PubMed Health⌕ Search

Biomedical subjects

C S Ogilvy

Publications and source records attributed to C S Ogilvy.

At least 19 recordsLinked to original sources
PubMed2005

SSRI and statin use increases the risk for vasospasm after subarachnoid hemorrhage.

BACKGROUND: Use of medications with vasoconstrictive or vasodilatory effects can potentially affect the risk for vasospasm after aneurysmal subarachnoid hemorrhage (SAH). METHODS: Using International Classification of Diseases-9 diagnostic codes followed by medical record review, the authors identified 514 patients with SAH admitted between 1995 and 2003 who were evaluated for vasospasm between days 4 and 14. The authors determined risks for vasospasm, symptomatic vasospasm, and poor clinical outcomes in patients with documented pre-hemorrhagic use of calcium channel blockers, beta-receptor blockers, ACE inhibitors, aspirin, selective serotonin reuptake inhibitors (SSRIs), non-SSRI vasoactive antidepressants, or statins. RESULTS: Vasospasm developed in 62%, and symptomatic vasospasm in 29% of the cohort. On univariate analysis, the risk for all vasospasm tended to increase in patients taking SSRIs (p = 0.09) and statins (p = 0.05); SSRI use increased the risk for symptomatic vasospasm (p = 0.028). The Cochran-Armitage trend test showed that the proportion of patients taking SSRIs and statins increased significantly across three worsening categories (none, asymptomatic, symptomatic) of vasospasm. Logistic regression analysis showed that SSRI use tended to predict all vasospasm (O.R. 2.01 [0.91 to 4.45]), and predicted symptomatic vasospasm (O.R. 1.42 [1.06 to 4.33]). Statin exposure increased the risk for vasospasm (O.R. 2.75 [1.16 to 6.50]), perhaps from abrupt statin withdrawal (O.R. 2.54 [0.78 to 8.28]). Age < 50 years, Hunt-Hess grade 4 or 5, and Fisher Group 3 independently predicted all vasospasm, symptomatic vasospasm, poor discharge clinical status, and death. CONCLUSION: Selective serotonin reuptake inhibitor and statin users have a higher risk for subarachnoid hemorrhage-related vasospasm. Whether the underlying disease indication, direct actions, or rebound effects from abrupt drug withdrawal account for the associated risk warrants further investigation.

Aged↗
PubMed2004

Computed tomographic demonstrated infarcts after surgical and endovascular treatment of aneurysmal subarachnoid hemorrhage.

BACKGROUND: Cerebral infarction is a sequela of vasospasm. Other etiologies for infarction after subarachnoid hemorrhage (SAH), however, have not been well-studied. To determine the incidence and etiologies for infarction after SAH, we reviewed the head CT scans of all SAH patients at our center from 1993-2000. METHODS: From 1993-2000, 679 consecutive patients were admitted with SAH, of which 619 patients underwent surgical or endovascular treatment. Two reviewers examined the head CT scans of all 619 patients for new infarct. Clinical outcome was collected from a prospective database. FINDINGS: 505 patients were treated with surgical clipping; 114 with endovascular coiling. There were CT findings of new infarct in 189 patients (30%): 140 in the surgical group (28%) and 49 in the endovascular group (43%). The etiologies for infarct in the surgical group were vasospasm 79 (15%), perforator occlusion 40 (8%), large vessel occlusion 14 (3%), elevated intracranial pressure 4 (1%), thromboembolism 2 (0.4%), and systemic hypotension 1 (0.2%). Infarcts in the endovascular group were due to vasospasm 20 (18%), thromboembolism 12 (11%), large vessel occlusion/dissection 9 (8%), elevated intracranial pressure 4 (4%), perforator occlusion 3 (3%), and systemic hypotension 1 (1%). Hunt Hess Grade (P < 0.001), Fisher Score (P < 0.0001), and MGH Grade (P < 0.001) were significantly associated with CT-demonstrated infarct. There was no significant difference in incidence of CT-infarcts when the period 1993-1996 was compared to 1997-2000. CONCLUSIONS: Despite advances in the treatment of SAH, there is still a significant incidence of associated radiographic infarcts. Hunt Hess Grade, Fisher Score, and MGH Grade were significantly associated with CT-demonstrated infarct.

Brain Infarction↗
PubMed2004

A modified technique for using elastase to create saccular aneurysms in animals that histologically and hemodynamically resemble aneurysms in human.

BACKGROUND: Treatment of intracranial aneurysms is evolving with the development of novel therapies. It is important to have an animal model which simulates human aneurysms. We describe a new modified technique to the elastase aneurysm model which creates aneurysms that histologically and hemodynamically resemble human aneurysms. METHODS: Twelve New Zealand white rabbits underwent the aneurysm creation procedure, and 2 underwent a control procedure. In the aneurysm creation procedure, the right common carotid artery (RCCA) origin is surgically exposed and temporarily occluded with a temporary aneurysm clip. The RCCA is ligated distally, and the trapped segment is infused with elastase for 20 minutes, after which the clip is removed. In the control procedure, the RCCA is ligated distally with no elastase. Animals were assessed neurologically using a previously described rabbit neurologic grading scale and food intake scale. Intravenous digital subtraction angiography (IVDSA) was performed 21 days after the procedure. Aneurysms were harvested and stained with H&E and Verhoeff's stain. FINDINGS: All 14 rabbits had normal neurologic and food intake assessments. All 12 rabbits that underwent aneurysm creation procedures demonstrated saccular aneurysms on IVDSA. Mean aneurysm size was 5.9+/-1.9 mm; range 4.3-10.8 mm. The close proximity of the LCCA to the origin of the RCCA on the aortic arch of the New Zealand white rabbit closely resembles a bifurcation aneurysm. Both rabbits that underwent control procedures showed no aneurysm and retrograde thrombosis of the RCCA. Histologic analysis showed the aneurysms had histology characteristic of true human aneurysms. CONCLUSION: We have developed a new modified technique to the elastase aneurysm model which creates aneurysms that hemodynamically and histologically resemble human aneurysms. There have been previous elastase models described, however we find our model is easier to perform and highly reproducible. The aneurysms can be accessed transfemorally making the model ideal for testing endovascular therapies.

Animals↗
PubMed2003

Incidence of residual intracranial AVMs after surgical resection and efficacy of immediate surgical re-exploration.

BACKGROUND: The true incidence of residual lesions after surgical resection of AVMs is not well documented in the literature. Partial surgical resection is thought to not confer any improvement over the natural history risk of hemorrhage of AVMs, and in certain cases may actually increase the risk of hemorrhage. Over the past 11 years, we have adopted a policy of immediate postoperative angiography with immediate surgical re-exploration if a residual lesion is seen. The purpose of the present study was to review our experience to determine the incidence of residual lesions and subsequent outcome. METHODS: From June 1991 to June 2002, 324 patients underwent craniotomy and surgical AVM resection. As per protocol, all patients underwent immediate postoperative angiography. We have a protocol for immediate surgical re-exploration if a residual lesion is seen on postoperative angiographic exam. FINDINGS: There were total six patients (1.8% of patients operated with intracranial AVMs) with residual lesions on postoperative angiography. All six patients underwent immediate surgical re-exploration with complete 100% obliteration; two patients required two re-exploration procedures. There was one operative complication: posterior cerebral artery and superior cerebellar artery infarcts after re-exploration of residual lesion after surgical resection of a large occipito-temperal-parietal AVM. There were no other morbidities and no mortalities. CONCLUSIONS: The incidence of residual lesions seen on postoperative angiography after AVM surgery at an experienced center is 1.8%. Because of the potential imminent danger of hemorrhage from a residual lesion, we recommend a policy of immediate postoperative angiography (or intraoperative angiography if image quality is satisfactory) for all AVM surgery and early surgical re-exploration if a residual lesion is seen.

Adult↗
PubMed2001

Fever in subarachnoid hemorrhage: relationship to vasospasm and outcome.

OBJECTIVE: To investigate the causes of fever in subarachnoid hemorrhage (SAH) and examine its relationship to outcome. BACKGROUND: Fever adversely affects outcome in stroke. Patients with SAH are at risk for cerebral ischemia due to vasospasm (VSP). In these patients, fever may be both caused by, and potentiate, VSP-mediated brain injury. METHODS: The authors prospectively studied patients admitted to a neurologic intensive care unit with nontraumatic SAH, documenting Hunt-Hess grade, Fisher group, Glasgow Coma Score, bacterial culture data, daily transcranial Doppler mean velocities, and maximum daily temperatures. Patients were classified as febrile (temperature above 38.3 degrees C for at least 2 consecutive days) or afebrile (no fever or isolated episodes of temperature above 38.3 degrees C). VSP was verified by either transcranial Doppler or angiographic criteria. Rankin scale scores on discharge were dichotomized into good (0 to 2) or poor (3 to 6) outcomes. RESULTS: Ninety-two consecutive patients were studied. Thirty-eight patients were classified as febrile. No source for infection was found in 10 of 38 (26%) patients. In a multivariate analysis, three variables independently predicted fever occurrence: ventriculostomy (OR, 8.5 [CI, 2.4 to 29.7]), symptomatic VSP (OR, 5.0 [CI, 1.03 to 24.5]), and older age (OR, 1.75 per 10 years [CI, 1.02 to 3.0]). Poor outcome was related to fever (OR, 1.4 per each day febrile [CI, 1.1 to 1.88]), older age (OR, 1.64 per 10 years [CI, 1.04 to 2.58]), and intubation (OR, 21.8 [CI, 5.6 to 84.5]). CONCLUSION: Fever in SAH is associated with vasospasm and poor outcome independently of hemorrhage severity or presence of infection.

Adult↗
PubMed2001

Results after surgical and endovascular treatment of paraclinoid aneurysms by a combined neurovascular team.

OBJECTIVE: Advances in surgical and endovascular techniques have improved treatment for paraclinoid aneurysms. A combined surgical and endovascular team can formulate individualized treatment strategies for patients with paraclinoid aneurysms. Patients who are considered to be at high surgical risk can be treated endovascularly to minimize morbidity. We reviewed the clinical and radiographic outcomes of 238 paraclinoid aneurysms treated by our combined surgical and endovascular unit. METHODS: From 1991 to 1999, the neurovascular team treated 238 paraclinoid aneurysms in 216 patients at the Massachusetts General Hospital. The modality of treatment for each aneurysm was chosen based on anatomic and clinical risk factors, with endovascular treatment offered to patients considered to have higher surgical risks. One hundred eighty aneurysms were treated by direct surgery, 57 were treated by endovascular occlusion, and one was treated by surgical extracranial-intracranial bypass and endovascular internal carotid artery balloon occlusion. Locations were transitional, 12 (5%); carotid cave, 11 (5%); ophthalmic, 131 (55%); posterior carotid wall, 38 (16%); and superior hypophyseal 46 (19%). Lesions contained completely within the cavernous sinus were excluded from this analysis. RESULTS: Using the Glasgow Outcome Scale (GOS), overall clinical outcomes were excellent or good (GOS 5 or 4), 86%; fair (GOS 3), 7%; poor (GOS 2), 4%; and death (GOS 1), 3%. Among the surgically treated patients, 90% experienced excellent or good outcomes (GOS 5 or 4), 6% had fair outcomes (GOS 3), 2% had poor outcomes (GOS 2), and 3% died (GOS 1). Among the endovascularly treated patients, 74% had excellent or good outcomes (GOS 5 or 4), 12% had fair outcomes (GOS 3), 10% had poor outcomes (GOS 2), and 4% died (GOS 1). The overall major and minor complication rate from surgery was 29%, with a 6% surgery-related permanent morbidity rate and a mortality rate of 0%. The overall major and minor complication rate from endovascular treatment was 21%, with a 3% endovascular-related permanent morbidity rate and a 2% mortality rate. Visual outcomes for patients who presented with visual symptoms were as follows: improved, 69%; no change, 25%; worsened, 6%; and new visual deficits, 3%. In general, angiographic efficacy was lower in the endovascular treatment group. CONCLUSION: A combined team approach of direct surgery and endovascular coiling can lead to good outcomes in the treatment for paraclinoid aneurysms, including high-risk lesions that might not have been treated in previous surgical series.

Adult↗
PubMed2001

Aneurysms of the lateral spinal artery: report of two cases.

OBJECTIVE AND IMPORTANCE: The goal of this report was to describe aneurysms arising from the lateral spinal artery. The locations of aneurysms contributing to subarachnoid hemorrhage (SAH) have been well characterized and are primarily in the circle of Willis or at the bifurcation points of the internal carotid artery or the vertebrobasilar system. Although the spinal arteries are also in direct communication with the subarachnoid space, aneurysms of these arteries that lead to SAH are rare. To date, only aneurysms of the anterior and posterior spinal arteries have been described. In this communication, we report two patients with aneurysms of the lateral spinal artery who presented with SAH. CLINICAL PRESENTATION: Review of our neurointerventional database from 1997 to the present revealed two patients with lateral spinal artery aneurysms. The medical records, as well as the operative and radiological findings, were reviewed for both patients. In both cases, the lateral spinal arteries were involved as collateral pathways for occlusive vertebral lesions, suggesting hemodynamic stress as a cause. INTERVENTION: Endovascular treatment was attempted in both cases and was successful in one; open surgery, with aneurysm resection, was performed in the other case. We review the vascular anatomic features of the spinal cord as they relate to the lateral spinal artery, as well as treatment options for lateral spinal artery aneurysms. CONCLUSION: Lateral spinal artery aneurysms are a rare cause of SAH. Both endovascular and surgical treatment options are available.

Aged↗
PubMed2001

Temporal clustering of hemorrhages from untreated cavernous malformations of the central nervous system.

OBJECTIVE: Hemorrhages from cerebral cavernous malformations (CMs) sometimes seem to occur in closely spaced "clusters" interspersed with long hemorrhage-free intervals. Clustering of hemorrhages could affect retrospective assessments of radiosurgery efficacy in prevention of CM rehemorrhage. However, this empirical observation had not been tested quantitatively. To test whether CM hemorrhages tend to cluster, we reviewed pretreatment rebleeding rates after a first symptomatic hemorrhage in CM patients who later underwent surgery or radiosurgery. METHODS: We performed a retrospective review of 141 patients with CMs who presented with clinically overt hemorrhage, and who subsequently underwent surgery or proton beam radiosurgery during an 18-year period. Statistical models were used to analyze all events per person and identify potential variation in rebleeding risk with time after a previous hemorrhage. RESULTS: Sixty-three of 141 patients experienced a second hemorrhage before treatment; 16 had additional hemorrhages. Five hundred thirty-eight patient years elapsed between first hemorrhages and treatment. The cumulative incidence of a second hemorrhage after the first CM hemorrhage was 14% after 1 year and 56% after 5 years. During the first 2.5 years after a hemorrhage, the monthly rehemorrhage hazard was 2%. The risk then decreased spontaneously to less than 1% per month, which represents a 2.4-fold decline (P < 0.001). Rehemorrhage rates were higher in younger patients (P < 0.01), but not in females or in patients with deep lesions. Shorter intervals between successive hemorrhages did not predict higher subsequent rehemorrhage risk. CONCLUSION: The rehemorrhage rate from untreated CMs is high initially, and it decreases 2 to 3 years after a previous hemorrhage. This hazard pattern generates the observed temporal clustering of hemorrhages from untreated CMs.

Adolescent↗
PubMed2001

Posterior fossa decompression and clot evacuation for fourth ventricle hemorrhage after aneurysmal rupture: case report.

OBJECTIVE AND IMPORTANCE: Massive intraventricular hemorrhage due to aneurysmal rupture is associated with a dismal prognosis. An intraventricular clot causing fourth ventricle dilation can cause compression to the brainstem similar to other posterior fossa masses such as cerebellar hemorrhage or infarction. The presence of fourth ventricle dilation carries a very high risk of death within 48 hours. Neither ventricular drainage nor fibrinolytic infusion has been successful in eliminating clots of the fourth ventricle. Posterior fossa decompression and direct evacuation of the clot could have good results in relieving brainstem compression caused by the clot. CLINICAL PRESENTATION: A 45-year-old woman was admitted to our intensive care unit after experiencing an aneurysmal subarachnoid hemorrhage. The neurological examination at admission revealed that she was in Grade V according to the World Federation of Neurological Surgeons grading system, but brainstem reflexes were present. Computed tomographic scanning revealed a massive intraventricular hemorrhage, with fourth ventricle dilation caused by an intraventricular clot. Bilateral external ventricular drains were placed to relieve elevated intracranial pressure. Cerebral angiography revealed a 1-cm basilar tip aneurysm, which was embolized with Guglielmi detachable coils (Boston Scientific, Boston, MA) during the same procedure. INTERVENTION: Given the patient's poor neurological condition, it was decided that brainstem compression should be relieved. A posterior fossa decompressive craniectomy was performed immediately after coil therapy, with direct evacuation of the intraventricular clot. The patient experienced a clear improvement in the level of consciousness and has achieved a good neurological result at early follow-up. CONCLUSION: Dilation of the fourth ventricle by an intraventricular clot is a sign of brainstem compression that can be relieved by posterior fossa decompression and direct clot evacuation.

Aneurysm, Ruptured↗
PubMed2001

Surgical and endovascular flow disconnection of intracranial pial single-channel arteriovenous fistulae.

INTRODUCTION: Intracranial pial single-channel arteriovenous (AV) fistulae are rare vascular lesions of the brain. They differ from AV malformations in that they lack a true "nidus" and are composed of one or more direct arterial connections to a single venous channel. They often are associated with a venous varix because of their high-flow nature. The pathological aspects of pial AV fistulae arise from their high-flow dynamics; therefore, we think that disconnection of the AV shunt is enough to obliterate the lesion, and that lesion resection is unnecessary. Flow disconnection can be accomplished via surgical or endovascular means. Certain lesions have angiogeometric configurations, however, that are unfavorable for endovascular treatment. We reviewed the experience in our combined neurosurgical and neuroendovascular unit in the treatment of patients with pial single-channel AV fistulae. METHODS: From 1991 to 1999, the combined neurovascular unit at the Massachusetts General Hospital treated nine consecutive patients with nontraumatic intracranial pial single-channel AV fistulae. Carotid-cavernous fistulae and vein of Galen malformations were excluded from this analysis. The combined neurovascular team planned the treatment strategy for each patient on the basis of the anatomic location and the angiogeometry of each lesion. We retrospectively reviewed the medical records, office charts, operative reports, endovascular reports, and x-rays for each patient. Radiographic outcome was assessed by use of posttreatment angiography. Clinical outcome was assessed by an independent nurse practitioner. RESULTS: A treatment strategy of flow disconnection was used in all nine patients and was accomplished surgically in six patients, endovascularly in two patients, and by combined techniques in one patient. All nine lesions were completely obliterated as demonstrated radiographically, including obliteration of the venous varices associated with three of the lesions. With a mean long-term clinical follow-up of 3.2 years (range, 0.3-8.4 yr), four patients were neurologically excellent with no deficits, two patients had pretreatment neurological deficits that did not worsen after treatment, one patient had transient dysphonia and dysphagia postoperatively that resolved, one patient had mild weakness after treatment, and one patient had moderate homonymous hemianopia after treatment. CONCLUSION: Single-channel pial AV fistulae can be treated by a strategy of flow disconnection. Resection of the lesion is not necessary. Flow disconnection can be accomplished either surgically or endovascularly; however, certain angiogeometric configurations are more favorable for surgical treatment. An experienced combined neurosurgical and neuroendovascular team can carefully determine the most appropriate treatment modality on the basis of patient-specific and angiospecific factors.

Adult↗
PubMed2001

Combined surgical and endovascular techniques of flow alteration to treat fusiform and complex wide-necked intracranial aneurysms that are unsuitable for clipping or coil embolization.

OBJECT: Certain intracranial aneurysms, because of their fusiform or complex wide-necked structure, giant size, or involvement with critical perforating or branch vessels. are unamenable to direct surgical clipping or endovascular coil treatment. Management of such lesions requires alternative or novel treatment strategies. Proximal and distal occlusion (trapping) is the most effective strategy. In lesions that cannot be trapped, alteration in blood flow to the "inflow zone," the site most vulnerable to aneurysm growth and rupture, is used. METHODS: From 1991 to 1999 the combined neurosurgical-neuroendovascular team at the Massachusetts General Hospital (MGH) managed 48 intracranial aneurysms that could not be clipped or occluded. Intracavernous internal carotid artery aneurysms were excluded from this analysis. By applying a previously described aneurysm rupture risk classification system (MGH Grades 0-5) based on the age of the patient, aneurysm size, Hunt and Hess grade, Fisher grade, and whether the aneurysm was a giant lesion located in the posterior circulation, the authors found that a significant number of patients were at moderate risk (MGH Grade 2; 31.3% of patients) and at high risk (MGH Grades 3 or 4; 22.9%) for treatment-related morbidity. The lesions were treated using a variety of strategies--surgical, endovascular, or a combination of modalities. Aneurysms that could not be trapped or occluded were treated using a paradigm of flow alteration, with flow redirected from either native collateral networks or from a surgically performed vascular bypass. Overall clinical outcomes were determined using the Glasgow Outcome Scale (GOS). A GOS score of 5 or 4 was achieved in 77.1%, a GOS score of 3 or 2 in 8.3%, and death (GOS 1) occurred in 14.6% of the patients. Procedure-related complications occurred in 27.1% of cases; the major morbidity rate was 6.3% and the mortality rate was 10.4%. Three patients experienced aneurysmal hemorrhage posttreatment; in two patients this event proved to be fatal. Aneurysms with MGH Grades 0, 1, 2, 3, and 4 were associated with favorable outcomes (GOS scores of 5 or 4) in 100%, 92.8%, 71.4%, 50%, and 0% of instances, respectively. CONCLUSIONS: Despite a high incidence of transient complications, intracranial aneurysms that cannot be clipped or occluded require alternative surgical and endovascular treatment strategies. In those aneurysms that cannot safely be trapped or occluded, one approach is the treatment strategy of flow alteration.

Adolescent↗
PubMed2001

Fluoroscopy-guided lumbar puncture: decreased frequency of traumatic tap and implications for the assessment of CT-negative acute subarachnoid hemorrhage.

BACKGROUND AND PURPOSE: In patients with suspected subarachnoid hemorrhage (SAH) and negative CT findings, the iatrogenic introduction of RBCs into the CSF during lumbar puncture may lead to a misdiagnosis. We tested the hypothesis that the risk of traumatic lumbar puncture is lower with the fluoroscopy-guided technique than with the standard bedside technique. METHODS: Data were collected retrospectively from two populations: adult inpatients undergoing standard bedside lumbar puncture for any reason and adult patients undergoing fluoroscopy-guided lumbar puncture for myelography. Patients with SAH and CSF samples with significant abnormalities other than erythrocytosis (ie, CSF leukocytosis, xanthochromia, or elevated protein) were excluded. In all, 1489 bedside procedures and 723 fluoroscopy-guided procedures met the criteria. RESULTS: We found a significant difference in the level of iatrogenic CSF erythrocytosis produced by the two procedures. Using a cutoff of 1000 cells/mm(3), the frequency of traumatic lumbar puncture was 10.1% for bedside lumbar puncture and 3.5% for fluoroscopy-guided lumbar puncture. With fluoroscopic guidance, the frequency of a traumatic tap varied significantly with the operator, ranging from 0% to 24%. CONCLUSION: The use of fluoroscopy-guided lumbar puncture in patients with suspected SAH and negative CT findings should reduce the frequency of false-positive diagnoses of acute SAH as well as the number of unnecessary angiograms for patients with suspected SAH but no underlying intracranial vascular malformation.

Fluoroscopy↗
PubMed2000

Post-treatment with nicotinamide (vitamin B(3)) reduces the infarct volume following permanent focal cerebral ischemia in female Sprague-Dawley and Wistar rats.

Delayed treatment with nicotinamide (NAm) protects male rats against cerebral ischemia. Since the preponderant use of male animals in stroke research may produce results not applicable to female stroke patients due to gender-related differences, we examined whether delayed NAm treatment could protect female rats against focal cerebral ischemia using a model of permanent middle cerebral artery occlusion (MCAo). NAm (500 mg/kg) given intravenously, 2 h after MCAo, significantly reduced the infarct volume of female Sprague-Dawley (55%, P<0.05) and Wistar rats (60%, P<0.05) rats when compared with saline-injected controls. These studies confirm that NAm is neuroprotective specifically at the dose of 500 mg/kg in rats. The novel findings are that this neuroprotection occurs in female, as well as male rats, and that the neuroprotection observed is more robust when administered as an intravenous bolus compared with intraperitoneal administration.

Animals↗