Microembolic signal detection in patients with symptomatic and asymptomatic lone atrial fibrillation.

BACKGROUND AND PURPOSE: There are few data on the occurrence of microembolic signals (MES) in patients with lone atrial fibrillation (LAF). The aim of this work was to systematically study the frequency of MES in patients with symptomatic and asymptomatic LAF and to compare it with that of nonvalvular atrial fibrillation (NVAF). METHODS: 37 consecutive acute stroke patients with LAF, 10 asymptomatic patients with LAF and 100 age-matched healthy controls were studied. Another 92 stroke patients with known NVAF were included in the study to compare patients with LAF regarding the presence of MES. Both middle cerebral arteries were monitored by transcranial Doppler ultrasound for at least 30 min at admission and after 1 week in symptomatic and asymptomatic patients with LAF. All patients with LAF were followed up for a mean duration of 18 months, and recurrent strokes were registered. RESULTS: MES was detected in 11 (29%) symptomatic patients with LAF but only in 1 asymptomatic patient with LAF (chi(2) = 11.3; p = 0.0008) and in no control subjects (chi(2) = 106; p = 0.00001). There was no difference in the frequency of MES-positive patients and the number of MES between subjects with symptomatic LAF and known NVAF (29% in both groups; mean count, 16 +/- 4 vs. 17 +/- 6; p = 0.73). In patients with symptomatic LAF and NVAF who underwent anticoagulant therapy, there was no difference in the frequency of MES after 1 week of hospitalization (chi(2) = 1.53; p = 0.2). During a mean follow-up period of 18 months, 1 patient with symptomatic LAF and MES had a recurrent ischemic event 1 year after the first stroke and none of those with asymptomatic LAF had any events. CONCLUSION: Our study suggests that asymptomatic and paroxysmal LAF with a lower frequency of MES is a benign disorder compared to chronic and symptomatic LAF with a higher frequency of MES. Further studies need to justify whether MES has a predictive value in patients with chronic LAF who are prone to ischemic stroke.

Microembolic signals in patients undergoing coronary artery bypass grafting. Effect of aortic atherosclerosis.

The aim of this prospective study was to determine whether aortic atherosclerotic plaques are associated with increased frequency of microembolic signals and stroke in patients who undergo coronary artery bypass grafting. A total of 69 such patients were monitored by transcranial Doppler ultrasonography for 30 minutes before and after surgery. To our knowledge, this study is the 1st in which in vivo pathologic analysis of aortic plaques was systematically performed-and microembolic signals monitored-before and after open-heart surgery. Plaques were assessed by transesophageal echocardiography and by biopsy of materials taken during surgery. The frequency of microembolic signals was evaluated with regard to the occurrence of postoperative stroke. In the preoperative phase, only 10 of 48 patients with aortic plaques had microembolic signals, and the mean count of microembolic signals was 3.2 +/- 1.2 per hour. At the conclusion of 24 postoperative hours, 29 patients (42%) displayed such signals (mean count, 9.8 +/- 3.1/h). Seven of the 48 patients (15%) with aortic atherosclerosis had cerebral ischemic events, but none of those with normal aorta (21 patients) experienced stroke during the postoperative phase. During postoperative monitoring, patients with stroke had higher microembolic-signal counts than did those with normal aorta (174 +/- 3.3/h vs 5.9 +/- 3.1/h; P <0.05). Our findings suggest that microembolic signals can be a marker of severe aortic atherosclerosis and that monitoring these signals should enable the application of appropriate surgical methods to coronary artery bypass patients who are at higher risk of stroke.

Bilateral thalamic infarction. Clinical, etiological and MRI correlates.

To determine clinical, behavioral, topographic and etiological patterns in patients with simultaneous bilateral thalamic infarction in varied thalamic artery territories, we studied 16 patients who were admitted to our stroke unit over a 7-year period. Patients with bithalamic infarction represented 0.6% of our registry which included 2,750 ischaemic stroke patients. On computed tomography and magnetic resonance imaging with gadolinium enhancement, there were 4 topographic patterns of infarction: 1) bilateral infarcts in the territory of paramedian artery (8 patients [50%]); 2) bilateral infarcts in the territory of thalamogeniculate arteries (3 patients [19%]); 3) bilateral infarcts involving territory of paramedian and thalamogeniculate arteries (3 patients [19%]); 4) bilateral infarcts involving territory of polar and thalamogeniculate arteries (2 patients [13%]). A specific clinical picture was found in up to 50% of the patients with bithalamic infarction. This included patients with bilateral paramedian infarction having disorder of consciousness, memory dysfunctions, various types of vertical gaze palsy and psychic changes. Bilateral sensory loss predicted accurately bilateral infarction in the territory of thalamogeniculate arteries. The main cause of bilateral thalamic infarction was small artery-disease, followed by cardioembolism. Cognitive functions in patients with bilateral paramedian infarction did not change significantly during the follow-up, in contrast to those with infarcts in varied arterial territories. Acute bilateral infarction involving both thalamus is uncommon, although they are often associated with specific neurologic-neuropsychological patterns, allowing diagnosis before radiological examination.

Transcranial Doppler detection of microembolic signals in patients with Behçet's disease.

We evaluated the prevalence of microembolic signals (MES) in patients with Behçet's disease (BD). We also attempted to determine the frequency of MES in BD patients with or without neurological involvement. This study enrolled 55 patients fulfilling the diagnostic criteria of International Study Group for BD. Bilateral transcranial Doppler ultrasound of the middle cerebral arteries was performed. MES were identified based on the criteria of International Consensus group on Microembolus Detection. Patients with BD were divided into two groups in respect of the presence of neurological involvement (n = 10) or not (n = 45), and counts of MES in the two were compared with each other and with normal subjects. We found MES in 16 patients (29%) with BD. The frequency was higher in patients with neurological involvement than in those without (80% vs. 17%, P< 0.001). In patients with neurological involvement there was a positive correlation in regression analysis between the prevalence of MES and disease duration (P = 0.025). There was a significantly higher prevalence of MES in BD patients than in control subjects. The frequency of MES was higher in patients with neurological involvement than in those without. TCD detection of MES may allow the recognition of subset of patients at high risk for the appearance of neurological involvement.

Acute caudate vascular lesions.

BACKGROUND AND PURPOSE: We sought to evaluate demographic features, risk factors, clinical profiles, and behavioral abnormalities in patients with caudate lesion, either with infarct or with hemorrhage involving the caudate nucleus. METHODS: We studied all patients with acute caudate stroke confirmed by CT or MRI who were admitted to our stroke unit over a 5-year period. A database containing risk factors, clinical features, type and mechanism of stroke, and caudate vascular territories was analyzed. RESULTS: Thirty-one patients had acute caudate stroke (24 men and 7 women; mean age, 62.3 years). Caudate infarct was present in 25 patients and caudate hemorrhage in 6. The main risk factors for caudate infarct were hypertension (64%), hypercholesterolemia (32%), diabetes mellitus (28%), and previous myocardial infarct (20%). Hypertension was present in 4 patients (67%) with caudate hemorrhage, and arteriovenous malformation was present in 1 patient (17%). Small-artery disease was diagnosed in 14 patients (59%), cardiac embolism in 5 patients (20%), and large-artery disease in 2 patients (8%), and 2 patients (8%) had mixed etiology. The most frequent neurological abnormalities were abulia and psychic akinesia (48%), frontal system abnormalities (26%), speech deficits in patients with left-sided lesions (23%), and neglect syndromes in those with right-sided lesions (10%). Fifteen patients with caudate infarct (60%) and 3 patients with hemorrhage (50%) were able to return to normal daily life. Patients with infarct in the territory of the lateral lenticulostriate arteries extending to neighboring structures showed more frequent motor and neuropsychological deficits than those with infarct in the territory of the anterior lenticulostriate arteries. CONCLUSIONS: The clinical presentation of patients with caudate hemorrhage mimicked subarachnoid hemorrhage with or without motor and neuropsychological signs. Caudate vascular lesions with concomitant neighboring structure involvement represent a specific stroke syndrome, usually caused by small-artery disease and in one fifth of the patients caused by cardiac embolism. The behavioral abnormalities were mostly due to medial, lateral, and ventral caudate subnuclei damage and coexisting lesion of the anterior limb of the internal capsule.