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Biomedical subjects

A J Furlan

Publications and source records attributed to A J Furlan.

At least 19 recordsLinked to original sources
PubMed1992

Further observations on the pathology of subcortical lesions identified on magnetic resonance imaging.

We performed postmortem magnetic resonance imaging and pathologic examinations on the brains of seven consecutive patients older than 50 years of age who died of non-neurologic causes. Multiple hyperintense subcortical lesions were identified in each patient, and a total of 29 lesions were examined histologically (eight rims, six caps, six punctate lesions, and nine patches). Rims were characterized by subependymal gliosis and loss of the ependymal lining; caps were associated with myelin pallor, gliosis, and arteriosclerosis; punctate lesions were characterized by dilated perivascular spaces and perivascular gliosis; and patches were associated with myelin pallor and dilated perivascular spaces. The pattern of myelin pallor defined the size and shape of caps and patches. Arteriosclerosis was identified in six of six caps, three of six punctate lesions, and in three of nine patches. These data indicate that (1) each type of hyperintense subcortical lesion has a distinct pathologic correlate; (2) arteriosclerosis is not invariably associated with all types of hyperintense subcortical lesions on magnetic resonance imaging; and (3) myelin pallor appears to contribute to the magnetic resonance imaging signal at 1.5 tesla.

Aged↗
PubMed1992

Recombinant tissue plasminogen activator in acute thrombotic and embolic stroke.

An open angiography-based, dose rate escalation study on the effect of intravenous infusion of recombinant tissue plasminogen activator (rt-PA) on cerebral arterial recanalization in patients with acute focal cerebral ischemia was performed at 16 centers. Arterial occlusions consistent with acute ischemia in the carotid or vertebrobasilar territory in the absence of detectable intracerebral hemorrhage were prerequisites for treatment. After the 60-minute rt-PA infusion, arterial perfusion was assessed by repeat angiography and computed tomography scans were performed at 24 hours to assess hemorrhagic transformation. Of 139 patients with symptoms of focal ischemia, 80.6% (112) had complete occlusion of the primary vessel at a mean of 5.4 +/- 1.7 hours after symptom onset. No dose rate response of cerebral arterial recanalization was observed in 93 patients who completed the rt-PA infusion. Middle cerebral artery division (M2) and branch (M3) occlusions were more likely to undergo recanalization by 60 minutes than were internal carotid artery occlusions. Hemorrhagic infarction occurred in 20.2% and parenchymatous hematoma in 10.6% of patients over all dose rates, while neurological worsening accompanied hemorrhagic transformation (hemorrhagic infarction and parenchymatous hematoma) in 9.6% of patients. All findings were within prospective safety guidelines. No dose rate correlation with hemorrhagic infarction, parenchymatous hematoma, or both was seen. Hemorrhagic transformation occurred significantly more frequently in patients receiving treatment at least 6 hours after symptom onset. No relationship between hemorrhagic transformation and recanalization was observed. This study indicates that site of occlusion, time to recanalization, and time to treatment are important variables in acute stroke intervention with this agent.

Acute Disease↗
PubMed1992

Intracranial hemorrhage after coronary thrombolysis with tissue plasminogen activator.

PURPOSE AND METHODS: We analyzed the clinical, laboratory, and radiologic data in nine patients who sustained an intracranial hemorrhage (ICH) after receiving intravenous recombinant tissue plasminogen activator (rt-PA) and heparin for treatment of acute myocardial infarction (MI). Our purpose was to delineate the clinical and radiologic features of the ICHs, as well as to determine their potential risk factors and mechanisms. RESULTS: Among 1,700 patients with an acute MI treated with an investigational two-chain rt-PA, duteplase (Burroughs Wellcome Co., Research Triangle Park, NC), nine (0.53%) developed symptomatic ICH. Neurologic symptoms occurred between 7 and 96 hours after onset of rt-PA therapy. All patients received heparin concomitantly for prevention of coronary reocclusion. The activated partial thromboplastin times (aPTTs) in five of eight (63%) patients at onset of ICH were excessively prolonged (greater than two times control); hypofibrinogenemia occurred in only one of five (20%) patients tested; and thrombocytopenia was present in only one of the nine (11%) patients. Fibrin degradation products (FDPs) were elevated in all five patients tested. Minor hemorrhage (not requiring transfusion) outside the central nervous system occurred in five of the nine patients with ICH. The ICHs were often of lobar location and of moderate to large size. They occurred at multiple sites in three patients, and were fatal in four instances (44%). CONCLUSIONS: The incidence of ICH in this series was low, and consistent with figures reported from studies with alteplase in patients with acute MI. The mechanisms of these hemorrhages remain unclear; while hypofibrinogenemia was not a uniform finding, excessive prolongation of the aPTT and elevated FDPs may have contributed to the occurrence of ICH in some patients. Still unidentified local cerebrovascular factors may play an additional role in causing ICH. In order to further clarify the mechanisms of ICH in the setting of thrombolytic therapy, prospective data collection on probable risk factors for ICH in patients with acute MI treated with rt-PA will be required.

Aged↗
PubMed1992

Hydroxyethyl starch 200/0.5 reduces infarct volume after embolic stroke in rats.

BACKGROUND AND PURPOSE: We evaluated isovolumic hemodilution with hydroxyethyl starch 200/0.5 in a rat model of focal cerebral ischemia. This compound avoids the unfavorable viscosity and erythrocyte aggregation abnormalities of low molecular weight dextran during administration over a period of several days. METHODS: Sprague-Dawley rats, anesthetized with 0.5-1% halothane and 70% N2O, were subjected to silicon cylinder (treated and control groups) or sham (sham group) embolization of the cerebral circulation. Thirty minutes after embolization, the treated group (n = 5) was infused with 11 ml/kg of 10% hydroxyethyl starch 200/0.5, and the control (n = 5) and sham (n = 4) groups were infused with saline for 1 hour. In the treated group, 7.1 ml/kg of blood was withdrawn. After 24 hours, the animals were reanesthetized, and cerebral blood flow was determined with [14C]iodoantipyrine. Alternative brain slices were either incubated with 2,3,5-triphenyltetrazolium chloride for infarct volume determination or frozen for ischemic volume and cerebral blood flow determination using autoradiography. RESULTS: The hematocrit in the treated group was reduced from (mean +/- SEM) 46 +/- 1% to 35 +/- 2% at 1.5 hours (p < 0.01). Cortical blood flow was within the normal range of 115-185 ml/min/100 g, except for the ischemic cortex in the embolized groups, treated and control. The ischemic and infarct volume of the treated group was reduced by 74% (p < 0.05) and 89% (p < 0.05), respectively, from the control group. The treated and sham ischemic and infarct volumes were not statistically different. CONCLUSIONS: These data suggest that hydroxyethyl starch 200/0.5 could be an effective treatment for ischemic stroke when administered early, because it reduces infarct and ischemic volumes from control values to levels indistinguishable from those of the sham group.

Animals↗
PubMed1992

Optic neuropathy: a rare paraneoplastic syndrome.

A 63-year-old man developed gradually progressive bilateral loss of vision, cerebellar ataxia, and downbeat nystagmus. Visual acuity was 20/400 OD and 20/200 OS, with cecocentral scotomas OU. Fundus examination showed bilateral optic atrophy and a vitreous cellular reaction. MRI of the brain was normal. CSF protein was elevated, with increased IgG levels but no malignant cells. Biopsy of a pulmonary lymph node showed undifferentiated small cell carcinoma. Neoplastic cells were positive for neuron-specific enolase. Serum contained IgG, which reacted with neuronal and glial cytoplasm and processes. IgG reactivity with systemic tissues and the patient's tumor was not different from that observed with control sera. Paraneoplastic optic neuropathy should be considered in patients with unexplained visual loss and malignancy, and our observations suggest a possible immunologic basis for this condition.

Antineoplastic Agents↗
PubMed1992

Neurologic complications related to cardiac surgery.

Neurologic complications are a major cause of morbidity, complicating open heart surgery, cardiac catheterization, and interventional techniques. Global or focal brain ischemia related to embolism or hypoperfusion predominates. Breakthrough cerebral hemorrhage and infection can complicate cardiac transplantation. Identifying individuals at risk for cerebrovascular complications may lead to more effective preventative and treatment measures.

Brain Damage, Chronic↗
PubMed1992

Cerebral vascular physiology in hypertensive disease.

Experimental advances during the last decade have greatly expanded our knowledge of mechanisms that control cerebral blood flow. In addition to local metabolites, many other factors are important in control of cerebral blood vessels. During chronic hypertension, several mechanisms of cerebral vascular control are altered, with both beneficial and detrimental consequences. The changes should be considered carefully during treatment of chronic hypertension.

Brain↗
PubMed1991

Sclerosing vasculopathy of the central nervous system in nonelderly demented patients.

Three nonelderly patients without hypertension whose clinical and radiologic features otherwise resembled Binswanger's subcortical arteriosclerotic encephalopathy underwent biopsy of the hyperintense periventricular lesions seen on magnetic resonance imaging. The pathologic findings of the periventricular lesions consisted of gliosis with mild rarefaction and edema of the white matter. All patients had a sclerosing vasculopathy of unknown cause, which involved numerous small vessels within the periventricular lesions. The vessels stained negatively for amyloid, amyloid precursors, desmin, vimentin, keratin, immunoglobulin, and complement. On electron microscopy, small arteries, arterioles, venules, and capillaries were characterized by swollen astrocytic foot processes surrounding the vessels; dense, perivascular collagen packing; crystalline arrays of filaments within basement membrane; giant lipid-laden lysosomes within perivascular cells; and narrowing of the vascular lumina. Similar changes were not seen in a control group of 19 patients. The pathologic features of the vessels in these cases are distinct from the vasculopathy associated with Binswanger's subcortical arteriosclerotic encephalopathy. We suggest that a spectrum of vasculopathies may be associated with dementia and periventricular hyperintense lesions on magnetic resonance imaging.

Adult↗
PubMed1991

Etiology of motor or sensory stroke: a prospective study of the predictive value of clinical and radiological features.

The diagnostic utility of clinical and radiological features for distinguishing penetrating artery disease from other causes of stroke has been questioned. To address this issue, we prospectively evaluated more than 40 features in 85 patients with pure motor, sensorimotor, or pure sensory syndromes. Nonischemic causes were present in 4 patients. The causes of ischemic stroke in the other 81 patients were penetrating artery disease (32 patients), large artery occlusive disease (17), cardioembolism (12), other causes (8), and undetermined (12). Of the features evaluated, frequent transient ischemic attacks (greater than or equal to 1/day), transient ischemic attacks occurring only within 1 week of stroke, pure motor hemiparesis (similar involvement of face, arm, and leg), pure sensory stroke, and round or oval infarction were associated (p less than 0.05) with penetrating artery disease. However, only pure sensory stroke involving two or more regions of the body and pure motor hemiparesis associated with subcortical infarction of less than 1.5 cm had positive predictive values exceeding 90% for penetrating artery disease. Carotid bruit ipsilateral to an anterior circulation infarction, monoparesis, and striatocapsular infarction had positive predictive values exceeding 90% for causes other than penetrating artery disease; however, half of the striatocapsular infarctions were of undetermined cause. These data suggest that certain clinical and radiological features are useful for distinguishing penetrating artery disease from other causes of stroke.

Aged↗
PubMed1991

Importance of freezing time when iodoantipyrine is used for measurement of cerebral blood flow.

The goal of the present study was to determine effects of delay of freezing of the brain on distribution of [14C]iodoantipyrine in the brain. Blood flow to parietal cerebral cortex (CBF) and choroid plexus was measured with the indicator fractionation technique and quantitative autoradiography. After injection of iodoantipyrine, each rat was decapitated, and the head was immersed in chlorodifluoromethane (-40 degrees C). The brain was removed from the skull after it was frozen. In some rats, heads were immersed immediately after decapitation, and CBF was markedly heterogeneous. In another group, heads were frozen 3 min after decapitation. In this case, CBF was uniform in its distribution. Average CBF was similar in groups with immediate and delayed freezing (90-104 ml.min-1 x 100 g-1). In contrast, delays in freezing decreased blood flow to choroid plexus from 551 +/- 115 to 261 +/- 48 ml.min-1 x 100 g-1. Our findings indicate that immediate freezing of the brain after decapitation is necessary to prevent diffusion of iodoantipyrine from regions of high blood flow to regions of lower blood flow and underestimations of blood flow in regions with high blood flow.

Animals↗
PubMed1991

Stroke in a young adult with familial plasminogen disorder.

BACKGROUND: We report a new plasminogen disorder detected in a 29-year-old man with a cerebellar infarct. To our knowledge, plasminogen disorders have not been previously linked with stroke. SUMMARY OF REPORT: Tests for well-recognized causes of stroke were negative. However, a screening hypercoagulation profile indicated low functional levels of plasminogen activity. Immunologic plasminogen (Laurell technique) was 64% of normal (normal level, 80-130%). The rate of plasmin generation induced by adding urokinase to plasma was also low. Plasminogen activator, free protease, and alpha 2-plasmin inhibitor levels were normal. Family studies detected a similar plasminogen abnormality in the patient's mother and 9-year-old son, both of whom are asymptomatic. CONCLUSIONS: Our patient shows a congenital, heterozygous, functionally abnormal plasminogen. Although the exact relationship to stroke is unclear, we suggest screening young patients with unexplained stroke for plasminogen defects using commercially available assay systems.

Adult↗
PubMed1991

Transcranial Doppler ultrasound identifies patients with right-to-left cardiac or pulmonary shunts.

We performed transcranial Doppler ultrasound (TCD) and transesophageal contrast echocardiography simultaneously in four patients. In one patient with a patent foramen ovale and another patient with pulmonary A-V fistulae, we detected micro air bubbles in the right middle cerebral artery three to five cardiac cycles after their appearance in the left atrium following intravenous injection of contrast. In two patients without right-to-left shunts, we did not detect air bubbles in the left atrium or middle cerebral artery following injection of contrast. These results show that TCD can identify patients with right-to-left cardiac or pulmonary shunts.

Adult↗
PubMed1990

Intracranial hypertension associated with unruptured cerebral arteriovenous malformations.

Only 6 patients with intracranial hypertension associated with unruptured cerebral arteriovenous malformations have been reported. We report 6 additional patients seen at the Cleveland Clinic during the past 10 years. The average age was 28 years (range, 19-44 years); 4 were women. Symptoms and signs included papilledema (6 patients), headache (6), transient nonepileptic focal symptoms (4), visual obscurations (3), ipsilateral carotid or ocular bruits (3), abnormal visual fields (3), focal seizures (2), and progressive visual loss (1). Enhanced computed tomography (CT) or magnetic resonance imaging (MRI) demonstrated the malformations in all 6 patients. The malformations were large, supplied by the branches of the middle and anterior cerebral arteries, with the posterior cerebral artery contributing in 3 patients, and all drained into the superior sagittal sinus. Associated venous obstruction was seen in 2 patients. Four patients underwent excision of the arteriovenous malformation, with resolution of papilledema in all 4. Measurements of cortical arterial and venous pressures during surgery in 3 patients showed decreased feeding artery pressures and elevated draining vein pressures, which normalized after removal of the malformation. Treatment in the 2 remaining patients consisted of medical therapy (acetazolamide, furosemide, steroids) alone in 1 patient, and in conjunction with proton beam radiation in the other. Papilledema resolved in the former patient, but the patient receiving proton beam radiation still had papilledema 2 years later. Intracranial hypertension associated with unruptured cerebral arteriovenous malformations occurs in young patients with high flow malformations that drain into the superior sagittal sinus, and is likely the result of increased cortical venous and superior sagittal sinus pressure. Excision of the malformation effectively reduces the intracranial pressure.

Adult↗
PubMed1990

Ipsilateral leg weakness associated with carotid stenosis.

Ipsilateral motor or sensory symptoms associated with carotid occlusive diseases are rare. We report a 52-year-old man who presented with aphasia, right hemiparesis, mild left leg weakness, and bilateral Babinski's signs. During the previous 10 days, he had experienced three episodes of left leg numbness and incoordination that occurred either alone or in association with right arm and leg weakness. Computed tomography showed infarcts in the right frontoparietal (parasagittal), left frontal, and left parietal lobes. Cerebral angiography revealed 60% stenosis of the right internal carotid artery, 80% stenosis of the left internal carotid artery, absence of the A1 segment of the right anterior cerebral artery, filling of the right anterior cerebral artery from the left carotid circulation only, and a normal vertebrobasilar system. This report illustrates that leg weakness may occur ipsilateral to carotid disease if the contralateral anterior cerebral artery is supplied by the ipsilateral carotid artery.

Carotid Arteries↗
PubMed1990

Mechanism of stroke in patients taking aspirin.

During a 1-year period, we prospectively studied the mechanism and severity of stroke in 47 patients sustaining a cerebral infarction while taking aspirin. The mechanism of stroke was undetermined in 12 patients (26%). In the remaining 35 patients, we identified 39 potential mechanisms: large-artery atherosclerosis (19 patients, 40%), cardioembolism (15 patients, 32%), and small-vessel occlusive disease (5 patients, 11%). Of 11 patients with carotid atherosclerosis and stroke, 9 (82%) had greater than 90% carotid stenosis or occlusion; of 12 patients with stroke of undetermined mechanism, 10 (83%) had previous stroke, of which 8 were also of undetermined mechanisms. Disability after stroke was moderate or severe in 27 patients (57%). These data suggest that (1) stroke in patients taking aspirin has a variety of etiologies and frequently causes moderate or severe disability; (2) patients with carotid disease failing aspirin often have high-grade carotid stenosis or occlusion; (3) stroke of undetermined mechanism may recur more frequently than other stroke subtypes in patients taking aspirin.

Adult↗
PubMed1990

Risk of cardiac surgery in patients with prior stroke.

We retrospectively examined the clinical outcome in 126 patients with a history of ischemic stroke undergoing open heart surgery (OHS). We classified prior strokes as recent or remote and by degree of neurologic deficit. Seventeen patients (13.4%) had new strokes or worsening of prior deficits, but only 4 were moderate-severe in degree (3.2%). There was no significant difference in new stroke rates between recent and remote stroke groups. New strokes more frequently involved worsening of prior deficits in the recent stroke group, while strokes in different areas of the brain occurred more often in the remote stroke group. Extracranial occlusive disease was not a factor. Intraoperative hypotension was more frequent in the recent stroke group, suggesting persistent hemodynamic vulnerability.

Adult↗
PubMed1989

Bimodal treatment with nimodipine and low-molecular-weight dextran for focal cerebral ischemia in the rat.

We compared the effects of intravenous treatment with combined low-molecular-weight dextran and nimodipine (n = 9), or placebo (n = 10), on local cerebral blood flow after occlusion of the left middle cerebral and common carotid artery in the rat. Treatment for a total of 4 hours with low-molecular-weight dextran (5 mg/kg/min) and nimodipine (0.25 microgram/kg/min) produced a decrease in hematocrit from 46 +/- 1 to 33 +/- 1% at the end of the study and a statistically significant increase in local cerebral blood flow, when compared to the control group, in 6 regions of interest: the territories of the right middle (p = 0.01), right anterior (p = 0.007), and left anterior cerebral arteries (p = 0.001); the superior (p = 0.03) and inferior border zone (p = 0.003); and white matter in the right hemisphere (p = 0.04). The ischemic volume, defined as brain volume with a cerebral blood flow of less than the critical level of 25 ml/min/100 gm was determined as a percentage of total brain volume for the control and treatment groups. The group treated with low-molecular-weight dextran and nimodipine showed a 31% decrease in ischemic volume (p = 0.03). These results indicate that a bimodal approach with low-molecular-weight dextran and nimodipine can be safely used in a model of acute stroke and has a beneficial effect on local cerebral blood flow and ischemic volume when compared with control subjects. After 4 hours, the potential exists that this treatment is therapeutic, assuming that the ischemic volume progresses to infarction.

Animals↗