Aneurysms of the Intracavernous Carotid Artery: Natural History and Indications for Treatment

Neurosurgery ◽  
1990 ◽  
Vol 26 (6) ◽  
pp. 933-938 ◽  
Author(s):  
Mark E. Linskey ◽  
Laligam N. Sekhar ◽  
William L. Hirsch ◽  
Howard Yonas ◽  
Joseph A. Horton

Abstract Of 37 patients with 44 intracavernous carotid artery aneurysms (ICCAAns) diagnosed between 1976 and 1988. patients with 20 aneurysms were followed without treatment for 5 months to 13 years (median, 2.4 years). Ten of the 20 ICCAAns were asymptomatic at diagnosis, and 10 were symptomatic. Three of the asymptomatic ICCAAns were symptomatic at follow-up. One of these required clipping because of a progressing cavernous sinus syndrome; the other 2 were minimally symptomatic and have not required treatment. Of the 10 initially symptomatic ICCAAns, 2 had not changed, 4 became more symptomatic, and 4 had symptomatically improved by follow-up. One patient with an ICCAAn that had not changed clinically was lost to follow-up 6 months after diagnosis. Of the 4 ICCAAns that became more symptomatic, 2 continue to be monitored, and 2 required intervention; one with detachable balloon occlusion of the aneurysm with preservation of the internal carotid artery lumen, and the other with gradual cervical internal carotid artery occlusion. The clinical course of this selected group of patients with ICCAAns suggests that the natural history of ICCAAns can be quite variable. Although clinical progression does occur, symptomatic ICCAAns also can improve spontaneously. Therapeutic intervention for asymptomatic ICCAAns should be reserved for patients with aneurysms arising at the anterior genu of the carotid siphon and/or extending into the subarachnoid space, where subarachnoid hemorrhage is most likely. Intervention for symptomatic ICCAAns should be reserved for patients with subarachnoid hemorrhage, epistaxis, severe facial or orbital pain, evidence of radiographic enlargement, progressive ophthalmoplegia, or progressive visual loss.

2019 ◽  
Vol 24 (2) ◽  
pp. 184-189 ◽  
Author(s):  
Daniel-Alexandre Bisson ◽  
Peter Dirks ◽  
Afsaneh Amirabadi ◽  
Manohar M. Shroff ◽  
Timo Krings ◽  
...  

OBJECTIVEThere are little data in the literature on the characteristics and natural history of unruptured intracranial aneurysms in children. The authors analyzed their experience with unruptured intracranial aneurysms in the pediatric population at their tertiary care pediatric institution over the last 18 years. The first objective was to assess the imaging characteristics and natural history of these aneurysms in order to help guide management strategies in the future. A second objective was to evaluate the frequency of an underlying condition when an incidental intracranial aneurysm was detected in a child.METHODSThe authors conducted a Research Ethics Board–approved retrospective review of incidental intracranial aneurysms in patients younger than 18 years of age who had been treated at their institution in the period from 1998 to 2016. Clinical (age, sex, syndrome) and radiological (aneurysm location, type, size, thrombus, mass effect) data were recorded. Follow-up imaging was assessed for temporal changes.RESULTSSixty intracranial aneurysms occurred in 51 patients (36 males, 15 females) with a mean age of 10.5 ± 0.5 years (range 9 months–17 years). Forty-five patients (88.2%) had a single aneurysm, while 2 and 3 aneurysms were found in 3 patients each (5.8%). Syndromic association was found in 22 patients (43.1%), most frequently sickle cell disease (10/22 [45.5%]). Aneurysms were saccular in 43 cases (71.7%; mean size 5.0 ± 5.7 mm) and fusiform in the remaining 17 (28.3%; mean size 6.5 ± 2.7 mm). Thirty-one aneurysms (51.7%) arose from the internal carotid artery (right/left 1.4), most commonly in the cavernous segment (10/31 [32.3%]). Mean size change over the entire follow-up of 109 patient-years was a decrease of 0.6 ± 4.2 mm (range −30.0 to +4.0 mm, rate −0.12 ± 9.9 mm/yr). Interval growth (2.0 ± 1.0 mm) was seen in 8 aneurysms (13.3%; 4 saccular, 4 fusiform). An interval decrease in size (8.3 ± 10.7 mm) was seen in 6 aneurysms (10%). There was an inverse relationship between aneurysm size and growth rate (r = −0.82, p < 0.00001). One aneurysm was treated endovascularly with internal carotid artery sacrifice.CONCLUSIONSUnruptured pediatric intracranial aneurysms are most frequently single but can occur in multiples in a syndromic setting. None of the cases from the study period showed clinical or imaging signs of rupture. Growth over time, although unusual and slow, can occur in a proportion of these patients, who should be identified for short-term imaging surveillance.


Neurosurgery ◽  
1985 ◽  
Vol 17 (4) ◽  
pp. 569-573 ◽  
Author(s):  
Ming-Ying Liu ◽  
Chun-Jen Shih ◽  
Yeou-Chih Wang ◽  
Shin-Han Tsai

Abstract Five cases of traumatic intracavernous carotid aneurysm are presented. All of the patients were young men with a history of severe head injury. The clinical manifestations were massive epistaxis and an ipsilateral cavernous sinus syndrome. The diagnosis was made correctly by carotid angiography. All of the patients developed another episode of massive epistaxis after admission. Emergency trapping of the internal carotid artery was performed. An urgent rescue method was used in one of our patients to prevent exsanguination before definitive surgical treatment. One patient died of exsanguination in spite of emergency ligation of the internal carotid artery. In the other four patients, no epistaxis was experienced after the operation.


Neurosurgery ◽  
1995 ◽  
Vol 36 (1) ◽  
pp. 23-30 ◽  
Author(s):  
Jeffrey J. Larson ◽  
John M. Tew ◽  
Thomas A. Tomsick ◽  
Harry R. van Loveren

2006 ◽  
Vol 59 (suppl_1) ◽  
pp. ONS-E168-ONS-E168 ◽  
Author(s):  
Raymond F. Sekula ◽  
David B. Cohen ◽  
Matthew R. Quigley ◽  
Peter J. Jannetta

Abstract OBJECTIVE: Blister-like aneurysms at nonbranching sites in the supraclinoid portion of the internal carotid artery are a rare but important cause of subarachnoid hemorrhage. We report a case of subarachnoid hemorrhage caused by a ruptured blister-type aneurysm, review the pertinent literature, and hope to remind readers of the wisdom of the use of an encircling clip as the primary treatment of these challenging lesions. CLINICAL PRESENTATION: A 41-year-old woman presented with sudden onset of headache. An admission computed tomographic (CT) scan revealed thick and diffuse subarachnoid hemorrhage involving primarily the carotid cistern and the proximal left sylvian fissure. A cerebral angiogram was initially interpreted as absent for aneurysm, but a follow-up angiogram performed 1 week later confirmed an enlarging aneurysm. INTERVENTION: A craniotomy with placement of an encircling clip graft around a blister-like aneurysm was performed. CONCLUSION: Although Sundt advocated the encircling clip graft for the blister-type aneurysm almost 40 years ago, use of an encircling clip graft in the treatment of blister-like aneurysms of the supraclinoid portion of the internal carotid artery seems to be reserved as a secondary or “rescue” measure in current practice. Neurosurgeons must familiarize themselves with this distinct entity (the blister-type aneurysm), recognize the possible risks associated with parallel clipping, and consider the use of an encircling clip graft as the primary treatment.


2010 ◽  
Vol 28 (4) ◽  
pp. E14 ◽  
Author(s):  
Robert E. Elliott ◽  
Jeffrey H. Wisoff

Object Fusiform dilation of the supraclinoid internal carotid artery (FDCA) is a reported occurrence following surgery for suprasellar tumors, in particular craniopharyngiomas. We report our experience of the incidence and natural history of FDCA following aggressive surgical resection of craniopharyngiomas in children. Methods Between 1986 and 2006, 86 patients under the age of 21 underwent radical resection of craniopharyngiomas at our institution. Ten cases with < 1 year of follow-up imaging (6), perioperative death (3), or nonsuprasellar tumors (1) were excluded. Data were retrospectively collected on the remaining 76 patients (43 male, 33 female; mean age 9.5 years; mean tumor size 3.3 cm) to determine the risk factors for and the rate and clinical significance of FDCA. Results Fifty patients had primary tumors and 26 patients received treatment before referral to our center. Sixty-six children (87%) had gross-total resection. At a mean follow-up time of 9.9 years, FDCA had developed in 7 patients (9.2%), all of whom had primary tumors and gross-total resection. The mean time to onset of FDCA was 6.8 months (range 3–11 months) with stabilization occurring at mean of 17.7 months (range 9–29.5 months). The mean size of the aneurysms was 9.1 mm (range 7.1–12 mm). After arrest, no lesions showed continued growth on serial imaging or produced symptoms or required treatment. There were no significant differences in age, sex, tumor size, pre- or retrochiasmatic location, extent of resection, or surgical approach (p > 0.05) between patients with and without FDCA. Conclusions Fusiform dilation of the supraclinoid internal carotid artery occurred in almost 10% of children following radical resection of craniopharyngiomas. In agreement with other reports, the authors concluded that FDCA probably occurs as a result of surgical manipulation of the supraclinoid carotid artery and should be managed conservatively because very few patients exhibit continued symptoms or experience growth or rupture of the lesion.


Author(s):  
Madeline B. Karsten ◽  
R. Michael Scott

Fusiform dilatation of the internal carotid artery (FDCA) is a known postoperative imaging finding after craniopharyngioma resection. FDCA has also been reported following surgery for other lesions in the suprasellar region in pediatric patients and is thought to be due to trauma to the internal carotid artery (ICA) wall during tumor dissection. Here, the authors report 2 cases of pediatric patients with FDCA. Case 1 is a patient in whom FDCA was visualized on follow-up scans after total resection of a craniopharyngioma; this patient’s subsequent scans and neurological status remained stable throughout a 20-year follow-up period. In case 2, FDCA appeared after resection and fenestration of a giant arachnoid cyst in a 3-year-old child, with 6 years of stable subsequent follow-up, an imaging finding that to the authors’ knowledge has not previously been reported following surgery for arachnoid cyst fenestration. These cases demonstrate that surgery involving dissection adjacent to the carotid artery wall in pediatric patients may lead to the development of FDCA. On very long-term follow-up, this imaging finding rarely changes and virtually all patients remain asymptomatic. Neurointerventional treatment of FDCA in the absence of symptoms or significant late enlargement of the arterial ectasia does not appear to be indicated.


Author(s):  
Enzo Emanuelli ◽  
Maria Baldovin ◽  
Claudia Zanotti ◽  
Sara Munari ◽  
Luca Denaro ◽  
...  

AbstractWhile the so-called pseudoaneurysms can result from arterial injury during trans-sphenoidal surgery or after a trauma, spontaneous aneurysms of cavernous–internal carotid artery (CICA) are rare. Symptoms vary and the differential diagnosis with other, more frequent, sellar lesions is difficult. We describe three cases of misdiagnosed CICA spontaneous aneurysm. In two cases the onset was with neuro-ophthalmological manifestations, classifiable as “cavernous sinus syndrome.” The emergency computed tomography scan did not show CICA aneurysm and the diagnosis was made by surgical exploration. The third patient came to our attention with a sudden severe unilateral epistaxis; endonasal surgery revealed also in this case a CICA aneurysm, eroding the wall and protruding into the sphenoidal sinus. When the onset was with a cavernous sinus syndrome, misdiagnosis exposed two patients to potential serious risk of bleeding, while the patient with epistaxis was treated with embolization, using coils and two balloons. Intracavernous nontraumatic aneurysms are both a diagnostic and therapeutic challenge, because of their heterogeneous onset and risk of rupture, potentially lethal. Intracavernous aneurysms can be managed with radiological follow-up, if asymptomatic or clinically stable, or can be surgically treated with endovascular or microsurgical techniques.


Author(s):  
Hashaam Arshad ◽  
Zhenhua Gui ◽  
Dakota Owens ◽  
Binod Wagle ◽  
Charles Donohoe

Introduction : A 51‐year‐old lady with a past medical history of Essential Hypertension, Hypothyroidism, prior Herpes Zoster infection 8 weeks ago was admitted with complaints of abdominal pain, bilateral flank pain, and restlessness. Her initial workup was significant for hyponatremia and hypokalemia. On the 3rd day of admission, she developed acute hypoxemic respiratory failure which led to intubation. At that time, CTA Chest was not done but CT Chest revealed prominent mucous plugging with left side glass ground opacities, Ultrasound of lower extremities revealed right common femoral vein DVT which led to concerns that she may have suffered from Pulmonary Embolism and led to starting Heparin drip. On the 6th day of admission, she developed Acute Encephalopathy, MRI Brain revealed acute infarcts in bilateral cerebral cortices and cerebella, CT Angiogram Head showed acute subarachnoid hemorrhage in the high posterior right parietal lobe, stenosis of the right high cervical internal carotid artery, and irregular, the appearance of the arterial vasculature throughout and CT Angiogram Neck abrupt change in caliber of the right ICA, 1.5 cm distal to the bifurcation with markedly severe narrowing of the majority of the extracranial right ICA throughout its course. A cerebral Angiogram was done which showed diffuse tandem segments of tandem cervical and intracranial portions of the right internal carotid artery and she was given nitroglycerin was administered as a therapeutic intervention. Lumbar Puncture showed WBC 2, RBC 7, Protein 162, Glucose 64, VZV PCR was negative, CSF VZV IgG Antibody positive at 303 IV (>165 IV indicative of current or past infection). Serum VZV IgG Antibody was positive at >4000 IV. Infectious Diseases were consulted after Lumbar Puncture, they initially started Acyclovir but once the Serum VZV IgG Antibody came back much higher than Serum VZV IgG Antibody levels, their assessment was that VZV vasculitis is unlikely and Acyclovir was discontinued. Eventually, the case was discussed at Neuroradiology which led to us getting a repeat MRA Neck without contrast which showed a concentric T1 and T2 hyperintensity along with a small and irregular caliber right cervical ICA consistent with dissection. She eventually completed a 21‐day course of Nimodipine due to underlying Subarachnoid Hemorrhage. Methods : NA Results : NA Conclusions : Our case demonstrates how it can become difficult to ascertain the etiology of stroke in certain patients. Our patient presented with multiple non‐specific symptoms initially and it was later on due to her Acute Encephalopathy that her Strokes and Subarachnoid Hemorrhage were discovered. It is still difficult to pinpoint whether the cause of strokes was dissection or VZV infection. Lumbar Puncture remains an essential tool to complete work up on uncommon etiologies of stroke.


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