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Biomedical subjects

I A Awad

Publications and source records attributed to I A Awad.

At least 19 recordsLinked to original sources
PubMed1999

A comparison of the clinical profile of cavernous malformations with and without associated venous malformations.

OBJECTIVE: Little is known about the clinical behavior of cavernous malformations (CMs) associated with venous malformations (VMs) of the brain. The aim of this study is to compare the clinical profile of patients harboring CMs with and without associated VMs. METHODS: A retrospective analysis of 55 consecutive patients harboring CMs of the brain who presented to a single neurovascular team during a 4-year period was performed. Forty-two patients (76%) had CMs alone (CM group), and 13 patients (24%) had CMs associated with VMs (CM + VM group). Detailed clinical information regarding each patient was gathered. Statistical analysis was performed using Fisher's exact test for binary variables and Mann-Whitney U test for continuous variables. RESULTS: The lesion location was infratentorial for 19 of the 70 CMs (27%) in the CM group and for 14 of the 21 CMs (67%) in the CM + VM group (P = 0.001). Familial histories of CMs were documented for 7 of the 42 patients (17%) in the CM group and none of the 13 patients in the CM + VM group. There was a female-to-male gender bias of 1.6:1 in the CM group and 3.3:1 in the CM + VM group. Sixteen of the 42 patients (38%) in the CM group and 8 of the 13 patients (62%) in the CM + VM group presented with symptomatic hemorrhage. Seizure presentation was documented in 11 of the 42 patients (26%) in the CM group and in 1 of the 13 patients (8%) in the CM + VM group. Repeated symptomatic hemorrhage was diagnosed in 4 of the 42 patients (9.5%) in the CM group and in 3 of the 13 patients (23%) in the CM + VM group. There were no apparent differences in the mean age at presentation, lesion size, or multiplicity between the two groups. CONCLUSION: Patients with CMs associated with VMs are more likely to be female patients, have associated symptomatic hemorrhage, have lesions in the posterior fossa (statistically significant), suffer from repeated symptomatic hemorrhage, and are less likely to present with seizures or to have familial histories when compared with patients with CMs alone. The possible mechanisms for these apparent differences in clinical profile are discussed.

Adult↗
PubMed1999

Spontaneous angiographic obliteration of cerebral arteriovenous malformations.

OBJECTIVE: The factors associated with spontaneous angiographic obliteration of cerebral arteriovenous malformations (AVMs) are not well understood. We present a review of the literature and a report of our experience with six cases (four with no previous treatment intervention and two postoperative residual malformations) that were identified as having occurred during a 20-year period and describe the clinical and lesion features associated with this rare phenomenon. We present the first detailed histological study of a spontaneously thrombosed AVM specimen, including immunohistochemical analysis of angiogenesis factor expression. METHODS: A combined experience in the management of approximately 700 AVMs during 20 years identified six cases of spontaneous angiographic obliteration of cerebral AVMs. A literature review revealed another 24 cases with angiographic documentation of the initial AVMs and follow-up data showing nonfilling of the lesions. Histological analysis of a recently excised lesion included immunostaining with monoclonal antibodies to the antigens of Factor VIII, Tie, vascular endothelial growth factor, and its receptors, Flt-1 and Flk. RESULTS: A single draining vein was a feature in each of our 6 cases and in 12 of 14 (86%) cases from the literature. Hemorrhage as the presenting symptom was identified in 5 of our 6 (83%) cases and in 17 of 24 (71%) of the literature cases. The size of the AVM was less than 6 cm in each of our 6 cases and in 22 of 24 (92%) of the literature cases. A histological examination of a thrombosed AVM surgical specimen revealed persistent patent vascular channels within the lesion. Immunohistochemical analysis with angiogenesis and endothelia-specific factors showed expression of these factors within the lumen of the thrombosed nidus vessels. CONCLUSION: We propose that the occlusion of a single draining vein may lead to total venous outflow obstruction and lesion thrombosis. Hemorrhagic presentation and small nidus may also predispose to this phenomenon. Immunohistochemical analysis of a thrombosed AVM revealed possible ongoing angiogenic changes within the AVM vessels 1 month after angiographically documented thrombosis. It is possible that neovascularization within a thrombosed AVM may lead to lesion recanalization; however, this phenomenon seems to be clinically exceedingly rare.

Adult↗
PubMed1999

De novo development of a cavernous malformation of the spinal cord following spinal axis radiation. Case report.

Analysis of recent reports has suggested that cavernous malformations (CMs) of the brain may have an acquired pathogenesis and a dynamic pathophysiological composition, with documented appearance of new lesions in familial cases and following radiotherapy. The authors report the first case of demonstrated de novo formation of an intramedullary CM following spinal radiation therapy. A 17 year-old boy presented with diabetes insipidus and delayed puberty. Evaluation of endocrine levels revealed hypopituitarism, and magnetic resonance (MR) imaging demonstrated an infundibular mass. The patient underwent a pterional craniotomy and removal of an infundibular germinoma. The MR image of the spine demonstrated normal results. The patient received craniospinal radiation therapy and did well. He presented 5 years later with acute onset of back pain, lower-extremity weakness and numbness, and difficulty with urination. An MR image obtained of the spine revealed an intramedullary T-7 lesion; its signal characteristics were consistent with a CM. The patient was initially managed conservatively but developed progressive myelopathy and partial Brown-Séquard syndrome. Although he received high-dose steroids and bed rest, his symptoms worsened. He underwent a costotransversectomy and excision of a hemorrhagic vascular lesion via an anterolateral myelotomy. Pathological examination confirmed features of a CM. The patient has done well and was walking without assistance within 4 weeks of surgery. De novo genesis of CMs may be associated with prior radiation therapy to the spinal cord.

Abnormalities, Radiation-Induced↗
PubMed1998

Failure of the hypotensive provocative test during temporary balloon test occlusion of the internal carotid artery to predict delayed hemodynamic ischemia after therapeutic carotid occlusion.

BACKGROUND: Extensive experience and critical evaluation of the efficacy of a pharmacologic hypotensive challenge during conventional balloon test occlusion (BTO) of the internal carotid artery (ICA) is lacking. This prompted us to review our institution's most recent experience with this adjunctive provocative test before planned therapeutic balloon occlusion of the ICA. METHODS: Twenty consecutive cases of endovascular therapeutic balloon occlusion of the ICA were retrospectively reviewed. Conventional BTO under normotension and with hypotensive challenge were performed within a standardized protocol. RESULTS: Sixteen patients underwent provocative testing, of which 13 had BTO with hypotensive challenge. All patients in this group tolerated these maneuvers without acute neurologic deficit. Two (15%) of these patients developed delayed permanent neurologic deficits, which seemed to be attributable to hemodynamic ischemia. One of seven patients not undergoing hypotensive challenge also developed transient neurologic deficits after carotid occlusion. CONCLUSIONS: Despite the conceptually attractive and early positive experience of the hypotensive challenge in attempting to increase sensitivity and specificity of risk for developing delayed hemodynamic ischemia, we have found two significant false-negative results. This experience is reviewed in the context of risks of permanent balloon occlusion of the carotid artery after balloon test occlusion.

Adolescent↗
PubMed1998

Multilocus linkage identifies two new loci for a mendelian form of stroke, cerebral cavernous malformation, at 7p15-13 and 3q25.2-27.

Cerebral cavernous malformation (CCM) is a Mendelian model of stroke, characterized by focal abnormalities in small intracranial blood vessels leading to hemorrhage and consequent strokes and/or seizures. A significant fraction of cases is inherited as an autosomal dominant trait with incomplete penetrance. Among Hispanic Americans, virtually all CCM is attributable to a founder mutation localized to 7q ( CCM1 ). Recent analysis of non-Hispanic Caucasian kindreds, however, has excluded linkage to 7q in some, indicating at least one additional CCM locus. We now report analysis of linkage in 20 non-Hispanic Caucasian kindreds with familial CCM. In addition to linkage to CCM1, analysis of linkage demonstrates linkage to two new loci, CCM2 at 7p13-15 and CCM3 at 3q25.2-27. Multilocus analysis yields a maximum lod score of 14.11, with 40% of kindreds linked to CCM1, 20% linked to CCM2 and 40% linked to CCM3, with highly significant evidence for linkage to three loci (linkage to three loci supported with an odds ratio of 2.6 x 10(5):1 over linkage to two loci and 1.6 x 10(9):1 over linkage to one locus). Multipoint analysis among families with high posterior probabilities of linkage to each locus refines the locations of CCM2 and CCM3 to approximately 22 cM intervals. Linkage to these three loci can account for inheritance of CCM in all kindreds studied. Significant locus-specific differences in penetrance are identified. These findings have implications for genetic testing of this disorder and represent an important step toward identification of the molecular basis of this disease.

Cerebrovascular Disorders↗
PubMed1998

Occipital lobe vascular malformations: prevalence of visual field deficits and prognosis after therapeutic intervention.

BACKGROUND: The prevalence of visual field (VF) deficits in association with vascular malformations of the occipital lobe is not known, and the prognosis of the VF after therapeutic intervention has not been systematically documented. METHODS: We reviewed the clinical records of 23 consecutive patients who were managed at a single institution during a 3-year period with intracranial vascular malformations extending within the anatomic borders of the occipital lobe. Lesion location and treatment rendered were correlated with formal VF testing performed before and after therapeutic intervention. RESULTS: Twenty-one of the 23 patients underwent treatment of their lesions. Treatment included resection after preoperative embolization (12 patients), resection alone (2 patients with arteriovenous malformations and 3 patients with cavernous malformations), and stereotactic radiosurgery (4 patients; preceded by embolization in 3 of the 4). One patient was followed expectantly, and another died as a result of hemorrhage soon after undergoing endovascular embolization. The VFs were assessed before and after therapeutic intervention (follow-up assessment, 2-29 mo). New VF deficits or worsening of preexisting VF deficits were documented in 5 of the 21 treated patients (24%), but only 2 of these patients (9.5%) had persistent deficits at the time of their follow-up examinations. Among the 10 patients with pretreatment VF deficits, 5 improved and the other 5 were unchanged after treatment. CONCLUSION: Patients with occipital lobe vascular malformations frequently present with associated VF deficits. Surgical resection or stereotactic radiosurgery (with or without previous embolization) of these lesions can be performed with little risk of causing new VF deficits or worsening of preexisting ones. Many VF deficits can be expected to improve or resolve after therapy.

Adult↗
PubMed1998

Endothelial cell culture from human cerebral cavernous malformations.

BACKGROUND AND PURPOSE: The cerebral cavernous malformation (CCM) is a common and frequently unrecognized cause of stroke and epilepsy. It consists of blood-filled caverns lined by endothelial cells (EC) and devoid of mature vessel wall structure. Cultured EC obtained from CCM may express phenotypic and genotypic alterations contributing to CCM pathogenesis. We report the first successful isolation and growth in vitro of primary EC lines from human CCM lesions. METHODS: We developed a procedure for the isolation and growth of EC from human CCM, confirmed their EC origin by a panel of molecular markers, and determined by immunocytochemistry the basic expression patterns of 6 transmembrane receptor protein kinases comparing brain, skin, and CCM primary EC lines grown identically. RESULTS: Several CCM EC lines were established from 2 patients after we treated the excised specimens with 0.3% trypsin/1% EDTA, selective cloning, and growth in MCDB107 containing 0.3 g/L heparin, 0.15 g/L endothelial cell growth supplement, and 15% FBS. The CCM EC showed contact inhibition and a rounded cobblestone appearance. The cells expressed CD31, CD105, von Willebrand factor, and binding sites for Ulex europaeus agglutinin, type 1 and acetylated LDL. They showed low levels of Flt-1, Flk-1, transforming growth factor (TGF)-beta RI, and TGF-beta RII expression but stained strongly with antibodies against Tie-1 and Tie-2. CONCLUSIONS: Cultured CCM EC retained their endothelial phenotype. Brain, skin, and CCM EC lines did not significantly differ in their staining patterns with antibodies against Flt-1, Flk-1, TGF-beta RI, TGF-beta RII, Tie-1, and Tie-2. These cell lines will assist in defining molecular phenotype and genotype alterations in association with CCM.

Antibodies, Monoclonal↗
PubMed1998

Surgery for intracerebral hemorrhage.

Intracerebral hemorrhage (ICH) represents 8 to 15% of all strokes in the United States and 20 to 30% of all strokes in Japan and China. Although ICH represents a relatively small fraction of total strokes, it is a formidable disease, with a 30-day mortality rate two- to sixfold higher than that for ischemic stroke. Furthermore, it is a major cause of disability, with only 20% of patients becoming independent at 6 months. The most common risk factors for ICH are age, hypertension, and amyloid angiopathy, which are associated with damage to and weakening of the arterial/arteriolar wall leading to vessel rupture. The pathology is a dynamic one that continues to evolve over the first few days after onset. In 20 to 30% of ICH, clot volume increases over the first 24 hours and is generally associated with neurologic worsening. The final outcome from ICH is related not only to clot volume, compression, and destruction but also to potential neurotoxicity from the blood degradation products and associated neuronal ischemia. The treatment of ICH has been one of the most controversial and least well-studied areas from a medical or surgical perspective. Surgical treatment has evolved over the years and can be grouped into open and stereotactically guided surgery for hematoma evacuation. Seven thousand operations per year are performed in the United States for hematoma evacuation, although this approach has not been adequately investigated. Adjuvant medical therapies with neuroprotective agents require further investigation and may potentially have additive benefits.

Cerebral Hemorrhage↗
PubMed1998

MR of hereditary hemorrhagic telangiectasia: prevalence and spectrum of cerebrovascular malformations.

PURPOSE: Our goal was to describe the prevalence and types of cerebral vascular malformations (CVMs) seen with MR imaging in patients with hereditary hemorrhagic telangiectasia (HHT). METHODS: We reviewed retrospectively the brain MR images of 184 consecutive patients with HHT. Catheter angiography was performed in 17 patients with CVMs detected on MR images. RESULTS: MR imaging revealed 63 CVMs in 42 patients. Classic arteriovenous malformations (n = 10) had a conspicuous network of vessels with flow voids and enlarged adjacent pial vessels. Apparent venous malformations (n = 5) were best seen after administration of contrast material as a prominent vessel coursing through normal brain parenchyma. Indeterminate vascular malformations (n = 48) had a spectrum of appearances characterized by variable combinations of heterogeneous signal intensity, enhancement, or hemosiderin. Angiography in 17 patients revealed 47 CVMs. Forty-six were arteriovenous malformations (AVMs), including 25 CVMs not seen with MR imaging and 21 CVMs that by MR criteria included 8 AVMs and 13 indeterminate vascular malformations. Angiography confirmed 1 venous malformation seen with MR imaging but failed to detect 3 indeterminate lesions revealed by MR imaging. CONCLUSION: MR imaging of a large cohort of consecutive patients with HHT revealed a CVM prevalence of 23% (42/184). Most CVMs (48/63) have an atypical appearance for vascular malformations on MR images. Angiographic correlation suggests that MR imaging underestimates the prevalence of CVMs and that the majority of indeterminate CVMs, despite their variable MR appearance, are AVMs.

Cerebral Angiography↗
PubMed1997

Cerebral vascular malformations adjacent to sensorimotor and visual cortex. Functional magnetic resonance imaging studies before and after therapeutic intervention.

BACKGROUND AND PURPOSE: It is not known how cerebral vascular malformations affect the function of the surrounding brain. Functional magnetic resonance imaging (fMRI) can provide information about normal functional neuroanatomy and its alteration by vascular lesions and therapeutic intervention. METHODS: We performed fMRI studies in 24 patients harboring vascular malformations adjacent to primary somatosensory, motor, and visual cortex. The fMRI studies consisted of the acquisition of an image time series coupled with functional activation of motor, sensory, or visual cortex in both hemispheres. Activated voxels were identified using frequency domain analyses, and their number and anatomic location were compared between the affected and unaffected hemispheres. RESULTS: Every patient capable of performing the desired task showed functional activation. Eight patients without neurological deficits showed a symmetrical pattern of activation between the hemispheres. Each had a vascular malformation located one or more gyri from the functional region imaged. Three patients showed hemispheric symmetry in the location of activated cortex but with a marked asymmetry in the number of activated voxels. Each harbored vascular malformations located within one gyrus of the functional region and showed either subtle or no neurological deficit. Eleven patients showed hemispheric asymmetry in the location of activated cortex. In 6, the anatomic displacement appeared to be due to a mass effect of the lesion. In 5, the activation occurred at a different anatomic locale, and the patients exhibited gross neurological deficit in the respective function. Posttherapeutic changes in functional activation reflected elimination of the mass effect or recovery of clinical function. CONCLUSIONS: Systematic fMRI studies are possible in patients with vascular malformations in brain regions adjacent to primary somatosensory, motor, and visual cortex. Displacement of the activated region and hemispheric asymmetry in the number of activated voxels in the functional regions appear to reflect the anatomic and physiological impact of the vascular malformation. Changes in fMRI findings after intervention reflect the consequences of therapy and parallel clinical recovery.

Adolescent↗
PubMed1996

A founder mutation as a cause of cerebral cavernous malformation in Hispanic Americans.

BACKGROUND: Cerebral cavernous malformation is a vascular disease of the brain causing headaches, seizures, and cerebral hemorrhage. Familial and sporadic cases are recognized, and a gene causing familial disease has been mapped to chromosome 7. Hispanic Americans have a higher prevalence of cavernous malformation than do other ethnic groups, raising the possibility that affected persons in this population have inherited the same mutation from a common ancestor. METHODS: We compared the segregation of genetic markers and clinical cases of cavernous malformation in Hispanic-American kindreds with familial disease; we also compared the alleles for markers linked to cavernous malformation in patients with familial and sporadic cases. RESULTS: All kindreds with familial disease showed linkage of cavernous malformation to a short segment of chromosome 7 (odds supporting linkage, 4X10(10).1). Forty-seven affected members of 14 kindreds shared identical alleles for up to 15 markers linked to the cavernous-malformation gene, demonstrating that they had inherited the same mutation from a common ancestor. Ten patients with sporadic cases also shared these same alleles, indicating that they too had inherited the same mutation. Thirty-three asymptomatic carriers of the disease gene were identified, demonstrating the variability and age dependence of the development of symptoms and explaining the appearance of apparently sporadic cases. CONCLUSIONS: Virtually all cases of familial and sporadic cavernous malformation among Hispanic Americans of Mexican descent are due to the inheritance of the same mutation from a common ancestor.

Adolescent↗
PubMed1996

Giant aneurysms of the anterior circle of Willis: management outcome of open microsurgical treatment.

BACKGROUND: There is no uniform agreement to date regarding the optimal management of giant aneurysms (GAs) of the anterior circle of Willis. Endovascular therapeutic techniques have yielded unacceptable rates of aneurysm growth and recanalization (endosaccular) or high rates of complications (distal parent vessel occlusion). Despite size, frequent thrombosis and calcification (incollapsibility), and splaying of parent vessels, these aneurysms are readily amenable to direct surgical exposure and control of parent vessels intracranially. Published series have not considered these lesions separately and have often reflected a mixture of management strategies for these and other GAs. METHODS: Thirty-eight consecutive patients with symptomatic GAs of the anterior circle of Willis were managed by the senior author over a 7-year period. Twenty-six of these patients (68%) presented with subarachnoid hemorrhage (SAH). Temporary occlusion was performed under a protocol to enhance brain protection. Direct clip reconstruction or trapping was used in all instances, with intraoperative angiographic control. Revascularization procedures and suture vascular reconstructions were not used in any case. RESULTS: All patients were considered for direct microsurgical treatment. One patient refused surgery, and two patients were deemed a prohibitive medical risk. Thirty-five patients were treated surgically with complete obliteration of the aneurysm in 34 cases (97%), and patency of all parent arteries in 30 cases (86%). Overall mortality was 6% in the surgical cohort, with good or excellent clinical outcome in 71%. Mortality and poor outcome occurred exclusively in the setting of recent hemorrhage. CONCLUSIONS: The results are compared to the natural history of these lesions and to outcome (safety and effectiveness) of currently available endovascular techniques. This experience supports direct microsurgical intervention as the primary therapeutic modality for these lesions.

Adult↗
PubMed1996

Expression of angiogenic factors and structural proteins in central nervous system vascular malformations.

Little is known of the molecular mechanisms mediating the genesis and subsequent biological behavior of central nervous system vascular malformations. The role of angiogenic and permeability-inducing factors in the pathogenesis of these lesions has not bee previously explored. In this study, we subject specimens from 12 cases of excised vascular malformation to a battery of immunostaining for vascular endothelial growth factor, basic fibroblast growth factor, and selected structural and matrix proteins. The lesions consisted of seven arteriovenous malformations (AVMs), including one angiographically occult AVM, one arterialized vein from a dural AVM, and five cavernous malformations (CMs). Vascular endothelial growth factor was expressed by all lesions and was localized predominantly in the subendothelial layer and in perivascular spaces. Four of seven AVMs and four of five CMs demonstrated faint basic fibroblast growth factor expression that was localized to the media of AVM vessels and the subendothelial layer and intercavernous matrix of CMs. This pattern of angiogenic factor immunostaining was correlated with the expression of structural and matrix proteins in the same lesions. Laminin was not expressed in any of the CMs, confirming previous reports from our laboratory. By contrast, fibronectin expression was more prominent in CMs than in AVMs. Collagen Type IV and alpha smooth muscle actin expression occurred in every lesion. We conclude that angiogenic growth factors are expressed in all types of vascular malformations of the central nervous system. The pattern of expression suggests diffuse activation of angiogenesis without specific relation to individual vessel types or recent clinical behavior. Defining the role of angiogenesis in vascular malformations might provide insight into their pathogenesis and suggest novel strategies for modification of their behavior.

Actins↗
PubMed1996

Genetic heterogeneity of inherited cerebral cavernous malformation.

OBJECTIVE: Cerebral cavernous malformation (CCM) is frequently an inherited disorder showing autosomal dominant transmission. Genetic analysis has localized a gene causing CCM to a segment of the long arm of human chromosome 7 (7q). This evidence derives from investigation of a small number of families, mostly of Hispanic American descent. In this study, we have tested whether inherited CCM is always due to mutation in this 7q gene, or whether mutation in other genes can cause CCM. METHODS: We have studied subjects from two non-Hispanic families with inherited CCM. The clinical features of CCM in these families are indistinguishable from those in kindreds in which CCM is due to mutation in the 7q gene. To test whether CCM in these kindreds is caused by a mutation on 7q, we compared the inheritance of CCM to the inheritance of genetic markers on 7q. RESULTS: Genetic analysis demonstrates independent inheritance of CCM and markers on 7q in both families studied. This evidence excludes mutation in the 7q gene as the cause of CCM in these families, with odds against CCM being due to mutation in 7q in each family of more than 100,000:1 and 100:1, respectively. CONCLUSION: These findings demonstrate that inherited CCM is not always caused by a mutant gene on 7q, indicating the presence of at least a second gene in which mutation can cause CCM. These results have implications for genetic testing and the pathogenesis of this disorder.

Adult↗
PubMed1996

Expression of angiogenesis factors and selected vascular wall matrix proteins in intracranial saccular aneurysms.

OBJECTIVE: Little is known about the biological mechanisms associated with the genesis, growth, and rupture of intracranial saccular aneurysms. It is postulated that the vascular wall pathological response of aneurysmal disease is associated with abnormal angiogenesis factor expression. METHODS: We have examined the expression and distribution of immunoreactivity to angiogenesis growth factors (vascular endothelial growth factor and basic fibroblast growth factor) and selected vascular wall matrix proteins (fibronectin, Type IV collagen, and alpha smooth muscle actin) in the walls of human intracranial aneurysms from surgical biopsy or autopsy specimens. Double antibody immunohistochemical stains were performed in contiguous fixed sections from three control circle of Willis arteries, five berry aneurysms, four giant aneurysms, and one mycotic aneurysm (three unruptured and seven ruptured lesions). RESULTS: The aneurysmal wall exhibited diffuse disorganized expression of matrix proteins as compared to their organization in control vessels. There was strong patchy expression of vascular endothelial growth factor within the walls of all aneurysms, including marked staining of capillaries and small vessels within the thickened walls of giant lesions. The expression of basic fibroblast growth factor was more diffuse and occurred around the fibrocytes and myocytes within the disrupted media of 9 of 10 aneurysms. CONCLUSIONS: These results confirm the gross architectural molecular disruption in the walls of intracranial aneurysms and illustrate an apparent biological response involving angiogenesis factors. Further research should elucidate the time course and possible causal relationships of these changes to aneurysm growth and rupture with the aim of possible therapeutic manipulation.

Actins↗
PubMed1996

Misdiagnosis of symptomatic cerebral aneurysm. Prevalence and correlation with outcome at four institutions.

BACKGROUND AND PURPOSE: It is not known what fraction of patients with symptomatic cerebral aneurysms are misdiagnosed at initial medical presentation. It is also not clear whether misdiagnosed patients more frequently deteriorate before definitive aneurysm diagnosis and therapy or achieve a poorer outcome than correctly diagnosed patients. METHODS: We reviewed records of consecutive patients with symptomatic cerebral aneurysms managed by four tertiary-care neurosurgical services during a recent 19-month period. Clinical course and outcome were analyzed according to misdiagnosis or correct diagnosis at initial medical evaluation. RESULTS: Fifty-four of 217 patients (25%) were misdiagnosed at initial medical evaluation, including 46 of 121 patients (38%) initially in good clinical condition (clinical grade 1 or 2). Forty-six of 54 patients (85%) in the misdiagnosis group were initially grade 1 or 2 compared with 75 of 163 patients (46%) with correct initial diagnosis (P < .01). Twenty-six of 54 misdiagnosed patients (48%) deteriorated or rebled before definitive aneurysm treatment compared with 4 of 165 correctly diagnosed patients (2%) (P < .001). Among patients initially presenting as clinical grade 1 or 2, overall good or excellent outcome was achieved in 91% of those with correct initial diagnosis and 53% of patients with initial misdiagnosis (P < .001). Deterioration before correct diagnosis accounted for 16 of 67 patients (24%) with poor or worse final outcome in this series. CONCLUSIONS: Patients in good clinical condition with symptomatic cerebral aneurysms were commonly misdiagnosed. Misdiagnosed patients were more likely than correctly diagnosed patients to deteriorate clinically and had a worse overall outcome. Misdiagnosed cases accounted for a significant fraction of overall poor outcomes among consecutive cases of symptomatic aneurysms.

Adult↗