In 20 adult cadavers (40 sides), dissection of the cervical ICA was performed, with special attention given to the relationship between this artery and the stylopharyngeus muscle. In addition, rotation of the head was performed while observing for any compression of the ICA by this muscle. Last, the segment of the ICA immediately adjacent to the stylopharyngeus was excised and evaluated for signs of gross compression. Five sides (12.5%) were found to have an ICA that was grossly compressed by the neighboring stylopharyngeus muscle, and this was confirmed on excised ICA specimens. Moreover, such compression was increased with ipsilateral rotation of the head. Effacement of the lumen of the ICA by the stylopharyngeus ranged from approximately 30 to 50%. Such compression was increased by approximately 25% with ipsilateral rotation of the head. To the authors' knowledge, compression of the cervical ICA by the stylopharyngeus muscle has not been previously described. Such a relationship should be appreciated by the clinician who treats patients with symptoms of ICA stenosis or occlusion as a potential extracranial site of compression. Based on this study, a subset of patients with occlusion of the cervical ICA but without elongation of the styloid process should be included within the definition of Eagle syndrome.

Factors affecting the transient hyperaemic response test of the cerebral autoregulation

The transient compression of the internal carotid artery (ICA) results in dilatation of cerebral arterioles by effect of autoregulation. In the THR test, the increase in middle cerebral artery (MCA) blood flow immediately after release of transient compression of the ICA is measured, which is proportional to cerebral autoregulation. The aim of the study was to determine the significance of several factors of the test - blood flow inertia (acceleration), dimensions (length and radius) of ICA, patency of the Circle of Willis (WC), and asynchrony between release of ICA compression and arterial pressure pulsations (phase shift).

Aberrant internal carotid artery in the middle ear with a deficiency in the origin of the anterior cerebral artery: A case report

An aberrant internal carotid artery (ICA) in the middle ear is rare and difficult to diagnose, and may lead to severe complications. We present here a case of aberrant ICA with a deficiency in the origin of the anterior cerebral artery. The only symptom was aural fullness, and a nonpulsatile and white tympanic mass in the anteroinferior area was noted. Computed tomography (CT) and magnetic resonance angiography (MRA) are useful tools that provide excellent visualization of the temporal bone for the diagnosis of aberrant ICA by the following features: intratympanic mass, enlarged inferior tympanic canaliculus, absence of the vertical segment of the ICA canal, and absence of bone covering the tympanic portion of the ICA. In addition, in this case, a deficiency in the origin of the anterior cerebral artery on the same side was identified by MRA, and cerebral arteriography and a carotid occlusion test were performed. Because of the deficiency in the origin of the anterior cerebral artery, the ICA compression revealed that there was almost no cross flow from the other ICA. Our experience illustrates that after confirmation of the diagnosis of aberrant ICA, localized treatment and/or surgical procedures should be considered carefully.

Pituitary Apoplexy Producing Internal Carotid Artery Compression: A Case Report

We report a case of pituitary apoplexy resulting in right internal carotid artery occlusion accompanied by hemiplegia and lethargy. A 43-yr-old man presented with a sudden onset of severe headache, visual disturbance and left hemiplegia. Investigations revealed a nodular mass, located in the sella and suprasellar portion and accompanied by compression of the optic chiasm. The mass compressed the bilateral cavernous sinuses, resulting in the obliteration of the cavernous portion of the right internal carotid artery. A border zone infarct in the right fronto-parietal region was found. Transsphenoidal tumor decompression following conservative therapy with fluid replacement and steroids was performed. Pathological examination revealed an almost completely infarcted pituitary adenoma. The patient's vision improved immediately after the decompression, and the motor weakness improved to grade IV+ within six months after the operation. Pituitary apoplexy resulting in internal carotid artery occlusion is rare. However, clinicians should be aware of the possibility and the appropriate management of such an occurrence.