Cavernous carotid aneurysm presenting with epistaxis

BACKGROUND: Carotid artery aneurysms are a rare cause of epistaxis. The most common presentation for nontraumatic cavernous internal carotid artery aneurysms is mass effect, with only 3% presenting with hemorrhage. We present a case of epistaxis caused by a nontraumatic cavernous internal carotid artery aneurysm. METHODS: A 73-year-old white woman was seen with a 1-month history of recurrent right-sided epistaxis. The patient had essential hypertension and a family history of intracranial aneurysm. A complete otolaryngologic, neurologic, and ophthalmologic examinations were normal. Contrast-enhanced CT of the paranasal sinuses revealed a trilobed aneurysm of the cavernous segment of the right internal carotid artery. Coil embolization of the cavernous aneurysm and right internal artery was performed. RESULTS: The patient has had no further episodes of epistaxis and has remained neurologically intact. CONCLUSION: Carotid artery aneurysms must be considered in the differential diagnosis of profuse epistaxis.     

Persistence of a mycotic aneurysm of the intracavernous carotid artery

Mycotic aneurysms of the intracavernous portion of the carotid artery are rare, especially in children. In reported cases, treatment has been by antibiotics alone, or by some form of carotid surgery. In the present case only antibiotic therapy was used. Subsequent angiography showed spontaneous thrombosis of the internal carotid artery, but persistence of the mycotic aneurysm. The implications of these findings are discussed with regard to the management of the condition.     

False aneurysms of the intracavernous carotid artery — Report of 7 cases

Summary We present 7 cases of false intracavernous carotid artery aneurysms. Four occurred after trauma and three were caused iatrogenically. Two of the latter occurred in patients with pituitary adenomas, one after transsphenoidal microsurgery and the other after yttrium [YI⁹⁰] seed implantation into the sella. The third iatrogenic aneurysm was seen shortly after transcavernous tumour surgery.In five of our seven patients massive, delayed, lifethreatening epistaxis was the leading symptom. All traumatic cases were associated with immediate unilateral blindness or blurred vision and with skull base fractures. One of these had a concomitant carotid cavernous fistula. Treatment of choice of our 5 recent cases was permanent balloon occlusion of the intracavernous carotid artery at the level of the lesion. Collateral circulation was evaluated prior to definitive carotid occlusion using a balloon test occlusion. During the balloon test adequate collateral circulation was defined as symmetric angiographic filling of both hemispheres. Awake patients were neurologically examined continuously. In unconscious patients transcranial Doppler sonography, electroencephalographic and somatosensory evoked potential monitoring was used in addition. Intra-operative heparin administration was not reversed with protamin. A postoperative continuous heparin infusion was not found necessary.In our two early cases this technique was not available: In the first case we accomplished aneurysm occlusion by a surgically introduced Fogarty balloon catheter. Our second patient needed surgical trapping of the involved carotid after early unsuccessful attempts of selective aneurysm occlusion, After treatment no further epistaxis occurred. Follow-up angiography showed persistent aneurysm occlusion. The results were excellent in 5 cases and good in 1 case. One patient with bilateral lesions suffered a stroke after occlusion of the second, remaining carotid artery, despite functioning bilateral extra-intracranial bypasses. Four years later there is a mild dysphasia still present in this patient. The mean follow-up time was 75.6 months.     

Thrombosed giant intracavernous aneurysm with subsequent spontaneous ipsilateral carotid artery occlusion

Summary We report a case of a 47-year-old man with a giant thrombosed aneurysm of the right cavernous internal carotid artery who initially presented with headache, double vision and trigeminal numbness. He experienced subsequent asymtomatic proximal occlusion of the parent vessel, revealed by follow-up angiography. This case illustrates the possibility that a giant thrombosed aneurysm may exert enough compression upon the parent vessel to induce flow stasis with resultant intraluminal thrombosis progressing to occlude the entire parent artery.     

Traumatic aneurysm of the intracavernous part of the internal carotid artery presenting with epistaxis. Case report

A 22-year-old Chinese man sustained a gunshot wound through his right eye followed by three episodes of massive epistaxis. Angiography showed a large aneurysm in the intracavernous segment of the left internal carotid artery which was successfully treated by thrombosis with copper wire.     

Iatrogenic dissecting aneurysm of the internal carotid artery

Summary A secondary dissecting aneurysm after arterial injury has been reported as a complication of surgery. We encountered this phenomenon in a patient with a meningioma of the sphenoid ridge. Despite successful clipping of a small rupture in the anterior wall of the proximal portion of the internal carotid artery, the patient became drowsy 30 days after surgery and developed right hemiparesis followed by fatal bleeding from the internal carotid artery. Histological examination revealed a traumatic dissecting aneurysm which had developed from the tear in the intima and extended into the dural ring and the bifurcation of the carotid artery. The characteristic clinical and histopathologic findings are shown. Methods for early recognition and the possibility of immediate treatment are briefly discussed.     

Severe otorrhagia resulting from a ruptured aneurysm of the extracranial internal carotid artery

Severe otorrhagia was the presenting sign of a ruptured aneurysm of the extracranial internal carotid artery. An unusual collateral circulation was demonstrated angiographically, and it complicated treatment. Satisfactory results were obtained by entrapment of the aneurysm.     

Traumatic postsurgical aneurysm of the intracavernous carotid artery: A delayed presentation

Sixteen years after transsphenoidal sellar implantation of yttrium-90 screws for acromegaly, a 56-year-old woman was examined because of severe headaches and diabetes insipidus. Intravenous digital subtraction angiography revealed a large intrasellar aneurysm of the cavernous segment of the internal carotid artery. The aneurysm was entrapped, with an excellent surgical outcome. Previous reports of postsurgical aneurysms of the intracavernous carotid artery are discussed.     

Intracranial internal carotid artery aneurysm as a cause of raeder's paratrigeminal syndrome

A 26-year-old woman was first seen with severe facial pain, partial Horner's syndrome, and restriction of ocular movements on the right side—all features of Raeder's paratrigeminal syndrome. Right carotid angiogram revealed an aneurysm of the internal carotid artery. This is the second reported case of Raeder's syndrome due to an aneurysm of the intracranial portion of the internal carotid artery. The mechanism of facial pain and sympathetic involvement are discussed.     

Ruptured intracranial aneurysm associated with spontaneous occlusion of internal carotid artery

Summary Out of 921 patients diagnosed and treated for intracranial aneurysm in 5 cases (0,5%) the co-existence of ruptured aneurysm and occlusion of the internal carotid artery was found. 4 patients were treated surgically-aneurysm clipping-without serious post-operative complications and 6 months follow-up showed satisfactory results. In 4 of 5 cases the aneurysm was located on the anterior communicating artery (ACA); this fact may support the hypothesis concerning a possible role of enhanced blood flow in aneurysm formation and rupture. In cases with good collateral blood flow extra-/intracranial bypass before aneurysm occlusion seems not to be necessary. The risk of operation in those patients is not as high, as might be expected.     

Aplasia of the internal carotid artery

Summary.  Background: The majority of previous reports on this rare agenesis of the internal carotid artery (ICA) have been limited to reporting upon its association with other congenital anomalies case by case. In order to collectively summarize this congenital anomaly of ICA, we have reviewed nine cases of ICA aplasia and their associated abnormalities.  Method: Nine cases of ICA aplasia were reviewed. The diagnosis of aplasia or agenesis of the ICA was based on angiographic findings and the presence of an absent or hypoplastic bony carotid canal by temporal bone computed tomography (TBCT). Their presumable embryological aetiologies, initial presenting symptoms, unusual collateral circulations, as demonstrated by angiographies, and various associated anomalies are reviewed.  Findings: The initial presentations were; subarachnoid haemorrhage in three patients, headache in one patient and ischemic symptoms and signs in three patients. The remaining two cases were found incidentally during angiography for other diseases. Collateral circulations to the middle cerebral artery ipsilateral to the ICA aplasia were via posterior communicating artery (P-com) or anterior communicating artery (A-com). On TBCT, all cases but one demonstrated agenesis of the bony carotid canal and the remaining case showed a hypoplastic canal. Cerebral aneurysms were found in six patients, four with A-com aneurysm, one with a basilar bifurcation aneurysm, and one with both a right P-com and a left cavernous ICA aneurysm; two incidentally found cases had no aneurysm. Other associated abnormalities were found in four cases; one case of hypoplasia of the common carotid artery (CCA) with an arachnoid cyst at the temporal pole, one case of abnormal origin of the right CCA from the aorta and the right subclavian artery from the descending aorta, one case of congenital temporomandibular joint (TMJ) ankylosis, and one case of nasopharyngeal angiofibroma with atresia of the upper basilar artery. Except for the atresia of the upper basilar artery, all such abnormalities were found on the same side as the ICA aplasia.  Interpretation: Agenesis or aplasia of ICA may be entirely harmless. However, associated conditions such as cerebral aneurysm or abnormal collateral channels should alert clinicians to the possibility of deterioration to life-threatening conditions, such as subarachnoid haemorrhage or irreversible ischemia. Other associated anomalies are commonly depicted on the same side as the ICA aplasia and may also give rise to issues of clinical importance. Published online February 10, 2003 Acknowledgment  This work is supported in part by a grant from the Seoul National University Hospital Research Fund.  Correspondence: Chang Wan Oh, M.D., Department of Neurosurgery, Seoul National University Hospital, 28 Yongon-dong, Chongno-ku, Seoul, 110-744, South Korea.     

Contralateral intracranial aneurysm formation as a late complication of carotid ligation

Ligation of the carotid artery was the treatment of choice for intracranial aneurysms for many years. While the literature recognizes many complications associated with this procedure, the late occurrence of aneurysms on the side opposite the ligation is only mentioned briefly. Animal studies are reviewed in an attempt to explain a possible cause of this observed phenomenon. The 3 cases presented seem to indicate that this complication may be more common than has been previously realized.     

支架辅助介入栓塞治疗外伤性血泡样动脉瘤合并迟发颈内动脉海绵窦瘘1例

正患者女,21岁,以"头面部撞伤、意识不清2 h"入院。查体:血压90/55 mmHg,浅昏迷,颌面部重度瘀肿,双侧瞳孔等大、直径3 mm,对光反射灵敏。头部CT:蛛网膜下腔出血(Fisher 3级),左上下颌骨骨折。DSA:左侧颈内动脉(internal carotid artery, ICA)床突见3.5 mm×2.5 mm瘤样突起,无瘤颈;诊断:血泡样动脉瘤(blood blister like aneurysm, BBA)     

Parinaud''s syndrome in hydrocephalus due to a basilar artery aneurysm

A 65-year-old woman appeared with a progressive dementia, gait disturbance, and Parinaud's syndrome. A computed tomography scan, an angiogram of the vertebral artery, and metrizamide ventriculography demonstrated a marked hydrocephalus. A giant aneurysm at the termination of the basilar artery projected into the third ventricle producing partial obstruction of the aqueduct. The symptoms were resolved by a ventriculoperitoneal shunt; but after a month, the patient again showed the upward-gaze palsies concomitant with occurrence of shunt malfunction. The possible mechanisms of Parinaud's syndrome observed in the patient are discussed.     

An unrecognized neurological syndrome: Sixth-nerve palsy and Horner's syndrome due to traumatic intracavernous carotid aneurysm

An unclassified type of ophthalmoplegia, composed of sixth-nerve paresis and Horner's syndrome without facial anhidrosis, was studied in an 18-year-old woman following cranial trauma. Carotid angiography disclosed a traumatic intracavernous carotid aneurysm. According to previous anatomical reports, an important sympathetic nerve joins the sixth cranial nerve in the posterior part of the cavernous sinus. An expansive process into the cavernous sinus at this point may cause this unclassified neurological syndrome. A review of the literature and a detailed clinical study were made.