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Familial occurrence of intracranial aneurysms.

Intracranial aneurysms occurring in three families are reported. As a result of the discovery of splenic artery aneurysms in one of the family members the relation between intracranial aneurysms and aneurysms in other sites is discussed. It is put forward that aneurysms might be a part of a generalized connective tissue disease, and the relation between aneurysms and some connective tissue diseases is stressed. At present extensive angiographic investigations in family cases cannot be recommended in every family.

Adult

Iatrogenic intracranial aneurysms.

Intracranial aneurysms following head trauma are not uncommon. Few cases of iatrogenic intracranial aneurysm have been reported however. This type of lesion is illustrated by three cases. If these lesions have the same poor prognosis as that proposed for the usual traumatic aneurysm, their early diagnosis and treatment is important.

Adult

Intracranial pressure in patients with diffuse cerebral arterial spasm following ruptured intracranial aneurysms.

Intracranial pressure (ICP) was recorded continuously in 12 pre-operative patients with angiographic evidence of diffuse cerebral arterial spasm due to a ruptured intracranial aneurysm. Recordings were made for 1 to 7 days, starting within 13 days after the haemorrhage. 1. An increased ICP was observed in the first week after subarachnoid haemorrhage (SAH) in 4 of the patients without any signs of angiographic arterial spasm. 2. This initial increase was regularly followed by a depression of ICP in between 7--12 days after SAH. In 11 out of 12 patients such a depression was concomitant with the beginning of arterial spasm. During the period of depressed ICP pattern, 6 patients showed little or no neurological deterioration, whereas 5 patients showed impaired consciousness or neurological deficits. 3. A secondary rise of ICP thereafter always followed due to ischaemic brain swelling or infarction, and was usually associated with a serious neurological deterioration. 4. Continuous ventricular drainage was performed to control the secondary increased ICP in 7 patients who survived, 4 of them with good clinical improvement and 3 with severe neurological deficits. 5. In the stage of depressed ICP, the administration of isoproterenol and steroids is recommended in order to try to alleviate the secondary rise of ICP.

Acute Disease

Multi-Omics Genome-Wide to Explore the Formation and Development Targets for Intracranial Aneurysms.

Intracranial aneurysms (IAs) represent a significant and potentially life-threatening category of disease, and there is currently a lack of effective treatment options aimed at preventing the progression of the disease. Accordingly, this study is dedicated to exploring and identifying effective drug targets that can help in the prevention of both the formation and rupture of IAs, along with a detailed examination of the underlying potential mechanisms involved in these processes. The data related to IAs for this research was obtained from the ISGC Biobank and UK Biobank. Then, we investigated the possible biological functions and unintended consequences of targeting the specific genes that were highlighted in IAs by using mediation analysis, virtual knockout experiments, and PW-MR studies. A total of 5 unique potential drug targets for IAs (FKTN, MAP3K1, PSMA4, SLC22A4, ADAM17), 4 unique potential drug targets for SAH (PSMA4, ADAM17, GPR160, SLC22A4), and 2 unique potential drug targets for UIA (SLC22A4, PRCP) were identified across brain or blood samples. Among the various candidates identified, SLC22A4 has emerged as a promising potential drug target, showing significant expression levels in both blood and brain tissues. Additionally, phenome-wide MR of SLC22A4 across 32 selected phenotypes did not identify statistically significant adverse associations after FDR correction. Virtual knockout (KO) experiments on SLC22A4 revealed that SLC22A4 KO disrupted 81 genes, all of which are involved in IAs-related pathways. Besides, we recognized BRD-K85337334 as potential candidates for targeting SLC22A4. This research indicates that an increase in SLC22A4 gene expression within the blood or brain is directly linked to a heightened risk of IAs rupture, which will aid in prioritizing the development of drugs for IAs.

Humans

Stereotaxic thrombosis of inaccessible intracranial aneurysms.

Some intracranial aneurysms that might be considered inoperable by open craniotomy are readily treatable by stereotaxic thrombosis. This is possible because the stereotaxic technique requires only that some point on the fundus of the aneurysm can be punctured with a needle. Illustrative cases are given describing the successful treatment of aneurysms arising at the origin of the ophthalmic artery, within the cavernous sinus, within the sella turcica, and from the vertebrobasilar and the posterior inferior cerebellar arteries ventral to the brain stem. The aneurysms within the sella or cavernous sinus can be approached through the sphenoid sinus, and the aneurysms ventral to the brain stem can be approached through the clivus without opening the dura.

Cavernous Sinus

[Intracranial pressure in patients with diffuse cerebral arterial spasm following ruptured intracranial aneurysms (author's transl)].

Intracranial pressure (ICP) was recorded continuously for 2 to days in 12 pre-operative patients with angiographic evidence of diffuse cerebral arterial spasm due to ruptured intracranial aneurysm. The ICP pattern of the low level (below 15 mmHg) and flat type was registered in the early stage of the arterial spasm in 11 patients in whom the ICP recording was made within 11 days after the hemorrhagic attack. During the period of low and flat ICP pattern, 6 patients showed little or no neurological deterioration whereas 5 patient showed impaired consciousness or neurological deficits. In 9 out 11 patients, the low level of ICP was followed by an abnormal deterioration. Continuous ventricular drainage was performed to control the secondary increased ICP in 7 patients and they survived, 4 of them with good results but remaining 3 with severe neurological deficits.

Adult

[On the miliary intracranial aneurysm --its significance in subarachnoid hemorrhage (author's transl)].

Clinical use of four-vessels angiography increased the frequency of detection of intracranial aneurysm in patients who had episode of subarachnoid hemorrhage. However, some cases of subarachnoid hemorrhage did not show intracranial and intraspinal source of bleeding angiographically. Bjökesten and Troupp pointed out that some cases who were negative in angiography may have a very small intracranial aneurysm. Hassler described the minute aneurysm sized less than 2 mm in diameter from finding autpsy of the cases of subarachnoid hemorrhage and he emphasized that source of subarachnoid hemorrhage in tow cases were ruptured minute aneurysm. From the authors' experiences of ten very small intracranial aneurysms, the authors' advocated a name of miliary intracranial aneurysm in clinical practice. The author's criteria of the miliary intracranial aneurysm are as follows: (1) the miliary aneurysm grew from the wall of main trunk of intracranial artery, (2) the maximum diameter and height of protrusion of the miliary intracranial aneurysm are less than the diameter of parent artery. Ten miliary intracranial aneurysms are divided into two groups, one is the miliary intracranial aneurysm which is source of subarachnoid hemorrhage and the other is an accessory aneurysm bedise the another ruptured main aneurysm. These two groups were 5 aneurysms respectively. The majority of the accessory miliary intracranial aneurysms were observed in middle cerebral artery but the ruptured miliary intracranial aneurysms were observed in internal carotid artery, anterior communicating artery and middle cerebral artery. When the clinical symptom occurred at the time of rupture of miliary intracranial aneurysm compare with the one by rupture of usual major intracranial aneurysm, clinical symptom due to meningeal irritation was not different with each other but disturbance of consciousness and other neurological symptom were slight in miliary intracranial aneurysm cases. Angiographic diagnosis of miliary intracranial aneurysm is difficult, because differentiation of the miliary intracranial aneurysm from the loop or angulation of small artery is difficult in routine angiogram. In the case who showed questionable shadow as miliary intracranial aneurysm, the repeated angiography under modified direction of X-ray and modified head position of patient is required. The magnification cerebral angiography of three fold is also useful in diagnosis of miliary intracranial aneurysm. The intracranial treatment of miliary intracranial aneurysms were done by coating except one case whose aneurysm was clipped.

Adult

Treatment of mycotic intracranial aneurysms.

Two patients with mycotic intracranial aneurysms were successfully treated with only antibiotic therapy. One patient, who had subacute bacterial endocarditis, rheumatic valvular disease, and an abscessed tooth, sustained a subarachnoid hemorrhage from a ruptured right middle cerebral artery trifurcation aneurysm. The other patient, who had Turner's syndrome and probable congenital aortic stenosis, developed multiple neurological findings during an ipisode of acute bacterial endocarditis precipitated by an infected ingrown toenail; a false aneurysm of the distal left middle cerebral artery and two lesions involving the left superior cerebellar artery were found. A study of the literature shows that only 45 patients with mycotic intracranial aneurysms have received adequate antibiotic therapy and angiographic documentation. Statistically, there does not appear to be a clear-cut advantage to antibiotic plus surgical therpy over antibiotic alone. In fact, in 21 patients who underwent serial angiography, lesions were smaller in six and not visualized in 11. In four patients the aneurysms increased in size; in two others fresh lesions formed. The author proposes the following diagnostic and therapeutic regimen: 1) earliest possible diagnosis of the underlying disorder; 2) appropriate antibiotic therapy; 3) early four-vessel cerebral angiography and follow-up studies every 2 to 3 weeks; study; 5) definitive operation upon completion of antibiotic therapy if the lesion is larger or the same size; and 6) postoperative angiography to evaluate the effectiveness of treatment and to search for interim lesions.

Adult

[Vasoconstriction of external carotid arteries after the rupture of intracranial aneurysm (author's transl)].

A patient in whom vasospasm of not only intracranial but also extracranial arteries was demonstrated after the rupture of an intracranial aneurysm was reported. A 55-year-old male was admitted with a ruptured left IC-PC aneurysm. Intracranial direct operation and continuous ventricular drainage were performed 33 hours after the rupture. Six days after the surgery, right hemiparesis and consciousness disturbances developed. Angiography revealed severe vasospasm of intra-and extracranial arteries, especially branches of the external carotid artery. The symptoms improved markedly following the superior cervical ganglionectomy and perivascular sympathectomy of cervical internal carotid artery on the left side. Vasospasm of the external carotid system, which has not been reported, was further investigated angiographically in 23 patients who had vasospasm of the intracranial arteries after aneurysm rupture. In about 50% of these patients was found vasospasm of the external carotid system too. These changes were not found in control cases without vasospasm of the intracranial arteries. Pathogenesis of the vasospasm of the external carotid system was discussed with particular emphasis on the relationship with the sympathetic nerves.

Carotid Artery Diseases

Treatment of intracranial aneurysms associated with other entities.

Considering the current state of surgery for intracranial aneurysm, a philosophy for treating intracranial aneurysms associated with other entities is presented. The premise is based on a comprehensive review of the literature relative to the risk factors applied to intracranial aneurysms and personal experience in dealing with the combination of problems of aneurysms diagnosed in association with other intracranial aneurysms, vascular malformations, neoplasms, trauma, and inflammatory diseases. A patient's problem must be considered individually and comprehensively, using all known prognostic factors and the specific features of the case for an appropriate therapeutic regimen to be designed. Current mortality and morbidity rates warrant the surgical intervention for the incidentally diagnosed aneurysm, but the occurrence of an aneurysm in conjunction with another serious entity demands careful, comprehensive evaluation. The surgical challenge of these complex problems should take second priority to a careful therapeutic deliberation to promote the best final outcome.

Aortic Coarctation

Hypervolemic hypotension in surgical treatment of intracranial aneurysm.

Fifty cases of intracranial aneurysms were operated upon under hypervolemic hypotension. The cerebral metabolism was maintained within normal range. The dissection and clipping of the aneurysm were considerably easier, and a premature rupture of the aneurysm could be handled without difficulty. The advantages and the surgical results are discussed.

Adult

Intracranial hypertension in patients with ruptured intracranial aneurysm.

Simultaneous continuous recording of intracranial pressure (ICP) and systemic blood pressure was carried out in 26 patients admitted within 1 week after subarachnoid hemorrhage (SAH) due to a ruptured intracranial aneurysm. The patients were graded as described by Hunt and Hess. Recordings were made for 1 to 5 days. The more impaired the consciousness, the higher the rate of ICP. In Grade III, IV, and V patients, the mean ICP level was in the range of 15 to 40 mm Hg, 30 to 75 mm Hg, and exceeded 75 mm Hg, respectively. A definite correlation between vasospasm shown by cerebral arteriogram and the clinical grade was not observed. In our series of ICP recordings, we never observed a typical plateau wave. The variations of ICP seen in Grade III and IV patients were the B- and C-waves (15 to 45 mm Hg in amplitude) described by Lundberg, and those in Grade V patients were the high amplitude monotonous waves synchronous with the arterial pulses (15 to 40 mm Hg in amplitude). These phenomena may indicate that Grade III and IV patients with SAH are in a condition of cerebral vasomotor instability, and Grade V patients have cerebral vasomotor paralysis.

Adult

[Congenital anomalies of cerebral artery and intracranial aneurysm].

It is well known that congenital anomalies such as polycystic kidney, aortic coarctation, Marfan syndrome, Ehler-Danlos syndrome are apt to be complicated by intracranial aneurysms. In this report we attempt to reveal the relation and incidence between cerebrovascular anomalies and intracranial aneurysms. The etiology of aneurysms has been discussed, too. 12 cases of persistent trigeminl artery, 2 cases of persistent hypoglossal artery and 11 cases of fenestration were obtained from 3841 patients who were angiographically examined in our clinic for 5 years. The incidence is 0.31%, 0.05% and 0.29%, respectively. Persistent trigeminal arteries were complicated by 2 cases of intracranial aneurysms and one case of arterivenous malformations (AVM), persistent hypoglossal arteries were complicated by one case of aneurysm, and fenestrations were complicated by 2 cases of aneurysms and one case of AVM. One case of congenital agenesis of right internal carotid artery was obtained which was complicated by aneurysm of anterior communicating artery. Totally, 8 cases of aneurysms and AVM were obtained from 26 cases of cerebrovascular anomalies (incidence 30.8%). On the other hand, thalamic or caudate hemorrhage revealed the highest incidence of complication of intracranial aneurysms among intracerebral hematomas (10.7%). Compared with the incidence of aneurysms between cerebro vascular anomalies (30.8%) and thalamic or caudate hemorrhage (10.7%), the difference is statistically signigicant (P less than 0.05). The cause of intracranial aneurysm has not yet been clarified. But it is well accepted that the defect of tunica media vasorum is most responsible factor as to the occurrence of intracranial aneurysms. We concluded that the genetic error of cerebral vessels including defect of media caused intracranial aneurysms, and this result was supported from the evidence that cerebrovascular anomalies showed statistically high incidence of complication of intracranial aneurysms.

Humans

Computed tomography with giant intracranial aneurysms.

Five patients with giant intracranial aneurysms were studied by computed tomography. Secondary intracranial changes such as hemorrhage, cerebral infarction and communicating hydrocephalus are easily demonstrated by computed tomography. In addition, computed tomography provides precise information concerning the actual size and location of large but partially thrombosed or calcified aneurysm to better advantage than angiography.

Adult

Perangiographic rupture of intracranial aneurysms.

The reports of perangiographic rupture of intracranial aneurysm are very few, but the actual incidence is doubtless higher than reported. We could find only 49 cases in the literature, all of which were recognized by extravasation of contrast media. Three of our own cases are documented; in all of them cerebral angiography was carried out soon after subarachnoid hemorrhages. The danger of cerebral angiography in patients with a recently hemorrhaged intracranial aneurysm is stressed.

Adult