Community use of intravenous tissue plasminogen activator for acute stroke: results of the brain matters stroke management survey.

BACKGROUND AND PURPOSE: Little is known of neurologists' viewpoints regarding intravenous tPA use or institutional readiness to evaluate potential thrombolytic candidates. METHODS: Surveys were distributed at the Brain Matters Stroke Management Workshops held in 16 cities in the United States. RESULTS: Intravenous tPA was administered by 46.9% of responding neurologists. Almost 30% (29.9%) of surveyed neurologists were "very convinced" of its efficacy, whereas 61.6% were "very concerned" about the risk of intracranial hemorrhage. Only half of the respondents believed their institutions could meet all NINDS-recommended stroke-evaluation time targets. CONCLUSIONS: Neurologists' enthusiasm for the efficacy of intravenous tPA is tempered by their concern about intracranial hemorrhage. Institutional readiness for evaluating acute stroke patients is not optimized.

Cooling for acute ischemic brain damage (cool aid): an open pilot study of induced hypothermia in acute ischemic stroke.

BACKGROUND AND PURPOSE: Hypothermia is effective in improving outcome in experimental models of brain infarction. We studied the feasibility and safety of hypothermia in patients with acute ischemic stroke treated with thrombolysis. METHODS: An open study design was used. All patients presented with major ischemic stroke (National Institutes of Health Stroke Scale [NIHSS] score >15) within 6 hours of onset. After informed consent, patients with a persistent NIHSS score of >8 were treated with hypothermia to 32+/-1 degrees C for 12 to 72 hours depending on vessel patency. All patients were monitored in the neurocritical care unit for complications. A modified Rankin Scale was measured at 90 days and compared with concurrent controls. RESULTS: Ten patients with a mean age of 71.1+/-14.3 years and an NIHSS score of 19.8+/-3.3 were treated with hypothermia. Nine patients served as concurrent controls. The mean time from symptom onset to thrombolysis was 3.1+/-1.4 hours and from symptom onset to initiation of hypothermia was 6.2+/-1.3 hours. The mean duration of hypothermia was 47.4+/-20.4 hours. Target temperature was achieved in 3.5+/-1.5 hours. Noncritical complications in hypothermia patients included bradycardia (n=5), ventricular ectopy (n=3), hypotension (n=3), melena (n=2), fever after rewarming (n=3), and infections (n=4). Four patients with chronic atrial fibrillation developed rapid ventricular rate, which was noncritical in 2 and critical in 2 patients. Three patients had myocardial infarctions without sequelae. There were 3 deaths in patients undergoing hypothermia. The mean modified Rankin Scale score at 3 months in hypothermia patients was 3.1+/-2.3. CONCLUSION: Induced hypothermia appears feasible and safe in patients with acute ischemic stroke even after thrombolysis. Refinements of the cooling process, optimal target temperature, duration of therapy, and, most important, clinical efficacy, require further study.

Unilateral visual loss in bright light. An unusual symptom of carotid artery occlusive disease.

Five patients with carotid artery occlusive disease had unilateral visual loss in bright light. All five had reduced retinal artery pressure on the side of the visual loss, and arteriograms showed either an occlusion or a high-grade stenosis of the ipsilateral internal carotid artery. Unilateral visual loss in bright light may indicate ipsilateral carotid artery occlusive disease and may reflect the inability of borderline circulation to sustain the increased retinal metabolic activity associated with exposure to bright light.

Acute areflexic paralysis. Association with hyperalimentation and hypophosphatemia.

Acute areflexic paralysis associated with diffuse sensory loss, cranial nerve paisies, and respiratory insufficiency occurred in two patients who developed hypophosphatemia during hyperalimentation. Prompt recovery followed replacement of serum phosphorus in both cases. An electromyogram performed on one patient revealed only decreased insertional activity. A muscle biopsy specimen from the same patient showed minor, nonspecific neurogenic changes.

Focal EEG abnormalities in Heidenhain's variant of Jakob-Creutzfeldt disease.

Serial EEGs obtained during a six-week period from a patient with Heidenhain's variant of Jakob-Creutzfeldt disease demonstrated periodic complexes confined to the occipital regions that at no time became generalized. The focal character of the discharges correlated with the site of maximal disease in the occipital cortex, suggesting that cortical damage is a necessary substrate for the production of periodic complexes in Jakob-Creutzfeldt disease.

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.

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.

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.

Long-term prognosis after carotid artery occlusion.

One hundred thirty eight patients with angiographically proved carotid artery occlusion and minimal or no neurologic deficit were followed up for an average of 5 years. For patients 35 years old or over, the observed 5-year survival rate on an actuarial basis was 77% compared with an expected rate of 85% in a matched normal population. For patients 35 years old or over, the subsequent stroke rate was 3% per year, and two-thirds of the strokes were ipsilateral to the carotid artery occlusion. The observed stroke rate for all patients 35 years old or over was eight times the expected rate for a matched normal population. The relative risk of stroke was much greater in the younger patients with atherosclerotic carotid artery occlusion than in the older patients.

Ischemic monomelic neuropathy.

Ischemic monomelic neuropathy (IMN) is an infrequently recognized type of ischemic neuropathy produced by the shunting of blood away from, or the acute noncompressive occlusion of, a major proximal limb artery. IMN consists of multiple axonal-loss mononeuropathies that develop acutely and simultaneously in the distal portion of a limb. We found stereotyped clinical and EMG features in 14 patients. In six the IMN was thromboembolic in nature, whereas in eight it was due to various vascular surgical procedures. Our experience with IMN suggests that distal axonal infarction can occur without significant muscle necrosis, supporting the hypothesis that in humans the distal nerve fibers are more vulnerable than muscle to acute noncompressive limb ischemia.

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.

Intra-arterial thrombolysis of embolic proximal middle cerebral artery occlusion from presumed atrial myxoma.

The role of thrombolysis in brain ischemia in patients with atrial myxoma is unknown. A patient with acute brain ischemia and previously undiagnosed atrial myxoma recanalized an occluded middle cerebral artery with intra-arterial thrombolysis. Arterial occlusion from presumed myxoma may be amenable to fibrinolysis. Angiography before treatment in patients with atrial myxoma excludes a myxomatous pseudoaneurysm and permits site-specific thrombolytic instillment.

Sensory seizure mimicking a psychogenic seizure.

A patient had episodes of bilateral paresthesias with retained consciousness. The attacks were clinically considered to be psychogenic seizures. Electroencephalography indicated that the attacks were epileptic, perhaps originating from the second sensory area. Electroencephalographic recording of a seizure is essential in differentiating epileptic from psychogenic episodes.

Hemorrhage and anticoagulation after nonseptic embolic brain infarction.

Among 54 consecutive patients with acute nonseptic embolic brain infarction, there was CT evidence of hemorrhagic infarction in 1 patient (2%). None had clinical or CT evidence of massive brain hemorrhage even when anticoagulation therapy was used immediately. Seven patients (13%) had recurrent brain emboli, all within 7 days of the initial stroke. None of these patients was adequately anticoagulated at the time of recurrence. Immediate anticoagulation therapy should be employed after nonseptic embolic brain infarction if CT does not show hemorrhage and there is a persistent cardiac source of emboli.

Is in-hospital stroke mortality an accurate measure of quality of care?

We examined the validity of using in-hospital stroke mortality as predicted by the Cleveland Hospital Outcomes Indicators of Care Evaluations (CHOICE) model as a measure of quality of care. A total of 223 patients admitted to the hospital for stroke were evaluated by the CHOICE model, which predicted that 19 stroke deaths would occur. We reviewed the 19 patients with the highest predicted mortality, according to CHOICE, and three additional patients who died following stroke. We found that The CHOICE model accurately predicts in-hospital stroke mortality for large populations but not for individual patients. CHOICE and other stroke outcome models rely heavily on early Do Not Resuscitate orders and coma but exclude important variables found in the literature on stroke. No correlation between in-hospital stroke mortality and quality of care was demonstrated. Mortality prediction models used to guide consumers on where to receive stroke care are potentially misleading, as they do not assess functional neurologic recovery or the process of care that are essential elements of quality.

Neurologic complications of endocarditis: a 12-year experience.

We reviewed the neurologic complications in 113 patients with native and 62 patients with prosthetic valve endocarditis. Neurologic complications occurred with the same frequency (35.3% vs 38.7%) and distribution among the two groups. Death occurred in 20.6% of patients with neurologic complications and in 13.6% of patients without neurologic complications (p = 0.23). Staphylococcus aureus endocarditis correlated statistically with the development of neurologic complications (p less than 0.01) and death (p less than 0.01). Among 50 patients discharged from the hospital after receiving only medical treatment for native valve endocarditis, and followed for a mean period of 48 months, there was one patient with mitral valve prolapse and stroke. We conclude that (1) neurologic complications occur with the same frequency in native and prosthetic valve endocarditis, (2) S aureus endocarditis increases the risk of neurologic complications and death, (3) mortality is not significantly increased in patients with neurologic complications, and (4) an episode of treated native valve endocarditis does not increase the natural history of stroke in valvular disease.

Transcranial Doppler assessment of cerebral perfusion reserve in patients with carotid occlusive disease and no evidence of cerebral infarction.

Using transcranial Doppler ultrasound (TCD), we measured bilateral middle cerebral artery mean blood flow velocities (MCAVs) before and 10 minutes after intravenous infusion of 1 gram of acetazolamide in 20 patients without cerebral infarction. Seven patients had normal carotid arteries (group 1), seven had unilateral internal carotid artery (ICA) stenosis > or = 75% (group 2), and six had unilateral ICA occlusion (group 3). Before acetazolamide infusion, side-to-side differences in MCAV were 0.06 cm/sec in group 1 (p = 0.98), 4.3 cm/sec in group 2 (p = 0.36), and 15.0 cm/sec in group 3 (p = 0.02). Bilateral MCAV increased in all three groups after acetazolamide infusion, and the side-to-side differences in MCAV were 3.2 cm/sec in group 1 (p = 0.40), 11.4 cm/sec in group 2 (p = 0.04), and 27.6 cm/sec in group 3 (p = 0.03). Patients with carotid stenosis or occlusion and ipsilateral transient ischemic attacks (TIAs) had higher side-to-side differences in MCAV before (p = 0.03) and after (p = 0.01) acetazolamide than did asymptomatic patients with carotid disease. The association of impaired cerebral perfusion reserve and TIAs suggests that the TCD-acetazolamide test may enable identification of a subgroup of patients with carotid occlusive disease who are at higher risk for stroke.

Ischemic optic neuropathy: a complication of cardiopulmonary bypass surgery.

Ischemic optic neuropathy followed cardiopulmonary bypass surgery in the postoperative period in 7 of 7685 consecutive procedures. Th visual loss was unilateral in four patients and bilateral in three and there was little improvement. This ischemic infarction of the optic nerve disk was attributed to hypotension, hypothermia, and activation of certain complement factors by the bypass procedure.

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.

The Warfarin-Aspirin Symptomatic Intracranial Disease Study.

We conducted a retrospective, multicenter study to compare the efficacy of warfarin with aspirin for the prevention of major vascular events (ischemic stroke, myocardial infarction, or sudden death) in patients with symptomatic stenosis of a major intracranial artery. Patients with 50 to 99% stenosis of an intracranial artery (carotid; anterior, middle, or posterior cerebral; vertebral; or basilar) were identified by reviewing the results of consecutive angiograms performed at participating centers between 1985 and 1991. Only patients with TIA or stroke in the territory of the stenotic artery qualified for inclusion in the study. Patients were prescribed warfarin or aspirin according to local physician preference and were followed by chart review and personal or telephone interview. Seven centers enrolled 151 patients; 88 were treated with warfarin and 63 were treated with aspirin. Median follow-up was 14.7 months (warfarin group) and 19.3 months (aspirin group). Vascular risk factors and mean percent stenosis of the symptomatic artery were similar in the two groups, yet the rates of major vascular events were 18.1 per 100 patient-years of follow-up in the aspirin group (stroke rate, 10.4/100 patient-years; myocardial infarction or sudden death rate, 7.7/100 patient-years) compared with 8.4 per 100 patient-years of follow-up in the warfarin group (stroke rate, 3.6/100 patient-years; myocardial infarction or sudden death rate, 4.8/100 patient-years). Kaplan-Meier analysis showed a significantly higher percentage of patients free of major vascular events among patients treated with warfarin (p = 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)