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R Leblanc

Publications and source records attributed to R Leblanc.

At least 19 recordsLinked to original sources
PubMed1992

Giant aneurysm of the distal anterior cerebral artery: associated with an anterior communicating artery aneurysm and a dural arteriovenous fistula.

We describe an unusual case of a giant pericallosal artery aneurysm, producing psychomotor depression from mass effect, associated with a smaller aneurysm of the anterior communicating artery, a dural arteriovenous fistula, and a meningioma. Magnetic resonance imaging (MRI) and cerebral angiography demonstrated the giant aneurysm and the meningioma. Cerebral angiography provided a detailed appreciation of the cerebral circulation, including both aneurysms, the dural arteriovenous fistula, and the potential collateral supply to the involved anterior cerebral distribution. The anterior communicating artery aneurysm was successfully clipped as was the distal anterior cerebral branch supplying the giant aneurysm before its resection. The patient made a full recovery but with persisting, slight dysphasia. We conclude that computed tomography, cerebral angiography, and MRI are of specific value in the assessment of giant aneurysms, but only angiography can provide detailed characterization of the aneurysm and demonstrate other possible cerebrovascular pathology such as multiple aneurysms and arteriovenous fistulas.

Adult↗
PubMed1992

Language localization with activation positron emission tomography scanning.

We report the first instance of the use of 3-dimensional magnetic resonance imaging anatomically correlated to positron emission tomography (PET) scanning to identify language areas in a patient with an arteriovenous malformation (AVM) in the posterior speech region. The patient was a 24-year-old right-handed woman with an angiographically proven AVM (3-4 cm) in the left mid-posterior second temporal convolution in whom a left intracarotid injection of sodium Amytal produced significant language disruption. A baseline PET cerebral blood flow study identified the AVM, and an activation PET scan performed during the reading and speaking of simple words showed increased activity in the left parastriate cortex (the second visual area), in the left posterior third frontal convolution (Broca's area), and in the left inferior and midtemporal gyri (Wernicke's area). Increased activity was also noted in the right and left transverse temporal (Heschl's) gyri, in the left precentral gyrus, in the left medial superior frontal gyrus (the supplementary motor area), and in the right cerebellum. We conclude that activation PET scanning is useful in the preoperative assessment of patients who harbor cerebral AVMs in classically described speech regions.

Adult↗
PubMed1992

Cerebral hemorrhage from amyloid angiopathy and coronary thrombolysis.

Coronary thrombolysis with streptokinase or tissue plasminogen activator is useful for the treatment of acute myocardial infarction in selected patients. This treatment is associated with local hemorrhagic complications and age-related cerebral hemorrhage. Coronary thrombolysis is contraindicated in patients with transient cerebral ischemia and stroke, arterial hypertension, cerebral trauma, cerebral aneurysms, and arteriovenous malformations, because of the risk of cerebral hemorrhage. We report the occurrence of a cerebral hemorrhage related to cerebral amyloid angiopathy in a patient who underwent thrombolysis and treatment with heparin for acute myocardial infarction. Despite normal coagulation parameters, the cerebral hematoma enlarged over 36 hours, as documented by sequential computed tomographic scans, to produce significant mass effect, which prompted surgical evacuation. Histological examination of the resected specimen demonstrated the strong affinity for Congo red and yellow-green birefringence that are characteristic of cerebral amyloid angiopathy. Hemostasis was difficult to achieve, as the divided or disrupted amyloid-laden cortical vessels failed to vasoconstrict, their contractile elements replaced by amyloid beta protein. The patient died of recurrent myocardial ischemia 3 days postoperatively. The incidence of cerebral amyloid angiopathy increases with advancing age. It must be considered as a potential source of cerebral hemorrhage in elderly patients undergoing thrombolysis for cardiac ischemia. Such an occurrence presents a difficult challenge because cardiac function is compromised, the coagulation profile may be altered, the cerebral hematoma is life threatening, and intracranial hemostasis is difficult to achieve.

Aged↗
PubMed1992

The relationship of ventricular drainage to aneurysmal rebleeding.

Given the widespread use of continuous external ventricular drainage in patients with aneurysmal subarachnoid hemorrhage (SAH), this investigation was undertaken to define the relationship of ventricular drainage to aneurysmal rebleeding. A historical cohort study of 128 patients with confirmed aneurysmal SAH was performed using a multivariate stepwise logistic regression analysis to examine the relationship between aneurysmal rerupture and ventricular drainage, while controlling for important clinical and radiological independent variables. The variables for ventricular drainage selected in the regression analysis were clinical grade, aneurysm size, and presence of hydrocephalus. The rate of rerupture was significantly higher in cases with ventricular drainage (odds ratio 5.31:1, p less than 0.05), poor clinical grade (odds ratio 4.90:1, p less than 0.02), and large aneurysm size (odds ratio 11.25:1, p less than 0.01). The significant effect of ventricular drainage was limited to patients with hydrocephalus. The increased risk of aneurysmal rebleeding in patients undergoing ventricular drainage may result from both: 1) a rise in aneurysmal transmural pressure, since intracranial pressure is lowered by ventricular drainage; and 2) an association between ventricular drainage and a more severely disrupted aneurysm which is more prone to rebleed as part of its natural history. This study found an increased risk of aneurysmal rebleeding among patients undergoing ventricular drainage, particularly in the presence of hydrocephalus.

Analysis of Variance↗
PubMed1992

MRI diagnosis of brainstem cavernous angiomas presenting as tumours.

We report experience with 11 patients misdiagnosed for years, on the basis of computed tomography (CT) and angiography, as harbouring brainstem tumours in whom magnetic resonance imaging (MRI) demonstrated cavernous angiomas. Seven had undergone external irradiation, 2 had a ventriculo-peritoneal shunt, 2 developed aseptic femur necrosis following corticosteroid treatment, 1 had undergone a biopsy with a pathological diagnosis of glioma. CT had depicted ill-defined, hyperdense, faintly enhancing lesions. Angiography was normal, or showed an avascular mass or subtle venous pooling. MRI delineated discrete lesions, typical of cavernous angiomas, with a mixed hyperintense, reticulated, central core surrounded by a hypointense rim. Six patients subsequently underwent stereotactic radiosurgery without changes in clinical status or lesion. Although hemorrhagic neoplasms may mimic the clinical course and MRI appearance of cavernous angiomas, MRI is useful in the diagnosis of brainstem cavernous angiomas and should be performed in patients with suspected brainstem tumours.

Adult↗
PubMed1992

Cerebral aneurysms and polycystic kidney disease: a critical review.

The pathogenic basis of the association between adult polycystic kidney disease (APKD) and cerebral aneurysms is unknown. We have compared cerebral aneurysms in 79 patients with APKD gleaned from the literature to the sporadic aneurysm cases reported by the Cooperative Study to determine if there are significant biological differences between these two groups. Sixty-eight patients had a single aneurysm and 11 (14%) had multiple aneurysms. In APKD patients with subarachnoid hemorrhage from a single aneurysm there was a significant over-representation of males (72%, p less than 0.01); and the APKD group had more aneurysms of the middle cerebral artery (37%, p less than 0.05). The peak decennial incidence and mean age of rupture of APKD-associated aneurysms was younger (mean age 39.7 years, p less than 0.01) and over 77% of APKD-associated aneurysms had ruptured by age 50 versus 42% for sporadic aneurysms (p less than 0.001). Cerebral aneurysms co-existed with APKD in the absence of hypertension in 25% of 45 cases where the presence or absence of hypertension was recorded. These biological differences and the occurrence of aneurysms in normotensive APKD patients suggests an etiology which may be independent of hypertension and that APKD-associated aneurysms may be genetically determined. It is hypothesized that cases of inherited, familial cerebral aneurysms could be linked to a genetic defect resembling that which occurs on chromosome 16 in APKD.

Adult↗
PubMed1992

Cerebral amyloid angiopathy and moyamoya disease.

The incidence, clinical manifestations, diagnosis, and management of cerebral hemorrhage from amyloid angiopathy and moyamoya disease are reviewed. Particular attention is given to pathophysiologic mechanisms producing cerebral hemorrhage in these conditions, the diagnosis based on characteristic CT and angiographic appearances, and the role of surgery in comprehensive management.

Brain↗
PubMed1991

Surgical treatment of intractable epilepsy associated with schizencephaly.

With the advent of magnetic resonance imaging, there has been an increased recognition of schizencephaly during life, especially in epileptic patients. We report our experience with the assessment and treatment of three patients with medically intractable seizures associated with this condition. The three men were aged 24 to 37 years. Two had delayed developmental milestones and hemiparesis or hemiplegia. One had normal development and a normal neurological examination. Seizures began between the ages of 15 and 19 years and lasted for 5 to 22 years before surgery. All had partial simple or generalized seizures with predominant electroencephalographic and electrocorticographic epileptic activity localized to temporal and frontal lobes on the side of the lesion. Neuropsychological assessment indicated widespread dysfunction maximal at the areas of predominant electroencephalographic abnormality. Magnetic resonance imaging demonstrated anterior parasagittal, parietal, and Rolandic cerebral clefts, with ventricular diverticuli, gray matter heterotopia, polymicrogyria, and a true agenesis of the corpus callosum in individual patients. The patients underwent temporal (one patient) and frontotemporal (two patients) lobectomies without additional neurological deficits or neuropsychological deterioration. Postoperative follow-up showed reduction in seizure frequency. We conclude that the surgical treatment of epilepsy is well tolerated in such patients, and their seizures can be alleviated by resection of epileptogenic areas.

Adult↗
PubMed1991

Surgical considerations in cerebral amyloid angiopathy.

In cerebral amyloid angiopathy, the contractile elements of the leptomeningeal and cortical arteries are replaced by noncontractile amyloid beta protein. The incidence of amyloid angiopathy increases with advancing age. It is associated with Alzheimer's disease and spontaneous cerebral hemorrhage. The latter can have the characteristic acute computed tomographic appearance of a hematoma at the cortex-white matter junction with extension of blood into the subarachnoid, subdural, and intraventricular spaces. Multiple hemorrhages are frequent. Additional bleeding can occur after evacuation of the hematoma, and postoperative hemorrhage can occur after cortical biopsy. To elucidate the role of surgery in this condition, we have reviewed 20 consecutive operated cases of cerebral amyloid angiopathy. A first group of 8 patients with senila dementia underwent cortical biopsy without resultant hemorrhage. A second group of 6 patients in good clinical condition had delayed evacuation of a spontaneous cerebral hematoma from cerebral amyloid angiopathy because of the radiological misdiagnosis of a hemorrhage within a tumor. One patient died of a pulmonary embolism, and another had subsequent multiple hemorrhages that were ultimately fatal. A third group of 6 patients in poor neurological condition had the acute evacuation of a spontaneous cerebral hematoma to relieve intracranial hypertension. All died or were severely disabled. One had repeated hemorrhages which added a progressively more severe organic dementia onto an initial hemiplegia.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Developmental anterobasal temporal encephalocele and temporal lobe epilepsy.

The authors describe the association between an antero-basal temporal lobe encephalocele and medically intractable temporal lobe epilepsy in three patients treated successfully by surgery. Two men and one woman, aged 26 to 37 years (mean 31 years), had onset of complex automatism and generalized seizures in their second and fourth decades (mean age 22.7 years). They had been epileptic for 6 to 14 years (mean 8.3 years) before surgery. Preoperative electroencephalograms localized ictal epileptic activity to the left mesial temporal lobe in all cases, and neuropsychological testing revealed dominant temporal lobe dysfunction. Magnetic resonance (MR) imaging demonstrated an anteromedial basal temporal encephalocele extending into the pterygopalatine fossa through a bone defect at the base of the greater sphenoid wing in the region of the foramen rotundum and pterygoid process, a discrete center of embryonal chondrification. At surgery, the encephaloceles were found in front of the uncus, and an area of gliosis extended from the encephalocele to the amygdalohippocampal region. All patients have been seizure-free following anterior temporal resection and amygdalohippocampectomy including the encephalocele. These three cases delineate a condition of disordered embryogenesis wherein a developmental anterobasal temporal encephalocele acts as the substrate for temporal lobe epilepsy. This lesion may be diagnosed preoperatively with MR imaging and should be considered in the differential diagnosis of late-onset temporal lobe epilepsy.

Adult↗
PubMed1991

Physiologic studies of cerebral ischemia.

Using the technology of his day, limited to direct observation and histological techniques, Fisher conclusively established the importance of the atherosclerotic carotid plaque in stroke. Recognizing the limits of his observations, he raised a number of questions as regards the degree of carotid disease necessary to adversely affect the brain and the effects of silent carotid occlusion. He also suggested the possible beneficial effects of revascularization. These questions have been addressed and in large part answered by PET. Thresholds of electrical activity and of cellular viability have been established both for cerebral blood flow and for oxygen metabolism. The effects of severe carotid stenosis have been found to be limited to the anterior border zone, where a decreased CBF and CBF to CBV ratio is seen in association with a trend towards rising OEF and declining CMRO2. The acute effects of a stroke and the passage of ischemia to infarction have been documented as they affect CBF, OEF, and CMRO2 in densely ischemic areas and in the penumbra region. An early pattern of elevated OEF in the face of diminished CBF is recognized and evolves into a later pattern of low OEF and CMRO2 characteristic of cell death. Silent carotid occlusion has been shown to produce widespread hypoperfusion and metabolic depression, the former improved by bypass, the latter not. Finally, the CBF to CBV ratio does not appear to be adequate in identifying patients who would benefit from EC-IC bypass, while an elevated preoperative OEF, an unusual event, does not clearly guarantee improved postoperative oxygen metabolism or the prevention of an ipsilateral stroke. Because the anterior border zone is selectively vulnerable to cerebral ischemia in patients with carotid stenosis, and since irreversible oxygen hypometabolism ensues once occlusion occurs, PET may be useful in identifying patients who may be at risk of further ischemic events should stenosis progress to occlusion. PET may also prove to be helpful in understanding the pathophysiology of ischemic complications associated with cerebral aneurysms and AVMs and may be a useful tool for deciding the timing of therapeutic intervention in these conditions.

Brain Ischemia↗
PubMed1990

Functional PET scanning in the assessment of cerebral arteriovenous malformations. Case report.

A case is presented which represents the first instance of the use of functional positron emission tomography (PET) scanning to precisely localize a structural brain lesion to the precentral gyrus, and the first validation of functional PET scanning by intraoperative cortical mapping. The lesion was a 3-cm arteriovenous malformation (AVM) that had produced a generalized seizure in an otherwise asymptomatic young woman. A first, resting H2(15)O PET scan identified the AVM. A second PET scan, performed during vibrotactile stimulation of the contralateral hand, identified the somatosensory area of the hand region and localized the AVM to that part of the precentral gyrus immediately in front of it. This relationship and localization were confirmed by cortical mapping at the time of craniotomy under local anesthesia. Functional PET scanning may prove to be useful to localize cortical lesions precisely and to help in determining preoperatively the best form of treatment for lesions, especially AVM's, in functionally important cortex.

Adult↗
PubMed1989

Hemodynamic and metabolic effects of extracranial carotid disease.

Cerebral blood flow (CBF), cerebral blood volume (CBV), the CBF/CBV ratio - an index of the hemodynamic reserve capacity - the rate of oxygen metabolism (CMRO2), and the fractional extraction of oxygen by the brain (OEF) were studied by positron emission tomography (PET) in the cortical territory of both internal carotid arteries in 15 cases of transiently symptomatic or progressive extracranial atherosclerotic carotid disease. None of the patients had a major stroke or had a significant neurological deficit except 1 whose damaged hemisphere is excluded from study. All were asymptomatic at the time of PET scanning. Values were obtained in the middle cerebral artery (MCA) distribution, and in the anterior and posterior borderzone regions. Eight cases had unilateral carotid stenosis of 80% or greater and 7 had unilateral or bilateral occlusion of the origin of the internal carotid artery. Results obtained in patients were compared using Student's t-test, to those obtained in neurologically normal, elderly volunteers. Patients with carotid stenosis had a significantly decreased CBF (p less than .025) and CBF/CBV ratio (p less than .025) selectively in the anterior borderzone regions. This was accompanied by a trend toward elevated OEF and declining CMRO2 values. Patients with carotid occlusion had significantly decreased CBF (p less than .005), decreased CBF/CBV ratio (p less than .005) and decreased CMRO2 (p less than .025) in the ipsilateral anterior borderzone and MCA territories. Similar changes were present in the opposite hemisphere of patients with bilateral carotid disease. These results indicate that carotid stenosis is associated with hypoperfusion and diminished hemodynamic reserve capacity in the anterior borderzone, and that carotid occlusion produces more widespread hypoperfusion and metabolic depression.

Aged↗
PubMed1989

Hemodynamic and metabolic effects of cerebral arteriovenous malformations studied by positron emission tomography.

Seventeen patients with an intracranial arteriovenous malformation were studied with positron emission tomography. Cerebral blood flow, cerebral blood volume, oxygen extraction fraction, and glucose and oxygen metabolism were evaluated in both hemispheres, excluding the area of the malformation itself. Patients were divided into three groups according to the size of their malformation, and results obtained were compared with studies in healthy volunteers. The glucose metabolism was significantly (p less than 0.01) decreased in the ipsilateral hemisphere in all patients. The cerebral blood volume was significantly increased (p less than 0.001) ipsilaterally in the three groups, and contralaterally in patients with medium- and large-sized arteriovenous malformations. The cerebral blood volume to cerebral blood flow ration, an index of vascular mean transit time, was significantly increased (p less than 0.005) ipsilaterally in patients with medium- and large-sized malformations and contralaterally in patients with large ones. Cerebral blood flow, oxygen extraction fraction, and oxygen metabolism were within the normal range bilaterally in all three groups, but oxygen extraction fraction tended to be higher in patients with larger lesions. The lack of significant change in oxygen metabolism suggests that oxygen metabolism in cortical areas remote from the arteriovenous malformation has been maintained by compensatory hemodynamic mechanisms. These data reveal widespread metabolic and hemodynamic consequences of arteriovenous malformations and suggest that they are associated with impairment of glucose metabolism, both in ipsilateral regions remote from the lesion and in the contralateral hemisphere in patients with large lesions.

Adult↗
PubMed1989

Absence of collagen deficiency in familial cerebral aneurysms.

It has been suggested that a deficiency in the expression of type III collagen may play a role in the pathogenesis of cerebral aneurysms. To test this hypothesis in cases of familial cerebral aneurysms, fibroblast cell cultures were established and the expression of collagen types I and III was studied in a patient with three cerebral aneurysms whose mother and sister also had cerebral aneurysms. Cultured skin fibroblasts were labeled with tritiated proline. The collagens and procollagens were precipitated and run on sodium dodecyl sulfate-polyacrylamide gel electrophoresis after reduction to analyze procollagen chains. Control cell lines were analyzed simultaneously. Quantitation of the ratios of type III to type I procollagen synthesis was achieved by integration of the intensities of the pro-alpha 1(III), pro-alpha 1(I), and pro-alpha 2(I) bands on fluorograms of electrophoretic gels of medium proteins. There was no difference in type I and III procollagen levels observed between the cells from the aneurysm patient and those from the control cell lines. These data do not support the hypothesis that familial cerebral aneurysms are caused by a deficiency of type III collagen.

Collagen↗