Tissue plasminogen activator reduces neurological damage after cerebral embolism.

Intravenous administration of tissue plasminogen activator immediately after the injection of numerous small blood clots into the carotid circulation in rabbit embolic stroke model animals caused a significant reduction in neurological damage. In vitro studies indicate that tissue plasminogen activator produced substantial lysis of clots at concentrations comparable to those expected in vivo, suggesting that this may be the mechanism of action of this drug. Drug-induced hemorrhages were not demonstrable. Tissue plasminogen activator may be of value for the immediate treatment of embolic stroke.

Bilateral paramedian thalamic contrast enhancement on CT after Intra-arterial thrombolysis.

A 58-year-old woman presented with an acute embolic occlusion of the distal basilar artery. She underwent angioplasty and intra-arterial thrombolysis. Angiography performed after recanalization revealed a single perforating thalamic artery. A nonenhanced CT scan carried out immediately after the procedure revealed hyperdense lesions in the bilateral paramedian portions of the thalami, which disappeared on the 24-hour follow-up CT scan. Three months later, the patient improved to functional independence, but had some memory dysfunction and vertical gaze palsy. This case suggests that contrast enhancement or extravasation can occur in the thalamus after intra-arterial thrombolysis performed to recanalize a basilar artery occlusion.

[Headache in patients with cerebral venous thrombosis]. / Céphalées au cours des thromboses veineuses cérébrales.

Headache is the most frequent symptom of cerebral venous thrombosis. They do not have particular characteristics and can mimic other numerous varieties of headache. Frequently associated with other neurological symptoms, such as intracranial hypertension, seizures, focal deficits or disorders of consciousness, they are sometimes isolated, which stresses the need for investigations in all recent and unusual headache.

Effects of acute percutaneous transluminal recanalization on cerebral embolism.

The effects of percutaneous transluminal recanalization (PTR) on critical hemodynamics of cerebral embolism were studied using stable xenon-enhanced computed tomography in patients within 6 hours after onset. PTR was conducted in 10 cases (PTR group) and not conducted 8 cases (non-PTR group). The development of infarction was followed by CT scan. In the cortical arterial regions, the lowest cerebral blood flow (CBF) value in regions of interests (ROIs) without development of infarction was 12.9 ml/100 g/min in the PTR group and 17.0 ml/100 g/min in the non-PTR group. In ROIs with a cerebrovascular reserve capacity (CRC) less than 0 ml/100 g/min, even with a CBF greater than 12.9 ml/100 g/min, 3 of 4 ROIs underwent cerebral infarction. PTR conducted within 6 hours after onset of cerebral embolism would prevent the cortical regions with a CBF greater than 12.9 ml/100 g/min and with a CRC greater than 0 ml/100 g/min from undergoing cerebral infarction.

Delayed hyperbaric treatment of cerebral air embolism: report of a case.

A 23-year-old woman with Eisenmenger's complex had a cerebral air embolism with resultant severe neurologic impairment while undergoing phlebotomy for secondary polycythemia. She was treated with hyperbaric therapy 29 hours after the original accident with almost complete recovery of neurologic function.

Cerebral air embolism treated by pressure and hyperbaric oxygen.

We used pressure and hyperbaric oxygen to treat 2 patients with cerebral air embolism, occurring as the result of invasive medical procedures, and neither suffered any permanent damage detectable by clinical examination and MRI. This outcome contrasts with reports of infarct and disability among untreated victims of air embolism.

Neurologic presentation of decompression sickness and air embolism in sport divers.

In a retrospective study of scuba divers with neurologic injuries, we found that mild symptoms were common. Seventy divers had decompression sickness, most often with paresthesias or numbness, rarely with paresis. Thirty-nine divers had air embolism that often caused unconsciousness or mild symptoms of cerebral injury. Many divers with neurologic decompression sickness gave histories of dives that were within conventional limits, and many with air embolism gave no history of breath-holding during ascent. Mild symptoms sometimes regressed spontaneously. Recompression delays were responsible for poor responses to therapy.

Stroke and intracranial venous thrombosis during pregnancy and puerperium.

OBJECTIVES: To determine nationally representative estimates of the incidence of stroke and intracranial venous thrombosis during pregnancy and the puerperium, and to identify potential risk factors for these conditions. METHODS: National Hospital Discharge Survey data were analyzed for the period 1979 to 1991. Nationally representative estimates of risk were calculated by age, race, presence of pregnancy-related hypertension, census region, hospital ownership, and number of hospital beds. Multivariate models were developed using logistic regression. RESULTS: There were an estimated 8,918 cases of stroke and 5,723 cases of intracranial venous thrombosis during pregnancy and the puerperium in the United States among 50,264,631 deliveries, giving risks of 17.7 cases of stroke and 11.4 cases of intracranial venous thrombosis per 100,000 deliveries. In the multivariate models, stroke was associated strongly with pregnancy-related hypertension, larger hospital size, and proprietary hospital ownership, and inversely associated with living in the South. Intracranial venous thrombosis was associated with maternal age. CONCLUSIONS: Stroke and intracranial venous thrombosis are relatively common complications of pregnancy and the puerperium. Collectively, rates for these conditions are about 50% greater for the entire period of pregnancy and the puerperium than for the immediate peripartum period.

Increased therapeutic efficacy with rt-PA and anti-CD18 antibody treatment of stroke in the rat.

OBJECTIVE: To examine the efficacy of an antileukocyte adhesion antibody (anti-CD18) as an adjuvant for delayed (2 hours and 4 hours) thrombolytic therapy (recombinant human tissue plasminogen activator [rt-PA]) in middle cerebral artery occlusion (MCAO) in rats. BACKGROUND: Thrombolytic therapy with rt-PA is limited in its application by a short therapeutic window. METHODS: Male Wistar rats were subjected to MCAO by a single fibrin-rich clot. The rats were assigned to the following experimental groups: Experiment 1 (treatment 2 hours after embolization), 1) rt-PA, 2) anti-CD18 antibody, 3) rt-PA and anti-CD18 antibody, 4) immunoglobulin (Ig) G, and 5) vehicle; Experiment 2 (treatment 4 hours after occlusion), 1) rt-PA alone, 2) rt-PA and anti-CD18 antibody, and 3) nontreated control group. Neurologic deficits, infarction volume, hemorrhage, and brain myeloperoxidase (MPO) immunoreactivity were measured. RESULTS: Administration of rt-PA and anti-CD18 antibody 2 hours later reduced significantly (p < 0.05) the infarct volume and improved neurologic deficits compared with the vehicle-treated group. Treatment with rt-PA alone improved neurologic deficits significantly and reduced mean infarct volume compared with the vehicle-treated group. However, treatment with anti-CD18 antibody neither reduced infarct volume nor improved neurologic deficits compared with the IgG-treated group. The combination of rt-PA and anti-CD18 antibody treatment at 4 hours reduced significantly the infarct volume and MPO immunoreactive cells compared with rt-PA treatment alone at 4 hours, and reduced neurologic deficits compared with rt-PA treatment alone and compared with the nontreated animals. CONCLUSIONS: The combination of antileukocyte adhesion antibody and thrombolytic therapy may increase the therapeutic window for the treatment of stroke.

Relation between cerebral blood flow and neurologic deficit resolution in acute ischemic stroke.

BACKGROUND AND OBJECTIVE: Early intervention remains the key to acute ischemic stroke therapy. Many patients whose deficits would later resolve without intervention are exposed to the risks of stroke treatment without benefit. The purpose of this study was to determine whether patients with transient deficits could be distinguished from patients with evolving strokes on the basis of acute cerebral blood flow (CBF) measurements before any clinical distinction could be made. METHODS: Fifty-three patients who presented with acute hemispheric stroke symptoms and who underwent xenon-enhanced CT (XeCT) CBF studies within 8 hours of onset of symptoms (and before any clinical improvement) were studied. RESULTS: Eight patients (15%) had a complete resolution of their symptoms within 24 hours (not related to treatment). All eight patients with deficits that resolved had normal CBF in the symptomatic vascular territories (mean time to XeCT = 3 hours, 51 min). Mean CBF in the regions of interest of the symptomatic vascular territories of patients who had deficits that resolved was 35.4 +/- 8.1 mL x 100 g(-1) x min(-1) compared with 17.3 +/- 9.3 mL x 100 g(-1) x min(-1) of patients with evolving strokes (p = 0.00058). CONCLUSIONS: Patients with ischemic neurologic deficits that will later resolve can be acutely distinguished from patients with evolving cortical infarctions using XeCT CBF measurements. CBF measurements may assist in the triage of patients for acute stroke therapy by selecting patients with a favorable prognosis and may not benefit from therapy but would still be exposed to the potential risks and expense of treatment.

Cardiac embolism: the neurologist's perspective.

Cardioembolic stroke represents a major healthcare challenge in the United States, accounting for significant morbidity and mortality, as well as economic and social costs. Determining the cause of ischemic stroke is often difficult because multiple potential etiologies are often present and available diagnostic tools are relatively insensitive. The diagnosis of cardioembolic stroke is based on a variety of clinical and laboratory clues that are significant, although not invariable, predictors of stroke etiology. Computed tomography scans help suggest etiology, and scans performed at 48 hours after stroke onset are essential to identify hemorrhagic infarctions. Cerebral angiograms may be helpful if performed early. Echocardiography is indicated only for selected patients who are more likely to demonstrate cardiac abnormalities on an echocardiogram. The management of acute cardioembolic stroke involves weighing the benefits of reducing stroke recurrence by anticoagulation against the risk of symptomatic brain hemorrhage. A management algorithm is provided that can help reduce both the risk of symptomatic brain hemorrhage and the incidence of potentially disabling stroke recurrence.

Role of transesophageal echocardiography in the management of thromboembolic stroke.

Cardiac causes of stroke account for approximately 20% of strokes occurring in the United States. Transthoracic echocardiography (TTE) remains the cornerstone of non-invasive cardiac imaging, but transesophageal echocardiography (TEE) is superior for identifying potential cardiac sources of emboli, including left atrial thrombi, valvular vegetations, thoracic aortic plaque, patent foramen ovale, and spontaneous left atrial echocardiographic contrast. The diagnostic yield of TEE for potential cardiac causes of thromboembolism exceeds 50%. The impact of TEE on the clinical management of this group, however, remains undefined for most TEE-specific diagnoses. Thus, routine use of TEE in these patients has been questioned. The diagnostic yield is highest if the clinical history/physical examination suggests a cardiac source. However, the clinical scenario often dictates patient management, and TEE data are used to "validate" the clinical impression. Data from large, prospective, randomized (aspirin/warfarin) studies, in which TEE data are obtained from patients with suspected cardiac thromboembolism, are needed. If specific TEE diagnoses can be identified in which defined therapies are beneficial, "source of embolism" will continue to be the most common indication for TEE referral. In this paradigm, TEE (without initial TTE) will probably become a more direct diagnostic pathway. However, if these studies demonstrate that all patients with suspected cardiac source benefit from one (or no) therapy, independent of TEE data, referrals for TEE will decline. Results of ongoing randomized trials to evaluate the efficacy of TEE in patients with cryptogenic stroke or transient ischemic attack are awaited.

Hyperbaric treatment of cerebral air embolism sustained during an open-heart surgical procedure.

A case of cerebral air embolism sustained during replacement of the mitral valve resulted in postoperative coma and seizures. Hyperbaric treatment, begun 30 hours after the occurrence of the air embolism, resulted in good immediate and long-term recovery. Mild deficits of the left hemisphere were present at follow-up 53 days after the embolus was sustained, and lesser, minimal residua were present at 14-month follow-up. Hyperbaric treatment is the definitive therapy for cerebral air embolism. Although it is most effective when administered early, the outcome may be excellent even with late treatment.

Hyperbaric oxygen therapy for massive arterial air embolism during cardiac operations.

BACKGROUND: Massive arterial air embolism is a rare but devastating complication of cardiac operations. Several treatment modalities have been proposed, but hyperbaric oxygen is the specific therapy. METHODS: The Israel Naval Medical Institute is the only referral hyperbaric center in this country for acute care patients. We reviewed our experience in the hyperbaric oxygen treatment of massive arterial air embolism during cardiac operations. RESULTS: Seventeen patients were treated between 1985 and 1998. Eight patients (47.1%) experienced a complete neurologic recovery; 6 patients (35.3%) remained unconscious at discharge, and 3 patients (17.6%) died. Mean (+/- SD) delay from the end of the operation to hyperbaric therapy was 9.6 +/- 7.4 hours (range, 1-20 hours). This delay was 4.0 +/- 3.4 hours (1-12 hours) for patients who had a full neurologic recovery, 12.8 +/- 7.1 hours (5-20 hours) for patients with severe neurologic disability, and 18.0 +/- 2.0 hours (16-20 hours) for patients who died (1-way analysis of variance; P =.002). The source of variance among the groups mainly resulted from the short delay for patients who experienced complete recovery compared with the other 2 groups (Tukey test). All 5 patients who were treated within 3 hours from the operation and 50% (2 of 4 patients) of those patients treated 3 to 5 hours from operation experienced a full neurologic recovery. With a delay of 9 to 20 hours, only 1 of 8 patients had a full neurologic recovery. The association between outcome and treatment delay was found to be statistically significant (tau = 0.65 with exact 2-sided P value =.0007). CONCLUSION: Hyperbaric oxygen therapy should be administered as soon as possible after massive arterial air embolism during cardiac operations.

Can retrograde perfusion mitigate cerebral injury after particulate embolization? A study in a chronic porcine model.

OBJECTIVE: We assessed the impact on histologic and behavioral outcome of an interval of retrograde cerebral perfusion after arterial embolization, comparing retrograde cerebral perfusion with and without inferior vena caval occlusion with continued antegrade perfusion. METHODS: Sixty Yorkshire pigs (27 to 30 kg) were randomly assigned to the following groups: antegrade cerebral perfusion control; antegrade cerebral perfusion after embolization; retrograde cerebral perfusion control; retrograde cerebral perfusion after embolization; retrograde cerebral perfusion with inferior vena cava occlusion, retrograde cerebral perfusion with inferior vena cava occlusion control, and retrograde cerebral perfusion with inferior vena cava occlusion after embolization. After cooling to 20 degrees C, a bolus of 200 mg of polystyrene microspheres 250 to 750 (microm diameter (or saline solution) was injected into the isolated aortic arch. After 5 minutes of antegrade cerebral perfusion, 25 minutes of antegrade cerebral perfusion, retrograde cerebral perfusion, or retrograde cerebral perfusion with inferior vena cava occlusion was instituted. After the operation, all animals underwent daily assessment of neurologic status until the time of death on day 7. RESULTS: Aortic arch return, cerebral vascular resistance, and oxygen extraction data during retrograde cerebral perfusion showed differences, suggesting that more effective flow occurs during retrograde cerebral perfusion with inferior vena cava occlusion, which also resulted in more pronounced fluid sequestration. Microsphere recovery from the brain revealed significantly fewer emboli after retrograde cerebral perfusion with inferior vena cava occlusion. Behavioral scores showed full recovery in all but one control animal (after retrograde cerebral perfusion with inferior vena cava occlusion) by day 7 but were considerably lower after embolization, with no significant differences between groups. The extent of histopathologic injury was not significantly different among embolized groups. Although no histopathologic lesions were present in either the antegrade cerebral perfusion control group or the retrograde cerebral perfusion control group, mild significant ischemic damage occurred after retrograde cerebral perfusion with inferior vena cava occlusion even in control animals. CONCLUSIONS: Although effective washout of particulate emboli from the brain can be achieved with retrograde cerebral perfusion with inferior vena cava occlusion, no advantage of retrograde cerebral perfusion with inferior vena cava occlusion after embolization is seen from behavioral scores, electroencephalographic recovery, or histopathologic examination; retrograde cerebral perfusion with inferior vena cava occlusion results in greater fluid sequestration and mild histopathologic injury even in control animals. Retrograde cerebral perfusion with inferior vena cava occlusion shows clear promise in the management of embolization, but further refinements must be sought to address its still worrisome potential for harm.

Hypothermia in conjunction with hyperbaric oxygenation in the treatment of massive air embolism during cardiopulmonary bypass.

Massive gas embolism during cardiopulmonary bypass is a rare but ever-present danger. Following this catastrophic event, the immediate institution of core cooling on bypass may be advantageous. The remarkable complete recovery of our patient is attributed to this technique, which was used in conjunction with standard therapy.

Postoperative management of cerebral air embolism: gas physiology for surgeons.

Cerebral gaseous microemboli are present in most, if not all, cardiopulmonary bypass-assisted operations. Fortunately, the great majority are subclinical. Clinically significant cases of cerebral air embolism are largely underdiagnosed, undertreated, and underreported. The management of cerebral air embolism has been challenged due to the lack of prospective, randomized studies. Preventive measures that have been implemented throughout the years, resulting from empirically acquired knowledge, have avoided frequent major mishaps. Perfusion accidents, in which massive amounts of gas are pumped into patients, are managed intraoperatively by common-sense heroic measures which, at best, remove 50% of the embolized gas. Postoperative confirmation of a neurologic insult after a cardiopulmonary bypass-assisted operation, in which a cerebral air embolism is likely the source, is one of the most distressing situations a surgical team has to confront, due in part to the lack of pathognomonic diagnostic tools and to the absence of a "scientifically proven" (supported by prospective, randomized studies) therapeutic regimen. In lieu of the latter, we present the physical and physiologic bases that will justify the use of several therapeutic tools when facing a suspected CAE. These tools, when applied rationally, will represent some of the most innocuous modalities in the medical armamentarium.

Percutaneous transluminal angioplasty adjunct to thrombolysis for acute middle cerebral artery rethrombosis.

PURPOSE: To report three patients, each of whom had acute rethrombosis of a reopened middle cerebral artery after urokinase treatment for proximal stenosis (percutaneous transluminal angioplasty of the stenosis was performed adjunctive to the thrombolytic treatment to preserve the success of the thrombolysis), and a fourth patient who had percutaneous transluminal angioplasty right after the completion of thrombolysis and had no rethrombosis despite a partial dilatation of the severe stenosis. METHODS: Thrombolytic treatment was carried out by a coaxial technique with a Tracker 18 catheter through a 5-F angiographic catheter; 80,000 U in 5 mL of urokinase were intermittently injected every 15 minutes after an initial dose of 250,000 U. All patients were given 3000 U of heparin with a booster dose of 1000 U every hour. Angioplasty was performed with a Stealth catheter balloon, 2 to 3 mm x 1.5 cm. RESULTS: Three patients recovered without hemorrhage after percutaneous transluminal angioplasty and thrombolytic treatment. Percutaneous transluminal angioplasty was unsuccessful in one patient because of the inability to pass a 2-mm Stealth balloon catheter, and the result was a second rethrombosis. This patient had a poor recovery. CONCLUSION: Acute thrombosis of the middle cerebral artery may be associated with severe proximal stenosis. Rethrombosis may occur even after complete thrombolysis. Percutaneous transluminal angioplasty may be safely performed to prevent rethrombosis.

Experimental models in interventional neuroradiology.

Various experimental models have been developed to test interventional neuroradiologic techniques. Most have been used to test various devices and embolic materials, and a small number of models have been designed for teaching or training purposes. Experimental models in endovascular techniques have seldom been used to stimulate disease processes in order to facilitate their understanding.

Giant serpentine aneurysms: a review and presentation of five cases.

We present five cases of giant serpentine aneurysms (large, partially thrombosed aneurysms containing tortuous vascular channels with a separate entrance and outflow pathway) and review 28 cases reported in the literature. Giant serpentine aneurysms should be considered as a subgroup of giant aneurysms, distinct from saccular and fusiform varieties, given their unique clinical presentation and radiographic features.