Find information on thousands of medical conditions and prescription drugs.

Cerebral aneurysm

A cerebral or brain aneurysm is a cerebrovascular disorder in which weakness in the wall of a cerebral artery or vein causes a localized dilation or ballooning of the blood vessel. A common location of cerebral aneurysms is on the arteries at the base of the brain, known as the Circle of Willis. Aneurysms may result from congenital defects, preexisting conditions such as high blood pressure and atherosclerosis (the buildup of fatty deposits in the arteries), or head trauma. Cerebral aneurysms occur more commonly in adults than in children and are slightly more common in women than in men, but they may occur at any age. more...

Home
Diseases
A
B
C
Angioedema
C syndrome
Cacophobia
Café au lait spot
Calcinosis cutis
Calculi
Campylobacter
Canavan leukodystrophy
Cancer
Candidiasis
Canga's bead symptom
Canine distemper
Carcinoid syndrome
Carcinoma, squamous cell
Carcinophobia
Cardiac arrest
Cardiofaciocutaneous...
Cardiomyopathy
Cardiophobia
Cardiospasm
Carnitine transporter...
Carnitine-acylcarnitine...
Caroli disease
Carotenemia
Carpal tunnel syndrome
Carpenter syndrome
Cartilage-hair hypoplasia
Castleman's disease
Cat-scratch disease
CATCH 22 syndrome
Causalgia
Cayler syndrome
CCHS
CDG syndrome
CDG syndrome type 1A
Celiac sprue
Cenani Lenz syndactylism
Ceramidase deficiency
Cerebellar ataxia
Cerebellar hypoplasia
Cerebral amyloid angiopathy
Cerebral aneurysm
Cerebral cavernous...
Cerebral gigantism
Cerebral palsy
Cerebral thrombosis
Ceroid lipofuscinois,...
Cervical cancer
Chagas disease
Chalazion
Chancroid
Charcot disease
Charcot-Marie-Tooth disease
CHARGE Association
Chediak-Higashi syndrome
Chemodectoma
Cherubism
Chickenpox
Chikungunya
Childhood disintegrative...
Chionophobia
Chlamydia
Chlamydia trachomatis
Cholangiocarcinoma
Cholecystitis
Cholelithiasis
Cholera
Cholestasis
Cholesterol pneumonia
Chondrocalcinosis
Chondrodystrophy
Chondromalacia
Chondrosarcoma
Chorea (disease)
Chorea acanthocytosis
Choriocarcinoma
Chorioretinitis
Choroid plexus cyst
Christmas disease
Chromhidrosis
Chromophobia
Chromosome 15q, partial...
Chromosome 15q, trisomy
Chromosome 22,...
Chronic fatigue immune...
Chronic fatigue syndrome
Chronic granulomatous...
Chronic lymphocytic leukemia
Chronic myelogenous leukemia
Chronic obstructive...
Chronic renal failure
Churg-Strauss syndrome
Ciguatera fish poisoning
Cinchonism
Citrullinemia
Cleft lip
Cleft palate
Climacophobia
Clinophobia
Cloacal exstrophy
Clubfoot
Cluster headache
Coccidioidomycosis
Cockayne's syndrome
Coffin-Lowry syndrome
Colitis
Color blindness
Colorado tick fever
Combined hyperlipidemia,...
Common cold
Common variable...
Compartment syndrome
Conductive hearing loss
Condyloma
Condyloma acuminatum
Cone dystrophy
Congenital adrenal...
Congenital afibrinogenemia
Congenital diaphragmatic...
Congenital erythropoietic...
Congenital facial diplegia
Congenital hypothyroidism
Congenital ichthyosis
Congenital syphilis
Congenital toxoplasmosis
Congestive heart disease
Conjunctivitis
Conn's syndrome
Constitutional growth delay
Conversion disorder
Coprophobia
Coproporhyria
Cor pulmonale
Cor triatriatum
Cornelia de Lange syndrome
Coronary heart disease
Cortical dysplasia
Corticobasal degeneration
Costello syndrome
Costochondritis
Cowpox
Craniodiaphyseal dysplasia
Craniofacial dysostosis
Craniostenosis
Craniosynostosis
CREST syndrome
Cretinism
Creutzfeldt-Jakob disease
Cri du chat
Cri du chat
Crohn's disease
Croup
Crouzon syndrome
Crouzonodermoskeletal...
Crow-Fukase syndrome
Cryoglobulinemia
Cryophobia
Cryptococcosis
Crystallophobia
Cushing's syndrome
Cutaneous larva migrans
Cutis verticis gyrata
Cyclic neutropenia
Cyclic vomiting syndrome
Cystic fibrosis
Cystinosis
Cystinuria
Cytomegalovirus
Dilated cardiomyopathy
Hypertrophic cardiomyopathy
Restrictive cardiomyopathy
D
E
F
G
H
I
J
K
L
M
N
O
P
Q
R
S
T
U
V
W
X
Y
Z
Medicines

A small, unchanging aneurysm will produce no symptoms. Before a larger aneurysm ruptures, the individual may experience such symptoms as a sudden and usually severe headache, nausea, vision impairment, vomiting, and loss of consciousness, or the individual may be asymptomatic, experiencing no symptoms at all. Onset is usually sudden and without warning. Rupture of a cerebral aneurysm is dangerous and usually results in bleeding into the meninges or the brain itself, leading to a subarachnoid hemorrhage or intracranial hematoma, either of which constitutes a stroke. Rebleeding, hydrocephalus (the excessive accumulation of cerebrospinal fluid), vasospasm (spasm of the blood vessels), or multiple aneurysms may also occur. An unruptured cerebral aneurysm has a 4% chance of rupturing each year.

In outlining symptoms of ruptured cerebral aneurysm, it is useful to make use of the Hunt and Hess scale of subarachnoid hemorrhage severity:

  • Grade 1: Asymptomatic; or minimal headache and slight nuchal rigidity. Approximate survival rate 70%.
  • Grade 2: Moderate to severe headache; nuchal rigidity; no neurologic deficit except cranial nerve palsy. 60%.
  • Grade 3: Drowsy; minimal neurologic deficit. 50%.
  • Grade 4: Stuporous; moderate to severe hemiparesis; possibly early decerebrate rigidity and vegetative disturbances. 20%.
  • Grade 5: Deep coma; decerebrate rigidity; moribund. 10%.

Emergency treatment for individuals with a ruptured cerebral aneurysm generally includes restoring deteriorating respiration and reducing intracranial pressure. Surgery is usually performed within the first three days to clip the ruptured aneurysm and reduce the risk of rebleeding. When aneurysms are discovered before rupture occurs, microcoil thrombosis or balloon embolization may be performed on patients for whom surgery is considered too risky. During these procedures, a thin, hollow tube (catheter) is inserted through an artery to travel up to the brain. Once the catheter reaches the aneurysm, tiny balloons or coils are used to block blood flow through the aneurysm. Other treatments may include bedrest, drug therapy, or hypertensive-hypervolemic therapy (which elevates blood pressure, increases blood volume, and thins the blood) to drive blood flow through and around blocked arteries and control vasospasm.

The prognosis for a patient with a ruptured cerebral aneurysm depends on the extent and location of the aneurysm, the person's age, general health, and neurological condition. Some individuals with a ruptured cerebral aneurysm die from the initial bleeding. Other individuals with cerebral aneurysm recover with little or no neurological deficit. However, estimates are, that of the 30,000 people per year in the United States who suffer a ruptured aneurysm, only 20% will be alive and well in one year's time. 20% will be alive but disabled, and 60% will have died.

Read more at Wikipedia.org


[List your site here Free!]


Comparison of prognosis and complications after warning leaks in subarachnoidal hemorrhage-experience with 214 patients following aneurysm clipping
From Neurological Research, 9/1/05 by Ritz, Rainer

Objectives: The 'warning leak', a smaller bleeding event from an aneurysm, which sometimes occurs before an acute massive subarachnoidal hemorrhage (SAH), was first described in 1967. The present study was performed to compare the complications and prognosis for 214 patients with and without a warning leak; aneurysm clipping had been performed in all.

Methods: The interval between the warning headache and the actual SAH was calculated. The following complications were examined: preoperative hemorrhage, intra-operative rupture of the aneurysm, postoperative re-bleeding, symptomatic vasospasm, shunt-requiring hydrocephalus, ventriculitis, postoperative wound infection, and outcome according to the Glasgow Outcome Scale (GOS).

Results: Sixty-seven (31%) out of the 214 patients had a warning leak with a median distance of 11 days before suffering from major SAH. Preoperative angiographie vasospasms occurred more frequently in the group with a warning bleeding (22.4 versus 6.1%; p

Discussion: To give patients the chance to start their treatment in a better clinical condition it is important to recognize the early warning signs. [Neurol Res 2005; 27: 620-624]

Keywords: Cerebral aneurysm; complications; outcome; subarachnoidal hemorrhage; warning leak

INTRODUCTION

Spontaneous subarachnoidal hemorrhage (SAH) is, with an incidence of ~5-10 cases/100,000 per year, a frequent disease1-8. SAH is with 22-25% a major constituent of cerebrovascular mortality9. The most frequent cause of SAH is a ruptured aneurysm of the intracranial brain-supplying arteries. The percentage of ruptured aneurysms as the cause of SAH varies in the literature between 72 and 95%10.

Despite modern microsurgical techniques and intensive care medicine, there still is high morbidity and mortality resulting from SAH. In several investigations a total mortality of 25% is described in SAH patients and a significant morbidity in 50% of the surviving patients11. It is generally accepted that the outcome correlates with the preoperative clinical status12,13. To improve the outcome, it is therefore important to diagnose endangered patients early and perform the operation while they are in a good clinical state. The aneurysmal SAH in most cases presents with a sudden event of severe headache, accompanied by meningism, photophobia, nausea and/or vomiting, and frequently by loss of consciousness14. Classically, the patients describe a sudden headache of an intensity that they had never experienced before.

Already in 1967, Gillingham15 described the phenomenon of the 'warning leak', a smaller bleeding event from an aneurysm, which sometimes occurs prior to an acute massive SAH. The warning leak is frequently recognizable as a headache14,16-18. As the symptomatology is not as impressive as with actual SAH, the symptoms are misinterpreted more frequently19. The aim of this investigation was to answer the following question: do patients with a "warning leak" differ in complications and outcome after SAH compared with patients without such a warning leak?

PATIENTS AND METHODS

Patients

In the period from 1 January 1986 to 30 May 1997 the senior author (J.R.) performed aneurysm clipping in a total of 273 patients. Of these, 252 patients had suffered from SAH. In 214 patients we were able to explore retrospectively whether or not a warning leak had existed. The authors established a database on the patients with SAH. For each patient the following data were analysed: age, sex, and clinical status according to the Hunt and Hess grading scale20. The pattern of hemorrhage on computed tomography (CT) was described according to Fisher et al.21. The localization of the ruptured aneurysm was identified by a transfemoral selective four-vessel cerebral angiography. The patients themselves or their relatives were questioned about a warning headache event. The quality of pain of the warning headache had to be different from the headache these patients were familiar with. In general, the warning leak was characterized as a sudden headache, rather less intensive than in the major bleeding, but also of sudden and short time quality. The interval between the warning headache and the actual SAH was calculated. We defined the actual SAH as the headache event that led to the diagnosis and hospitalization.

The following complications were checked: preoperative hemorrhage, intra-operative rupture of the aneurysm, symptomatic vasospasm (defined as impaired vigilance and/or a new neurological deficit such as a hemiparesis or aphasia), hydrocephalus requiring the implantation of a shunt, ventriculitis, postoperative wound infection, and re-bleeding. The outcome was examined according to the Glasgow Outcome Scale (GOS)22 at the time of dismissal and in the follow-up.

Statistical analysis

Contingency analysis was performed by comparing the categorical variables using the Pearson's chisquared test or the Fisher's exact test. Differences with a p

RESULTS

In 214 out of a total of 273 patients, the patients themselves or their relatives were able to precisely describe a warning headache event. In 21 out of 273 patients, elective aneurysm surgery was performed. In 38 patients, no information about a warning leak was available; H&H grade at permission and outcome was similar to the remaining 214 patients. Subsequently, 214 patients were analysed. Sixty-seven (31.3%) out of the 214 patients in whom aneurysm clipping had been performed had had a warning bleeding before the acute SAH. The median interval between the warning leak and the acute SAH amounted to 11 days (Figure 7). Table 1 gives a comparative overview of the patients with and without a warning leak. Twenty-three (34%) of the 67 patients with a warning leak had visited a physician before the acute SAH happened. The following diagnoses without recognition of the aneurysm were stated: seven times cervicocephalgias, seven times cranial nerve disturbances of unclear genesis, twice each an ischemic event, a cerebral convulsion, and a drop attack. Once a trauma was assumed as causal. In one case the warning leak was misinterpreted as cervicocephalgia in combination with a drop attack, and in another case as cervicocephalgia in combination with a cerebral convulsion. The mean interval between acute SAH and aneurysm clipping was 2 days in the group with a warning bleeding. Of these, 43 patients were treated early, i.e. between days 0 and 3, and 24 patients were treated later. In the group without a warning bleeding the mean distance between SAH and clipping of the ruptured aneurysm amounted to 1 day. 113 patients were treated early and 34 patients were treated later.

Fifteen out of the 67 patients with a warning bleeding showed an early preoperative angiographic vasospasm. Of these patients, five had a local vasospasm and five showed an ipsilateral vasospasm over a long distance of the vessels on the side of the ruptured aneurysm. Also, five patients had multiple vasospasms. The mean time between the SAH, which led to hospitalization and the angiography amounted to 1 day. In contrast, only nine of the 147 patients without a warning bleeding had an early angiographie vasospasm. Five patients had a regional vasospasm, four over a long distance of the ipsilateral vessel, and no patient had multiple vasospasms. The mean time between the SAH and submission to hospital was O days. In summary, patients with a warning bleeding showed a statistically significant higher frequency of early preoperative angiographic vasospasms than patients without a warning leak.

Preoperative re-bleeding and intra-operative rupture was statistically significantly more frequent in the warning leak group (see also Table 2).

Hypodensities suspect of ischemic lesions in CT were preoperatively seen in three patients of the group with a warning bleeding. Two of these patients showed the hypodensity in the area supplied by the ruptured aneurysm, the third showed multiple vasospasms in the angiography. Postoperatively, 11 patients with warning bleeding showed hypodensities in the CT scan, nine of them in the area supplied by the vessel with the ruptured aneurysm. Five of these patients had a manifest vasospasm already in the preoperative angiography (two times multiply, two times regionally, one time long distance). In the group without a warning bleeding, seven patients showed hypodensities in the preoperative CT scan, in two cases the hypodensities were located in the territory of the supplying vessel where the ruptured aneurysm was located. Three of the seven patients had angiographically proven vasospasms.

Postoperatively, 31 patients without warning bleeding showed hypodensities in the CCT. Fifteen of these were outside the territory supplied by the vessel of the ruptured aneurysm, the other 16 were within the territory supplied by the vessel of the ruptured aneurysm. In the preoperative angiography only two of these patients had an angiographically proven vasospasm.

Table 2 summarizes the complications. Two patients without a warning bleeding had a re-bleeding after aneurysm clipping. The outcome after a mean time of 22 months according to the GOS is shown in Figure 2. There was no significant difference between the two groups with and without warning bleeding.

DISCUSSION

The proportion of patients with a warning bleeding previous to SAH varies widely in the literature. Depending upon the examiner it varies between 15 and 58.8%17,18,23,25-28. This great variability may be explained mainly by the anamnestical evaluation of warning bleedings. In our investigation the proportion of patients with warning bleeding was 31.3%, while the true rate might be higher, because warning bleedings in patients with a disturbance of consciousness could not be verified if these patients had not told their relatives about a sudden headache experience. Our data are within the range of proportions reported in the literature. In contrast to previous investigations, objective differences during the acute treatment interval, e.g. incidence of preoperative vasospasm, confirming the difference between the two groups, are demonstrated. The outcome after a mean follow-up time of 22 months did not show any differences between the two groups.

EFFECT ON PREOPERATIVE VASOSPASM AND INTRA-OPERATIVE COMPLICATIONS

Preoperative angiographie vasospasms were more common in the group with a warning bleeding (22.4 versus 6.1%). This might be caused by inducing reactions after a warning bleeding similar to those after SAH. The number of hypodensities in the preoperative CT did not differ between the two groups (see also Table 2).

Intra-operative aneurysm rupture was more frequent in the group of patients with a warning bleeding than in the group without a warning bleeding (28.4 versus 15%). This might be due to a perianeurysmal scar formation by the earlier event, with the local reactions resulting in a higher vulnerability. An example for the intra-operative findings after a warning leak is shown in Figure 3.

EFFECT ON POSTOPERATIVE COMPLICATIONS AND THE OUTCOME

The patients without a warning bleeding did not have postoperative symptomatic vasospasms (15%) more often than the patients with a warning bleeding (14.9%), although in CT scan hypodensities in patients with no warning leak were more frequent (21.1 versus 16.4%). More of the patients with no warning leak developed a shunt-requiring hydrocephalus malresorptivus (18.4 versus 10.5%) corresponding to the varying grades of SAH (see also Table 1). In the postoperative courses no statistically significant differences could be seen.

The outcome of both groups after a follow-up time of nearly 2 years did not vary (Figure 2). This may be explained by the fact that both groups had a similar clinical condition when arriving at the hospital (see Table 1, H&H grade at admission). While patients with a warning leak more frequently had preoperative angiographie vasospasms and intra-operative aneurysm ruptures, CT scans showed more postoperative hypodensities in patients with no warning leak.

Thirty out of the 67 patients with warning bleeding were graded H&H III-V at the time of admission to the hospital. This is 14% of the total number of 214 SAH patients. Comparing the total mortality of the H&H I and Il patients (3.6%) with the total mortality of the H&H UI-V patients (22.1%), the better outcome of the patients with a good initial clinical grading is shown. The difference in prognosis is more clearly shown when the favorable outcome (GOS GR or MD) is separated from the unfavorable (GOS SD, PVS, and D). Here the patients graded H&H I and II in 92% achieved a favorable long time outcome already when dismissed from hospital, whereas only 54% of the H&H III-V patients could achieve this status. Therefore, theoretically 30 more patients (14%) could have been treated under better prognostic conditions if a warning leak had been correctly diagnosed early before major SAH occurred.

CONCLUSION

The warning leak and non-warning leak group differ in early perioperative course. In summary, the warning leak group showed a higher percentage of preoperative angiographically proven vasospasm. In the end, the outcome of both groups did not differ after a period of almost 2 years.

It is important to recognize the warning signs early and to use the nowadays well available diagnostic possibilities such as CT or MR angiography with the aim to perform surgery before the patients suffer from the major bleeding. If this is accomplished, a considerable proportion of aneurysm patients will have the chance to undergo surgery in a better clinical status.

ACKNOWLEDGEMENTS

The authors thank Prof. Dr K. Dietz, Department of Medical Biometry, Eberhard-Karls University Tuebingen, for his assistance with the statistical analysis.

REFERENCES

1 Anderson CS, Jamrozik KD, Burvill PWS, et al. Determining the incidence of different subtypes of stroke: results from the Perth Community Stroke Study, 1989-1990. Med J Aust 1993; 158: 85-89

2 Bamford J, Sandercock P, Dennis M, et al. A prospective study of acute cerebrovascular disease in the community: The Oxfordshire Community Stroke Project-1981-86. II: Incidence, case fatality rates and overall outcome at one year of cerebral infarction, primary intracerebral and subarachnoid hemorrhage. J Neurol Neurosurg Psychiatry 1990; 53: 16-22

3 Broderick JP, Brott T, Tomsick T, et al. Intracerebral hemorrhage more than twice as common as subarachnoid hemorrhage. J Neurosurg 1993; 78: 188-191

4 Davis PH, Hachinski V. Epidemiology of cerebrovascular disease. In: Anderson DW, ed. Neuroepidemiology: A Tribute to Bruce Schoenberg. Boca Rotan, FL: CRC Press, Inc., 1991; 27-53

5 Jerntrop P, Berglund G. Stroke registry in Malmö, Sweden. Stroke 1992; 23: 357-361

6 Longstreth WT Jr, Nelson LM, Koepsell TD, et al. Cigarette smoking, alcohol use and subarachnoid hemorrhage. Stroke 1992; 23: 1242-1249

7 Mathieu J, Perusse L, Allard P, ef al. Epidemiological study of ruptured intracranial aneurysms in the Saguenay-Lac-Saint-Jean region (Quebec, Canada). Can J Neurol Sci 1996; 23: 184-188

8 Menghini VV, Brown RD Jr, Sicks JD, et al. Incidence and prevalence of intracranial aneurysms and hemorrhage in Olmsted County, Minnesota, 1965 to 1995. Neurology 1988; 51: 405-411

9 Weaver JP, Fisher M: Subarachnoid hemorrhage: An update of pathogenesis, diagnosis and management. J Neural Sci 1994; 1 25: 119-131

10 Schwartz TH, Solomon RA. Perimesencephalic nonaneurysmal subarachnoid hemorrhage. Review of the literature. Neurosurgery 1996; 39: 433-440

11 Mayberg MR, Batjer HH, Dacey R, et al. Guidelines for the mangement of aneurysmal subarachnoid hemorrhage. A statement for healthcare professionals from a special writing group of the Stroke Council, American Heart Association. Stroke 1994; 25: 2315-2328

12 Kassell NF, Torner JC, Haley E Jr, et al. The International Cooperative Study on the Timing of Aneurysm Surgery: Part 1. Overall management results. J Neurosurg 1990; 73: 18-36

13 Kassell NF, Torner JC, Jane JA, et al. The International Cooperative Study on the Timing of Aneurysm Surgery: Part 2. Surgical results. J Neurosurg 1990; 73: 37-47

14 Leblanc R. The minor leak preceding subarachnoid hemorrhage. J Neurosurg 1987; 66: 35-9

15 Cillingham FJ. The management of ruptured intracranial aneurysms. Scoff Med J 1967; 12: 377-383

16 Lyrer PH, Gratzl O. Gibt es eine Frühdiagnose bei zerebralen Aneurysmen? Symptome sakkulärer zerebraler Aneurysmen vor Auftreten einer massiven Subarachnoidalblutung. Schweiz Rundschau Med (Praxis) 1993; 82: 3-7

17 Ostergaard JR. Warning leak in subarachnoid hemorrhage. Br Med J 1990; 301: 190-191

18 Waga S, Ohtsubo K, Handa H. Warning signs in intracranial aneurysms. Surg Neurol 1975; 3: 15-20

19 Walter G, Stober T, Schimrigk K. Fehldiagnosen bei Subarachnoidalblutungen. Eine Untersuchung an 154 Fällen. Dtsch Med Wochenschr 1987; 112: 585-589

20 Hunt WE, Hess RM. Surgical risk as related to time of intervention in the repair of intracranial aneurysms. J Neurosurg 1968; 28: 14-20

21 Fisher CM, Kistler JP, Davis JM. Relation of cerebral vasospasm to subarachnoid hemorrhage visualized by computerized tomographic scanning. Neurosurgery 1980; 6: 1-9

22 Jennett B, Bond M. Assessment of outcome after severe brain damage: A practical scale. Lancet 1975; 1: 480-484

23 Duffy GP. The 'warning leak' in spontaneous subarachnoid hemorrhage. Med I Aust 1983; 1: 514-516

24 Edner G and Ronne-Engstrom E. Can early admission reduce aneurysmal rebleeds? A prospective study on aneurysmal incidence, aneurysmal rebleeds, admission and treatment delays in a defined region. Br J Neurosurg 1991; 5: 601-608

25 Hauerberg J, Andersen BB, Eskesen V. Importance of the recognition of a warning leak as a sign of a ruptured intracranial aneurysm. Acta Neurol Scand 1991; 83: 61-64

26 Jakobsson KE, Säveland H, Hillman J. Warning leak and management outcome in aneurysmal subarachnoid hemorrhage. J Neurosurg 1996; 85: 995-999

27 Juvela S. Minor leak before rupture of an intracranial aneurysm and subarachnoid hemorrhage of unknown etiology. Neurosurgery 1992; 30: 7-11

28 Tolias CM, Choksey MS. Will increased awareness among physicans of the significance of sudden agonizing headache affect the outcome of subarachnoid hemorrhage? Stroke 1996; 27: 807-812

Rainer Ritz* and Johannes Reif[dagger]

* Department of Neurosurgery, Eberhard-Karls University Tuebingen, 72076 Tuebingen, Germany

[dagger] Department of Neurosurgery, University of Saarland, 66421 Homburg/Saar, Germany

Correspondence and reprint requests to: Rainer Ritz, Department of Neurosurgery, University Hospital Tuebingen, Hoppe-Seyler-Strasse 3, 72076 Tuebingen, Germany. [rainer.ritz@med.uni-tuebingen.de] Accepted for publication September 2004.

Copyright Maney Publishing Sep 2005
Provided by ProQuest Information and Learning Company. All rights Reserved

Return to Cerebral aneurysm
Home Contact Resources Exchange Links ebay